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Jan. 15, 2004 -- For the first time, researchers have linked a gene that regulates a specific chemical in the brain to a person's risk of alcoholism.

This new finding gives greater credence to theories that predisposition to alcoholism may be inherited as part of a general state of brain overexcitability, writers lead researcher Danielle M. Dick, PhD, a professor of psychiatry at Washington University School of Medicine in St. Louis.

Her report appears in the current issue of the journal Alcoholism: Clinical and Experimental Research.

Alcohol may normalize these overactive brain circuits, which would put a drinker at greater risk of alcohol abuse and dependence, she adds.

In fact, previous studies have identified a major brain chemical known as gamma-amino butyric acid (GABA) that is involved in many nerve pathways affecting alcohol abuse and dependence, writes Dick.

Many effects from alcohol involve GABA -- the difficulty walking, the lessened anxiety, the sleepiness, and even alcohol preference. GABA is also involved in alcohol withdrawal and in the craving for greater amounts of alcohol to soothe nervousness, she explains.

There are several versions of GABA genes. However, the role of these genes in alcohol abuse has been somewhat unclear, she writes.

Her newest study is the first to identify the specific gene variation linked with alcoholism.

Positron emission tomography (PET) shows different effects of depression treatments on the brain, according to the results of a study published in the January issue of the Archives of General Psychiatry. Patients who recover after cognitive behavioral therapy (CBT) show a pattern of brain changes that is distinct from that of patients who respond to paroxetine.

"When treating clinical depression we know that one type of treatment doesn't fit all. Our imaging study shows that you can correct the depression network along a variety of pathways," senior author Helen Mayberg, MD, formerly from the University of Toronto in Ontario, Canada, and currently with Emory University in Atlanta, Georgia, says in a news release. "Antidepressant drugs change the chemical balance in the brain through effects at very specific target sites. CBT also changes brain activity; it's just tapping into a different component of the same depression circuit board."

By modifying attention and memory functions, affective bias, and maladaptive information processing, CBT teaches patients cognitive strategies to reduce automatic reactivity to negative thoughts. Unlike this "top-down" approach, which focuses on cortical brain areas and uses thought processes to modulate abnormal mood states, drug therapy is considered a "bottom-up" approach because it alters neurochemistry in the brain stem and limbic regions driving basic emotional and circadian behaviors.

Of 17 adults with clinical depression who were not taking antidepressant drugs and who were enrolled in this study, 14 underwent a full course of CBT consisting of 15 to 20 individualized outpatient sessions. Mean improvement in Hamilton Depression Rating Scale score was 6.7 ± 4. As an independent, post-hoc comparison group, 13 paroxetine-treated responders also had PET scans.

PET scanning before beginning CBT and after the full course of therapy revealed that CBT targets many of the same limbic and cortical regions affected by paroxetine therapy. However, metabolism decreased in the limbic area and increased in the cortical area with paroxetine, whereas CBT was associated with limbic system increases in the hippocampus and dorsal cingulate regions, and with decreases in the dorsolateral, ventrolateral and medial orbital frontal, inferior temporal, and parietal cortex.

Each treatment also showed changes in unique brain regions supporting the top-down, bottom-up mechanisms of action for CBT versus paroxetine. The investigators suggest that CBT allows patients to suppress the thinking paradigm associated with dwelling on negative thoughts and attitudes, which is reflected in decreased activity in cortical regions.

Younger women who suffer
migraines may have a slightly higher stroke risk than other
women their age, but the risk may depend on the type and
frequency of women's early migraines, new research
suggests.

There is some evidence that, while strokes
are rare among women of childbearing age, younger women who
suffer migraines may face a somewhat higher risk. In
addition, some research has suggested that this stroke risk
may be particularly tied to migraine with aura--tell-tale
symptoms, such as visual disturbances, that signal an
impending migraine attack.

In this latest study, UK
researchers again found a connection between migraine with
aura and a higher risk of ischemic stroke, the form of
stroke caused by a blockage in the blood vessels feeding
the brain. The tie was particularly strong, however, among
women whose first migraines were accompanied by aura,
especially if these initial attacks occurred more than 12
times a year.

