Mind-Body Medicine

If the mind, that rules the body, ever so far forgets itself as to trample on its slave, the slave is never generous enough to forgive the injury, but will rise and smite the oppressor. Henry Wadsworth Longfellow

In the 1600s, philosopher René Descartes gave the world the concept of mind-body dualism. The body was composed of physical substance, visible, weighable and measurable. The mind was something else. Over the next three centuries, as scientists deconstructed the body to discover its secrets, the mind reclaimed its place as an inseparable part of the body. (Soul is another matter, not open to scientific inquiry.) Some rudimentary examples of the mind-body connection are the blush of embarrassment, the adrenaline rush following a near miss accident or the receipt of bad news, and the cotton mouth that accompanies emotional distress. The mind perceives and the body reacts. The mind decides and the body acts. Not only are mind and body inseparable, but most often the body responds to a vast subconscious system rather than to the aware part of the mind known as consciousness.

The powerful subconscious mind

In Sigmund Freud’s (1856-1939) introductory rendering, the unconscious mind was a cauldron of seething resentments that gave rise to neurotic behaviors and bad dreams. Modern research softened this view and today the unconscious mind seems more like an executive secretary who relieves the boss of routine work. It sorts through incoming information, keeps track of the environment and runs the motor system that operates the body, all with such subtlety that much of the time you, the boss, think you are in charge. But if you have an electrode placed in your brain recording the action of the nerve cells that put your arm in motion, the recording will show activation of those cells before you are consciously aware of your decision to reach for that candy bar. Before you “know” it, the choice has been made in your subconscious mind. But this doesn’t mean we are automatons – after all, you can still decide not to eat the candy.

The neuropeptide network: connection of mind to body

The subconscious mind may have even more power than we suspect. The same chemicals that transmit information in the brain are found in virtually every organ of the body. This neuropeptide network, discovered around 1980, bridges the gap between the brain and the body, making a psycho(mind)somatic(body) connection. Since the time of Freud, the word psychosomatic has a bad reputation, often synonymous with “hysterical” or “without physical cause.” All symptoms, however, are technically psychosomatic because they arise in the body and are perceived in the mind. The discovery of the chemical interplay between brain and other body organs forces us to consider whether the flow of information goes the other way too. Can the mind cause diseases to happen? Can it help heal disease?

Placebo effect

Eastern medical practices have always regarded the body/mind as one entity. Since the 1950s, Western medicine has acknowledged the mind’s influence over the body by taking into account the placebo effect in studies of new treatments. The placebo effect is the relief that happens when a patient believes he has received a real treatment, despite the treatment being a sham. The phenomenon may reflect the power of belief or it may reflect the fact that many disease processes get better on their own – the only way to tell is to add a third, no-treatment group to each study. The fact that the placebo effect occurs in more than 30% of patients in many studies demonstrates the mind’s significant role in disease and health.

Conventional medicine takes a look at the alternatives

Western medicine’s gradual acceptance the mind/body connection culminated in the establishment of a National Center for Complementary and Alternative Medicine (NCCAM) within the National Institute of Health (http://nccam.nih.gov/) in 1991. The center conducts controlled studies on subjects such as the effect of regular meditation on chronic pain, anxiety, high blood pressure, cholesterol, health care use, substance abuse, post-traumatic stress syndrome in Vietnam veterans. It offers objective descriptions of Eastern medical theories which for which science has no proof. Part of the NCCAM’s mission is also to educate the public to become discerning customers within the vast alternative care and wellness industries that capitalize on the tantalizing possibility that good health may be a byproduct the “right” frame of mind.

The alternative and the conventional medical industries operate side-by-side, sometimes, but not always complementing each other. Conventional medicine is increasingly fragmented, with care delivered on an organ by organ basis. The whole person and his mind- body relationship can get lost in the process; unwanted side effects occur, and sometimes treatments hurt more than they help. But conventional methods save many lives and provide much needed comfort. Alternative practices that teach wellness via mind-body wholeness also do much good, mostly in preventing disease by emphasizing the back- to- basics factors: nutrition, sleep, exercise, relaxation, relationships and environment. Importantly, most of them do no harm except if they keep patients from seeking conventional help when necessary.

