Tag Archives: neuroplasticity

MIGRAINE AND DEPRESSION: It’s All The Same Brain – Gale Scott * Migraine May Permanently Change Brain Structure – American Academy of Neurology * Migraine: Multiple Processes, Complex Pathophysiology – Rami Burstein, Rodrigo Noseda, and David Borsook.

The symptoms that accompany migraine suggest that multiple neuronal systems function abnormally. Neuroimaging studies show that brain networks, brain morphology, and brain chemistry are altered in episodic and chronic migraineurs. As a consequence of the disease itself or its genetic underpinnings, the migraine brain is altered structurally and functionally.

Migraine tends to run in families and as such is considered a genetic disorder. Genetic predisposition to migraine resides in multiple susceptible gene variants, many of which encode proteins that participate in the regulation of glutamate neurotransmission and proper formation of synaptic plasticity.

Migraine is a leading cause of suicide, an indisputable proof of the severity of the distress that the disease may inflict on the individual. 40% of migraine patients are also depressed.

Migraine and Depression: It’s All The Same Brain

Gale Scott

When a patient suffers from both migraines and depression or other psychiatric comorbidities, physicians have to treat both. It’s a common situation, since 40% of migraine patients are also depressed. Anxiety is even more prevalent in these patients. An estimated 50% of migraine patients are anxious whether with generalized anxiety, phobias, panic attacks. or other forms of anxiety, said Mia Minen, MD Director of Headache Services at NYU Langoni Medical Center.

Health care costs in treating these co-morbid patients are 1.5 times higher than for migraine patients without accompanying psychiatric disorders.

But sorting out whether one problem is causing the other is not always easy, she said in a recent interview at NYU Langone. “it’s really interesting, which came first,” she said, “We really don’t know.”

There may be a bidirectional relationship with depression. Anxiety may precede migraines, then depression may follow.

Fortunately, she said, the question of which problem came first doesn’t really matter that much.

“It’s all one brain, one organ, and some of the same neurotransmitters are implicated in both disorders.” Serotonin is affected in migraine just as it is in depression and anxiety, she said. Dopamine and norepinephrine are also related both to migraines and psychiatric comorbidities.

“So it’s really one organ that’s controlling all these things,” Minen said.

The first step in treatment is having patients keep a headache diary to track the intensity and frequency and what they take when they feel it coming on.

For a mild migraine that might be ibuprofen or another over-the-counter pain killer.

If the migraine is moderately severe there are 7 migraine-specifuc medications that are effective, she said. There are oral, nasal, and injectable forms of triptans a family of tryptamine-based drugs. “We sometimes tell patients to combine the triptan with Naprosyn,” she said.

If triptans are contraindicated because the patient has other health problems, there are still more pharmaceutical options.

Those include some classes of beta blockers, antiseizure medications, and tricyclic antidepressants at low doses.

The drug regimen may vary with the particular comorbidity. For instance, for migraines with anxiety, venlafaxine might work. If patients have sleep disturbances, amitriptyline might be effective. “Lack of sleep is also a trigger for migraine,” she noted.

The toughest co-morbidity to treat in patients with migraine is finding a regimen that works for patients who are taking a lot of psychiatric medications, like SSRIs and antipsychotics.

For older patients with migraines plus cardiovascular disease, drug choices are also limited.

Botox injections seem promising, but Minen is cautious. “It’s a great treatment for patients with chronic migraines but they have to have failed 2 or 3 medications before they qualify for Botox.” Treatment involves 31 injections over the forehead, the back of the head and the neck. Relief lasts about 3 months, she said.

In addition to pharmaceutical treatment, there are cognitive behavior approaches that can work, like biofeedback and progressive muscle relaxation therapy.

Opioids are not the treatment of choice, she said. They have not been shown to be effective, Minen said and reduce the body’s ability to respond to triptans.

“For chronic migraine, studies don’t show opioids enable patients to return to work; there is no objective study showing they work,” and their uses raises other problems. Patients used to taking opioids who go to an emergency room and request them may find themselves suspected of drugseeking behavior. “It’s hard for doctors and patients,” she said, when patients ask for opioids “It puts doctors in a predicament.”

New drugs are on the horizon, she said. “Calcitonin gene related peptide antagonists look good,” and unlike triptans are not contraindicated for people at risk of strokes or heart attacks.

For now, said Minen, treating migraine and comorbidities “is more an art than a science,” she said, “But a large majority of patients do get better.”

Migraine May Permanently Change Brain Structure

American Academy of Neurology

Migraine may have longlasting effects on the brain’s structure, according to a study published in the August 28, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Traditionally, migraine has been considered a benign disorder without long-term consequences for the brain,” said study author Messoud Ashina, MD, PhD, with the University of Copenhagen in Denmark. “Our review and meta-analysis study suggests that the disorder may permanently alter brain structure in multiple ways.”

The study found that migraine raised the risk of brain lesions, white matter abnormalities and altered brain volume compared to people without the disorder. The association was even stronger in those with migraine with aura.

Migraine with aura
A common type of migraine featuring additional neurological symptoms. Aura is a term used to describe a neurological symptom of migraine, most commonly visual disturbances.
People who experience ‘migraine with aura’ will have many or all the symptoms of a ‘migraine without aura‘ and additional neurological symptoms which develop over a 5 to 20 minute period and last less than an hour.
Visual disturbances can include: blind spots in the field of eyesight, coloured spots, sparkles or stars, flashing lights before the eyes, tunnel vision, zig zag lines, temporary blindness.
Other symptoms include: numbness or tingling, pins and needles in the arms and legs, weakness on one side of the body, dizziness, a feeling of spinning (vertigo).
Speech and hearing can be affected and some people have reported memory changes, feelings of fear and confusion and, more rarely, partial paralysis or fainting.
These neurological symptoms usually happen before a headache, which could be mild, or no headache may follow.

For the meta-analysis, researchers reviewed six population-based studies and 13 clinic-based studies to see whether people who experienced migraine or migraine with aura had an increased risk of brain lesions, silent abnormalities or brain volume changes on MRI brain scans compared to those without the conditions.

The results showed that migraine with aura increased the risk of white matter brain lesions by 68 percent and migraine with no aura increased the risk by 34 percent, compared to those without migraine. The risk for infarct-like abnormalities increased by 44 percent for those without aura. Brain volume changes were more common in people with migraine and migraine with aura than those with no migraines.

“Migraine affects about 10 to 15 percent of the general population and can cause a substantial personal, occupational and social burden,” said Ashina. “We hope that through more study, we can clarify the association of brain structure changes to attack frequency and length of the disease. We also want to find out how these lesions may influence brain function.”

The study was supported by the Lundbeck Foundation and the Novo Nordisk Foundation.

To learn more about migraine, please visit American Academy of Neurology.

Migraine: Multiple Processes, Complex Pathophysiology

Rami Burstein (1,3), Rodrigo Noseda (1,3) and David Borsook (2,3)
1 – Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, Boston
2 – Department of Anesthesiology, Perioperative and Pain Medicine, Boston Children’s Hospital
3 – Harvard Medical School

Migraine is a common, multifactorial, disabling, recurrent, hereditary neurovascular headache disorder. It usually strikes sufferers a few times per year in childhood and then progresses to a few times per week in adulthood, particularly in females. Attacks often begin with warning signs (prodromes) and aura (transient focal neurological symptoms) whose origin is thought to involve the hypothalamus, brainstem, and cortex.

Once the headache develops, it typically throbs, intensifies with an increase in intracranial pressure, and presents itself in association with nausea, vomiting, and abnormal sensitivity to light, noise, and smell. It can also be accompanied by abnormal skin sensitivity (anodynia) and muscle tenderness.

Collectively, the symptoms that accompany migraine from the prodromal stage through the headache phase suggest that multiple neuronal systems function abnormally.

As a consequence of the disease itself or its genetic underpinnings, the migraine brain is altered structurally and functionally. These molecular, anatomical, and functional abnormalities provide a neuronal substrate for an extreme sensitivity to fluctuations in homeostasis, a decreased ability to adapt, and the recurrence of headache.

Homeostasis is the state of steady internal conditions maintained by living things.

Advances in understanding the genetic predisposition to migraine, and the discovery of multiple susceptible gene variants (many of which encode proteins that participate in the regulation of glutamate neurotransmission and proper formation of synaptic plasticity) define the most compelling hypothesis for the generalized neuronal hyperexcitability and the anatomical alterations seen in the migraine brain.

Regarding the headache pain itself, attempts to understand its unique qualities point to activation of the trigeminovascular pathway as a prerequisite for explaining why the pain is restricted to the head, often affecting the periorhital area and the eye, and intensities when intracranial pressure increases.

Introduction

Migraine is a recurrent headache disorder affecting 15% of the population during the formative and most productive periods of their lives, between the ages of 22 and 55 years. It frequently starts in childhood, particularly around puberty, and affects women more than men.

It tends to run in families and as such is considered a genetic disorder.

In some cases, the headache begins with no warning signs and ends with sleep. In other cases, the headache may be preceded by a prodromal phase that includes fatigue; euphoria; depression; irritability; food cravings; constipation; neck stiffness; increased yawning; and/or abnormal sensitivity to light, sound, and smell and an aura phase that includes a variety of focal cortically mediated neurological symptoms that appear just before and/or during the headache phase. Symptoms of migraine aura develop gradually, feature exeitatory and inhibitory phases, and resolve completely. Positive (gain of function) and negative (loss of function) symptoms may present as scintillating lights and scotomas when affecting the visual cortex; paresthesia, and numbness of the face and hands when affecting the somatosensory cortex; tremor and unilateral muscle weakness when affecting the motor cortex or basal ganglia; and difficulty saying words (aphasia) when affecting the speech area.

The pursuant headache is commonly unilateral, pulsating, aggravated by routine physical activity, and can last a few hours to a few days (Headache Classification Committee of the International Headache Society, 2013). As the headache progresses, it may be accompanied by a variety of autonomic symptoms (nausea, vomiting, nasallsinus congestion, rhinorrhea, lacrimation, ptosis, yawning, frequent urination, and diarrhea), affective symptoms (depression and irritability), cognitive symptoms (attention deficit, difficulty finding words, transient amnesia, and reduced ability to navigate in familiar environments), and sensory symptoms (photophobia, phonophobia, osmophobia, muscle tenderness, and cutaneous allodynia).

The extent of these diverse symptoms suggests that migraine is more than a headache. It is now viewed as a complex neurological disorder that affects multiple cortical, subcortical, and brainstem areas that regulate autonomic, affective, cognitive, and sensory functions. As such, it is evident that the migraine brain differs from the non-migraine brain and that an effort to unravel the pathophysiology of migraine must expand beyond the simplistic view that there are “migraine generator” areas.

In studying migraine pathophysiology, we must consider how different neural networks interact with each other to allow migraine to commence with stressors such as insufficient sleep, skipping meals, stressful or post stressful periods, hormonal fluctuations, alcohol, certain foods, flickering lights, noise, or certain scents, and why migraine attacks are sometimes initiated by these triggers and sometimes not.

We must tackle the enigma of how attacks are resolved on their own or just weaken and become bearable by sleep, relaxation, food, and/or darkness. We must explore the mechanisms by which the frequency of episodic migraine increases over time (from monthly to weekly to daily), and why progression from episodic to chronic migraine is uncommon.

Disease mechanisms

In many cases, migraine attacks are likely to begin centrally, in brain areas capable of generating the classical neurological symptoms of prodromes and aura, whereas the headache phase begins with consequential activation of meningeal nociceptors at the origin of the trigeminovascular system.

A nociceptor is a sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals to the spinal cord and the brain. If the brain perceives the threat as credible, it creates the sensation of pain to direct attention to the body part, so the threat can hopefully be mitigated; this process is called nociception.
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The meninges are the three membranes that envelop the brain and spinal cord. In mammals, the meninges are the dura mater, the arachnoid mater, and the pia mater. Cerebrospinal fluid is located in the subarachnoid space between the arachnoid mater and the pia mater. The primary function of the meninges is to protect the central nervous system.

While some clues about how the occurrence of aura can activate nociceptors in the meninges exist, nothing is known about the mechanisms by which common prodromes initiate the headache phase or what sequence of events they trigger that results in activation of the meningeal nociceptors. A mechanistic search for a common denominator in migraine symptomatology and characteristics points heavily toward a genetic predisposition to generalized neuronal hyperexcitability. Mounting evidence for alterations in brain structure and function that are secondary to the repetitive state of headache can explain the progression of disease.

Prodromes

In the context of migraine, prodromes are symptoms that precede the headache by several hours. Examination of symptoms that are most commonly described by patients point to the potential involvement of the hypothalamus (fatigue, depression, irritability, food cravings, and yawning), brainstem (muscle tenderness and neck stiffness), cortex (abnormal sensitivity to light, sound, and smell), and limbic system (depression and anhedonia) in the prodromal phase of a migraine attack. Given that symptoms such as fatigue, yawning, food craving, and transient mood changes occur naturally in all humans, it is critical that we understand how their occurrence triggers a headache; whether the routine occurrence of these symptoms in migraineurs (i.e., when no headache develops) differs mechanistically from their occurrence before the onset of migraine; and why yawning, food craving, and fatigue do not trigger a migraine in healthy subjects.

Recently, much attention has been given to the hypothalamus because it plays a key role in many aspects of human circadian rhythms (wake sleep cycle, body temperature, food intake, and hormonal fluctuations) and in the continuous effort to maintain homeostasis. Because the migraine brain is extremely sensitive to deviations from homeostasis, it seems reasonable that hypothalamie neurons that regulate homeostasis and circadian cycles are at the origin of some of the migraine prodromes.

Unraveling the mechanisms by which hypothalamic and brainstem neurons can trigger a headache is central to our ability to develop therapies that can intercept the headache during the prodromal phase (i.e., before the headache begins. The ongoing effort to answer this question focuses on two very different possibilities (Fig. 1). The first suggests that hypothalamic neurons that respond to changes in physiological and emotional homeostasis can activate meningeal nociceptors by altering the balance between parasympathetic and sympathetic tone in the meninges toward the predominance of parasympathetic tone. Support for such a proposal is based on the following: (1) hypothalamic neurons are in a position to regulate the firing of preganglionic parasympathetic neurons in the superior salivatory nucleus (SSN) and sympathetic preganglionic neurons in the spinal intermediolateral nucleus. (2) the SSN can stimulate the release of acetylcholine, vasoactive intestinal peptide, and nitric oxide from meningeal terminals of postganglionic parasympathetic neurons in the Spheno palatine ganglion (SPG), leading to dilation of intracranial blood vessels, plasma protein extravasation, and local release of inflammatory molecules capable of activating pial and dural branches of meningeal nociceptors; (3) meningeal blood vessels are densely innervated by para sympathetic fibers. (4) activation of SSN neurons can modulate the activity of central trigeminovascular neurons in the spinal trigeminal nucleus. (5) activation of meningeal nociceptors appears to depend partially on enhanced activity in the SPG. (6) enhanced cranial parasympathetic tone during migraine is evident by lacrimation and nasal congestion, and, finally, (7) blockade of the sphenopalatine ganglion provides partial or complete relief of migraine pain.

