This page contains news items of interest from neuroscience publications. The focus is on research findings about how our brains work, how to avoid brain damage and how to fix or compensate for effects of brain damage.

CONTENTS:

Testing the Fetal Brain
Take Aspirin after Stroke
Nitric Oxide Gas Triggers Alzheimers
Brain Disorders Top Worldwide Disability List
Self Recognition and the Brain
Workers' Fetus May Sue Employer
Can Mold Cause Brain Damage?
Biologic Treatment for Addiction
Wartime TBI and Alzheimers
Pets Reduce Caregiver Stress
When Words Hurt the Brain
Record Gift for Cognitive Treatment
Moving Robot Limbs with the Mind
Head Trauma and Brain Tumors
Improving Hospital Pain Relief
Imitation Circuits
Avoid Some Plane Flights
Exercise and Brain Repair
Zapping Away Depression
California TBI Planning Grant
Loneliness and Longevity
Depression and Tooth Decay
Jog Your Brain
SAM-e for Depression?
Unblocking Synaptic Regrowth
Steroid Side Effects
Head Injury Protection
Air Bags
Curing Blindness
Heros with TBI
Cell Phones
When Pain Control Hurts
Biological Limits on Healing TBI
New Brain Cells!
Fight Strokes with O.J.
Preventing Fatal DVT
Jaw Dysfunction after Neurosurgery
Preventing Falls by the Elderly
Gender and Brain Anatomy
Patients can sue their HMOs
Blocking Neuropathic Pain
Headaches and the Hypothalmus
Supermouse and Memory Genes
Better Headache Medication
Help Your Neurologist
TBI and Alzheimer's Disease
Relief for Insomnia
Nicotine and the Brain
fMRI Maps Math and Attention Circuits
Self-Managing Chronic Pain
Remedy for Coma?
Pitfalls of Medicating Apathy
A New Anti-Depressant
Anti-Depressants and Cognition
Off Label Prescriptions
Kids of Parents with a TBI
Telephonic Monitoring
Migraine and Triptans
Estrogen and Memory
Bicycle Helmets
Prosthetic Memory
Brain Implant
Brain Death
Credit Card Abuse
ID Cards
Hand held computers store memorable info
Creatine Risks to Young Athletes
Court Appointed guardians
Soccer Injuries
Herbal Remedies
Mandatory helmet law for skiers?
New location for Nat’l Brain Injury Assoc., Inc
Toy Guide for Differently-abled Kids
Apathy widespread among Brain Injured
Donepezil helpful in short term memory

Testing the Fetal Brain In Sept. 2002 Dr. Curtis Lowery of the University of Arkansas for Medical Sciences announced that he was able to test the responsiveness of the brain of live fetuses in utero by shining a light into the womb and measuring their brain activation with MEG (magneto-encephalography), a harmless scanning device that picks up the tiny magnetic fields given off by working brain cells. This is hoped to be the neurologic equivalent of the fetal heart monitor, but instead of detecting a fetus at risk due to abnormal heart rate or rhythym, this technique would detect a fetus at risk due to emerging or actual brain damage.

Take aspirin after stroke Stroke kills 160,000 Americans a year and is the leading cause of disability in adults. 80% of strokes are "ischemic" and result from a blocked blood vessel, while just 20% are hemmorhagic (due to a burst vessel). The clot busting drug TPA helps only when given within 3 hours of a stroke, and as a practical matter is hard to access because you have to get to a hospital in time. Recent research shows that taking a couple of aspirin right after an ischemic stroke improves outcomes better than any other remedy. Stroke may manifest itself by suddent onset of severe heachache, dizziness, blurred vision or slurred speech. Anyone who thinks he has suffered a stroke should call 911. If you cannot get to a hospital within 3 hours of a stroke to receive TPA, it makes sense to take a couple of aspirin, which could save your life.

Nitric oxide gas triggers Alzheimers On radio and TV, one can hear adverstisements promoting the use of nitric oxide for health effects. Research published in August 2002 in the Journal Science by the Burhnam Institute in LaJolla, CA, should give us pause. The research showed that buildup of nitric oxide gas in rat brains triggered activation of enzymes that chewed up brain cells in the same manner seen in Alzheimer's Disease, multiple sclerosis and HIV-dementia.

Brain disorders top worldwide disability list WHO (the World Health Organization) just published a study showing that the foremost cause of disability from diseases that do not involve infectious or parasitic transmission is brain disorders. In developing countires neuropsychiatric disorders account for just 1.3% of all deaths but generate 11.5% of all disability in the living. In developed countries, where neuropsychiatric disorders cause 25% of all cases of disability, 8 out of the top 10 ten disability causing disorders are brain based. The higher figure in developed countries is attributed in part to greater demands on the brain from more complex laws, regulations and institutions; the stressful time demands of modern life; and requirement of ever faster information processing from computerization and the Internet. Even slight impairment of cognitive or emotional functioning from a brain disorder can significantly limit and interfere with our activities in this densely populated, highly technological and fast paced world.

Self recognition and the brain Dr. Julian Keenan and colleagues at Harvard Medical School have established that the right cerebral hemisphere is activated when we see and recognize ourselves in a mirror or photo, whereas the left hemisphere is activated when we recognize another person. This was done by selectively anesthetizing different hemispheres of the brain and asking volunteers about to undergo epilepsy surgery to identify the person depicted in photos. Volunteers with an anesthetized left hemisphere could recognize only themselves. Those with an anesthetized right hemisphere could only recognize a celebrity but not themselves.

Workers' fetus can sue employer Normally, an employee hurt on the job cannot sue her employer, because she is limited by law to workers' compensation insurance. However, in Meyers v. Burger King Corp. decided 7/12/01 the Supreme Court of the state of Washington held that when a pregnant employee slipped and fell at work and struck her abdomen against a table, and her baby was born with severe brain damage as a direct consequence, the baby could sue the employer for negligence because the baby was not an employee and because the baby's injuries were personal to her and not derivative of work-related injury to her mother.