The importance of habits

In this century, the commercial spotlight is trained on the role of the mind in sickness and in health, which may obscure an important fact: most of the mind’s effects on health are subconscious, embedded in long years of mental and physical habits and not amenable to conscious adjustment over short periods of time. The right thinking and attitudes will help only insofar as they can work their way into the subconscious underpinnings of the mind by the diligent practice that leads to habit formation. Whether the mind-body practices are called meditation, yoga, Tai-chi, guided imagery, art and music therapy, biofeedback or acupuncture, they should be undertaken as long term projects requiring persistence, just like all those other low-tech habits that promote good health. The mind may be the body’s master, but it cannot change the laws of nature that govern all biologic systems. There are no quick and easy fixes.

Interesting Reading

Blink: The Power of Thinking Without Thinking, Malcolm Gladwell, Little Brown, Boston, 2005

Anatomy of an Illness as Perceived by the Patient, Norman Cousins and Rene Dubos, W.W. Norton & Co., NY, 1979.

Posted by medical plaintalk

Physician turned medical writer.

Pain in the Neck: More than a Metaphor

The cervical spine is a slender stack of fragile bones that balances the 15-17 lb. skull atop the body. Each bone has a round thick body and an arch of thinner bone projecting from its backside. The knobs of bone you feel in your own spine are just the tips of each bony arch, called the spinous processes. A wide array of ligaments, tendons and muscles hold the vertebrae together, and thirty-seven separate joints allow the head to move through a wide range of finely calibrated movements. Arthritic changes accumulate in most necks over the years, particularly in the lower regions where most movement takes place. In scans of people over 50, almost all will show some degree of wear and tear change in the lower vertebrae.

Aging changes in bones neck bones and ligaments

Wear and tear takes form of thickening of bony edges of the vertebrae and degeneration of the discs between them. These changes may put pressure on the nerves that exit from the spinal cord through bony canals between the stacked vertebrae, and occasionally on the spinal cord itself, which travels through a canal formed by the centers of the stacked arches. The ligaments that line this canal also thicken with age and create ridges inside the canal that press on the spinal cord. Degenerative changes contribute to episodic neck pain, and sometimes to more severe symptoms that require medical attention.

Why the neck hurts

The neck is second only to the low back pain as a common source of pain. Most neck pain is benign and episodic, coming from muscles, tendons, ligaments and joints. Painful episodes usually occur after some unaccustomed activity, such as painting a ceiling or suddenly twisting or bending the neck, or after sustaining a neck position for an unusual amount of time – for example, over a long drive. Even an unaccustomed head position occasioned by wearing new bifocals can trigger a bout of stiff neck.

Other symptoms

Neck pain requires medical attention when it persists or is associated with neurological symptoms in the arms or legs. Sensory symptoms like numbness or tingling in fingers and arms are quite common when underlying degenerative changes are present in the neck. While they may indicate pressure on nerve roots, sensory symptoms also occur when neck pain is simply a reflection of tight muscles and ligaments. The same nerve fibers that carry pain sensations also carry sensory messages and pain seems to have a kind of spillover effect into other sensory pathways. That same spillover effect also can also cause a wide variety of sensory and pain symptoms in the head. Headaches, pain in the back of the head, and even eye pain can be attributed to some neck problems.

Red flag symtoms: weakness and bladder control problems

Neurological symptoms indicating trouble in the motor nerves or in the spinal cord, in the setting of neck pain and degenerative changes, often indicate a more serious degree of trouble. Weakness in arm or hand muscles may mean that motor nerve roots are being squeezed as they exit the spinal column. Weakness, fatigue and stiffness in the legs, and new trouble with bladder control are symptoms of pressure on the spinal cord. Sensory problems usually recover when the painful cause is successfully treated, but motor nerves and the spinal cord are more fragile and less reliably improve even after surgical decompression. When motor problems are part of the picture, medical attention should be sought sooner rather than later.