The second proposal suggests that hypothalamic and brainstem neurons that regulate responses to deviation from physiological and emotional homeostasis can lower the threshold for the transmission of nociceptive trigeminovascular signals from the thalamus to the cortex, a critical step in establishing the headache experience. This proposal is based on understanding how the thalamus selects, amplifies, and prioritizes information it eventually transfers to the cortex, and how hypothalamic and brainstem nuclei regulate relay thalamocortical neurons. It is constructed from recent evidence that relay trigeminothalamic neurons in sensory thalamie nuclei receive direct input from hypothalamic neurons that contain dopamine, histamine, orexin, and melanin concentrating hormone (MCH), and brainstem neurons that contain noradrenaline and serotonin. In principle, each of these neuropeptides/neurotransmitters can shift the activity of thalamic neurons from burst to tonic mode if it is excitatory (dopamine, and high concentration of serotonin, noradrenaline, histamine, orexin, and from tonic to burst mode if it is inhibitory (MCH and low concentration of serotonin). The opposing factors that regulate the firing of relay trigeminovascular thalamic neurons provide an anatomical foundation for explaining why prodromes give rise to some migraine attacks but not to others, and why external (e.g., exposure to strong perfume) and internal conditions (e.g., skipping a meal and feeling hungry, sleeping too little and being tired, or simple stress) trigger migraine attacks so inconsistently.

In the context of migraine, the convergence of these hypothalamic and brainstem neurons on thalamic trigeminovascular neuruns can establish high and low set points for the allostatic load of the migraine brain. The allostatic load, defined as the amount of brain activity required to appropriately manage the level of emotional or physiological stress at any given time, can explain why external and internal conditions only trigger headache some of the times, when they coincide with the right circadian phase of cyclic rhythmicity of brainstem, and hypothalamic and thalamic neurons that preserve homeostasis.

Cortical spreading depression

Clinical and preclinical studies suggest that migraine aura is caused by cortical spreading depression (CSD), a slowly propagating wave of depolarization/excitation followed by hyperpolarization/inhibition in cortical neurons and glia. While specific processes that initiate CSD in humans are not known, mechanisms that invoke inflammatory molecules as a result of emotional or physiological stress, such as lack of sleep, may play a role. In the cortex, the initial membrane depolarization is associated with a large efflux of potassium; influx of sodium and calcium; release of glutamate, ATP, and hydrogen ions; neuronal swelling ; upregulation of genes involved in inflammatory processing; and a host of changes in cortical perfusion and enzymatic activity that include opening of the megachannel Panxl, activation of caspase-1, and a breakdown of the blood brain barrier.

Outside the brain, caspase-1 activation can initiate inflammation by releasing high mobility group protein B1 and interleukin-1 into the CSF, which then activates nuclear factor KB in astrocytes, with the consequential release of cyclooxygenase-2 and inducible nitric oxide swithase (iNOS) into the subarach noid space. The introduction into the meninges of these proinflammatory molecules, as well as calcitonin gene related peptide (CGRP) and nitric oxide, may be the link between aura and headache because the meninges are densely innervated by pain fibers whose activation distinguishes headaches of intracranial origin (e.g., migraine, meningitis, and subaraeh noid bleeds) from headaches of extracranial origin (e.g., tension type headache, cervicogenic headache, or headaches caused by mild trauma to the cranium).

Anatomy and physiology of the trigeminovascular pathway: from activation to sensitization

Anatomical description

The trigeminovascular pathway conveys nociceptive information from the meninges to the brain. The pathway originates in trigeminal ganglion neurons whose peripheral axons reach the pia, dura, and large cerebral arteries, and whose central axons reach the nociceptive dorsal horn laminae of the SpV. In the SpV, the nociceptors converge on neurons that receive additional input from the periorbital skin and pericranial muscles. The ascending axonal projections of trigeminovascular SpV neurons transmit monosynaptic nocieeptive signals to (1) brainstem nuclei, such as the ventro lateral periaqueductal gray, reticular for mation, superior salivatory, parabrachial, cuneiform, and the nucleus of the solitary tract; (2) hypothalamic nuclei, such as the anterior, lateral, perifornical, dorsome dial, suprachiasmatic, and supraoptic; and (3) basal ganglia nuclei, such as the caudate putamen, globus pallidus, and sub stantia innominata. These projections maybe critical for the initiation of nausea, vomiting, yawning, lacrimation, urination, loss of appetite, fatigue, anxiety, irritability, and depression by the headache itself.

Additional projections of trigeminovascular SpV neurons are found in the thalamic ventral posteromedial (VPM), posterior (PO), and parafascicular nuclei. Relay trigeminovascular thalamic neurons that project to the somatosensory, insular, motor, parietal association, retrosplenial, auditory, visual, and olfactory cortices are in a position to construct the specific nature of migraine pain (i.e., location, intensity, and quality) and many of the cortically mediated symptoms that distinguish between migraine headache and other pains. These include transient symptoms of motor clumsiness, difficulty focusing, amnesia, allodynia, phonophobia, photophobia, and osmophobia. Figure 2A illustrates the complexity of the trigeminovascular pathway.

Activation

Studies in animals show that CSD initiates delayed activation (Fig. 2D, 2B,C) and immediate activation (Fig. 2D) of peripheral and central trigeminovascular neurons in a fashion that resembles the classic delay and occasional immediate onset of headache after aura, and that systemic administration of the M type potassium channel opener KCNQ2/3 can prevent the CSD induced activation of the nociceptors.

These findings support the notion that the onset of the headache phase of migraine with aura coincides with the activation of meningeal nociceptors at the peripheral origin of the trigeminovascular pathway. Whereas the vascular, cellular, and molecular events involved in the activation of meningeal nocieeptors by CSD are not well under stood, a large body of data suggests that transient constriction and dilatation of pial arteries and the development of dural plasma protein extravasation, neurogenic inflammation, platelet aggregation, and mast cell degranulation, many of which may be driven by CSD dependent peripheral CGRP release, can introduce to the meninges proinflammatory molecules, such as histamine, bradykinin, serotonin, and prostaglandins (prostaglandin E2), and a high level of hydrogen ions thus altering the molecular environment in which meningeal nociceptors exist.

Sensitization

When activated in the altered molecular environment described above, peripheral trigeminovascular neurons become sensitized (their response threshold decreases and their response magnitude increases) and begin to respond to dura stimuli to which they showed minimal or no response at base line. When central trigeminovascular neurons in laminae I and V of SpV (Fig. 2F) and in the thalamic PO/VPM nuclei (Fig. 2G) become sensitized, their spontaneous activity increases, their receptive fields expand, and they begin to respond to innocuous mechanical and thermal stimulation of cephalic and extracephalic skin areas as if it were noxious. The human correlates of the electrophysiological measures of neuronal sensitization in animal studies are evident in contrast analysis of BOLD signals registered in MRI scans of the human trigeminal ganglion (Fig. 2H), spinal trigeminal nucleus (Fig. 2I), and the thalamus (Fig. 2J), all measured during migraine attacks.

The clinical manifestation of peripheral sensitization during migraine, which takes roughly 10 mins to develop, includes the perception of throbbing headache and the transient intensiflcation of headache while bending over or coughing, activities that momentarily increase intracranial pressure.

The clinical manifestation of sensitization of central trigeminovascular neurons in the SpV, which takes 30-60 min to develop and 120 min to reach full extent, include the development of cephalic allodynia signs such as scalp and muscle tenderness and hypersensitivity to touch. These signs are often recognized in patients reporting that they avoid wearing glasses, earrings, hats, or any other object that come in contact with the facial skin during migraine.

The clinical manifestation of thalamic sensitization during migraine, which takes 2-4 h to develop, also includes extracephalic allodynia signs that cause patients to remove tight clothing and jewelry, and avoid being touched, massaged, or hugged.

Evidence that triptans, 5HT agonists that disrupt communications between peripheral and central trigeminovascular neurons in the dorsal horn, are more effective in aborting migraine when administered early (i.e., before the development of central sensitization and allodynia) rather than late (i.e., after the development of allodynia) provides further support for the notion that meningeal nociceptors drive the initial phase of the headache. Further support for this concept was provided recently by studies showing that humanized monoclonal antihodies against CGRP, molecules that are too big to penetrate the bloodbrain barrier and act centrally (according to the companies that developed them), are effective in preventing migraine. Along this line, it was also reported that drugs that act on central trigeminovascular neurons, e.g., dihydroergotamine (DHE), are equally effective in reversing an already developed central sensitization a possible explanation for DHE effectiveness in aborting migraine after the failure of therapy with triptans.

Genetics and the hyperexcitable brain

Family history points to a genetic predisposition to migraine. A genetic association with migraine was first observed and defined in patients with familial hemiplegic migraine (FHM).

The three genes identified with FHM encode proteins that regulate glutamate availability in the synapse. FHM1 (CACNAIA) encodes the pore-forming a1 subunit of the P/Q type calcium channel; FHM2 (ATP1A2) encodes the 112 subunit of the Na+/K+ ATPase pump; and the FHM3 (SCNIA) encodes the a1 sub unit of the neuronal voltage gated Nav1.1 channel.

Collectively, these genes regulate transmitter release, glial ability to clear (reuptake) glutamate from the synapse, and the generation of action potentials.

Since these early findings, large genome wide association studies have identified 13 susceptibility gene variants for migraine with and without aura, three of which regulate glutaminergic neurotransmission (MTDH/AEG-1 downregulates glutamate transporter, LPRI modulates synaptic transmission through the NMDA receptor, and MEF-2D regulates the glutamatergic excitatory synapse), and two of which regulate synaptic development and plasticity (ASTN2 is involved in the structural development of cortical layers, and FHI5 regulates cAMP sensitive CREB proteins involved msynaptic plasticity).

These findings provide the most plausible explanation for the “generalized” neuronal hyperexcitability of the migraine brain.

In the context of migraine, increased activity in glutamalergic systems can lead to excessive occupation of the NMDA receptor, which in turn may amplify and reinforce pain transmission, and the development of allodynia and central sensitization. Network wise, wide spread neuronal hyperexcitability may also be driven by thalamocortical dysrhythmia, defective modulatory brainstem circuits that regulate excitability at multiple levels along the neuraxis; and inherently improper regulation/habituation of cortical, thalamic, and brainstem functions by limbic structures, such as the hypothalamus, amygdala, nucleus accumbens, caudate, putamen, and globus pallidus. Given that 2 of the 13 susceptibility genes regulate synaptic development and plasticity, it is reasonable to speculate that some of the networks mentioned above may not be properly wired to set a normal level of habituation throughout the brain, thus explaining the multi factorial nature of migraine. Along this line, it is also tempting to propose that at least some of the structural alterations seen in the migraine brain may be inherited and, as such, may be the “cause” of migraine, rather than being secondary to (i.e., being caused by) the repeated headache attacks. But this concept awaits evidence.

Structural and functional brain alterations

Brain alterations can be categorized into the following two processes: (1) alteration in brain function and (2) alterations in brain structure (Fig. 3). Functionally, a variety of imaging techniques used to measure relative activation in different brain areas in migraineurs (vs control subjects) revealed enhanced activation in the periaqueductal gray; red nucleus and substantia nigra; hypothalamus; posterior thalamus; cerebellum, insula, cingulate and prefrontal cortices, anterior temporal pole, and the hippocampus; and decreased activation in the somatosensory cortex, nucleus cuneiformis, caudate, putamen, and pallidum. All of these activity changes occurred in response to nonrepetitive stimuli, and in the cingulate and prefrontal cortex they occurred in response to repetitive stimuli.

Collectively, these studies support the concept that the migraine brain lacks the ability to habituate itself and consequently becomes hyperexcitable. It is a matter of debate, however, if such changes are unique to migraine headache. Evidence for nearly identical activation patterns in other pain conditions, such as lower back pain, neuropathic pain, Hbromyalgia, irritable bowel syndrome, and cardiac pain, raises the possibility that differences between somatic pain and migraine pain are not due to differences in central pain processing.

Anatomically, voxel based morphometry and diffusion sensor imaging studies in migraine patients (vs control subjects) have revealed thickening of the somatosensory cortex; increased gray matter density in the caudate; and gray matter volume loss in the superior temporal gyms, inferior frontal gyms, precentral gyms, anterior cingulate cortex, amygdala, parietal operculum, middle and inferior frontal gyrus, inferior frontal gyrus, and bilateral insula.

Changes in cortical and subcortical structures may also depend on the frequency of migraine attacks for a number of cortical and subcortical regions. As discussed above, it is unclear whether such changes are genetically predetermined or simply a result of the repetitive exposure to pain/stress. Favoring the latter are studies showing that similar gray matter changes occurring in patients experiencing other chronic pain conditions are reversible and that the magnitude of these changes can be correlated with the duration of disease.

Further complicating our ability to determine how the migraine brain differs from the brain of a patient experiencing other chronic pain conditions are anatomical findings showing decreased gray matter density in the prefrontal cortex, thalamus, posterior insula, secondary somatosensory cortex, precentral and posteentral gyms, hippocampus, and temporal pole of chronic back pain patients; anterior insula and orbitofrontal cortex of complex regional pain syndrome patients; and the insula, midanterior cingulate cortex, hippocampus and inferior temporal coxtex in osteoarthritis pa tients with chronic back pain.

Whereas some of the brain alterations seen in migraineurs depend on the sex of the patient, little can he said about the role played by the sex of patients who experience other pain conditions.

Treatments in development

Migraine therapy has two goals: to terminate acute attacks; and to prevent the next attack from happening. The latter can potentially prevent the progression from episodic to chronic state. Regarding the effort to terminate acute attacks, migraine represents one of the few pain conditions for which a specific drug (i.e., triptan) has been developed based on understanding the mechanisms of the disease. In contrast, the effort to prevent migraine from happening is likely to face a much larger challenge given that migraine can originate in an unknown number of brain areas (see above), and is associated with generalized functional and structural brain abnormalities.

A number of treatments that attract attention are briefly reviewed below.

Medications The most exciting drug currently under development is humanized monoclonal antibodies against CGRP. The development of these monoclonal antibodies are directed at both CGRP and its receptors. The concept is based on CGRP localization in the trigeminal ganglion and its relevance to migaine patho-physiology. In recent phase II randomized placebo-controlled trials, the neutralizing humanized monoclonal antibodies against CGRP administered by injection for the prevention of episodic migraine, showed promising results. Remarkably, a single injection may prevent or significantly reduce migraine attacks for 3 months.

Given our growing understanding of the importance of prodromes (likely representing abnormal sensitivity to the fluctuation in hypothalamically regulated homeostasis) and aura (likely representing the inherited conical hyperexcitability) in the pathophysiology of migraine, drugs that target ghrelin, leptin, and orexin receptors may be considered for therapeutic development which is based on their ability to restore proper hypothalamic control of stress, hyperphagia, adiposity, and sleep. All may be critical in reducing allostatic load and, consequently, in initiating the next migraine attack.

Brain modification

Neuroimaging studies showing that brain networks, brain morphology, and brain chemistry are altered in episodic and chronic migraineurs justify attempts to develop therapies that widely modify brain networks and their functions. Transcranial magnetic stimulation, which is thought to modify cortical hyperexcitability, is one such approach. Another approach for generalized brain modification is cognitive behavioral therapy.

Conclusions

Migraine is a common and undertreated disease. For those who suffer, it is a major cause of disability, including missing work or school, and it frequently has associated comorbidities such as anxiety and depression. To put this in context, it is a leading cause of suicide, an indisputable proof of the severity of the distress that the disease may inflict on the individual.