Can Mold cause Brain Damage? The May 2001 issue of California Laywer reports there are 2,000 plaintiffs in California currently pursuing toxic mold cases against the builders, owners and landlords of infected building - suits modeled after a trio of highly successful cases in Florida. One case is currently in suit against Tulare County for injuries to employees of the Visalia Courthouse. The injuries alleged include headache and cognitive dysfunction. In the 19th century British archaelogists who excavated the tombs of Pharohs died from "King Tut's Curse," when they inhaled toxic molds. The likely route of travel for toxins in the mold would be through the lung tissue into the bloodstream and across the blood-brain barrier to the brain itself. One government agency that may have more information is the National Institute of Environmental Health Sciences (NIEHS) in Bethesda, Maryland.

Biologic Treatment for Addiction Two new discoveries hold promise for future biologic treatments for addiction. In March 2001 James Bibb and Paul Greengard at the Rockefeller University in Mahattan announced they had identified an enzyme called cyclin-dependent kinase 5 (Cdk5) which increased in the brains of mice in direct proportion to the amount of cocaine fed to them. Mice fed lots of coke had much higher levels of Cdk5. They postulate that Cdk5 blocks the body's response to cocaine thus forcing the addict to ingest ever larger quantitites to get the same high. To block Cdk5 without disturbing essential activities of the dopamine pathways (such as attention and mood) will require a lot of work. The Neuroscience Newsletter (May-June 2001) reports another development, the trial of a vaccine to stimulate antibodies that will detect, trap and inactivate target drugs such as cocaine. Experiments with the vaccine have rendered rats indifferent to cocaine and PCP. The vaccine has not yet been tested on humans. Improved treatment is needed, since some 13 million Americans abuse drugs on a regular basis, because of the euphoria they experience from taking them.

Wartime TBI and Alzheimers Scientists at the National Institute on Aging and Duke University just published a retrospective study on the link between head injuries in American soliders who fought in world war II and onset of Alzheimers Disease. Instead of relying on participant's recollections, they studied the actual medical records of the 548 Navy and Marine vetrans with wartime head injuries (many of them 50 years old).
This group was compared to a control group of 1,228 WWII veterans with no history of tbi. Following statistical analysis they found the risk of developing AD correlated directly with the severity of the tbi. The risk was low for mild, increased for moderate (30 min to 24 hours Loss of Consciousness or Post Traumatic Amnesia) and highest for severe (LOC or PTA over 24 hours). Unlike several other studies they found no enhanced risk for development of AD in tbi survivors with the APOE-e4 gene. Alcohol use, tabacco use and positive family history for dementia, were also found not to increase the risk.

Pets Reduce Caregiver Stress Karen Allen, PhD, a clinical pharmacologist at the Univsersity of Buffalo, informed the Society of Psychophysiogical Research, at its annual meeting on 10/19/00, of her research into the beneficial cardio-vascular effects of owning a pet dog for caregivers of brain-injured spouses. She monitored the blood pressure of 60 caregiving spouses, all of them taking anti-hypertension medication, over a period of 6 months. 30 were given dogs; the other 30 had none. After 6 months the dog owning caregivers showed a much lower rise in blood pressure during stressful situations than the non-dog owners, an average of 40 mmHg difference. The controls were then given dogs. After 12 months, all 60 participants (now all dog owners) had equivalent improvement in their cardio-vascular responses to stress.

When Words Hurt the Brain In elementary school we were often told by parents and teachers that "sticks and stones may break my bones, but names will never hurt me." Like so many other bits of "folk wisdom," this one turns out to be wrong. On 12/15/00 Dr. Martin Teicher, Director of the Biopsychiatry Dept. at McLean Hospital in Boston, released a paper finding that children who suffered harsh verbal abuse showed the same brain abnormalities as those who had been sexually abused or brutally beaten. On MRI scans, the traumatized children (including recipients of verbal abuse only) showed stunted development of their corpus callosum compared to normal kids. The corpous callosum in the "fiber bridge" linking the left (logical) and right (emotional) hemispheres of the brain, and enabling them to work in sync. The traumatized kids tended to "live" primarily in the left hemisphere (acting unemotional most of the time), but will become completely unglued when faced with reminders of their trauma by moving completely into the right hemisphere with no logic to guide them. Dr. Teicher recommends therapies which get the youngsters to use both hemispheres in a seamless whole, like playing music.

Record Gift for Cognitive Treatment On 1/17/01 Bill Coleman, a Silicon Valley entrepreneur who has a niece with mental retardation, pledged a donation of $250 million to the University of Colorado to fund a state of the art program for research into technological advances for people with cognitive disabilities. This is the largest ever one time donation from a private source to a public university. Mr Colemand and his wife Claudia are to be thanked for their tremendous generosity. The research should one day bear fruit for all persons with cognitive disabilities, including those with tbi.

Moving Robot Limbs with the Mind Following stroke, spinal cord injury or tbi to a portion of the motor cortex, a person becomes "paralyzed," and cannot move the affected arm or leg. Scientists have been working on ways to move robotic limbs to enable people to compensate for such paralysis. The cyber approach has been to program a network of computers with a program resembling the neural signal for limb movement, which can trigger motion in a robotic arm. A more biological approach was reported in November 2000 by Dr. Miguel Nicolelis, a neuroscientist at Duke University, who used motor signals from the brains of living owl monkeys to move a robotic arm. This an important first step in the development of a neural prosthesis, which may one day be used by human beings.

Head Trauma and Brain Tumors The legal view of the connection between trauma and cancer mirrors the medical one. While most doctors will not accept the view that trauma can cause (i.e. create new) cancer; many are prepared to agree that trauma can activate and spread a latent or slow growing tumor which otherwise would have remained quiescent. A recent court decision in Michigan is an example. In Wilkinson v. Lee, decided 9/26/00, the Supreme Court of Michigan upheld a $175,000 jury verdict for a man who was diagnosed with a brain tumor 1.5 years after suffering head trauma in a car accident. The Court stated that a latent pre-existing tumor made the man an "eggshell plaintiff," who was entitled to recover because the trauma "triggered" or "precipitated" the extra growth of the tumor and worsening of symptoms.