Diagnosis

Careful history and physical examination are crucial to the proper diagnosis. Diagnosis of a painful, stiff neck begins with taking a history. Most people do this before they ever see a doctor. What did I do yesterday? Did I sleep sitting up on a plane? In a strange bed? What movement makes this worse? What makes it better? Do I have any other funny symptoms? Most people also do the right thing by avoiding maneuvers that cause pain, applying either heat or ice, and even trying a soft cervical collar, which does not really immobilize the neck, but gives the head a temporary place to rest. Most often the neck improves and no medical attention is required.

Medical attention, when sought, should begin with a very detailed history, not only of the current episode, but of past problems, and other medical problems which might cause or complicate neck problems. Important facts include history of trauma, rheumatoid arthritis, cancer, vascular disease, infections and past radiation treatment. Evaluation then moves to a physical examination, not only of the neck, but a general physical exam and a neurological exam. Imaging studies, electrical evaluation of nerves and muscles, and blood work follow under some circumstances. These include symptoms persisting more than 6 weeks, severe symptoms involving a single joint, presence of fever and weight loss, suspected fracture or dislocation, associated neurological symptoms or findings, and failure of simple treatments over a course of 4-6 weeks.

Treatment

Conservative measures are effective for treating common types of neck pain, especially if carried out conscientiously. Massage, hot or cold applications, topical pain relieving and muscle relaxing creams and intermittent use of aspirin or non-steroidal anti-inflammatory agents are all helpful but they are play a only a supporting role. The major goal is to correct posture, not only of the neck, but of the whole spine, by strengthening and stretching of the muscles that support the spine and those that suspend and move the shoulders. An effective exercise program, under supervision of a qualified physical therapist, involves the entire spine, as well as legs and arms. In addition, supporting the neck’s normal curve in sleep with a good cervical pillow is crucial.

When conservative measures fail, more invasive means of treatment such as injections of anti-inflammatory and analgesic drugs are often added. Surgical treatment of neck pain problems is reserved for situations in which a nerve root or the spinal cord must be decompressed, or ones in which pain is so severe and unremitting that fusing the bones to decrease movement of the neck is considered the only option. In comparison to the number of people with neck pain at some point in their lives, surgically treated neck complaints are actually few and far between. Considering how much the neck moves, how much wear and tear it sustains and how little protection it has, this is a remarkable measure of its resilience.

Posted by medical plaintalk

Physician turned medical writer.

Alzheimer’s Disease: A Power Failure?

Like Willy Sutton, the bank robber famed for his explanation of why he robbed banks (because that’s where the money is), Alzheimer’s disease researchers have aimed most of their efforts at the well-known, visible pathology of the disease, the collections of debris scattered among the dying cells in the brains of patients suffering from the dementing illness. Made of a protein known called beta-amyloid, these plaques are the cause of the progressive death of brain cells and consequent loss of mental function – or so it has been thought. Research focus on amyloid plaques has been disappointing, though, yielding neither effective treatments nor preventive strategies. Moreover, the dramatic rise in the incidence of Alzheimer’s disease (AD), from 2% of people over age 85 in 1960 to 50% in 2000 indicates that something else is in play, something other than bad genetic luck that supposedly causes beta-amyloid to accumulate and nerve cells to die.

Energy production in the brain

As attention has turned to other potential causes of AD, older research findings seemingly unrelated to AD have assumed new importance, particularly discoveries related to brain energy metabolism. The preferred fuel for the brain is glucose. Until the 1980s, researchers thought that the brain, unlike other organs, did not need use the hormone insulin to allow glucose to enter its cells. But in the 1970s insulin receptors were discovered in brain cells and insulin was found in the spinal fluid, implying that the brain did indeed use the hormone. Because progressive resistance to insulin and difficulty getting glucose into cells to provide energy are the hallmarks of type 2 diabetes, and because the rise in AD incidence paralleled rising rates of type 2 diabetes in the last few decades, researchers began to wonder if AD might be rooted in insulin resistance and impaired energy production in brain cells. Insulin resistance in the brain might also explain the results of glucose metabolism studies in the brains of people at high genetic risk for AD, showing as much as 25% decrease in the use of glucose in areas concerned with memory and learning – long before any symptoms suggestive of AD have appeared.