There is currently no objective diagnosis or treatment that is universally effective in aborting or preventing attacks. As an intermittent disorder, migraine represents a neurological condition wherein systems that continuously evaluate errors (error detection) frequently fail, thus adding to the allostatic load of the disease.

Given the enormous burden to society, there is an urgent imperative to focus on better understanding the neurobiology of the disease to enable the discovery of novel treatment approaches.

OFC, Brain Stimulation for Depression – Janice Wood * Direct Electrical Stimulation of Lateral OFC Acutely Improves Mood.

“You could see the improvements in patients’ body language. They smiled, they sat up straighter, they started to speak more quickly and naturally. They said things like ‘Wow, I feel better,’ ‘I feel less anxious,’ ‘I feel calm, cool and collected.”

An important step toward developing a therapy for people with treatment-resistant depression.

Converging lines of evidence from lesion studies, functional neuroimaging, and intracranial physiology point to a role of OFC in emotion processing. Clinically depressed individuals have abnormally high levels of activity in OFC as ascertained by functional neuroimaging, and recovery from depression is associated with decreased OFC activity.

We found that lateral OFC stimulation acutely improved mood in subjects with baseline depression and that these therapeutic effects correlated with modulation of large-scale brain networks implicated in emotion processing.

Our results suggest that lateral OFC stimulation improves mood state at least partly through mechanisms that underlie natural mood variation, and they are consistent with the notion that OFC integrates multiple streams of information relevant to affective cognition.

Unilateral stimulation of lateral OFC consistently produced acute, dose-dependent mood-state improvement across subjects with baseline depression traits.

In a new study, patients with moderate to severe depression reported significant improvements in mood when researchers stimulated the orbitofrontal cortex (OFC).

The orbitofrontal cortex (OFC) is a prefrontal cortex region in the frontal lobes in the brain, which is involved in the cognitive processing of decision-making.

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Researchers at the University of California San Francisco say the study’s findings are “an important step toward developing a therapy for people with treatment-resistant depression, which affects as many as 30 percent of depression patients.”

Using electrical current to directly stimulate affected regions of the brain has proven to be an effective therapy for treating certain forms of epilepsy and Parkinson’s disease, but efforts to develop therapeutic brain stimulation for depression have so far been inconclusive, according to the researchers.

“The OFC has been called one of the least understood regions in the brain, but it is richly connected to various brain structures linked to mood, depression, and decision making, making it very well positioned to coordinate activity between emotion and cognition.”

Two additional observations suggested that OFC stimulation could have therapeutic potential.

First, the researchers found that applying current to the lateral OFC triggered wide-spread patterns of brain activity that resembled what had naturally occurred in volunteers’ brains during positive moods in the days before brain stimulation. Equally promising was the fact that stimulation only improved mood in patients with moderate to severe depression symptoms but had no effect on those with milder symptoms.

“These two observations suggest that stimulation was helping patients with serious depression experience something like a naturally positive mood state, rather than artificially boosting mood in everyone.

This is in line with previous observations that OFC activity is elevated in patients with severe depression and suggests electrical stimulation may affect the brain in a way that removes an impediment to positive mood that occurs in people with depression.”

Psych Central

Direct Electrical Stimulation of Lateral Orbitofrontal Cortex Acutely Improves Mood in Individuals with Symptoms of Depression

Vikram R. Rao, Kristin K. Sellers, Deanna L. Wallace, Maryam M. Shanechi, Heather E. Dawes, Edward F. Chang.

Mood disorders cause significant morbidity and mortality, and existing therapies fail 20%–30% of patients. Deep brain stimulation (DBS) is an emerging treatment for refractory mood disorders, but its success depends critically on target selection. DBS focused on known targets within mood-related frontostriatal and limbic circuits has been variably efficacious.

Here, we examine the effects of stimulation in orbitofrontal cortex (OFC), a key hub for mood-related circuitry that has not been well characterized as a stimulation target. We studied 25 subjects with epilepsy who were implanted with intracranial electrodes for seizure localization. Baseline depression traits ranged from mild to severe. We serially assayed mood state over several days using a validated questionnaire. Continuous electrocorticography enabled investigation of neurophysiological correlates of mood-state changes.

We used implanted electrodes to stimulate OFC and other brain regions while collecting verbal mood reports and questionnaire scores. We found that unilateral stimulation of the lateral OFC produced acute, dose-dependent mood-state improvement in subjects with moderate-to-severe baseline depression. Stimulation suppressed low-frequency power in OFC, mirroring neurophysiological features that were associated with positive mood states during natural mood fluctuation. Stimulation potentiated single-pulse-evoked responses in OFC and modulated activity within distributed structures implicated in mood regulation.

Behavioral responses to stimulation did not include hypomania and indicated an acute restoration to non-depressed mood state.

Together, these findings indicate that lateral OFC stimulation broadly modulates mood-related circuitry to improve mood state in depressed patients, revealing lateral OFC as a promising new target for therapeutic brain stimulation in mood disorders.

Experimental Design and Locations of Stimulated Sites

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Introduction

A modern conception of mood disorders holds that the signs and symptoms of emotional dysregulation are manifestations of abnormal activity within large-scale brain networks. This view, evolved from earlier hypotheses based on chemical imbalances in the brain, has fueled interest in selective neural network modulation with deep brain stimulation (DBS). Although the potential for precise therapeutic intervention with DBS is promising, its efficacy is sensitive to target selection. In treatment-resistant depression (TRD), for example, well-studied targets for DBS include the subgenual cingulate cortex (SCC) and subcortical structures, but the benefits of DBS in these areas are not clearly established.

A major challenge in this regard relates to the fact that clinical manifestations of mood disorders like TRD are heterogeneous and involve dysfunction in cognitive, affective, and reward systems. Therefore, brain regions that represent a functional confluence of these systems are attractive targets for therapeutic brain stimulation.

Residing within prefrontal cortex, the orbitofrontal cortex (OFC) shares reciprocal connections with amygdala, ventral striatum, insula, and cingulate cortex, areas implicated in emotion regulation. As such, OFC is anatomically well positioned to regulate mood. Functionally, OFC serves as a nexus for sensory integration and has myriad roles related to emotional experience, including predicting and evaluating outcomes, representing reward-driven learning and behavior, and mediating subjective hedonic experience.

Converging lines of evidence from lesion studies, functional neuroimaging, and intracranial physiology point to a role of OFC in emotion processing. Clinically depressed individuals have abnormally high levels of activity in OFC as ascertained by functional neuroimaging, and recovery from depression is associated with decreased OFC activity.

Repetitive transcranial magnetic stimulation (rTMS) of OFC was shown to improve mood in a single-subject case study and in a series of patients who otherwise did not respond to rTMS delivered to conventional (non-OFC) targets, but whether intracranial OFC stimulation can reliably alleviate mood symptoms is not known.

Furthermore, OFC is relatively large, and functional distinctions between medial and lateral subregions are known, raising the possibility that subregions of OFC may play distinct roles in mood regulation.

More generally, it remains poorly understood how direct brain stimulation affects local and network-level neural activity to produce complex emotional responses.

We hypothesized that brain networks involved in emotion processing include regions, like OFC, that represent previously unrecognized stimulation targets for alleviation of neuropsychiatric symptoms. To test this hypothesis, we developed a system for studying mood-related neural activity in subjects with epilepsy who were undergoing intracranial electroencephalography (iEEG) for seizure localization. In addition to direct recording of neural activity, iEEG allows delivery of defined electrical stimulation pulses with high spatiotemporal precision and concurrent measurement of behavioral correlates.

Using serial quantitative mood assessments and continuous iEEG recordings, we investigated the acute effects of OFC stimulation on mood state and characterized corresponding changes in neural activity locally and in distributed brain regions. We found that lateral OFC stimulation acutely improved mood in subjects with baseline depression and that these therapeutic effects correlated with modulation of large-scale brain networks implicated in emotion processing.

Our results suggest that lateral OFC stimulation improves mood state at least partly through mechanisms that underlie natural mood variation, and they are consistent with the notion that OFC integrates multiple streams of information relevant to affective cognition.

Discussion

Here, we show that human lateral OFC is a promising target for brain stimulation to alleviate mood symptoms. Unilateral stimulation of lateral OFC consistently produced acute, dose-dependent mood-state improvement across subjects with baseline depression traits. Locally, lateral OFC stimulation increased cortical excitability and suppressed low-frequency power, a feature we found to be negatively correlated with mood state. At the network level, lateral OFC stimulation modulated activity within a network of limbic and paralimbic structures implicated in mood regulation.

Relief of mood symptoms afforded by lateral OFC stimulation may arise from OFC acting as a hub within brain networks that mediate affective cognition.

Previous studies identify OFC as a key node within an emotional salience network activated by anticipation of aversive events. Within this network, OFC is thought to integrate multimodal sensory information and guide emotion-related decisions by evaluating expected outcomes.

Stimulation of other brain regions that encode value information, such as SCC and ventral striatum, has also been found to improve mood, highlighting the relevance of reward circuits to mood state.

Here, using iEEG, we extend previous studies that employed indirect imaging biomarkers, such as glucose metabolism or blood oxygen level, to show that direct OFC stimulation modulates neural activity within a distributed network of brain regions. Our finding that lateral OFC stimulation was more effective than medial OFC stimulation for mood symptom relief advances the idea that these regions have differential contributions to depression, likely due to differences in network connectivity.

We did not observe consistent differences based on laterality of stimulation, but future studies powered to discern such differences may reveal additional layers of specificity.

Although few behavioral variables have been identified to predict which individuals will respond to stimulation of a given target for depression, we found that only patients with significant trait depression experienced mood-state improvement with lateral OFC stimulation. Based on speech-rate analysis, lateral OFC stimulation did not produce supraphysiological mood states, as can be seen with stimulation of other targets, but did specifically elevate speech rate in trait-depressed subjects, resulting in a level similar to that of the non-depressed subjects. Local neurophysiological changes induced by stimulation were opposite of those observed during spontaneous negative mood states. Taken together, these findings suggest that the effect of lateral OFC stimulation is to normalize or suppress pathological activity in circuits that mediate natural mood variation.

Our observations provide potential clues about how lateral OFC stimulation may impact mood. Although functional imaging biomarkers of depression are not firmly established, increased activity in lateral OFC is seen in patients with depression and normalizes with effective antidepressant treatment, and lateral OFC hyperactivity has been proposed as a mood-state marker of depression.

Thus, a speculative possibility is that our stimulation paradigm works by decreasing OFC theta power in a way that may impact baseline hyperactivity. We cannot exclude the possibility that the mechanisms underlying mood improvement with lateral OFC stimulation involve multiple regions and may at least partially overlap with mechanisms responsible for mood improvement with stimulation of SCC. In fact, based on anatomic and functional connectivity between these regions, and the constellation of white matter tracts likely affected by stimulation of these sites, some mechanistic overlap seems probable.

Our results have potential implications for interventional treatments for psychiatric disorders like TRD and anxiety. DBS efficacy for TRD is inconsistent, and a major thrust of the field has been to understand and circumvent inter-subject variability. For example, the heterogeneous responses seen with SCC stimulation may relate to laterality and precise anatomic electrode position. In our study, positive mood responses were induced by unilateral stimulation of the OFC in either hemisphere, and although stimulation of lateral OFC improved mood more than stimulation of medial OFC, we observed mood improvement with stimulation across lateral OFC and did not see evidence of fine subregion specificity. These findings suggest that lateral OFC may be a more forgiving site for therapeutic stimulation than previously reported targets.

Another practical advantage of OFC relative to other targets is that the cortical surface is generally more surgically accessible than deep brain targets and that the ability to forego parenchymal penetration may impart lower risk during electrode implantation. Although seizures are a theoretical risk with any cortical stimulation, this risk is thought to be acceptably low, and we did not observe seizures during OFC stimulation.

Despite the widespread use of DBS in clinical and research applications, the mechanisms by which focal brain stimulation modulates network activity to produce complex behavioral changes remain largely unknown. The effects of stimulation are not limited to the targeted region, and stimulation-induced activity can propagate through anatomical connections to influence distributed networks in the brain. Previous studies have shown that target connectivity may determine likelihood of response to DBS.

Deciphering the precise mechanism of mood improvement with OFC stimulation requires future study, but our observation that stimulation suppresses low-frequency activity broadly across multiple sites suggests a possible local inhibitory effect that reverberates through connected brain regions. Consistent with this, inhibitory transcranial magnetic stimulation of OFC was recently reported to improve mood in one depressed patient. Since the OFC is relatively large and bilateral, it is possible that the mood effects we observed could be improved by more widespread stimulation.

Our study has limitations. The sample size was relatively small, reflecting the rare opportunity to directly and precisely target brain stimulation in human subjects. Although electrode coverage was generally extensive in our subjects, basal ganglia structures known to be important for mood are not typically implanted with electrodes for the purposes of seizure localization. Subjective self-report of mood has intrinsic limitations but remains the best instrument available to measure internal experience.

Our subjects, who had medically refractory epilepsy, may not be representative of all patients with mood disorders. While we cannot rule out the possibility that mood symptoms in our subjects had a seizure-specific etiology, the observed effects of lateral OFC stimulation were robust in a patient group with diverse underlying seizure pathology. To establish generalizability, our findings will need to be replicated in other cohorts.

Finally, it is possible that the acute effects of stimulation we observed may not translate into chronic efficacy for mood disorders in clinical settings. Indeed, rapid mood changes have been previously reported in TRD patients treated with bilateral DBS of SCC and subcortical targets. Whether chronic OFC stimulation can produce durable mood improvement is an important question for future study, ideally under controlled clinical trial conditions with appropriate monitoring of relevant outcomes and adverse events.

The clinical heterogeneity of mood disorders suggests that brain stimulation paradigms may need to be tailored for individual patients. Importantly, this study is one of few to assess the functional consequences of brain stimulation with direct neural recordings. The approach we used for serial quantitative mood state assessment may be useful for sensitively tracking symptoms of mood disorders during clinical interventions, including DBS trials. Our identification of a novel, robust stimulation target and our observation of stimulation-induced changes in endogenous mood-related neural features together set the stage for the next generation of stimulation therapies. OFC theta power may be useful for optimization of stimulation parameters for non-invasive stimulation modalities targeting the OFC in depression, and further characterization of mood biomarkers might enable personalized closed-loop stimulation devices that ameliorate debilitating mood symptoms.

Although the OFC is currently among the least understood brain regions, it may ultimately prove important for the treatment of refractory mood disorders.

Study: Current Biology

University of California, San Francisco (UCSF)

OUR EARLIEST EXPERIENCES SHAPE WHO WE ARE. Babies, Their Wonderful World – Dr Guddi Singh * The Six Faces of Maternal Narcissism – Karyl McBride Ph.D.

Love and attention.

One of the most important things that we know about early brain development is that the first two years of life are crucial.

Our brains are literally built on experience from the moment we are born. Experiences help build strong neural pathways between brain cells and allow brain material to expand.

Strong initial attachment bonds are crucial to making a happy secure adult.

Babies aren’t just eating and sleeping machines. Instead, we know they are like mini computers taking in everything that is going on around them.

In the first few months of life, personality traits start to show like caution, or bravery.