Improving Hospital Pain Relief For years patient advocates have complained that hospitals under-medicate pain due to excessive fear of causing addiction. Commencing January 1, 2001 all hospitals and nursing homes must comply with new rules issued by the Joint Commission on Accreditation of Hospitals requiring them to properly treat patients' pain. Should they fail to honor the right of each patient to have his pain properly assessed and treated, they can be sanctioned by JCAH. Pain assessment is to be done on a zero to 10 scale with 10 being the "worst pain imaginable." For tbi patients who suffered painful nerve damage or orthopedic injuries during the traumatic event, this is welcome news. Unrelieved pain is unpleasant, debilitating and blocks effective rehabilitation.

Imitation Circuits brain mapper Marco Iacoboni at UCLA announced on 5/18/00 that using functional MRI scanning he had isolated the human brain's "imitation circuits" in the left posterior frontal lobe (Broca's area where the commands for muscle movement of the mouth, lips and tongue are given for articulate speech) and the right parietal lobe (where sensory data are integrated with precise muscle movements of the body in space in response to perceptions). This makes sense, because imitation is at the root of learning any human language and learning motor skills like hitting a golf ball.

Avoid Some Plane Flights Oxygen deprivation, of sufficient proportion, is a cause of brain damage. Hyberbaric oxygen chambers, of the kind used to treat the "bends" in scuba divers, have been used with some success for victims of severe TBI in the acute phase at trauma centers. Our brains thrive with plentiful O2, and function poorly when supplies run low. All things being equal, if a person with TBI can avoid low O2 situations, he is better off. On 6/9/00 the Wall Street Journal ran an article quoting physicians who said stale (high CO2, low O2) air on planes is making more people sick, and the problem only grows worse because of long delays, planes stuck motionless on runways, and many airlines cutting back on the percentage of fresh air for passengers. WSJ quoted a United Airlines flight attendant who spoke of people "passing out" due to poor air quality on long flights to Europe. WSJ says a group of 26 Alaska Airlines flight attendants sued their employer in June 1998 for illnesses (including headache, blurry vision, confusion, impaired motor skills and nausea) which they attribute to stale air. Doctors advise people to fly less, if they can. If you must fly, they suggest avoiding alcohol, drinking lots of water. Some people wear surgical masks. A few even bring oxygen tanks or air purifiers on board! Anyone who must fly frequently is encouraged to let the airlines know you want better ventilation and more, not less, fresh air pumped into the plane.

Exercise and Brain Repair Exercise is known to improve mood and boost cognitive performance. Scientists hypothesized this resulted from increased blood flow and oxygenation of brain tissue, and perhaps to release of endorphins. Research just published in the Journal of Neuroscience (4/15/2000 Vol 20(8):2926-2933) shows that physical exercise liberates large quantities of a peptide called IGF-1 (insulin-like growth factor I) into the bloodstream, from the liver and other organs. The IGF-1 crosses the blood brain barrier and saturates receptor sites in the choroid plexus (the lining of the brain's ventricular system where cerebro-spinal fluid is made). From there it gains entry to many parts of the brain, where it triggers the release of BDNF (a neuro-trophic growth factor) and other substances which promote the health and vigor of  brain cells, synaptic circuits and neural pathways. It is believed that boosting of trophic factors in the brain, following traumatic brain injury, would protect the survival of damaged brain cells and assist in the rebuilding of damaged neural connections.

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Zapping away Depression

Approximately 1,000,000 people suffer from "intractible" depression, about 15% of which will commit suicide. These are people who have not responded to medication, psychotherapy or hospitalization. In March 2000, it was announced by University of Texas, Southwestern Medical Center of Dallas, and 3 sister research institutions that promising results for treating such patients had been reached through surgical implantation of a small pace-maker like device in the chest which emits a mild current to the vagus nerve every 5 minutes, 24 hours a day.  According to device manufacturer  Cyberonics, Inc. of Houston, the total cost of the device, surgery and follow-up is $15,000 and an application for FDA approval of the device in now pending. Although the mood enhancing effect of vagus nerve stimulation is not understood, and was discovered accidentally, it appears to work dramatic improvement. Out of 30 patients hospitalized recurrently for chronic severe depression, 17 are doing much better and have been able to stay out of the hospital. 200 new patients will be tested later this year at the Medical University of South Carolina at Charleston.

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California TBI Planning Grant

In July 1996 the federal government enacted the Traumatic Brain Injury Act (Public Law 104-166). A purpose of the law was to issue grants of money to the states for "planning" and "implementation" of core infrastructure to provide services for state residents with a brain injury. California just obtained a "planning" grant for the year 2000. It will hold 11 focus groups around the state plus 4 large scale public forums. To attend or submit your own suggestions as to how the grant money should be spent, please contact Marita McElvain, TBI Project Coordinator, California Dept. of Mental Health, 1600 - 9th Street, Room 100 Sacramento, CA 96814 (916) 654-3168, fax (916) 653-6486.

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Loneliness and Longevity

According to the Harvard Mental Health Letter (4/2000 edition Vol. 16 No. 10) people with good social connections tend to be healthier, to live longer and to survive heart attacks, breast cancer and other serious illnesses much longer than people who live alone. Whether the social network consists of friends or a support group, having people to be with and talk to has a real and tangible effect on our health and longevity. The risk of becoming socially disconnected and lonely is high for people with a TBI. No one wants to admit they feel  lonely and its hard to risk the rejection that goes with trying to make new friends. Nevertheless your life may depend on doing something about it.  Joining a TBI support group is a totally acceptable and less threatening way to make new friends. Many of these groups go on successfully for years, because they enable their members to share experiences, feelings,   concerns and observations with others who are going through similar situations.  