Insulin resistance

By 2005, the idea that insulin resistance in the brain plays a significant role in the development of AD gained traction. Since not all type 2 diabetics get AD and not all AD patients have type 2 diabetes, insulin resistance cannot be the sole cause of AD. But a high blood insulin level is one of the two biggest risk factors for the disease. The other is a genetic factor – the gene for the E4 version of a protein called apolipoprotein B (apoB). Like insulin, apoB’s function is moving the building blocks for energy production into place in the various cells of the body. ApoB is like a delivery vehicle, packed with fats and cholesterol which are necessary for building the cellular machinery in the brain and providing fatty fuel for use when glucose is unavailable.

The tie between glucose, insulin and amyloid

Does impairment of glucose metabolism in the brain have any relationship to the classic pathological components of the disease – the amyloid plaques littering the brain, the destruction of nerve cell architecture, and the non-specific inflammatory changes? There are tantalizing clues. In the brain amyloid protein is a normal waste product. What is not normal is its accumulation in clumps around nerve cells. Beta-amyloid is usually broken down by an enzyme called IDE, insulin destroying enzyme. IDE breaks down insulin much more readily than it does amyloid proteins and when insulin is present in high amounts, the amyloid waits longer to be cleaned up and precipitates out of solution, forming clumps. Uncleared amyloid also prevents insulin from attaching to nerve cells to let more glucose in, depriving them of fuel.

Competition for IDE may not explain beta-amyloid accumulation completely, but it is a link between insulin, glucose metabolism and AD. In addition, high levels of glucose in all parts of the body prompt the development of abnormal collections of proteins/glucose combinations called advanced glycation products which trigger inflammatory damage to tissues in all organs. The brain is no exception.

A link between poor sleep and AD?

Sleep is another subject beginning to gain attention in the prevention and treatment of AD. Lack of good sleep contributes to the development of the metabolic syndrome, including type 2 diabetes, though disruption of normal hormonal rhythms. In normal people and in people with sleep apnea, sleep deprivation produces measurable impairments in working memory, thinking speed, attention, vigilance, and higher cognitive functions – the same functions affected by dementing illnesses such as AD.

Reasons for optimism

Do changing theories about AD have any practical consequences? Indeed. First, there is more reason for optimism about the future. If AD rates have risen because of changing dietary habits and lifestyles, we can change them again. The factors known to produce the metabolic syndrome are weight gain, lack of exercise and poor diet. Regular exercise is recognized as a deterrent to the development of AD. Some people are beginning to feel that the low fat dietary recommendations must also be changed since they have resulted in diets high in processed foods and carbohydrates, and low in foods with high amounts of antioxidants which counter inflammation. Fat metabolism, abnormal in the metabolic syndrome, is also important in the brain, which contains 25% of the body’s cholesterol. It needs sufficient healthy fats in the diet for normal function.

The second practical implication of the changing view of AD is the application of known drug treatments for type 2 diabetes, both for attempted prevention and for treatment of AD. Clinical studies in AD patients are already under way, using medications that improve insulin resistance. Intranasal insulin has also been tried. It is delivered directly into the brain, without fear of lowering body glucose levels and has shown some promise in improving AD symptoms. These approaches are entirely new and evidence of shifting focus in research. If Willy Sutton were an AD researcher he would be changing his targets.

Terminal Lucidity and Lucid Intervals

Caregivers of Alzheimer’s patients have long reported episodes of the patient returning briefly to “themselves,” for periods of hours to days. Some dramatic cases of such returns have been reported in the terminal phases of life. All of these cases have fallen into the “we don’t know why that happens” category of clinical observations. The concept of brain cells failing to function because of lack of energy is one that fits the appearance of lucid intervals better than a theory of the disease that implicates cellular destruction alone as the underlying cause of symptoms.