Babies who are not exposed to enough stimulation in their environment do not have the chance to develop the ‘hardware’ they need to be effective adults. Our brains are literally built on experience from the moment we are born. Experiences help build strong neural pathways between brain cells and allow brain material to expand. Stress and neglect can also inhibit brain growth because high levels of the stress hormone cortisone inhibits brain cells, although ironically it may encourage the over development of areas that are involved in the fight or flight response, increasing the likelihood that an individual will be prone to anxiety.

When it comes to smart phones and screens in baby cots, the issue is not so much that technology inhibits brain growth but that it causes a problem when it is a stand-in for parental involvement and love. That’s when we see problems when mobile phones and screens are used as babysitters for long periods while carers divert their attention elsewhere. From observational studies, it seems that it interferes with normal attachment and socialisation as well as inhibiting sleep, and the brain needs sleep for normal growth.

Babies who have siblings may benefit from socialisation and to a baby, nothing is funnier than a sibling. But single children can also be stimulated in a busy, challenging environment where they can still get this type of input including in a nursery environment.

The strongest evidence we have about developmental milestones early in life surround attachment theory. It has been shown time and time again that strong initial attachment bonds are crucial to making a happy secure adult. This is why paediatricians advocate close skin to skin contact in the early days and weeks of life. And we know that babies who are separated from a strong parental figure early on can have all sorts of emotional and social problems later in life.

However, that figure does not have to be the parent but can be someone from an extended family or even the community. It is really helpful to look at different cultures and how they parent their kids, there isn’t a one perfect solution and it can be done in different ways. In the west, there is a fetishisation of biological bonds, but adopted or looked after children can benefit from this strong bond as long as it includes love and attention.

Hippocratic Post

Dr Guddi Singh is a paediatrician based at East London NHS Foundation Trust. She is one of the advisers on the new BBC 2 series, Babies – Their Wonderful World. She is a member of the Royal Society of Medicine’s Paediatrics and Child Health Section Council.

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Also on TPPA = CRISIS

The Six Faces of Maternal Narcissism – Karyl McBride Ph.D.

“We Will Change The World , Starting From The Very Beginning.” Building Babies Brains . Criança Feliz, Brazil’s Audacious Plan To Fight Poverty – Jenny Anderson

Life After Severe Childhood Trauma . I Think I’ll Make It. A True Story Of Lost And Found – Kat Hurley

Chronic Childhood Stress And A Dysfunctional Family – Kylie Matthews * Different Adversities Lead To Similar Health Problems – Donna Jackson Nakazawa

How Our Brains Grow – Ruby Wax

The Deepest Well. Healing The Long Term Effects Of Childhood Adversity – Dr Nadine Burke Harris

Childhood Adversity Can Change Your Brain. How People Recover From Post Childhood Adversity Syndrome – Donna Jackson Nakazawa * Future Directions In Childhood Adversity and Youth Psychopathology – Katie A. McLaughlin

Childhood Disrupted . How Your Biography Becomes Your Biology , And How You Can Heal – Donna Jackson Nakazawa * The Origins Of Addiction . Evidence From The Adverse Childhood Experiences Study – Vincent J. Felitti MD.

MIND IN THE MIRROR * Neuroplasticity in a Nutshell * Mindsight, Change Your Brain and Your Life – Daniel J. Siegel MD.

We come to know our own minds through our interactions with others.

As we welcome the neural reality of our interconnected lives, we can gain new clarity about who we are, what shapes us, and how we in turn can shape our lives.

Riding the Resonance Circuits

It’s folk wisdom that couples in long and happy relationships look more and more alike as the years go by. Peer closely at those old photographs, and you’ll see that the couples haven’t actually grown similar noses or chins. Instead, they have reflected each other’s expressions so frequently and so accurately that the hundreds of tiny muscle attachments to their skin have reshaped their faces to mirror their union. How this happens gives us a window on one of the most fascinating recent discoveries about the brain, and about how we come to “feel felt” by one another.

Some of what I’ll describe here is still speculative, but it can shed light on the most intimate ways we experience mindsight in our daily lives.

Neurons That Mirror Our Minds

In the mid-1990s, a group of Italian neuroscientists were studying the premotor area of a monkey’s cortex. They were using implanted electrodes to monitor individual neurons, and when the monkey ate a peanut, a certain electrode fired. No surprise there, that’s what they expected. But what happened next has changed the course of our insight into the mind. When the monkey simply watched one of the researchers eat a peanut, that same motor neuron fired. Even more startling: The researchers discovered that this happened only when the motion being observed was goal-directed. Somehow, the circuits they had discovered were activated only by an intentional act.

This mirror neuron system has since been identified in human beings and is now considered the root of empathy. Beginning from the perception of a basic behavioral intention, our more elaborated human prefrontal cortex enables us to map out the minds of others. Our brains use sensory information to create representations of others’ minds, just as they use sensory input to create images of the physical world. The key is that mirror neurons respond only to an act with intention, with a predictable sequence or sense of purpose. If I simply lift up my hand and wave it randomly, your mirror neurons will not respond. But if I carry out any act you can predict from experience, your mirror neurons will “figure out” what I intend to do before I do it. So when I lift up my hand with a cup in it, you can predict at a synaptic level that I intend to drink from the cup. Not only that, the mirror neurons in the premotor area of your frontal cortex will get you ready to drink as well.

We see an act and we ready ourselves to imitate it. At the simplest level, that’s why we get thirsty when others drink, and why we yawn when others yawn. At the most complex level, mirror neurons help us understand the nature of culture and how our shared behaviors bind us together, mind to mind. The internal maps created by mirror neurons are automatic, they do not require consciousness or effort. We are hardwired from birth to detect sequences and make maps in our brains of the internal state, the intentional stance, of other people. And this mirroring is “cross-modal”, it operates in all sensory channels, not just vision, so that a sound, a touch, a smell, can cue us to the internal state and intentions of another.

By embedding the mind of another into our own firing patterns, our mirror neurons may provide the foundation for our mindsight maps.

Now let’s take another step. Based on these sensory inputs, we can mirror not only the behavioral intentions of others, but also their emotional states. In other words, this is the way we not only imitate others’ behaviors but actually come to resonate with their feelings, the internal mental flow of their minds. We sense not only what action is coming next, but also the emotional energy that underlies the behavior. In developmental terms, if the behavioral patterns we see in our caregivers are straightforward, we can then map sequences with security, knowing what might happen next, embedding intentions of kindness and care, and so create in ourselves a mindsight lens that is focused and clear. If, on the other hand, we’ve had parents who are confusing and hard to “read,” our own sequencing circuits may create distorted maps.

So from our earliest days, the basic circuitry of mindsight can be laid down with a solid foundation, or created on shaky ground.

Knowing Me, Knowing You

I once organized an interdisciplinary think tank of researchers to explore how the mind might use the brain to perceive itself. One idea we discussed is that we make maps of intention using our cortically based mirror neurons and then transfer this information downward to our subcortical regions. A neural circuit called the insula seems to be the information superhighway between the mirror neurons and the limbic areas, which in turn send messages to the brainstem and the body proper. This is how we can come to resonate physiologically with others, how even our respiration, blood pressure, and heart rate can rise and fall in sync with another’s internal state.

These signals from our body, brainstem, and limbic areas then travel back up the insula to the middle prefrontal areas. I’ve come to call this set of circuits, from mirror neurons to subcortical regions, back up to the middle prefrontal areas, the “resonance circuits.” This is the pathway that connects us to one another. Notice what happens when you’re at a party with friends. If you approach a group that is laughing, you’ll probably find yourself smiling or chuckling even before you’ve heard the joke. Or perhaps you’ve gone to dinner with people who’ve suffered a recent loss. Without their saying anything, you may begin to sense a feeling of heaviness in your chest, a welling up in your throat, tears in your eyes. Scientists call this emotional contagion. The internal states of others, from joy and play to sadness and fear, directly affect our own state of mind. This contagion can even make us interpret unrelated events with a particular bias, so that, for example, after we’ve been around someone who is depressed we interpret someone else’s seriousness as sadness.

For therapists, it’s crucial to keep this bias in mind. Otherwise a prior session may shape our internal state so much that we aren’t open and receptive to the new person with whom we need to be resonating.

Our awareness of another person’s state of mind depends on how well we know our own. The insula brings the resonating state within us upward into the middle prefrontal cortex, where we make a map of our internal world. So we feel others’ feelings by actually feeling our own, we notice the belly fill with laughter at the party or with sadness at the funeral home. All of our subcortical data, our heart rate, breathing, and muscle tension, our limbic coloring of emotion, travels up the insula to inform the cortex of our state of mind. This is the main reason that people who are more aware of their bodies have been found to be more empathic.

The insula is the key: When we can sense our own internal state, the fundamental pathway for resonating with others is open as well.

The mind we first see in our development is the internal state of our caregiver. We coo and she smiles, we laugh and his face lights up. So we first know ourselves as reflected in the other. One of the most interesting ideas we discussed in our study group is that our resonance with others may actually precede our awareness of ourselves. Developmentally and evolutionarily, our modern self-awareness circuitry may be built upon the more ancient resonance circuits that root us in our social world.

How, then, do we discern who is “me” and who is “you”? The scientists in our group suggested that we may adjust the location and firing pattern of the prefrontal images to perceive our own mind. Increases in the registration of our own bodily sensations combined with a decrease in our mirror neuron response may help us know that these tears are mine, not yours, or that this anger is indeed from me, not from you. This may seem like a purely philosophical and theoretical question until you are in the midst of a marital conflict and find yourself arguing about who is the angry one, you or your spouse. And certainly, as a therapist, if I do not track the distinction between me and other, I can become flooded with my patients’ feelings, lose my ability to help, and also burn out quickly.

When resonance literally becomes mirroring, when we confuse me with you, then objectivity is lost. Resonance requires that we remain differentiated, that we know who we are, while also becoming linked. We let our own internal states be influenced by, but not become identical with, those of the other person.

It will take much more research to elucidate the exact way our mindsight maps make this distinction, but the basic issues are clear. The energy and information flow that we sense both in ourselves and in others rides the resonance circuits to enable mindsight.

As I consider the resonance circuits, two mind lessons stand out for me. One is that becoming open to our body’s states, the feelings in our heart, the sensations in our belly, the rhythm of our breathing, is a powerful source of knowledge. The insula flow that brings up this information and energy colors our cortical awareness, shaping how we reason and make decisions. We cannot successfully ignore or suppress these subcortical springs. Becoming open to them is a gateway to clear mindsight.

The second lesson is that relationships are woven into the fabric of our interior world. We come to know our own minds through our interactions with others. Our mirror neuron perceptions, and the resonance they create, act quickly and often outside of awareness. Mindsight permits us to invite these fast and automatic sources of our mental life into the theater of consciousness. As we welcome the neural reality of our interconnected lives, we can gain new clarity about who we are, what shapes us, and how we in turn can shape our lives.

Neuroplasticity in a Nutshell – Daniel J. Siegel MD

Change Your Brain and Your life – Daniel J. Siegel MD

from

Mindsight, change your brain and your life

by Daniel J. Siegel MD

get it at Amazon.com

MINDING THE BRAIN. Neuroplasticity in a Nutshell – Daniel J. Siegel MD * Neuroplasticity – Wikipedia.

“The brain is so complicated it staggers its own imagination.”

“Neurons that fire together, wire together”, “neurons that fire out of sync, fail to link”.

We can use the power of our mind to change the firing patterns of our brain and thereby alter our feelings, perceptions, and responses. The power to direct our attention, focus, has within it the power to shape our brain’s firing patterns, as well as the power to shape the architecture of the brain itself.

The causal arrows between brain and mind point in both directions. When we focus our attention in specific ways, we create neural firing patterns that permit previously separated areas to become linked and integrated. The synaptic linkages are strengthened, the brain becomes more interconnected, and the mind becomes more adaptive.

Daniel J. Siegel, MD, is a clinical professor of psychiatry at the UCLA School of Medicine, co-director of the UCLA Mindful Awareness Research Center, and executive director of the Mindsight Institute.

Neuroplasticity

/,njuaraupla’stisiti/ noun

The ability of the brain to form and reorganize synaptic connections, especially in response to learning or experience or following injury. “neuroplasticity offers real hope to everyone from stroke victims to dyslexics”

It’s easy to get overwhelmed thinking about the brain. With more than one hundred billion interconnected neurons stuffed into a small, skull-enclosed space, the brain is both dense and intricate. And as if that weren’t complicated enough, each of your average neurons has ten thousand connections, or synapses, linking it to other neurons. In the skull portion of the nervous system alone, there are hundreds of trillions of connections linking the various neural groupings into a vast spiderweb-like network. Even if we wanted to, we couldn’t live long enough to count each of those synaptic linkages.

Given this number of synaptic connections, the brain’s possible on-off firing patterns, its potential for various states of activation, has been calculated to be ten to the millionth power, or ten times ten one million times. This number is thought to be larger than the number of atoms in the known universe. It also far exceeds our ability to experience in one lifetime even a small percentage of these firing possibilities. As a neuroscientist once said, “The brain is so complicated it staggers its own imagination.” The brain’s complexity gives us virtually infinite choices for how our mind will use those firing patterns to create itself. ‘If we get stuck in one pattern or the other, we’re limiting our potential.

Patterns of neural firing are what we are looking for when we watch a brain scanner “light up” as a certain task is being performed. What scans often measure is blood flow. Since neural activity increases oxygen use, an increased flow of blood to a given area of the brain implies that neurons are firing there. Research studies correlate this inferred neural firing with specific mental functions, such as focusing attention, recalling a past event, or feeling pain.

We can only imagine how a scan of my brain might have looked when I went down the low road in a tense encounter with my son one day: an abundance of limbic firing with increased blood flow to my irritated amygdala and a diminished flow to my prefrontal areas as they began to shut down. Sometimes the out-of-control firing of our brain drives what we feel, how we perceive what is happening, and how we respond. Once my prefrontal region was off-Iine, the firing patterns from throughout my subcortical regions could dominate my internal experience and my interactions with my kids. But it is also true that when we’re not traveling down the low road we can use the power of our mind to change the firing patterns of our brain and thereby alter our feelings, perceptions, and responses.

One of the key practical lessons of modern neuroscience is that the power to direct our attention has within it the power to shape our brain’s firing patterns, as well as the power to shape the architecture of the brain itself.

As you become more familiar with the various parts of the brain, you can more easily grasp how the mind uses the firing patterns in these various parts to create itself. It bears repeating that while the physical property of neurons firing is correlated with the subjective experience we call mental activity, no one knows exactly how this actually occurs. But keep this in the front of your mind:

Mental activity stimulates brain firing as much as brain firing creates mental activity.

When you voluntarily choose to focus your attention, say, on remembering how the Golden Gate Bridge looked one foggy day last fall, your mind has just activated the visual areas in the posterior part of your cortex. On the other hand, if you were undergoing brain surgery, the physician might place an electrical probe to stimulate neural firing in that posterior area, and you’d also experience a mental image of some sort.

The causal arrows between brain and mind point in both directions.

Keeping the brain in mind in this way is like knowing how to exercise properly. As we work out, we need to coordinate and balance the different muscle groups in order to keep ourselves fit. Similarly, we can focus our minds to build the specific “muscle groups” of the brain, reinforcing their connections, establishing new circuitry, and linking them together in new and helpful ways. There are no muscles in the brain, of course, but rather differentiated clusters of neurons that form various groupings called nuclei, parts, areas, zones, regions, circuits, or hemispheres.