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Depression and Tooth Decay

During the 1970s and part of the 1980s the most prescribed anti-depressants were known at tri-cyclics because they had 3 rings of carbon atoms - e.g. imipramine, desipramine, nortriptyline and amitriptyline. These caused severe dry mouth. The newer generation of anti-depressants which became popular in the later 1980s (the SSRIs such as Prozac, Paxil and Zoloft) also cause dry mouth, but less extreme and obvious. Why is this important? Saliva is filled with anti-microbial substances, and in the absence of a normal quantity of saliva, people are prone to develop cavities, gum disease and fungal infections of the mouth. The dry mouth effect of anti-depressants is compounded and greatly increased when the patient is taking other medications to relieve anxiety, lower blood pressure, lower cholesterol and reduce allergic symptoms. Coffee is another culprit. Since it is common for doctors to prescribe anti-depressants to people who have suffered a TBI, please remember to drink lots of water and see your dentist regularly. Some users of anti-depressants are shocked to learn that cavities and dentures in their adult life were related to the medications they were talking for depression.

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Jog Your Brain

Neuroscientist Fred Gage of the Salk Institute in La Jolla, CA, has demonstrated in juvenile mice that jogging improves recent memory and new learning by greatly increasing the number of cells in the dentate gyrus of the hippocampus, and priming those cells for more efficient firing in response to stimulii. Mice that ran a treadmill intermittently over a 5 week period performed much better in navigating a water maze than sedentary mice that did not exercise, and on autopsy the runners had more robust brain growth and development in the specific area for associative memory (learning by experience) than the couch potatos - as reported in the Proceedings of the National Academy of Sciences. So go out and take a jog. It may jog your brain.

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SAM-e for Depression?

Doctors in Europe have been prescribing a synthetic version of S-adenosylmethionine (SAM-e), a naturally occuring bodily chemical, for depression, liver disease and arthritis. The manufacturers of this product have just brought it to America, touting it in health food stores across the country as a highly effective, natural remedy against depression with no side effects. Scientific testing of its safety and effectiveness have only just begun, so it is way too early to accept or reject these claims, but caution is advised. The UC Berkeley Wellness Letter advises that reports of stomach upset have been made, and that SAM-e appears to increase the risk of heart attacks by increasing the concentration of homocysteine in the body. They also caution not to drop your anti-depressant in favor of SAM-e or start taking SAM-e with your anti-depressant without first consulting your physician. If you decide to take SAM-e the Wellness letter suggests taking a B vitamin or eating Vitamin B rich foods like broccoli to lower homocysteine levels.

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Unblocking Synaptic Regrowth

In the Feb. 2000 issue of the journal Nature, it was reported that molecular biologists in Zurich, Philadelphia and Yale University had simultaneously isolated the gene (which they named NoGo) which blocks axonal regeneration following traumatic damage. Nerve cells taken out of synaptic contact with other nerve cells self-destruct, so regrowth of damaged axons is imperative to save damaged cells. NoGo codes for the production of a protein inside the myelin sheath which coats the axons of brain cells. Although myelin, an insulation material,  is necessary for lightening fast transmission of nerve impulses from one brain cell to another and down the spinal cord, it inhibits the sprouting or regrowth of damaged axons. Pediatric brain cells in the infant and toddler can rewire themselves to a remarkable extent following TBI, brain surgery or other brain insult, precisely because they are only partially myelinated. Adult brain cells are fully myelinated, and do not regrow to any appreciable extent after neurologic injury. It is hoped by the discoverers of Nogo that methods can be devised in the future which will block NoGo receptors, prevent the formation of the growth inhibiting protein and pave the way for robust regeneration of damaged nerve cells in the brain and spinal cord. One group of patients likely to benefit in the near term from this research are people with Parkinson's Disease. This is because blockade of NoGo could allow fetal brain tissue transplants to take root, grow and hook up with surrounding cells, with consequent increase in the production and effective transmission of dopamine.

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Steroid Side Effects

TBI patients may be taking prednisone or other steroids for conditions ranging from bulging spinal disc pain to stress rash of the skin to joint inflammation, all common after a trauma serious enough to damage the brain. Are steroids harmless? Far from it. In the past they have been linked with side effects including weight gain, diabetes, glaucoma and osteoporosis. When taken in very high doses they have been known to cause temporary psychosis withdelusions and hallucinations. Recent research indicates they can cause depression, irritability, emotional lability and memory loss in patients who were free of those problems before taking the drug. The Harvard Mental Health Letter (Feb. 2000) cautions people taking steroid therapy to monitor themselves for memory and mood problems, and recommends lithium as a way of stabilizing  in ents who must take steroids on a chronic basis.

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Head Injury Protection

Each year there are 60,000 head injuries from vehicle interior impactsof which 3,000 are "serious" and 2,500 are fatal, involving contact between an occupants's head and Upper Interior Impact Zones such as the A-Pillar, B-Pillar, Front Header, and Front Side Rail. In 1995 federal regulations were adopted requiring auto makers to pad those danger spots with energy absorbing materials meeting minimum safety standards. Unfortunately the regulations are not fully effective until Sept. 2002, and tey do not go far enough. Consumer safety advocates have recommended that consumers seek to puchase vehicles which exceed the standards. One place to look for crashworthiness data is www.hwysafety.org/vehicle-ratings.

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Air Bags

Air bags tucked into the steering wheel have saved lives in high speed front end collisions. However, they remain of no protective value against brain injury from head trauma in side impact, rear end or roll over crashes, or in frontal collisions when the occupant is out of position. They became a source of increased injury or even death to adult drivers not wearing their seatbelts and to seatbelted children under age 12 sitting in front. Litigation for extra injury (TBI, spinal cord damage or both) has been brought when the air bag failed to deploy as intended or deployed when not intended in low speed crashes. Deployment in low speed crashes can be highly injurious, because the occupant is not expecting anything, when the air bag hits him like a huge boxing glove at 180-200 mph. Apart from always wearing your seatbelt and making sure children under age 12 always sit in the rear, can you do anything else to reduce the risk of  air bag injury? The answer is yes. According to an article in the Jan. 2000 issue of Trial, you can select a car which has the following safety features: tailored gas flow bag inflators which equilibrate air bag inflation rate to the severity of the collision; use of cloth straps inside the air bag to tether it and restrain from moving too far rearward into the occupant; contouring the shape of the bag  to prevent excursion into your body during inflation; telescoping steering wheels; and less aggressive air bags deploying at 150 mph or less instead of 200 mph.