Arch Gerontol Geriatr. 2012 Jul-Aug;55(1):138-42. doi: 10.1016/j.archger.2011.06.031. Epub 2011 Jul 20. Terminal lucidity: a review and a case collection.

Nahm M¹, Greyson B, Kelly EW, Haraldsson E.

Posted by medical plaintalk

Physician turned medical writer.

Parkinson’s Disease: a New Research Era

In the 1980s, a designer street drug* derived from the narcotic Demerol appeared in California and caused immediate and irreversible Parkinson’s disease in the young heroin addicts who used it. At that time, scientific research into Parkinson’s disease had plateaued. The excitement surrounding the use of the drug L-Dopa to treat the disease in the 1960s had faded as the long term problems with its use became apparent. But the Demerol derivative, called MPTP (short for 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) gave researchers a new tool. For the first time in history they had the ability to create an animal model of the disease. A new flurry of research began, providing hope for all patients with the progressive and debilitating disease.

The clinical picture

Most people know someone who has Parkinson’s disease because it is a relatively common ailment, affecting approximately one out of every 100 people over the age of 65 in all parts of the world. To doctors, Parkinson’s disease is a “doorway diagnosis,” meaning that when all of its core components have developed, and there are no unusual features, the diagnosis can be made from the first sight of the patient.

The typical Parkinsonian patient sits quietly, with none of the spontaneous gestures or shifting of the trunk or extremities that most people exhibit when confined to a chair. His face is smooth and expressionless, and he looks slightly wide-eyed, blinking only 5-10 times a minute, about half the normal frequency. Both seated and standing, he has a forward flexed posture of head neck and trunk. His hands shake rhythmically unless he is using them, a problem known as a resting tremor.

When he gets up to walk he does not make preliminary movements to adjust his foot position. Walking seems hard to start, but once started, his upper body may move ahead of his feet, and his steps “hurry up” to catch up to the body, a “festinating” gait. His gait is simultaneously “shuffling,” since his feet barely clear the floor. His elbows are bent with arms held slightly forward of his body. They do not swing as he walks. Should someone tap him on the chest, he does not make any quick postural adjustments such as stepping back with one foot, and he may topple over if someone does not catch him.

His voice is soft and monotonous, and his words are hurried. While he has normal muscular strength, he cannot generate any speed, so an action like clapping appears weak. All of his motions are slow, a phenomenon called bradykinesia.

Parkinson disease begins most commonly in the sixth decade and is rare before age thirty. Many of the characteristics of the disease, in minor form, are also characteristics elderly people: forward flexed postures, shorter step lengths, softer voices, and slower, less forceful movements. But these signs in people who have Parkinson disease appear earlier and progress enough to impair normal activities within about 10 years. Parkinsonian symptoms can also be side effects of drugs used in the treatment of some psychiatric disorders.

Where the symptoms originate

The symptoms of Parkinson’s disease come from nerve cell death a tiny area in the brain stem called the substantia nigra. These cells contain neuromelanin, a substance similar to the pigment in the skin, and they produce a chemical neurotransmitter called dopamine. When the cells die, the substantia nigra loses its black color and dopamine levels decline. The drugs that improve symptoms in Parkinson’s disease either raise dopamine levels or make it more effective at the junction between nerve cells where dopamine works to transmit information from cell to cell.

Replacing the lost dopamine

However, the pharmacologic treatment of Parkinson’s disease has limitations. Initially, the drugs that elevate dopamine levels work in most patients, but sooner or later they became less effective and dose increases produce unwanted movements called dyskinesias. The drugs also have a peculiar tendency to produce an “on-off effect,” causing symptoms to reappear random times. Nevertheless, L-Dopa (in the form of Sinemet) and drugs that improve dopamine’s actions (like Eldepryl) remain the mainstays of treatment, supplemented by a few other drugs that alter the levels of another brain chemical called acetylcholine. Drug treatment of Parkinson disease requires patience and close attention to timing of doses, with frequent adjustments of schedules. Since dietary protein can interfere with the drugs, many doctors also suggest confining dietary protein to the evening meal.