And just as we can intentionally activate our muscles by flexing them, we can “flex” our circuits by focusing our attention to stimulate the firing in those neuronal groups. Using mindsight to focus our attention in ways that integrate these neural circuits can be seen as a form of “brain hygiene.”

WHAT FIRES TOGETHER, WIRES TOGETHER

You may have heard this before: As neurons fire together, they wire together. But let’s unpack this statement piece by piece. When we have an experience, our neurons become activated; What this means is that the long length of the neuron, the axon, has a flow of ions in and out of its encasing membrane that functions like an electrical current. At the far end of the axon, the electrical flow leads to the release of a chemical neurotransmitter into the small synaptic space that joins the firing neuron to the next, postsynaptic neuron. This chemical release activates or deactivates the downstream neuron. Under the right conditions, neural firing can lead to the strengthening of synaptic connections. These conditions include repetition, emotional arousal, novelty, and the careful focus of attention! Strengthening synaptic linkages between neurons is how we learn from experience.

One reason that we are so open to learning from experience is that, from the earliest days in the womb and continuing into our childhood and adolescence, the basic architecture of the brain is very much a work in progress.

During gestation, the brain takes shape from the bottom up, with the brainstem maturing first. By the time we are born, the limbic areas are partially developed but the neurons of the cortex lack extensive connections to one another.

This immaturity, the lack of connections within and among the different regions of the brain, is what gives us that openness to experience that is so critical to learning.

A massive proliferation of synapses occurs during the first years of life. These connections are shaped by genes and chance as well as experience, with some aspects of ourselves being less amenable to the influence of experience than others. Our temperament, for example, has a nonexperiential basis; it is determined in large part by genes and by chance. For instance, we may have a robust approach to novelty and love to explore new things, or we may tend to hang back in response to new situations, needing to “warm up” before we can overcome our initial shyness. Such neural propensities are set up before birth and then directly shape how we respond to the worId-and how others respond to us.

From our first days of life, our immature brain is also directly shaped by our interactions with the world, and especially by our relationships. Our experiences stimulate neural firing and sculpt our emerging synaptic connections. This is how experience changes the structure of the brain itself, and could even end up having an influence on our innate temperament.

As we grow, then, an intricate weaving together of the genetic, chance, and experiential input into the brain shapes what we call our “personality,” with all its habits, likes, dislikes, and patterns of response. If you’ve always had positive experiences with dogs and have enjoyed having them in your life, you may feel pleasure and excitement when a neighbor’s new dog comes bounding toward you. But if you’ve ever been severely bitten, your neural firing patterns may instead help create a sense of dread and panic, causing your entire body to shrink away from the pooch. If on top of having had a prior bad experience with a dog you also have a shy temperament, such an encounter may be even more fraught with fear. But whatever your experience and underlying temperament, transformation is possible. Learning to focus your attention in specific therapeutic ways can help you override that old coupling of fear with dogs.

The intentional focus of attention is actually a form of self-directed experience: It stimulates new patterns of neural firing to create new synaptic linkages.

You may be wondering, “How can experience, even a mental activity such as directing attention, actually shape the structure of the brain?” As we’ve seen, experience means neural firing. When neurons fire together, the genes in their nuclei, their master control centers, become activated and “express” themselves. Gene expression means that certain proteins are produced. These proteins then enable the synaptic linkages to be constructed anew or to be strengthened.

Experience also stimulates the production of myelin, the fatty sheath around axons, resulting in as much as a hundredfold increase in the speed of conduction down the neuron’s length. And as we now know, experience can also stimulate neural stem cells to differentiate into wholly new neurons in the brain.

This neurogenesis, along with synapse formation and myelin growth, can take place in response to experience throughout our lives. As discussed before, the capacity of the brain to change is called neuroplasticity. We are now discovering how the careful focus of attention amplifies neuroplasticity by stimulating the release of neurochemicals that enhance the structural growth of synaptic linkages among the activated neurons.

Epigenesis

An additional piece of the puzzle is now emerging. Researchers have discovered that early experiences can change the long-term regulation of the genetic machinery within the nuclei of neurons through a process called epigenesis.

If early experiences are positive, for example, chemical controls over how genes are expressed in specific areas of the brain can alter the regulation of our nervous system in such a way as to reinforce the quality of emotional resilience. If early experiences are negative, however, it has been shown that alterations in the control of genes influencing the stress response may diminish resilience in children and compromise their ability to adjust to stressful events in the future.

The changes wrought through epigenesis will continue to be in the science news as part of our exploration of how experience shapes who we are.

In sum, experience creates the repeated neural firing that can lead to gene expression, protein production, and changes in both the genetic regulation of neurons and the structural connections in the brain. By harnessing the power of awareness to strategically stimulate the brain’s firing, mindsight enables us to voluntarily change a firing pattern that was laid down involuntarily. When we focus our attention in specific ways, we create neural firing patterns that permit previously separated areas to become linked and integrated. The synaptic linkages are strengthened, the brain becomes more interconnected, and the mind becomes more adaptive.

THE BRAIN IN THE BODY

It’s important to remember that the activity of what we’re calling the “brain” is not just in our heads. For example, the heart has an extensive network of nerves that process complex information and relay data upward to the brain in the skull. So, too, do the intestines, and all the other major organ systems of the body. The dispersion of nerve cells throughout the body begins during our earliest development in the womb, when the cells that form the outer layer of the embryo fold inward to become the origin of our spinal cord. Clusters of these wandering cells then start to gather at one end of the spinal cord, ultimately to become the skull-encased brain. But other neural tissue becomes intricately woven with our musculature, our skin, our heart, our lungs, and our intestines. Some of these neural extensions form part of the autonomic nervous system, which keeps the body working in balance whether we are awake or asleep; other circuitry forms the voluntary portion of the nervous system, which allows us to intentionally move our limbs and control our respiration. The simple connection of sensory nerves from the periphery to our spinal cord and then upward through the various layers of the skull-encased brain allows signals from the outer world to reach the cortex, where we can become aware of them. This input comes to us via the five senses that permit us to perceive the outer physical world.

The neural networks throughout the interior of the body, including those surrounding the hollow organs, such as the intestines and the heart, send complex sensory input to the skull-based brain. This data forms the foundation for visceral maps that help us have a “gut feeling” or a “heartfelt” sense. Such input from the body forms a vital source of intuition and powerfully influences our reasoning and the way we create meaning in our lives.

Other bodily input comes from the impact of molecules known as hormones. The body’s hormones, together with chemicals from the foods and drugs we ingest, flow into our bloodstream and directly affect the signals sent along neurai routes. And, as we now know, even our immune system interacts with our nervous system. Many of these effects influence the neurotransmitters that operate at the synapses. These chemical messengers come in hundreds of varieties, some of which, such as dopamine and serotonin, have become household names thanks in part to drug company advertising. These substances have specific and complex effects on different regions of our nervous system. For example, dopamine is involved in the reward systems of the brain; behaviors and substances can become addictive because they stimulate dopamine release. Serotonin helps smooth out anxiety, depression, and mood fluctuations. Another chemical messenger is oxytocin, which is released when we feel close and attached to someone.

Throughout this book, I use the general term brain to encompass all of this wonderful complexity of the body proper as it intimately intertwines with its chemical environment and with the portion of neural tissue in the head. This is the brain that both shapes and is shaped by our mind. This is also the brain that forms one point of the triangle of well-being that is so central to mindsight.

By looking at the brain as an embodied system beyond its skull case, we can actually make sense of the intimate dance of the brain, the mind, and our relationships with one another. We can also recruit the power of neuroplasticity to repair damaged connections and create new, more satisfying patterns in our everyday lives.

from

Mindsight, change your brain and your life

by Daniel J. Siegel MD

get it at Amazon.com

See also: MINDSIGHT, OUR SEVENTH SENSE, an introduction. Change your brain and your life – Daniel J. Siegel MD.

Neuroplasticity – Wikipedia

Neuroplasticity, also known as brain plasticity and neural plasticity, is the ability of the brain to change throughout an individual’s life, e.g., brain activity associated with a given function can be transferred to a different location, the proportion of grey matter can change, and synapses may strengthen or weaken over time.

Research in the latter half of the 20th century showed that many aspects of the brain can be altered (or are “plastic”) even through adulthood.“ However, the developing brain exhibits a higher degree of plasticity than the adult brain.

Neuroplasticity can be observed at multiple scales, from microscopic changes in individual neurons to larger-scale changes such as cortical remapping in response to injury. Behavior, environmental stimuli, thought, and emotions may also cause neuroplastic change through activity-dependent plasticity, which has significant implications for healthy development, learning, memory, and recovery from brain damage.

At the single cell level, synaptic plasticity refers to changes in the connections between neurons, whereas non-synaptic plasticity refers to changes in their intrinsic excitability.

Neurobiology

One of the fundamental principles underlying neuroplasticity is based on the idea that individual synaptic connections are constantly being removed or recreated, largely dependent upon the activity of the neurons that bear them. The activity-dependence of synaptic plasticity is captured in the aphorism which is often used to summarize Hebbian theory: “neurons that fire together, wire together”/”neurons that fire out of sync, fail to link”. If two nearby neurons often produce an impulse in close temporal proximity, their functional properties may converge. Conversely, neurons that are not regularly activated simultaneously may be less likely to functionally converge.

Cortical maps

Cortical organization, especially in sensory systems, is often described in terms of maps. For example, sensory information from the foot projects to one cortical site and the projections from the hand target another site. As a result, the cortical representation of sensory inputs from the body resembles a somatotopic map, often described as the sensory homunculus.

In the late 1970s and early 1980s, several groups began exploring the impact of interfering with sensory inputs on cortical map reorganization. Michael Merzenich, Jon Kaas and Doug Rasmusson were some of those researchers. They found that if the cortical map is deprived of its input, it activates at a later time in response to other, usually adjacent inputs. Their findings have been since corroborated and extended by many research groups. Merzenich’s (1984) study involved the mapping of owl monkey hands before and after amputation of the third digit. Before amputation, there were five distinct areas, one corresponding to each digit of the experimental hand. Sixty-two days following amputation of the third digit, the area in the cortical map formerly occupied by that digit had been invaded by the previously adjacent second and fourth digit zones. The areas representing digit one and five are not located directly beside the area representing digit three, so these regions remained, for the most part, unchanged following amputation. This study demonstrates that only those regions that border a certain area invade it to alter the cortical map. In the somatic sensory system, in which this phenomenon has been most thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. Reorganization is not cortically emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.“

Merzenich and William Jenkins (1990) initiated studies relating sensory experience, without pathological perturbation, to cortically observed plasticity in the primate somatosensory system, with the finding that sensory sites activated in an attended operant behavior increase in their cortical representation. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the rodent whisker barrel cortex (also part of the somatosensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, and Kevin Fox. Great inroads were made in identifying the locus of change as being at cortical synapses expressing NMDA receptors, and in implicating cholinergic inputs as necessary for normal expression. The work of Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations causing a substantial impact on the cortical plasticity in that system.

Merzenich and DT Blake (2002, 2005, 2006) went on to use cortical implants to study the evolution of plasticity in both the somatosensory and auditory systems. Both systems show similar changes with respect to behavior. When a stimulus is cognitively associated with reinforcement, its cortical representation is strengthened and enlarged. In some cases, cortical representations can increase two to threefold in 1-2 days when a new sensory motor behavior is first acquired, and changes are largely finalised within at most a few weeks. Control studies show that these changes are not caused by sensory experience alone: they require learning about the sensory experience, they are strongest for the stimuli that are associated with reward, and they occur with equal ease in operant and classical conditioning behaviors.

An interesting phenomenon involving plasticity of cortical maps is the phenomenon of phantom limb sensation. Phantom limb sensation is experienced by people who have undergone amputations in hands, arms, and legs, but it is not limited to extremities. Although the neurological basis of phantom limb sensation is still not entirely understood it is believed that cortical reorganization plays an important role.

Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of “positive plasticity”. Changes such as an excessive level of neuronal growth leading to spasticity or tonic paralysis, or excessive neurotransmitter release in response to injury that could result in nerve cell death, are considered as an example of “negative” plasticity. In addition, drug addiction and obsessive-compulsive disorder are both deemed examples of “negative plasticity” by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive.

A 2005 study found that the effects of neuroplasticity occur even more rapidly than previously expected. Medical students’ brains were imaged during the period of studying for their exams. In a matter of months, the students’ gray matter increased significantly in the posterior and lateral parietal cortex.

Applications and example

The adult brain is not entirely “hard-wired” with fixed neuronal circuits. There are many instances of cortical and subcortical rewiring of neuronal circuits in response to training as well as in response to injury. There is solid evidence that neurogenesis (birth of brain cells) occurs in the adult mammalian brain, and such changes can persist well into old age. The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well. However, the degree of rewiring induced by the integration of new neurons in the established circuits is not known, and such rewiring may well be functionally redundant.

There is now ample evidence for the active, experience-dependent reorganization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex. The specific details of how this process occurs at the molecular and ultrastructural levels are topics of active neuroscience research. The way experience can influence the synaptic organization of the brain is also the basis for a number of theories of brain function including the general theory of mind and Neural Darwinism. The concept of neuroplasticity is also central to theories of memory and learning that are associated with experience-driven alteration of synaptic structure and function in studies of classical conditioning in invertebrate animal models such as Aplysia.

Treatment of brain damage

A surprising consequence of neuroplasticity is that the brain activity associated with a given function can be transferred to a different location; this can result from normal experience and also occurs in the process of recovery from brain injury. Neuroplasticity is the fundamental issue that supports the scientific basis for treatment of acquired brain injury with goal-directed experiential therapeutic programs in the context of rehabilitation approaches to the functional consequences of the injury.

Neuroplasticity is gaining popularity as a theory that, at least in part, explains improvements in functional outcomes with physical therapy post-stroke. Rehabilitation techniques that are supported by evidence which suggest cortical reorganization as the mechanism of change include constraint-induced movement therapy, functional electrical stimulation, treadmill training with body-weight support, and virtual reality therapy. Robot assisted therapy is an emerging technique, which is also hypothesized to work by way of neuroplasticity, though there is currently insufficient evidence to determine the exact mechanisms of change when using this method.

One group has developed a treatment that includes increased levels of progesterone injections in brain-injured patients. “Administration of progesterone after traumatic brain injury (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhances spatial reference memory and sensory motor recovery.” In a clinical trial, a group of severely injured patients had a 60% reduction in mortality after three days of progesterone injections?” However, a study published in the New England Journal of Medicine in 2014 detailing the results of a multi-center NIH-funded phase III clinical trial of 882 patients found that treatment of acute traumatic brain injury with the hormone progesterone provides no significant benefit to patients when compared with placebo.”

Vision

For decades, researchers assumed that humans had to acquire binocular vision, in particular stereopsis, in early childhood or they would never gain it. In recent years, however, successful improvements in persons with amblyopia, convergence insufficiency or other stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements and stereopsis recovery are now active areas of scientific and clinical research.

Brain training

Several companies have offered so-called cognitive training software programs for various purposes that claim to work via neuroplasticity; one example is Fast ForWord which is marketed to help children with learning disabilities. A systematic metaanalytic review found that “There is no evidence from the analysis carried out that Fast ForWord is effective as a treatment for children‘s oral language or reading difficulties”. A 2016 review found very little evidence supporting any of the claims of Fast ForWord and other commercial products, as their task-speciflc effects fail to generalise to other tasks.