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Curing Blindness

When facial trauma causes sufficient damage to eye structures such as the retina, blindness results because of dysfunction in the machinery for registering the dots of light (of which images are made), converting them to neural impulses and sending them to occipital lobes at the back of the brain for re-processisng into color images. After 30 years of work Dr. William Dobelle (bio-medical inventor and professor at Columbia University School of Medicine in New York) has created a working prototype of an artificial visions system. In a remarkable demonstration, Dr. Dobelle's patient (who was rendered legally blind by injury) was able to read large type words, pick out  objects against a contrasting background, and safely navigate his way onto a subway from the platform without assistance. The system he used, and which he trained on extensively before the demonstration, consist of a miniature light sensor and ultrasonic distance sensor built into a pair of glasses, which transmit data through a cable along the eyeglass frame to a tiny computer worn on the hip. The computer pre-processes the data, and transmits it through another cable to a series of electrodes implanted directly onto the surface of the patient's occipital lobes through a small hole drilled in his skull. His occipital lobes take it from there, and recreate simplified, black and white (only) images of the world. Dr. Dobelle is confident he can refine the device and vastly increase its resolution over time. For more information check out his website at www.artificialvision.com

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Heros With TBI

After acute recovery from a severe TBI, Julie "Butterfly" Hill, a 25 year old woman from Arkansas came to Humboldt County, California, and made history through heroic, non-violent civil disobdience. Julie built a shelter 180 feet up a giant redwood tree in Stafford, California, which she named "Luna" and lived there for the past 2 years, until the owner of the ancient redwood grove, Pacific Lumber/Maxxam, promised in writing never to cut down Luna or the small grove where the tree stood, and to convert from clearcutting to more eco-friendly, sustainable logging practices. Harper will publish her story in April 200 under the title "The Legacy of Luna." Congratulations and hats off to Julie Hill for showing everyone that life does not end with a brain injury, and that people with a TBI are capable of creativity, courageous acts and admirable deeds which inspire others.

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Cell Phones

Do  cell phones harm the brain? Recent reports contain conflicting evidence regarding the alleged risk of growing a brain tumor from holding a cell phone with a built in antenae to your ear; and so far the data is inconclusive either way. However, we do know that using a cell phone while driving your car increases the risk of a car crash by four times, according to a 1997 study in the New England Journal of Medicine. We also know that traffic accidents account for half of all TBIs. If you must speak on the phone while in the car, it is recommended that you do it only while gridlocked in stopped traffic or pull over if you are in fast moving traffic.

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When Pain Control Hurts

Chronic pain often follows a TBI, in the form of migraines, spinal pain from disc herniations or myofascial pain disorder involving inflammation and fibrous scarring of muscle tissue. Such pain must be brought under control, because pain and its sequelae (depression, insomnia and fatigue) distract survivors from concetrating on rehab tasks such as cognitive, speech or physical therapy. However, not all pain remedies are created equal, and some have the potential to cause new injuries or problems. Overuse of narcotic analgesics like Vicodin or Codeine can create addiction and dull cognition. Rebound headache can result from overuse of OTC (over-the-counter) migraine pills such as Excedrin Migraine. In the Oct. 1999 issue of Headache, Excedrin Migraine maker Bristol-Myers conceded that daily use of its pill was likely to increase the frequency of migraine, and should not be taken more than 2-3 times per week.  Overuse of Excedrin, Anacin, Tylenol and Advil have  all been associated with  "rebound headache." Why does rebound headache occur? There are several theories: withdrawal symptoms from addiction to caffeine in these pills; build-up of a "false tolerance" to pain accompanied by an extreme response to slight pain; or growth of extra pain receptors in response to chronic blockade of pain by these pills. So far, the clinical solution to rebound headache is to wean the user off the particular pill being overused, and then start him on a alternating combo of new medications. Another pain control technique that can backfire is accupuncture. In the hands of unskilled practitioners accupuncture needles can puncture and deflate the lungs or fracture ribs. Chiropractors who use high force adjustments to the upper neck can cause stroke or paralysis. There is a new neurosurgical procedure aimed at fibromyalgia patients which allegedly cures headache and depression by sawing bone away from the base of the skull to reduce "pressure" on the brain. This procedure poses many risks including brain damage, infection and reducing skull protection against future trauma. While effective pain control is a vital component of recovering from a TBI, attention must be paid to the efficacy, safety and potential complications of using a given technique or using the services a particular practitioner. One way of exercising caution is to consult a licensed physician who is Board Certified in rehabilitation medicine (physiatry) or in pain medicine. 

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Biological Limits to Healing TBI

Compared to adults, the neural plasticity of the child's brain is vastly superior. There are many clinical cases on record in which a neurosurgeon removed the entire left hemisphere of a severely epileptic child, who went on to speak normally because all his language functions were transferred to and taken over by his remaining right hemisphere. Such a thing is utterly impossible in an adult. Why? When the adult brain loses a pocket of nerve cells from trauma, glial cells migrate to the area and create a glial scar which acts as a physical barrier to rewiring and reorganization of surviving brain tissue. Experimentation with grafts of healthy brain tissue into the space left behind by dead neurons has failed largely because of glial scarring. Recent research has shed light on the reason for this. The developing human embryo undergoes an explosive proliferation of neurons which migrate along genetically predetermined paths with the assistance of glial cells which act as a kind of scaffolding. When they reach their targets, they begin hooking up with (synapsing with) other brain cells in response to genetic coding and experience. Some of these connections are normal and adaptive (useful), while others are abnormal and maladaptive. During late embryonic development and early childhood, the human brain undergoes a kind of self-pruning of maladaptive neural connections. The failure of this pruning processs to occur as it should is believed to be a factor in the genesis of schizophrenia. Recent research indicates that certain glial cells (those containing a substance called chondroitin sulfate) block axons from sprouting new connections which would be harmful to the organism. These glial cells continue to be produced into adulthood, and continue to block axonal regeneration following brain trauma. Neuroscientists are now at the point where they can breed glial cells in vitro without the protein which inhibits new grwoth of damaged axons. These could be injected into a damaged brain. Such experiments will now occur in rats for a long time before they are attempted in humans.

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New Brain Cells!