The limitations of pharmaceutical treatment spurred a number of different surgical procedures aimed at restoring balance to the complicated interplay of brain signals that, under normal circumstances, control balance, speed and fluidity of movement. These procedures involve destruction of tiny localized areas in deep centers of motor control (pallidotomy), or stimulation with tiny electrodes of other nearby areas. Implants of dopamine-producing fetal stem cells have caused devastating side effects in some patients and enthusiasm for this approach has waned.

How the ‘frozen addicts” advanced Parkinson’s research

Because Parkinson’s disease does not run in families, researchers have long suspected that it is triggered by some type of environmental factor. They have examined the role of neurotoxins such as heavy metals and fertilizers because Parkinson disease is more common in industrialized countries and also in agrarian areas, but they have never been able to pin blame on any specific substance. Now, though, they know that the California street drug MPTP destroys the dopamine producing cells in the substantia nigra by damaging their mitochondria, the power houses of all cells. Mitochondria are susceptible to damage by other toxins. They also contain DNA, with all its variations from person to person, perhaps explaining why some people might be more susceptible to toxic damage than others.

New ideas for treating the disease pharmacologically will eventually emerge from animal models of Parkinson’s disease. For interested readers, the medical mystery posed by the young people who developed Parkinson disease after using MPTP is recorded in a fascinating book, The Case of the Frozen Addicts. ** The research born from their tragic losses will someday help all Parkinsonian patients.

*a drug produced by modification of the chemical structure just enough to make it no longer identical to drug regulated by the FDA

** The Case of the Frozen Addicts, by J. William Langston & Jon Palfreman, New York, Pantheon, 1995.

Posted by medical plaintalk

Physician turned medical writer.

Concussion: Temporary Power Outage

One of the most dramatic conditions in medicine is the concussion – the total and immediate paralysis of brain function that follows a blow to the head. Typically, the victim loses consciousness and all reflexive muscle activity for seconds to moments. Blood pressure and heart rate may fall and breathing might stop, effects that are usually brief and unnoticed but which on rare occasion cause immediate death. As consciousness returns, the victim seems confused. He does not recall the fall or the blow. Depending on the seriousness of the injury, he suffers a variable period of time during which he remembers nothing new. He asks repetitive questions about what happened and may seem aggressive or out of character. Normality may reassert itself quickly after a concussion, but sometimes several weeks or months of irritability, insomnia, mood change, headaches, and dizziness follow. In other cases, a period of normality, the lucid interval, may be followed by headache, confusion and drowsiness, indicating more severe trauma to the brain and its surrounding tissues.

Concussion of some degree occurs in almost all “closed head injuries,” defined those in which there are no skull fractures or penetrating injuries to the brain. Depending on the trauma involved, symptoms vary from momentary stunning to prolonged coma, but the mechanism of initial paralysis of brain function is always the same. Understanding that mechanism makes it easier to understand delayed worsening and persistent symptoms that sometimes occur afterwards.

How concussions happen

Concussions happen because the brain has the consistency of Jello and is only loosely tethered inside the rigid skull, mainly at the base. When the head accelerates after a blow, or decelerates because of a fall, the brain keeps moving after the skull has stopped. First the cerebral hemispheres slam into the skull in one direction, and then they rebound in the opposite direction. The temporal lobes, where memories form, are particularly vulnerable to impact damage.

Loss of consciousness, however, comes from movement of the tiny brain stem, which emerges from beneath the two large cerebral hemispheres and connects them with the spinal cord. As the heavy cerebral hemispheres above move, the brainstem bends, rotating first in one direction and then in the other. Inside the midbrain, the top part of the brainstem, a group of cells called the reticular activating system reacts with shock and shuts down all communication between brain and body. The power failure lasts anywhere from seconds to weeks, depending on the degree of rotational force in the midbrain and the amount of stretching and shearing of nerve cell connections.