Sensory prostheses

Neuroplasticity is involved in the development of sensory function. The brain is born immature and it adapts to sensory inputs after birth. In the auditory system, congenital hearing impairment, a rather frequent inborn condition affecting 1 of 1000 newborns, has been shown to affect auditory development, and implantation of a sensory prostheses activating the auditory system has prevented the deficits and induced functional maturation of the auditory system. Due to a sensitive period for plasticity, there is also a sensitive period for such intervention within the first 2-4 years of life. Consequently, in prelingually deaf children, early cochlear implantation, as a rule, allows the children to learn the mother language and acquire acoustic communication.

Phantom limb sensation

In the phenomenon of phantom limb sensation, a person continues to feel pain or sensation within a part of their body that has been amputated. This is strangely common, occurring in 60-80% of amputees. An explanation for this is based on the concept of neuroplasticity, as the cortical maps of the removed limbs are believed to have become engaged with the area around them in the postcentral gyrus. This results in activity within the surrounding area of the cortex being misinterpreted by the area of the cortex formerly responsible for the amputated limb.

The relationship between phantom limb sensation and neuroplasticity is a complex one. In the early 1990s V.S. Ramachandran theorized that phantom limbs were the result of cortical remapping. However, in 1995 Hertz Flor and her colleagues demonstrated that cortical remapping occurs only in patients who have phantom pain.” Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization. This phenomenon is sometimes referred to as maladaptive plasticity.

In 2009 Lorimer Moseley and Peter Brugger carried out a remarkable experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible configurations. Four of the seven subjects succeeded in performing impossible movements of the phantom limb. This experiment suggests that the subjects had modified the neural representation of their phantom limbs and generated the motor commands needed to execute impossible movements in the absence of feedback from the body. The authors stated that: “In fact, this finding extends our understanding of the brain’s plasticity because it is evidence that profound changes in the mental representation of the body can be induced purely by internal brain mechanisms, the brain truly does change itself.”

Chronlc pain

Individuals who suffer from chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from the periphery then elicits a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.“ For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth.

Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus. However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain, chronic low back pain and carpal tunnel syndrome.

Meditation

A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter. One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000. Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest that long-term or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as attention, anxiety, depression, fear, anger, and the ability of the body to heal itself. These functional changes may be caused by changes in the physical structure of the brain.

Fitness and exercise

Aerobic exercise promotes adult neurogenesis by increasing the production of neurotrophic factors (compounds that promote growth or survival of neurons), such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor (IGF-1), and vascular endothelial growth factor (VEGF). Exercise-induced neurogenesis in the hippocampus is associated with measurable improvements in spatial memory. Consistent aerobic exercise over a period of several months induces marked clinically significant improvements in executive function (i.e., the “cognitive control” of behavior) and increased gray matter volume in multiple brain regions, particularly those that give rise to cognitive control. The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex and hippocampus; moderate improvements are seen in the anterior cingulate cortex, parietal cortex, cerebellum, caudate nucleus, and nucleus accumbens. Higher physical fitness scores (measured by V02 max) are associated with better executive function, faster processing speed, and greater volume of the hippocampus, caudate nucleus, and nucleus accumbens.

Human echolocation

Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010 and 2011 using functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation. Studies with blind patients, for example, suggest that the click-echoes heard by these patients were processed by brain regions devoted to vision rather than audition.

ADHD stimulants

Reviews of MRI studies on individuals with ADHD suggest that the long-term treatment of attention deficit hyperactivity disorder (ADHD) with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudatenucleus of the basal ganglia.

In children

Neuroplasticity is most active in childhood as a part of normal human development, and can also be seen as an especially important mechanism for children in terms of risk and resiliency. Trauma is considered a great risk as it negatively affects many areas of the brain and puts strain on the sympathetic nervous system from constant activation. Trauma thus alters the brain’s connections such that children who have experienced trauma may be hyper vigilant or overly aroused. However a child’s brain can cope with these adverse effects through the actions of neuroplasticity.

In animals

In a single lifespan, individuals of an animal species may encounter various changes in brain morphology. Many of these differences are caused by the release of hormones in the brain; others are the product of evolutionary factors or developmental stages. Some changes occur seasonally in species to enhance or generate response behaviors.

Seasonal brain changes

Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals. These changes can improve the chances of mating during breeding season. Examples of seasonal brain morphology change can be found within many classes and species.

Within the class Aves, black-capped chickadees experience an increase in the volume of their hippocampus and strength of neural connections to the hippocampus during fall months. These morphological changes within the hippocampus which are related to spatial memory are not limited to birds, as they can also be observed in rodents and amphibians?“ In songbirds, many song control nuclei in the brain increase in size during mating season. Among birds, changes in brain morphology to influence song patterns, frequency, and volume are common. Gonadotropin-releasing hormone (GnRH) immunoreactivity, or the reception of the hormone, is lowered in European starlings exposed to longer periods of light during the day.

The California sea hare, a gastropod, has more successful inhibition of egg-laying hormones outside of mating season due to increased effectiveness of inhibitors in the brain. Changes to the inhibitory nature of regions of the brain can also be found in humans and other mammals. In the amphibian Bufo japonicus, part of the amygdala is larger before breeding and during hibernation than it is after breeding.

Seasonal brain variation occurs within many mammals. Part of the hypothalamus of the common ewe is more receptive to GnRH during breeding season than at other times of the year.

Humans experience a change in the size of the hypothalamic suprachiasmatic nucleus and vasopressin-immunoreactive neurons within it during the fall, when these parts are larger. In the spring, both reduce in size.

Traumatic brain injury research

Randy Nudo’s group found that if a small stroke (an infarction) is induced by obstruction of blood flow to a portion of a monkey’s motor cortex, the part of the body that responds by movement moves when areas adjacent to the damaged brain area are stimulated. In one study, intracortical microstimulation (ICMS) mapping techniques were used in nine normal monkeys. Some underwent ischemic-infarction procedures and the others, ICMS procedures. The monkeys with ischemic infarctions retained more finger flexion during food retrieval and after several months this deficit returned to preoperative levels.

With respect to the distal forelimb representation, “postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex.” Understanding of interaction between the damaged and undamaged areas provides a basis for better treatment plans in stroke patients. Current research includes the tracking of changes that occur in the motor areas of the cerebral cortex as a result of a stroke. Thus, events that occur in the reorganization process of the brain can be ascertained. Nudo is also involved in studying the treatment plans that may enhance recovery from strokes, such as physiotherapy, pharmacotherapy, and electrical-stimulation therapy.

Jon Kaas, a professor at Vanderbilt University, has been able to show “how somatosensory area 3b and ventroposterior (VP) nucleus of the thalamus are affected by longstanding unilateral dorsal-column lesions at cervical levels in macaque monkeys.” Adult brains have the ability to change as a result of injury but the extent of the reorganization depends on the extent of the injury. His recent research focuses on the somatosensory system, which involves a sense of the body and its movements using many senses. Usually, damage of the somatosensory cortex results in impairment of the body perception. Kaas’ research project is focused on how these systems (somatosensory, cognitive, motor systems) respond with plastic changes resulting from injury.

One recent study of neuroplasticity involves work done by a team of doctors and researchers at Emory University, specifically Dr. Donald Stein and Dr. David Wright. This is the first treatment in 40 years that has significant results in treating traumatic brain injuries while also incurring no known side effects and being cheap to administer. Dr. Stein noticed that female mice seemed to recover from brain injuries better than male mice, and that at certain points in the estrus cycle, females recovered even better. This difference may be attributed to different levels of progesterone, with higher levels of progesterone leading to the faster recovery from brain injury in mice. However, clinical trials showed progesterone offers no significant benefit for traumatic brain injury human patients.

History

Origin

The term “plasticity” was first applied to behavior in 1890 by William James in The Principles of Psychology. The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.

See also: William James’s Revolutionary 1884 Theory of How Our Bodies Affect Our Feelings – Maria Popova * What is an Emotion? – William James (1884).

In 1793, Italian anatomist Michele Vicenzo Malacarne described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. He discovered that the cerebellums of the trained animals were substantially larger. But these findings were eventually forgotten.

The idea that the brain and its function are not fixed throughout adulthood was proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected. Until around the 1970s, neuroscientists believed that the brain’s structure and function was essentially fixed throughout adulthood.

The term has since been broadly applied:

“Given the central importance of neuroplasticity, an outsider would be forgiven for assuming that it was well defined and that a basic and universal framework served to direct current and future hypotheses and experimentation. Sadly, however, this is not the case. While many neuroscientists use the word neuroplasticity as an umbrella term it means different things to different researchers in different subflelds. In brief, a mutually agreed upon framework does not appear to exist.”

Research and discovery

In 1923, Karl Lashley conducted experiments on rhesus monkeys that demonstrated changes in neuronal pathways, which he concluded were evidence of plasticity. Despite this, and other research that suggested plasticity took place, neuroscientists did not widely accept the idea of neuroplasticity.

In 1945, Justo Gonzalo concluded from his research of brain dynamics, that, contrary to the activity of the projection areas, the “central” cortical mass (more or less equidistant from the visual, tactile and auditive projection areas), would be a “maneuvering mass”, rather unspecific or multisensory, with capacity to increase neural excitability and re-organize the activity by means of plasticity properties. He gives as a first example of adaptation, to see upright with reversing glasses in the Stratton experiment, and specially, several first-hand brain injuries cases in which he observed dynamic and adaptive properties in their disorders, in particular in the inverted perception disorder. He stated that a sensory signal in a projection area would be only an inverted and constricted outline that would be magnified due to the increase in recruited cerebral mass, and re-inverted due to some effect of brain plasticity, in more central areas, following a spiral growth.

Marian Diamond of the University of California, Berkeley, produced the first scientific evidence of anatomical brain plasticity, publishing her research in 1964.

Other significant evidence was produced in the 1960s and after, notably from scientists including Paul Bach-y-Rita, Michael Merzenich along with Jon Kaas, as well as several others.

In the 1960s, Paul Bach-y-Rita invented a device that was tested on a small number of people, and involved a person sitting in a chair, in which were embedded nubs that were made to vibrate in ways that translated images received in a camera, allowing a form of vision via sensory substitution.

Studies in people recovering from stroke also provided support for neuroplasticity, as regions of the brain that remained healthy could sometimes take over, at least in part, functions that had been destroyed; Shepherd Ivory Franz did work in this area.

Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London’s layout in local taxi drivers. A redistribution of grey matter was indicated in London Taxi Drivers compared to controls. This work on hippocampal plasticity not only interested scientists, but also engaged the public and media worldwide.

Michael Merzenich is a neuroscientist who has been one of the pioneers of neuroplasticity for over three decades. He has made some of “the most ambitious claims for the field that brain exercises may be as useful as drugs to treat diseases as severe as schizophrenia, that plasticity exists from cradle to the grave, and that radical improvements in cognitive functioning, how we learn, think, perceive, and remember are possible even in the elderly.

Merzenich’s work was affected by a crucial discovery made by David Hubel and Torsten Wiesel in their work with kittens. The experiment involved sewing one eye shut and recording the cortical brain maps. Hubel and Wiesel saw that the portion of the kitten’s brain associated with the shut eye was not idle, as expected. Instead, it processed visual information from the open eye. It was “…as though the brain didn’t want to waste any ‘cortical real estate’ and had found a way to rewire itself.”

This implied neuroplasticity during the critical period. However, Merzenich argued that neuroplasticity could occur beyond the critical period. His first encounter with adult plasticity came when he was engaged in a postdoctoral study with Clinton Woosley. The experiment was based on observation of what occurred in the brain when one peripheral nerve was cut and subsequently regenerated. The two scientists micromapped the hand maps of monkey brains before and after cutting a peripheral nerve and sewing the ends together. Afterwards, the hand map in the brain that they expected to be jumbled was nearly normal. This was a substantial breakthrough. Merzenich asserted that, “If the brain map could normalize its structure in response to abnormal input, the prevailing view that we are born with a hardwired system had to be wrong. The brain had to be plastic.” Merzenich received the 2016 Kavli Prize in Neuroscience “for the discovery of mechanisms that allow experience and neural activity to remodel brain function.”

MINDSIGHT, OUR SEVENTH SENSE, an introduction. Change your brain and your life – Daniel J. Siegel MD.

Mindsight, the brain’s capacity for both insight and empathy.

How can we be receptive to the mind’s riches and not just reactive to its reflexes? How can we direct our thoughts and feelings rather than be driven by them?

And how can we know the minds of others, so that we truly understand “where they are coming from” and can respond more effectively and compassionately?

Mindsight is a kind of focused attention that allows us to see the internal workings of our own minds, making it possible to see what is inside, to accept it, and in the accepting to let it go, and finally, to transform it.

When we develop the skill of mindsight, we actually change the physical structure of our brain. How we focus our attention shapes the structure of the brain.

Mindsight has the potential to free us from patterns of mind that are getting in the way of living our lives to the fullest.

Mindsight, our ability to look within and perceive the mind, to reflect on our experience, is every bit as essential to our wellbeing as our six senses. Mindsight is our seventh sense.

What is Mindsight?

“Mindsight” is a term coined by Dr. Dan Siegel to describe our human capacity to perceive the mind of the self and others. It is a powerful lens through which we can understand our inner lives with more clarity, integrate the brain, and enhance our relationships with others. Mindsight is a kind of focused attention that allows us to see the internal workings of our own minds. It helps us get ourselves off of the autopilot of ingrained behaviors and habitual responses. It lets us “name and tame” the emotions we are experiencing, rather than being overwhelmed by them.

“I am sad” vs. “I feel sad”

Mindsight is the difference between saying “I am sad” and ”I feel sad.” Similar as those two statements may seem, they are profoundly different. “I am sad” is a kind of limited selfdefinition. “I feel sad” suggests the ability to recognize and acknowledge a feeling, without being consumed by it. The focusing skills that are part of mindsight make it possible to see what is inside, to accept it, and in the accepting to let it go, and finally, to transform it.

Mindsight: A Skill that Can Change Your Brain

Mindsight is a learnable skill. It is the basic skill that underlies what we mean when we speak of having emotional and social intelligence. When we develop the skill of mindsight, we actually change the physical structure of the brain. This revelation is based on one of the most exciting scientific discoveries of the last twenty years: How we focus our attention shapes the structure of the brain. Neuroscience has also definitively shown that we can grow these new connections throughout our lives, not just in childhood.

What’s Interpersonal Neurobiology?

Interpersonal neurobiology, a term coined by Dr. Siegel in The Developing Mind, 1999, is an interdisciplinary field which seeks to understand the mind and mental health. This field is based on science but is not constrained by science. What this means is that we attempt to construct a picture of the ”whole elephant” of human reality. We build on the research of different disciplines to reveal the details of individual components, while also assembling these pieces to create a coherent view of the whole.

The Mindsight Institute

Through the Mindsight Institute, Dr. Siegel offers a scientificaliy-based way of understanding human development. The Mindsight Institute serves as the organization from which interpersonal neurobiology first developed and it continues to be a key source for learning in this area. The Mindsight Institute links science, clinical practice, education, the arts, and contemplation, serving as an educational hub from which these various domains of knowing and practice can enrich their individual efforts. Through the Mindsight Institute’s online program, people from six continents participate weekly in our global conversation about the ways to create more health and compassion in the world.