Despite these findings, however, women
who experience migraines face a small risk of stroke
overall. The study authors estimate that, based on existing
evidence, about 15 per 100,000 of these women will suffer a
first stroke every year.

Dec. 17, 2003 — Spontaneous intracranial hypotension (SIH) is often misdiagnosed, causing significant delay in treatment and risks of mistreatment, according to the results of a study published in the December issue of the Archives of Neurology.

"Spontaneous intracranial hypotension is an important cause of 'new daily persistent headaches' but is not a well-recognized entity," writes Wouter I. Schievink, MD, from the Cedars-Sinai Medical Center in Los Angeles, California. "The misdiagnosis of SIH can have serious consequences."

From Jan. 1, 2001, through June 30, 2002, 18 consecutive patients with SIH were evaluated for definitive surgical treatment of spontaneous spinal cerebrospinal fluid (CSF) leak. The initial diagnosis was incorrect in 17 patients (94%), with a diagnostic delay ranging from four days to 13 years (median, five weeks).

Migraine, meningitis, and psychogenic disorder were the most common misdiagnoses. Procedures performed for conditions mimicking SIH included cerebral arteriography in two patients, craniotomy for Chiari malformation in two patients and for evacuation of subdural hematoma in one patient, and brain biopsy in one patient.

"The patients in this report were well educated, had medical insurance with ready access to medical care, and had symptoms severe enough to warrant consideration of surgical correction of the underlying spinal CSF leak and thus were more likely to be diagnosed," Dr. Schievink writes. "It is likely that for other patients with SIH, the diagnostic delay is even more pronounced, or the correct diagnosis is never established."

The management of SIH includes bed rest, oral hydration, caffeine, and steroids, with placement of one or more lumbar epidural blood patches, followed by directed epidural blood patch or percutaneous placement of fibrin glue if there is still no relief.

"Surgical treatment is reserved for those patients in whom these nonsurgical measures have failed," according to Dr. Schievink.

researchers have made great progress in elucidating the underlying causes of the disorder. The first big advance occurred in the early 1990s, when epidemiological studies revealed that 90 to 95 percent of individuals with the disorder carry a genetic marker associated with autoimmune disease—self-inflicted damage that occurs when the body mistakes its own tissues for a foreign invader and attacks them.

The next big clue came when Mignot of Stanford University tracked down a gene for narcolepsy in dogs and discovered it caused a mutation in a receptor for hypocretin, a neuropeptide involved in prodding the central nervous system awake and maintaining alertness and good muscle tone. Although humans with narcolepsy do not possess the same genetic mutation, this finding still proved instrumental in unraveling the disease’s fundamental cause. In most human cases, as research by Mignot and his colleague Seiji Nishino soon showed, the sufferer is deficient in hypocretin. Further sleuthing revealed that the cells that normally produce it in the brain seem to have been destroyed in narcoleptics.

That knowledge, coupled with evidence that narcolepsy in humans might be an autoimmune disorder, has led many researchers to suspect that sufferers have immune systems that are genetically predisposed to attack and destroy hypocretin-producing cells. “That’s just a theory,” says Mignot. “We’ve not been able to prove it, but it’s our best hunch for now.”

These revelations about the underpinnings of the disease have in turn led doctors to rethink the prevalence of the disorder. In recent sleep lab studies of 600 people age 30 or older, Mignot was surprised to find that 1 percent—or 20 times as many as with classic narcolepsy—suffered from inordinate sleepiness, had a high frequency of the autoimmune marker linked to narcolepsy, and went very rapidly into REM when they napped. Yet none reported cataplexy. Even when the researchers took into account shift work and other environmental causes of daytime fatigue, the association held up. “It may be that a mild form of narcolepsy happens much more often than we realize and is an unappreciated cause of excessive sleepiness in the general population,” says Mignot.