Added Problems

Prolonged symptoms, however , usually indicate more widespread damage to the brain in the form of contusions (bruises) and hemorrhages, which cause delayed swelling and worse symptoms. In addition, bleeding from small veins on the surface of the brain (subdural hemorrhage) or between the skull and the dura mater, the tough fibrous lining around the brain (epidural hemorrhage) can occur after seemingly minor concussions. The bleeding stretches, then ruptures more blood vessels, and the growing accumulation of blood puts increasing pressure on the brain. In 2009, the actress Natasha Richardson died from this kind of complication, soon after a relatively minor fall while skiing. Ronald Reagan suffered much slower development of a subdural accumulation of blood following a fall from a horse. Surgical evacuation of the accumulated blood returned him to normal.

After The Concussion

After a head injury, it is very important for the victim to be accompanied by someone who knows him, in order to alert medical personnel to subtle changes in personality or cognitive ability. Most people suffering loss of consciousness will undergo CT or MRI scans, though this is probably unnecessary in mild cases in which the victim has returned to normality quickly. But even after a normal scan, observation, including waking and checking the victim every few hours at night for the first 24 hours, is prudent. If confusion persists after a concussion, the victim should be hospitalized until it clears, and observed carefully after discharge for 24-48 hours.

Most post concussive symptoms like headache, insomnia, irritability and lightheadedness resolve over a few months, requiring only simple medications like ibuprofen and sensible habits such as avoiding alcohol, eating well, sleeping enough, exercising and managing stress.

Repetitive concussions over a lifetime, as suffered in a sport like boxing, clearly damage the brain, producing decline in memory and cognitive abilities, as well as slurred speech and motor symptoms resembling Parkinson’s disease. Recent research suggests that brain injuries may induce progressive change some brain proteins, producing, over a long period, an Alzheimer’s like deterioration in function. The recent attention to the long term effects of other sports related head injuries, especially in professional athletes, stems from this research.

Do Helmets Help

Do helmets protect people from concussions? Helmets do reduce brain damage from trauma in sports like biking and rock climing, but they do it by protecting the skull from fracturing. To dampen the movement of the brain within the skull – the mechanism of injury in concussion- the diameter of the helmet would have to be so large that it would be impossible to wear. I have heard many people express surprise about concussions they experienced while wearing helmets in sports like skiing. But if you understand that the skull stops moving in a fall before the brain inside does, you understand that, no, a helmet does not stop a concussion from happening.

Posted by medical plaintalk

Physician turned medical writer.

The Problem with Stress: No Fighting or Fleeing

…grant me the serenity
to accept the things I cannot change;
courage to change the things I can;
and wisdom to know the difference….

from The Serenity Prayer, by Reinhold Niebuhr

Picture an early human moving through the quiet forest, intent on the prey he’s tracking. His pace is steady and his mind focused. Suddenly a bear bursts through the trees. Emotional centers in primitive parts the hunter’s brain fire off threat messages which race through the sympathetic nervous system to his adrenal glands—little thumb size organs buried in fat and sitting on top of the kidneys. Almost instantly, each gland responds with a burst of adrenalin from its central core, the adrenal medulla. Danger also prompts his pituitary gland to pour out a big dose of adrenocorticotropin (ACTH), a hormone that speeds through the blood to the adrenal cortex, the outer 80% of the gland. In response, the gland releases cortisol, a powerful glucocorticoid hormone involved in energy regulation.

The hunter’s pulse and blood pressure shoot up. His airways dilate and he breathes faster. His vision narrows and sharpens. Anticipating action, his muscles and liver free glucose and fat from storage. By the time he races to a nearby tree to haul himself to safety, the cascade of neural and hormonal events has shifted his metabolism from quiet homeostasis (maintenance of normal function) to an active state designed for fleeing….or for fighting if the bear climbs too. When the bear loses interest and wanders away, our early man’s activated physiology reverts to routine functioning. He climbs down, resumes his methodical hunt and cooks his game over an open fire. From sundown to sunup, he sleeps.