Mindsight Institute

Daniel J. Siegel, MD, is a clinical professor of psychiatry at the UCLA School of Medicine, co-director of the UCLA Mindful Awareness Research Center, and executive director of the Mindsight Institute. A graduate of Harvard Medical School, he is the author of the internationally acclaimed professional texts The Mindful Brain and The Developing Mind, and the co-author of Parenting from the Inside Out.

The groundbreaking bestseller on how your capacity for insight and empathy allows you to make positive changes in your brain and in your life.

Daniel J. Siegel, widely recognised as a pioneer in the field of mental health, coined the term ‘mindsight’ to describe the innovative integration of brain science with the practice of psychotherapy. Combining the latest research findings with case studies from his practice, he demonstrates how mindsight can be applied to alleviate a range of psychological and interpersonal problems from anxiety disorders to ingrained patterns of behaviour.

With warmth and humour, Dr Siegel shows us how to observe the working of our minds, allowing us to understand why we think, feel, and act the way we do; and how, by following the proper steps, we can literally change the wiring and architecture of our brains.

Both practical and profound, Mindsight offers exciting new proof that we have the ability at any stage of our lives to transform our thinking, our wellbeing, and our relationships.

Mindsight, change your brain and your life

Daniel J. Siegel MD

FOREWORD by Daniel Goleman

The great leaps forward in psychology have come from original insights that suddenly clarify our experience from a fresh angle, revealing hidden patterns of connection. Freud’s theory of the unconscious and Darwin’s model of evolution continue to help us understand the findings from current research on human behavior and some of the mysteries of our daily lives. Daniel Siegel’s theory of Mindsight, the brain’s capacity for both insight and empathy, offers a similar “Aha!” He makes sense for us out of the cluttered confusions of our sometimes maddening and messy emotions.

Our ability to know our own minds as well as to sense the inner world of others may be the singular human talent, the key to nurturing healthy minds and hearts. I’ve explored this terrain in my own work on emotional and social intelligence. Self-awareness and empathy are (along with seIf-mastery and social skills) domains of human ability essential for success in life. Excellence in these capacities helps people flourish in relationships, family life, and marriage, as well as in work and leadership.

Of these four key life skills, self-awareness lays the foundation for the rest. If we lack the capacity to monitor our emotions, for example, we will be poorly suited to manage or learn from them. Tuned out of a range of our own experience, we will find it all the harder to attune to that same range in others. Effective interactions depend on the smooth integration of selfawareness, mastery, and empathy. Or so I’ve argued. Dr. Siegel casts the discussion in a fresh light, putting these dynamics in terms of mindsight, and marshals compelling evidence for its crucial role in our lives.

A gifted and sensitive clinician, as well as a master synthesizer of research findings from neuroscience and child development, Dr. Siegel gives us a map forward. Over the years he has continually broken new ground in his writing on the brain, psychotherapy, and childrearing; his seminars for professionals are immensely popular.

The brain, he reminds us, is a social organ. Mindsight is the core concept in “interpersonal neurobiology,” a field Dr. Siegel has pioneered. This two-person view of what goes on in the brain lets us understand how our daily interactions matter neurologically, shaping neural circuits. Every parent helps sculpt the growing brain of a child; the ingredients of a healthy mind include an attuned, empathetic parent, one with mindsight. Such parenting fosters this same crucial ability in a child.

Mindsight plays an integrative role in the triangle connecting relationships, mind, and brain. As energy and information flow among these elements of human experience, patterns emerge that shape all three (and the brain here includes its extensions via the nervous system throughout the body). This vision is holistic in the true sense of the word, inclusive of our whole being. With mindsight we can better know and manage this vital flow of being.

Dr. Siegel’s biographical details are impressive. Harvard-trained and a clinical professor of psychiatry at UCLA and co-director of the Mindful Awareness Research Center there, he also founded and directs the Mindsight Institute. But far more impressive is his actual being, a mindful, attuned, and nurturing presence that is nourishing in itself. Dr. Siegel embodies what he teaches.

For professionals who want to delve into this new science, I recommend Dr. Siegel’s 1999 text on interpersonal neurobiology, The Developing Mind: Toward a Neurobiology of Interpersonal Experience. For parents, his book with Mary Hartzell is invaluable: Parenting from the Inside Out: How a Deeper Self-Understanding Can Help You Raise Children Who Thrive. But for anyone who seeks a more rewarding life, the book you hold in your hands has compelling and practical answers.

Daniel Goleman

INTRODUCTION

Diving into the Sea Inside

Within each of us there is an internal mental world that I have come to think of as the sea inside, that is a wonderfully rich place, filled with thoughts and feelings, memories and dreams, hopes and wishes. Of course it can also be a turbulent place, where we experience the dark side of all those wonderful feelings and thoughts, fears, sorrows, dreads, regrets, nightmares. When this inner sea seems to crash in on us, threatening to drag us down below to the dark depths, it can make us feel as if we are drowning.

Who among us has not at one time or another felt overwhelmed by the sensations from within our own minds? Sometimes these feelings are just a passing thing, a bad day at work, a fight with someone we love, an attack of nerves about a test we have to take or a presentation we have to give, or just an inexplicable case of the blues for a day or two.

But sometimes they seem to be something much more intractable, so much part of the very essence of who we are that it may not even occur to us that we can change them. This is where the skill that I have called “mindsight” comes in, for mindsight, once mastered, is a truly transformational tool. Mindsight has the potential to free us from patterns of mind that are getting in the way of living our lives to the fullest.

WHAT IS MINDSIGHT?

Mindsight is a kind of focused attention that allows us to see the internal workings of our own minds. It helps us to be aware of our mental processes without being swept away by them, enables us to get ourselves off the autopilot of ingrained behaviors and habitual responses, and moves us beyond the reactive emotional loops we all have a tendency to get trapped in. It lets us “name and tame” the emotions we are experiencing, rather than being overwhelmed by them. Consider the difference between saying “I am sad” and “I feel sad.” Similar as those two statements may seem, there is actually a profound difference between them. “I am sad” is a kind of seIf-definition, and a very limiting one. “I feel sad” suggests the ability to recognize and acknowledge a feeling, without being consumed by it. The focusing skills that are part of mindsight make it possible to see what is inside, to accept it, and in the accepting to let it go, and, finally, to transform it.

You can also think of mindsight as a very special lens that gives us the capacity to perceive the mind with greater clarity than ever before. This lens is something that virtually everyone can develop, and once we have it we can dive deeply into the mental sea inside, exploring our own inner lives and those of others. A uniquely human ability, mindsight allows us to examine closely, in detail and in depth, the processes by which we think, feel, and behave. And it allows us to reshape and redirect our inner experiences so that we have more freedom of choice in our everyday actions, more power to create the future, to become the author of our own story. Another way to put it is that mindsight is the basic skill that underlies everything we mean when we speak of having social and emotional intelligence.

Interestingly enough, we now know from the findings of neuroscience that the mental and emotional changes we can create through cultivation of the skill of mindsight are transformational at the very physical level of the brain. By developing the ability to focus our attention on our internal world, we are picking up a “scalpel” we can use to resculpt our neural pathways, stimulating the growth of areas of the brain that are crucial to mental health. I will talk a lot about this in the chapters that follow because I believe that a basic understanding of how the brain works helps people see how much potential there is for change.

But change never just happens. It’s something we have to work at. Though the ability to navigate the inner sea of our minds, to have mindsight, is our birthright, and some of us, for reasons that will become clear later, have a lot more of it than others, it does not come automatically, any more than being born with muscles makes us athletes. The scientific reality is that we need certain experiences to develop this essential human capacity. I like to say that parents and other caregivers offer us our first swimming lessons in that inner sea, and if we’ve been fortunate enough to have nurturing relationships early in life, we’ve developed the basics of mindsight on which we can build. But even if such early support was lacking, there are specific activities and experiences that can nurture mindsight throughout the lifespan. As you will see, mindsight is a form of expertise that can be honed in each of us, whatever our early history.

When I first began to explore the nature of the mind professionally, there was no term in our everyday language that captured the way we perceive our thoughts, feelings, sensations, memories, beliefs, attitudes, hopes, dreams, and fantasies. Of course, these activities of the mind fill our day-to-day lives, we don’t need to learn a skill in order to experience them. But how do we actually develop the ability to perceive a thought, not just have one, and to know it as an activity of our minds so that we are not taken over by it? How can we be receptive to the mind’s riches and not just reactive to its reflexes? How can we direct our thoughts and feelings rather than be driven by them?

And how can we know the minds of others, so that we truly understand “where they are coming from” and can respond more effectively and compassionately? When I was a young psychiatrist, there weren’t many readily accessible scientific or even clinical terms to describe the whole of this ability. To be able to help my patients, I coined the term mindsight so that together we could discuss this important ability that allows us to see and shape the inner workings of our own minds.

Our first five senses allow us to perceive the outside world, to hear a bird’s song or a snake’s warning rattle, to make our way down a busy street or smell the warming earth of spring. What has been called our sixth sense allows us to perceive our internal bodily states, the quickly beating heart that signals fear or excitement, the sensation of butterflies in our stomach, the pain that demands our attention.

Mindsight, our ability to look within and perceive the mind, to reflect on our experience, is every bit as essential to our wellbeing. Mindsight is our seventh sense.

As I hope to show you in this book, this essential skill can help us build social and emotional brainpower, move our lives from disorder to well-being, and create satisfying relationships filled with connection and compassion. Business and government leaders have told me that understanding how the mind functions in groups has helped them be more effective and enabled their organizations to become more productive. Clinicians in medicine and mental health have said that mindsight has changed the way they approach their patients, and that putting the mind at the heart of their healing work has helped them create novel and useful interventions. Teachers introduced to mindsight have learned to “teach with the brain in mind” and are reaching and teaching their students in deeper and more lasting ways.

In our individual lives, mindsight offers us the opportunity to explore the subjective essence of who we are, to create a life of deeper meaning with a richer and more understandable internal world. With mindsight we are better able to balance our emotions, achieving an internal equilibrium that enables us to cope with the small and large stresses of our lives. Through our ability to focus attention, mindsight also helps the body and brain achieve homeostasis, the internal balance, coordination, and adaptiveness that forms the core of health. Finally, mindsight can improve our relationships with our friends, colleagues, spouses, and children, and even the relationship we have with our own selves.

A NEW APPROACH TO WELLBEING

Everything that follows rests on three fundamental principles.

The first is that mindsight can be cultivated through very practical steps. This means that creating wellbeing in our mental life, in our close relationships, and even in our bodies, is a learnable skill. Each chapter of this book explores these skills, from basic to advanced, for navigating the sea inside.

Second, as mentioned above, when we develop the skill of mindsight, we actually change the physical structure of the brain. Developing the lens that enables us to see the mind more clearly stimulates the brain to grow important new connections. This revelation is based on one of the most exciting scientific discoveries of the last twenty years: How we focus our attention shapes the structure of the brain. Neuroscience supports the idea that developing the reflective skills of mindsight activates the very circuits that create resilience and wellbeing and that underlie empathy and compassion as well. Neuroscience has also definitively shown that we can grow these new connections throughout our lives, not just in childhood. The short Minding the Brain sections interspersed throughout part 1 are a traveler’s guide to this new territory.

The third principle is at the heart of my work as a psychotherapist, educator, and scientist. Wellbeing emerges when we create connections in our lives, when we learn to use mindsight to help the brain achieve and maintain integration, a process by which separate elements are linked together into a working whole.

I know this may sound both unfamiliar and abstract at first, but I hope you’ll soon find that it is a natural and useful way of thinking about our lives. For example, integration is at the heart of how we connect to one another in healthy ways, honoring one another’s differences while keeping our lines of communication wide open. Linking separate entities to one another, integration, is also important for releasing the creativity that emerges when the left and right sides of the brain are functioning together.

Integration enables us to be flexible and free; the lack of such connections promotes a life that is either rigid or chaotic, stuck and dull on the one hand or explosive and unpredictable on the other. With the connecting freedom of integration comes a sense of vitality and the ease of wellbeing. Without integration we can become imprisoned in behavioral ruts, anxiety and depression, greed, obsession, and addiction.

By acquiring mindsight skills, we can alter the way the mind functions and move our lives toward integration, away from these extremes of chaos or rigidity. With mindsight we are able to focus our mind in ways that literally integrate the brain and move it toward resilience and health.

MINDSIGHT MISUNDERSTOOD

It’s wonderful to receive an email from an audience member or patient who says, “My whole view of reality has changed.” But not everyone new to mindsight gets it right away. Some people are concerned that it’s just another way to become more self-absorbed, a form of navel-gazing, of becoming preoccupied with “reflection” instead of living fully. Perhaps you’ve also read some of the recent research (or the ancient wisdom) that tells us that happiness depends on “getting out of yourself.” Does mindsight turn us away from this greater good?

While it is true that being selfobsessed decreases happiness, mindsight actually frees you to become less self-absorbed, not more. When we are not taken over by our thoughts and feelings, we can become clearer in our own internal world as well as more receptive to the inner world of another. Scientific studies support this idea, revealing that individuals with more mindsight skills show more interest and empathy toward others. Research has also clearly shown that mindsight supports not only internal and interpersonal wellbeing but also greater effectiveness and achievement in school and work.

Another quite poignant concern about mindsight came up one day when I was talking with a group of teachers. “How can you ask us to have children reflect on their own minds?” one teacher said to me. “Isn’t that opening a Pandora’s box?” Recall that when Pandora’s box was opened, all the troubles of humanity flew out. Is this how we imagine our inner lives or the inner lives of our children? In my own experience, a great transformation begins when we look at our minds with curiosity and respect rather than fear and avoidance. Inviting our thoughts and feelings into awareness allows us to learn from them rather than be driven by them. We can calm them without ignoring them; we can hear their wisdom without being terrified by their screaming voices. And as you will see in some of the stories in this book, even surprisingly young children can develop the ability to pause and make choices about how to act when they are more aware of their impulses.

HOW DO WE CULTIVATE MINDSIGHT?

Mindsight is not an all-or-nothing ability, something you either have or don’t have. As a form of expertise, mindsight can be developed when we put in effort, time, and practice.

Most people come into the world with the brain potential to develop mindsight, but the neural circuits that underlie it need experiences to develop properly. For some, such as those with autism and related neurological conditions, the neural circuits of mindsight may not develop well even with the best caregiving. In most children, however, the ability to see the mind develops through everyday interactions with others, especially through attentive communication with parents and caregivers. When adults are in tune with a child, when they reflect back to the child an accurate picture of his internal world, he comes to sense his own mind with clarity. This is the foundation of mindsight. Neuroscientists are now identifying the circuits of the brain that participate in this intimate dance and exploring how a caregiver’s attunement to the child’s internal world stimulates the development of those neural circuits.

If parents are unresponsive, distant, or confusing in their responses, however, their lack of attunement means that they cannot reflect back to the child an accurate picture of the child’s inner world. In this case, research suggests, the child’s mindsight lens may become cloudy or distorted. The child may then be able to see only part of the sea inside, or see it dimly. Or the child may develop a lens that sees well but is fragile, easily disrupted by stress and intense emotions.

The good news is that whatever our early history, it is never too late to stimulate the growth of the neural fibers that enable mindsight to flourish. You’ll soon meet a ninety-two-year-old man who was able to overcome a painful and twisted childhood to emerge a mindsight maven. Here we see living evidence for another exciting discovery of modern neuroscience: that the brain never stops growing in response to experience. And this is true for people with happy childhoods, too. Even if we had positive relationships with our caregivers and parents early on-and even if we write books on the subject, we can continue as long as we live to keep developing our vital seventh sense and promoting the connections and integration that are at the heart of wellbeing.