Brain scans show that putting negative emotions into words calms the brain's emotion center. That could explain meditation’s purported emotional benefits, because people who meditate often label their negative emotions in an effort to “let them go.”

Psychologists have long believed that people who talk about their feelings have more control over them, but they don't know why it works.

UCLA psychologist Matthew Lieberman and his colleagues hooked 30 people up to functional magnetic resonance imaging (fMRI) machines, which scan the brain to reveal which parts are active and inactive at any given moment.

They asked the subjects to look at pictures of male or female faces making emotional expressions. Below some of the photos was a choice of words describing the emotion—such as “angry” or “fearful”—or two possible names for the people in the pictures, one male name and one female name.

When presented with these choices, the subjects were asked to pick
the most appropriate emotion or gender-appropriate name to fit the face
they saw.

When the participants chose labels for the negative emotions,
activity in the right ventrolateral prefrontal cortex region—an area
associated with thinking in words about emotional experiences—became
more active, whereas activity in the amygdala, a brain region involved
in emotional processing, was calmed.

By contrast, when the subjects picked appropriate names for the
faces, the brain scans revealed none of these changes—indicating that
only emotional labeling makes a difference.

“In the same way you hit the brake when you’re driving when you see
a yellow light, when you put feelings into words, you seem to be
hitting the brakes on your emotional responses,” Lieberman said of his
study, which is detailed in the current issue of Psychological Science.

In a second experiment, 27 of the same subjects completed questionnaires to determine how “mindful” they are.

Meditation and other “mindfulness” techniques are designed to help
people pay more attention to their present emotions, thoughts and
sensations without reacting strongly to them. Meditators often
acknowledge and name their negative emotions in order to “let them go.”

When the team compared brain scans from subjects who had more
mindful dispositions to those from subjects who were less mindful, they
found a stark difference—the mindful subjects experienced greater
activation in the right ventrolateral prefrontral cortex and a greater
calming effect in the amygdala after labeling their emotions.

“These findings may help explain the beneficial health effects of
mindfulness meditation, and suggest, for the first time, an underlying
reason why mindfulness meditation programs improve mood and health,”
said David Creswell, a UCLA psychologist who led the second part of the
study, which will be detailed in Psychosomatic Medicine.

Indeed, PET scans of people in a non-REM state show a decline in brain energy compared with REM sleep and increased activity in those dormant schoolmarmish lobes. Does this affect the content of dreams? Yes, say researchers from Harvard and the Boston University School of Medicine.

Since people should theoretically be more uninhibited when the controlling prefrontal cortex is quiet, the team tracked participants for two weeks to see if their REM dreams were more socially aggressive than the ones they reported during non-REM sleep. The REM dreams, in fact, were much more likely to involve social interactions and tended to be more aggressive.

Sometimes, dreams can be a helpful diagnostic tool, a way of taking the emotional temperature of a patient. The dreams of clinically depressed people are notable for their utter lack of activity, for example.

Might there be a physiological reason? Eric Nofzinger, director of the Sleep Neuroimaging Research Program at the University of Pittsburgh medical school, has studied PET scans of depressed patients and has found that the difference between their waking and sleeping states is far less dramatic than normal. On the one hand, he says, "we were shocked, surprised, and amazed at how much activity" there was in the emotional brain of healthy people during sleep. In depressed patients, by contrast, the vigilant prefrontal cortex, which normally is not active during sleep, worked overtime. Never surrendering to the soothing power of dreams, the brain is physically constrained, and its dream life shows it.

Healing power. Is it possible that dreaming can actually heal? "We know tthat 60 to 70 percent of people who go through a depression will recover without treatment," says Cartwright, who recently tested her theory that maybe they are working through their troubles while asleep. In a study whose results were published this spring in the journal Psychiatry Research, she recruited 30 people going through a divorce and asked them to record their dreams over five months. Depressed patients whose dreams were rich with emotion--one woman reported seething while her ex-husband danced with his new girlfriend--eventually recovered without the need for drugs or extensive psychotherapy. But those whose dreams were bland and empty of feeling were not able to recover on their own.