Now consider a modern man as he rushes through his urban environment. He becomes anxious and then angry when his train is late. As he hails a cab he narrowly misses being hit by an oncoming car. Horns blare. He flops down in the back seat of the cab, fumbling for his ringing cell phone, only to hear that his boss is angry because he is late. Inside our overweight modern man’s body, early hunter physiology whips his adrenal glands into action – over and over and over. But he does not get to fight or flee. Worse yet, the threats in his environment do not lose interest and wander away. He will be on edge all day, and perhaps late into the night. After a few drinks, a few smokes, a fast food meal and some paperwork, he falls asleep in front of the TV, finally stumbling into bed in the wee hours of the morning. By 6AM he’s starting over, sleep-deprived.

The adrenal gland connection

In both early and modern humans, the brain-adrenal connection is heavily influenced by environment, genetic makeup, lifestyle and memory of previous experiences. We learn fear and make habits of emotional responses. While animal research can’t take into account human mental components of stress, it has provided useful physical insights, especially about the adrenal connection to chronic stress. Experiments in “rat micro-societies” refined the fight-or-flight concept and divided it into aggressive defense and passive defeat responses, an important distinction because each type activates different parts of the adrenal glands.

Rats responded with passive defeat when a task like pushing a lever sometimes produced food, sometimes didn’t, sometimes in one place, sometimes in another, and sometimes not at all. The consequences of the rats’ actions were uncontrollable and feedback didn’t help them learn. In these circumstances the adrenal cortex overproduced cortisol. If you think the passive defeat experiments resemble average life, then you’ll guess, correctly, that chronic stress in people might also trigger elevated cortisol levels.

Aggressive defense responses to the rat equivalent of being mugged, in contrast, activated primarily the adrenal medulla, which takes charge of the immediate activity necessary to survive a threat by producing an adrenalin rush – a burst of the hormones epinephrine and norepinephrine. In states of fear and/or anger, we experience this rush as rapid pulse, elevated blood pressure, increased breathing rate, flushing, pallor and dry mouth.

In our early hunter these adrenal responses are sequential. First comes the adrenalin rush which helps him survive. Following just behind, the adrenal cortex ramps up hormone production to help restore normality–to restock energy supplies, dampen pain and divert resources from routine activities.The system is designed for short bursts of danger, not for chronic immersion in mental stress.

The metabolic syndrome connection

Beginning in 2002, researchers began to correlate adrenal hormone abnormalities with the modern plague of the metabolic syndrome—abdominal obesity, insulin resistance, diabetes and high blood pressure, all reliable side effects of exposure to excessive cortisol, whether it comes from drugs like prednisone or from pituitary or adrenal gland diseases. (See note on Cushing’s disease below). No one thinks cortisol and stress are wholly responsible for our metabolic epidemic, but many hope that the stress connection will help lead to a solution.

Counteracting the stress response

Stress researchers uniformly conclude that short of retreating from the world, the only major defense that counteracts the effects of stress is regular physical activity which dissipates some of the energy mobilized for action. The best results come from superimposing physical activity on a lifestyle that accommodates enduring human needs: sufficient sleep, diet suitable for an ancient physiology, good social network and engagement in focused activity that has personal value. Even then, coping strategies are necessary.

A Note on Cushing’s Disease

The most dramatic demonstration of the results of too much cortisol occurs in patients with Cushing’s disease, usually caused by a pituitary gland tumor which overstimulates the adrenal cortex. In these patients, muscles are thin and weak, and excess weight is concentrated in the trunk and face and neck. Patients have red, jowly faces and skin scored by purplish stretch marks and poorly healed wounds. Bones are robbed of calcium and osteoporotic upper backs round forward under the characteristic “buffalo hump” of fat. The adrenal cortex hormones also have weak male hormone effects causing male pattern baldness and excess facial hair in women. The immune system is weakened and health is further damaged by diabetes, high blood pressure and heart disease.

Posted by medical plaintalk

Physician turned medical writer.

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