We’ll begin our journey in part 1 by exploring situations in which the vital skills of mindsight are absent. These stories reveal how seeing the mind clearly and being able to alter how it functions are essential elements in the path toward wellbeing. Part 1 is the more theoretical section of the book, where I explain the basic concepts, give readers an introduction to brain science, and offer working definitions of the mind and mental health. Since I know that my readers will come from a wide variety of backgrounds and interests, I realize that some of you may want to skim or even skip much of that material in order to move directly to part 2.

In part 2, we’ll dive deeply into stories from my practice that illustrate the steps involved in developing the skills of mindsight. This is the section of the book in which I share the knowledge and practical skills that will help people understand how to shape their own minds toward health. At the very end of the book is an appendix outlining the fundamental concepts and a set of endnotes with the scientific resources supporting these ideas.

Our exploration of mindsight begins with the story of a family that changed my own life and my entire approach to psychotherapy. Looking for ways to help them inspired me to search for new answers to some painful questions about what happens when mindsight is lost. It also led to my search for the techniques that can enable us to reclaim and recreate mindsight in ourselves, our children, and our communities. I hope you’ll join me on this journey into the inner sea. Within those depths awaits a vast world of possibility.

PART I

THE PATH TO WELLBEING: MINDSIGHT ILLUMINATED

1. A BROKEN BRAIN, A LOST SOUL The Triangle of WellBeing

Barbara’s family might never have come for therapy if seven year old Leanne hadn’t stopped talking in school. Leanne was Barbara’s middle child, between Amy, who was fourteen, and Tommy, who was three. They had all taken it hard when their mother was in a near fatal car accident. But it wasn’t until Barbara returned home from the hospital and rehabilitation center that Leanne became “selectively mute.” Now she refused to speak with anyone outside the family, including me.

In our first weekly therapy sessions, we spent our time in silence, playing some games, doing pantomimes with puppets, drawing, and just being together. Leanne wore her dark hair in a single jumbled ponytail, and her sad brown eyes would quickly dart away whenever I looked directly at her. Our sessions felt stuck, her sadness unchanging, the games we played repetitive. But then one day when we were playing catch, the ball rolled to the side of the couch and Leanne discovered my video player and screen. She said nothing, but the sudden alertness of her expression told me her mind had clicked on to something.

The following week Leanne brought in a videotape, walked over to the video machine, and put it into the slot. I turned on the player and her smile lit up the room as we watched her mother gently lift a younger Leanne up into the air, again and again, and then pull her into a huge, enfolding hug, the two of them shaking with laughter from head to toe. Leanne’s father, Ben, had captured on film the dance of communication between parent and child that is the hallmark of love: We connect with each other through a give-and-take of signals that link us from the inside out. This is the joy filled way in which we come to share each other’s minds.

Next the pair swirled around on the lawn, kicking the brilliant yellow and burnt-orange leaves of autumn. The mother-daughter duet approached the camera, pursed lips blowing kisses into the lens, and then burst out in laughter. Five-year-old Leanne shouted, “Happy birthday, Daddy!” at the top of her lungs, and you could see the camera shake as her father laughed along with the ladies in his life. In the background Leanne’s baby brother, Tommy, was napping in his stroller, snuggled under a blanket and surrounded by plush toys. Leanne’s older sister, Amy, was off to the side engrossed in a book.

“That’s how my mom used to be when we lived in Boston,” Leanne said suddenly, the smile dropping from her face. It was the first time she had spoken directly to me, but it felt more like I was overhearing her talk to herself. Why had Leanne stopped talking?

It had been two years since that birthday celebration, eighteen months since the family moved to Los Angeles, and twelve months since Barbara suffered a severe brain injury in her accident, a head-on collision. Barbara had not been wearing her seat belt that evening as she drove their old Mustang to the local store to get some milk for the kids. When the drunk driver plowed into her, her forehead was forced into the steering wheel. She had been in a coma for weeks following the accident.

After she came out of the coma, Barbara had changed in dramatic ways. On the videotape I saw the warm, connected, and caring person that Barbara had been. But now, Ben told me, she “was just not the same Barbara anymore.” Her physical body had come home, but Barbara herself, as they had known her, was gone.

During Leanne’s next visit I asked for some time alone with her parents. It was clear that what had been a close relationship between Barbara and Ben was now profoundly stressed and distant. Ben was patient and kind with Barbara and seemed to care for her deeply, but I could sense his despair. Barbara just stared off as we talked, made little eye contact with either of us, and seemed to lack interest in the conversation. The damage to her forehead had been repaired by plastic surgery, and although she had been left with motor skills that were somewhat slow and clumsy, she actually looked quite similar, in outward appearance, to her image on the videotape. Yet something huge had changed inside.

Wondering how she experienced her new way of being, I asked Barbara what she thought the difference was. I will never forget her reply: “

Well, I guess if you had to put it into words, I suppose I’d say that I’ve lost my soul.”

Ben and I sat there, stunned. After a while, I gathered myself enough to ask Barbara what losing her soul felt like.

“I don’t know if I can say any more than that,” she said flatly. “It feels fine, I guess. No different. I mean, just the way things are. Just empty. Things are fine.”

We moved on to practical issues about care for the children, and the session ended.

A DAMAGED BRAIN

It wasn’t clear yet how much Barbara could or would recover. Given that only a year had passed since the accident, much neural repair was still possible. After an injury, the brain can regain some of its function and even grow new neurons and create new neural connections, but with extensive damage it may be difficult to retrieve the complex abilities and personality traits that were dependent on the now destroyed neural structures.

Neuroplasticity is the term used to describe this capacity for creating new neural connections and growing new neurons in response to experience. Neuroplasticity is not just available to us in youth: We now know that it can occur throughout the lifespan. Efforts at rehabilitation for Barbara would need to harness the power of neuroplasticity to grow the new connections that might be able to reestablish old mental functions. But we’d have to wait awhile for the healing effects of time and rehabilitation to see how much neurological recovery would be possible.

My immediate task was to help Leanne and her family understand how someone could be alive and look the same yet have become so radically different in the way her mind functioned. Ben had told me earlier that he did not know how to help the children deal with how Barbara had changed; he said that he could barely understand it himself. He was on double duty, working, managing the kids’ schedules, and making up for what Barbara could no longer do. This was a mother who had delighted in making homemade Halloween costumes and Valentine’s Day cupcakes. Now she spent most of the day watching TV or wandering around the neighborhood. She could walk to the grocery store, but even with a list she would often come home empty-handed. Amy and Leanne didn’t mind so much that she cooked a few simple meals over and over again. But they were upset when she forgot their special requests, things they’d told her they liked or needed for school. It was as if nothing they said to her really registered.

As our therapy sessions continued, Barbara usually sat quietly, even when she was alone with me, although her speech was intact. Occasionally she’d suddenly become agitated at an innocent comment from Ben, or yell if Tommy fidgeted or Leanne twirled her ponytail around her finger. She might even erupt after a silence, as if some internal process was driving her. But most of the time her expression seemed frozen, more like emptiness than depression, more vacuous than sad. She seemed aloof and unconcerned, and I noticed that she never spontaneously touched either her husband or her children. Once, when three-year-old Tommy climbed onto her lap, she briefly put her hand on his leg as if repeating some earlier pattern of behavior, but the warmth had gone out of the gesture.

When I saw the children without their mother, they let me know how they felt. “She just doesn’t care about us like she used to,” Leanne said. “And she doesn’t ever ask us anything about ourselves,” Amy added with sadness and irritation. “She’s just plain selfish. She doesn’t want to talk to anyone anymore.” Tommy remained silent. He sat close to his father with a drawn look on his face.

Loss of someone we love cannot be adequately expressed with words. Grappling with loss, struggling with disconnection and despair, fills us with a sense of anguish and actual pain. Indeed, the parts of our brain that process physical pain overlap with the neural centers that record social ruptures and rejection. Loss rips us apart.

Grief allows you to let go of something you’ve lost only when you begin to accept what you now have in its place. As our mind clings to the familiar, to our established expectations, we can become trapped in feelings of disappointment, confusion, and anger that create our own internal worlds of suffering. But what were Ben and the kids actually letting go of? Could Barbara regain her connected way of being? How could the family learn to live with a person whose body was still alive, but whose personality and “souI”, at least as they had known her, were gone?

“YOU-MAPS” AND “ME-MAPS”

Nothing in my formal training, whether in medical school, pediatrics, or psychiatry, had prepared me for the situation I now faced in my treatment room. I’d had courses on brain anatomy and on brain and behavior, but when I was seeing Barbara’s family, in the early 1990s, relatively little was known about how to bring our knowledge of such subjects into the clinical practice of psychotherapy. Looking for some way to explain Barbara to her family, I trekked to the medical library and reviewed the recent clinical and scientific literature that dealt with the regions of the brain damaged by her accident.

Scans of Barbara’s brain revealed substantial trauma to the area just behind her forehead; the lesions followed the upper curve of the steering wheel. This area, I discovered, facilitates very important functions of our personality. It also links widely separated brain regions to one another, it is a profoundly integrative region of the brain.

The area behind the forehead is a part of the frontal lobe of the cerebral cortex, the outermost section of the brain. The frontal lobe is associated with most of our complex thinking and planning. Activity in this part of the brain fires neurons in patterns that enable us to form neural representations, “maps” of various aspects of our world. The maps resulting from these clusters of neuronal activity serve to create an image in our minds. For example, when we take in the light reflected from a bird sitting in a tree, our eyes send signals back into our brain, and the neurons there fire in certain patterns that permit us to have the visual picture of the bird.

Somehow, in ways still to be discovered, the physical property of neurons firing helps to create our subjective experience, the thoughts, feelings, and associations evoked by seeing that bird, for example. The sight of the bird may cause us to feel certain emotions, to hear or remember its song, and even to associate that song with ideas such as nature, hope, freedom, and peace. The more abstract and symbolic the representation, the higher in the nervous system it is created, and the more forward in the cortex.

The prefrontal cortex, the most damaged part of the frontal lobe of Barbara’s brain, makes complex representations that permit us to create concepts in the present, think of experiences in the past, and plan and make images about the future. The prefrontal cortex is also responsible for the neural representations that enable us to make images of the mind itself. I call these representations of our mental world “mindsight maps.” And I have identified several kinds of mindsight maps made by our brains.

The brain makes what I call a “me-map” that gives us insight into ourselves, and a “you-map” for insight into others. We also seem to create “we-maps,” representations of our relationships. Without such maps, we are unable to perceive the mind within ourselves or others. Without a me-map, for example, we can become swept up in our thoughts or flooded by our feelings. Without a you-map, we see only others’ behaviors, the physical aspect of reality, without sensing the subjective core, the inner mental sea of others. It is the you-map that permits us to have empathy. In essence, the injury to Barbara’s brain had created a world without mindsight. She had feelings and thoughts, but she could not represent them to herself as activities of her mind. Even when she said she’d “lost her soul,” her statement had a bland, factual quality, more like a scientific observation than a deeply felt expression of personal identity. (I was puzzled by that disconnect between observation and emotion until I learned from later studies that the parts of our brain that create maps of the mind are distinct from those that enable us to observe and comment on self-traits such as shyness or anxiety or, in Barbara’s case, the lack of a quality she called “soul.”)

In the years since I took Barbara’s brain scans to the library, much more has been discovered about the interlinked functions of the prefrontal cortex. For example, the side of this region is crucial for how we pay attention; it enables us to put things in the “front of our mind” and hold them in awareness. The middle portion of the prefrontal area, the part damaged in Barbara, coordinates an astonishing number of essential skills, including regulating the body, attuning to others, balancing emotions, being flexible in our responses, soothing fear, and creating empathy, insight, moral awareness, and intuition. These were the skills Barbara was no longer able to recruit in her interactions with her family.

I will be referring to, and expanding on, this list of nine middle prefrontal functions throughout our discussion of mindsight. But even at first glance, you can see that these functions are essential ingredients for wellbeing, ranging from bodily processes such as regulating our hearts to social functions such as empathy and moral reasoning.

After Barbara emerged from her coma, her impairments had seemed to settle into a new personality. Some of her habits, such as what she liked to eat and how she brushed her teeth, remained the same. There was nothing significantly changed in how her brain mapped out these basic behavioral functions. But the ways in which she thought, felt, behaved, and interacted with others were profoundly altered. This affected every detail of daily life, right down to Leanne’s crooked ponytail. Barbara still had the behavioral moves necessary to fix her daughter’s hair, but she no longer cared enough to get it right.

Above all, Barbara seemed to have lost the very map-making ability that would enable her to honor the reality and importance of her own or others’ subjective inner lives. Her mindsight maps were no longer forming amid the now jumbled middle prefrontal circuitry upon which they depended for their creation. This middle prefrontal trauma had also disrupted the communication between Barbara and her family, she could neither send nor receive the connecting signals enabling her to join minds with the people she had loved most.

Ben summed up the change: “She is gone. The person we live with is just not Barbara.”

A TRIANGLE OF WELLBEING: MIND, BRAIN, AND RELATIONSHIPS

The videotape of Ben’s birthday had revealed a vibrant dance of communication between Barbara and Leanne. But now there was no dance, no music keeping the rhythm of two minds flowing into a sense of a “we.” Such joining happens when we attune to the internal shifts in another person, as they attune to us, and our two worlds become linked as one. Through facial expressions and tones of voice, gestures and postures, some so fleeting they can be captured only on a slowed-down recording, we come to “resonate” with one another. The whole we create together is truly larger than our individual identities. We feel this resonance as a palpable sense of connection and aliveness. This is what happens when our minds meet.

A patient of mine once described this vital connection as “feeling felt” by another person: We sense that our internal world is shared, that our mind is inside the other. But Leanne no longer “felt felt” by her mom.

The way Barbara behaved with her family reminded me of a classic research tool used to study infant-parent communication and attachment. Called the “still-face” experiment, it is painful both to participate in and to watch.

A mother is asked to sit with her four-month-old infant facing her and when signaled, to stop interacting with her child. This “still” phase in which no verbal or nonverbal signals are to be shared with the child is profoundly distressing. For up to three minutes, the child attempts to engage the now nonresponsive parent in a bid for connection. At first the child usually amps up her signals, increasing smiles, coos, eye contact. But after a period of continuing nonresponse, she becomes agitated and distressed, her organized bids for connection melting into signs of anguish and outrage. She may then attempt to soothe herself by placing her hand in her mouth or pulling at her clothes. Sometimes researchers or parents call off the experiment at this time, but sometimes it goes on until the infant withdraws, giving up in a kind of despondent collapse that looks like melancholic depression. These stages of protest, self-soothing, and despair reveal how much the child depends upon the attuned responses of a parent to keep her own internal world in equilibrium.

We come into the world wired to make connections with one another, and the subsequent neural shaping of our brain, the very foundation of our sense of self, is built upon these intimate exchanges between the infant and her caregivers. In the early years this interpersonal regulation is essential for survival, but throughout our lives we continue to need such connections for a sense of vitality and well-being.

. . .

from

Mindsight, change your brain and your life

by Daniel J. Siegel MD

get it at Amazon.com