For many years it has been a bedrock principal of neuroscience that all 100 billion of our brain cells exist at birth, that the adult human brain cannot grow new cells and that memory works by a rewiring of old brain brain cells rather than by growing new brain cells to record new data.  As of 10/15/99 this is now in question. On that date Princeton neuroscientists Elizabeth Gould and Charles Gross published a study in Science dealing announcing their discovery of the daily growth of new brain cells in the adult macaque monkey brain. Using a chemical tracer, these researchers found a rim-like layer of stem cells over the ventricles deep within the macaques' brain which produced a steady stream of new neurons. The new brain cells migrated up into the cortex at the surface of the brain and established synapses with older cells in the frontal lobes (where personality, planning, decisionmaking and working memory are located) and in the parietal lobes (where visual recognition memory exists). They speculate that this ceaseless train of new brain cells enables the brain to imprint and store new memories in a continuous sequence much like supplying a video camera with fresh video cassettes. If true, then a supply  of healthy neurons may exist for treatment of degenerative brain diseases like Alzheimer's and Parkinson's, if they could be channeled to the damages portions of the brain. Since the discovery has not yet been confirmed in human beings, no definite anwsers are possible now, but an exciting new area of research has been opened up.

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Fight Strokes with O.J.

A 3 year study at Harvard's School of Public Health, shows that drinking at least 6 ounces of orange juice every day has the same strong protective effect against ischemic stroke as eating cruciferous vegetables like broccoli or brussel sprouts, two foods that are good for you, but which many people have disliked intensely since childhood and still refuse to eat as adults no how much cheese is sprinkled over them.

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Preventing Fatal DVT

Persons hospitalized for major TBI are at very high risk of developing life threatening deep vein thrombosis. As a group their risk level is higher than patients with major injuries to the face, chest or abdomen, but slightly lower than those with significant spinal cord injuries. The period of highest risk is 2-3 weeks after the injury for which the patient was hospitalized. It is during this time frame that a patient with no clinical manifestation of DVT can die of a pulmonary embolism (PE). Therefore, recent studies recommend preventive measures. Use of high dose heparin is appropriate for patients without brain bleeding who have not undergone brain surgery. Use of unfractionated low dose Heparin or low molecular weight heparin was recommended for the patients with brain bleeding or post brain surgery.    

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Jaw Dysfunction after Neurosurgery

Persons who develop a large, compressive epidural or subdural hematoma after head trauma must have neurosurgery to evacuate the blood clot before irreversible brain damagae or death occurs. The surgery involves cutting a horseshoe shaped flap in the skull directly over the clot, allowing the clot to ooze out and gently suctioning any residual blood. When the clot is located under the temporal bone at the side of the head, the neurosurgeon will cut through the large temporalis muscle to gain access to the underlying bone. Although this seems a trivial matter to the surgeon who is saving the patient's life, patients are rarely told to expect jaw pain while chewing advised to get physical therapy for their jaw to break up scar tissue and mobilise the jaw. 

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Preventing Falls Among the Elderly

Falls account for nearly 20% of TBIs across all age groups, but make up a much higher proportion among small children and the elderly. For teens and young adults the main cause is motor vehicle accidents followed by violence. The Centers for Disease Control have issued a policy statement regarding fall prevention in the elderly. The key steps towards reducing risk are: a regular exercise program with attention to strength and balance; making the home safer (e.g., by use of non-slip tub mats and grab bars near the toilet, removingsmall throw rugs, better lighting, installation of handrails on stairs and wearing shoes with non-slip soles); having regular vision check ups; and having medications reviewed to weed out those which cause drowsiness or lightheadedness.

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Gender Differences in Brain Anatomy

Neuroscientists Ruben and Raquel Gur of the University of Pennsylvania Medical
Center, a married couple, just published a study of anatomical differences between the brains of men and women. Evolutionary anthropologists have noted that the larger the brain the more intelligent the creature. Yet while men have larger brain volume than women they test the same in IQ and while men excel at spatial tasks, women do better on verbal tests. Why? The Gurs used a group of 40 healthy men and women to answer the question. They gave the subjects a battery of cognitive and performance tests and Took MRIs of their brains. The conclusion was that male brains are larger because of more white matter connections (which make men better at finding places without maps), and that female brains have a greater number of cells more densely packed in their  gray matter (making them superior at verbal tasks) The study was published the May 15, 1999 issue of the Journal of Neuroscience.

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Patients Can Sue Their HMOs

On 9/27/99 California passed a law authorizing patients to obtain a second medical opinion paid for by their HMO, and to sue their HMOs for actual and even punitive damages for delaying or refusing treatment in certain circumstances. Governor Gray Davis signed the measure to "make   the health of the patient the bottom line with HMOs, not saving costs."   It is anticipated that the fear of being held financially accountable in patient lawsuits for damages, will deter HMOs from always opting for cost savings versus spending extra for quality care. Other states with new laws on the books having some elements of the California reform package are Georgia, Louisiana and Texas. At this time 34 other states are considering legislation to regulate HMO decisionmaking for protection of patients' rights TBI patients who are denied rehab services on the grounds that they are experimental or unproven, should check with medical and legal specialists to see if they have statutory grounds for a legal challenge. The California law mandates the creation of a new state agency to oversee and regulate managed care with the help of an Advisory Council. As of this moment (11/6/99) the agency is so new it does not even have a Director, and the Advisory Council has not yet been formed. A new coalition of advocacy groups called the California Neuro Alliance was formed on 11/5/99 to represent persons living with chronic neurologic conditions, such as TBI,   Cerebral Palsy, ALS, AD, epilepsy and MS. The California Neuro Alliance will be seeking a seat on the Advosory Council for the new Dept. of Managed Care. Persons with a TBI who are interested in the alliance should contact Harvey Hyman for more information. Go to Contact Us.

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Blocking Neuropathic Pain

Persons who suffer a TBI may suffer stretch damage to a cervical nerve root, the brachial plexus or other large nerve tracts as a result of the same traumatic event, especially if the trauma involved an object forcibly hitting the person's head so as to flex her neck or knock her to the ground. Nerve pain, known as neuropathic pain, is much worse than muscle pain and harder to treat.  It feels like an electric buzz rather than a dull ache and does not respond to customary pain treatments like Tylenol, Motrin or Vicodin. A recent discovery offers new hope to persons with this type of pain disorder. Researchers working with the venom of a poisonous sea snail, have discovered that it effectively blocks nerve pain by binding directly to receptors which admit the extra calcium into the nerve cell necessary to propagate the pain signal to the brain.  By injecting a small quantity of the snail venom into the spinal cord during a hospital visit, the nerve pain is stopped for a long time.

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Headaches and the Hypothalmus

Neurologists have believed for years that severe headaches such as migraines were a vascular phenomenon, in which transient release of chemical substances caused transient, reversible expansion of blood vessels surrounding the brain, which could be relieved each time the headache occurred by adminsitration of drugs which constrict the swollen blood vessels. Peter Goadsby of the National Hospital for Neurology and Neurosurgery in London, published a paper in Nature on July 1, 1999, which for the first time establishes the existence of permanent anatomic changes in the brain tissue associated with one type of severe headache, known as cluster headache. A cluster headache attacks one small area on one side of the head (such as the temple near the left eye) and causes excruciating pain in that spot for weeks or months, sometimes driving the victim to thoughts of suicide. Using PET scans Dr. Goadsby found abnormal metabolism going on in the hypothalmus on the same side of the  brain as the headaches. Then, applying  a new technique called voxel-based morphometry to brain MRIs of cluster headache patients, he found tiny anatomic changes in the same area of the hypothalmus consisting of unusually dense concentrations of grey matter neurons, i.e. far more than the expected number of brainc ells in that one spot. This could lead one day to better treatments for cluster headache, and to greater understanding of migraine headache as well.

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Super Mouse and Memory Genes

This September 1999, the media is abuzz with stories about "Doogie" the genetically modified mouse with superior memory created by teams at Princeton, MIT and Washington University led by Dr. Joe Tsien of Princeton. During the 1970s research on sea slugs (withdrawing their siphons  from a mild shock) showed that short term memory involved  the neural encoding of a life experience by means of strengthening the synpatic  connection between two nerve cells, and making it easier for them to "fire" in unison when the learned stimulus is repeated. During the 1980s research on mice (learning to navigate a water maze) and baby chicks (learning to avoid pecking a bead treated with a foul tasting liquid) uncovered the phenomemon of LTP (long term potentiation) in the hippocampal area of the brain. LTP involves biochemical and structural alterations of the cells in the hippocampus which underly the simplest form of memory, the kind of "associative memory" in which one bee sting will make us move away when we next see a bee. It is not equivalent to all forms of memory.  It is one important   segment of the neural process of encoding short term memory en route to further processing for long term storage outside of the hippocampus. LTP occurs when an attention grabbing  stimulus triggers upstream neurons to release  an excitatory neurotransmitter called glutamate, which binds to NMDA receptors on the dendrites of the downstream neurons, causing them to admit an influx of calcium ions into the cells. The calcium ions signal genes in the downstream cell nucleus to "remodel" the synapse by synthesizing new proteins which go to form new dendrites or dendritic spines. The downstream neuron sends nitric oxide back to the upstream neuron to replicate the process, which involves formation of new vessicles for increased storage of glutamate, and  formation of new terminal boutons at the end of the axon. The process also involves the binding of phosphate to proteins in the receptors in the snaptic membrane and the creation of phosphoproteins which change the shape of the receptors, thereby making it easier for calcium to enter and lowering the threashold for nerve cell firing.

What Dr. Tsien and his colleagues did in the late 1990s was to insert a gene called NR2B into the hipppocampal neurons of mice. This boosted the mouse's natural supply of NMDA protein, which in turn increased the number and strength of NMDA receptors to bind with glutamate from the upstream nerve cells, and enhance the vigor of the LTP process. This one tiny change in the mouse DNA produced observable change at the level of the mouse's learning behavior. Mice with the bigger, stronger  NMDA receptors, recalled successful strategies for running a maze better and longer than the untreated mice. This made them learn better and outperform the untreated mice at maze running and other equivalent tests of mouse prowess. There is no evidence this made the new mice smarter or boosted their rodentine IQ. However, it clearly did improve their memory of successful strategies employed in dealing with certain challenging and  complex tasks, like navigating a maze. What are the implications of the results? Undoubtedly this adds to our growing store of useful knowledge about the molecular and cellular processes which underly encoding and storage of memory. Continued extension of our knowledge of these processes may indeed lead to gene therapy for persons with ALzheimers, and beyond. However, there is need for caution. It is known that too much glutamate and too much calcium can kill brain cells, as happens in stroke. The possibility also exists that a proliferation of NMDA receptors may increase the tendency of some persons to become addicted to narcotics like cocaine and heroin. Finally, boosting memory power by itself, out of sync with other brain capacities, may create a Frankenstein.

In "The Making of Memory, " (1992, Anchor Books) the molecular  neurobiologist Steven Rose of the Open University of London, discusses the tragic cases of two men who both died young from the curse of too much memory. These individuals could not forget anything they had every been exposed to, and were greatly burdened by this excess of memory and the heaps of trivia flashing through their minds. We assuredly do not need to remember every passing detail of our daily experiences. Human memory and animal memory were designed to store long term only those memories which were significant for survival such  as which predators to avoid, and how to avoid them. The massive cognitive machinery in the human brain for analytic   reasoning, creative thinking, and the like could be gummed up by too much memory. Hence the supermouse is controversial, and the scientific and medical communities will have much to debate. Philospher of science, Stephen J. Gould of Harvard, commented upon Dr. Tsien's research by cautioning us not to equate any single gene with highly complex, multi-factorial systems like intelligence or memory; and instructing us not to search for  short cuts like "smart pills" in the hope of becoming educated without attending school. The content of what we learn and the values that guide how we use it, will always matter a great deal.  Even Mark McGuire will tell you that taking androgens did not by itself let him hit 70 home runs. He still had to train, practice and work with coaches.

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Better Headache Medication

A new generation of anti-migraine drugs known as 5-HT receptor agonists shows great promise in reducting the severity and intensity of the severe headaches which accompany traumatic migraine from a blow to the head. These medications imitate the action of serotonin without the side effects of introducing extra serotonin into the system. They constrict swollen blood vessels in the meninges, the membranes covering the brain. They also block the leakage of inflammatory substances from intra-cranial blood vessels. Finally, they inhibit the firing of neurons in the trigeminal nerve which send pain messages to the brain. The drugs are named Imitrex (sumaptriptan), Amerge (naratriptan) and Maxalt (rizatriptan). The 3 drugs differ as to rate of absorption and rate of action. Current research indicates that Maxalt is aborbed faster and stops migraines more quickly than the others. However, all 3 are a vast improvement over earlier headache medications. To prevent migraines from starting in the first place, doctors prescribe an anti-convulsant medication called  Deptakote. If you have suffered frequent epsidoes of severe headache following a blow to the head (which may or may not be accompanied by hypersensitivity to light, nausea or vomiting), you should ask your neurologist about these medications.

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HELP YOUR NEUROLOGIST

Chronic neurologic disorders afflict a tremendous cross-section of  persons in our society (if you total up TBI, stroke, Alzheimer's disease, epilepsy, Parkinson's disease, Multiple Sclerosis, Autism and major psychiatric disorders such as schizophrenia, bi-polar and major depression). As a whole they disable more people at all age groups than any other kind of illness. Yet neurology is a very small subspecialty of medicine and there is only a handful of neurologists to take care of these patients. Still worse HMOs discourage neurologists from utilizing the great advances in diagnosis and treatment. HMOs exclude most patients from qualifying for an MRI of the central nervous sytem. In order to prescribe Imitrex, a powerful and highly effective new medication which stops migraine attacks in progress, your neurologist has to comb through your chart and spend the time necessary to recreate your whole history of migraine drugs, explaining why earlier drugs failed and why Imitrex is now necessary and likely to help when the others did not. Not knowing what neurologists must contend with, many patients express anger at them for not doing enough quickly enough. In a recent forum, the President of the Association of California Neurologists, asked for understanding and support from neurologic patients, and suggested that they take the following steps to better help their neurologists help them: (a) if needed tests or therapies get denied, appeal directly to the Patient-Family Services dept. of their HMO to contest the denial and give factual reasons why the denied service is necessary; (b) provide their neurologist with any factual information from their prior medical history to bolster the request; (c) provide their neurologist with any supportive medical information from the internet, support groups, or otherwise, such as new treatment standards for specific diseases, reviews of new medications, case reports; and (d) provide their neurologist with the name, address and phone number of disease specific patient advocacy organizations. From time to time we all have good grounds to complain, but while complaining lets off steam, it cannot substitute for a win-win alliance with your neurologist to overcome the tendency of HMOs to focus on short term cost savings above long terms treatment benefits. Educating your neurologist will help him or her help you.

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TBI and Alzheimer's Disease

Some, but not all, cases of Alzheimer's disease (AD) are familial and have a clear genetic component, which gets activated or switched on by an environmental trigger. Recent medical research has shown that traumatic brain injury is a trigger in persons having one specific form of one specific gene known as APOE-e4. In such persons sustaining a TBI will increase their risk of developing AD by 7.7 to 10 times according to various studies. The good news is that this greatly heightened risk has not been found with any of the many other forms of the same gene. It has been suggested that persons with chronic TBI who are refractory to treatment, and manifest little or no spontaneous healing following their brain injury, should be tested for the presence of APOE-e4. Such advice is controversial, at least in part because there is no cure for AD. Being tested is an individual decision.

There are other interesting connections between TBI and AD. Shortage of acetylcholine in the brain is a factor in the poor and progessively worsening memories of patients with AD.  Companies that manufacture and market neuropharmaceuticals, have distributed drugs to increase AcH in the brain by, among other ways, blocking the enzyme acetylcholinesterase which breaks down AcH. Such drugs help some patients to some extent. No magic cure has been found to stop the decline of memory dead in it tracks and reverse it, i.e. restore normal memory function. There has been some "off label" experimentation with these drugs in patients with TBI with some positive indications. Very recently it was discovered that rats have a tremendous number of insuline receptors in their brain, especially in the hippocampus, the part of the brain responsible for encoding short term memory for long term storage elsewhere in the cortex. It was also found that drugs which block insulin signaling in the rat brain impair short term memory function, and that drugs which enhance insulin transmission improve short term memory. Studies are now under way to try insulin enhancing drugs on patients with AD in hopes of boosting their short term memory. One reason for trying this   approach, aside from the rat studies, is that patients with AD have abnormal insulin levels in their spinal fluid, suggesting their brains do not process insulin normally. Everyone who has been forced to keep working until 2 or 3 pm in the afternoon with no lunch can attest to feeling their cognitive speed and efficiency fall off due to hypoglycemia. Studies of college students with slight abnormalities in insulin functioning show these students perform less well on memory tests than their peers. Does TBI cause abnormalities in insulin production or utilization, and can insulin enhancing drugs boost short term memory function in patients with TBI? This is not known, but would seem to be a fruitful area for future biomedical research.

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Relief for Insomnia

Following a traumatic brain injury, most persons experience insomnia on a chronic basis. It appears that multiple causes are probably at work. The most obvious factors to consider would be anxiety, depression and chronic pain. These can be treated with medications, and in some instances medications can lessen sleep problems, even if they do not eliminate them. It has been suggested by some physicians that chronic insomnia in TBI patients is due to complex neurotransmitter imbalances, which cause such patients to wake up as much as 40, 45 or 50 times a night, rendering them fatigued rather than refreshed in the morning. Whether or not this is occuring in a given patient can be measured in a sleep laboratory. Unfortunately, even if such a maladaptive sleep of constantly broken sleep is detected, there is at present no sure fire cure for the problem.

Until a therapy is designed to return people with TBI to a normal sleep pattern, doctors will tend to resort to traditional sleep remedies. It has been pointed out that sleep medications may have a negative rebound effect by impairing short term memory or causing day-time drowsiness or mental cloudiness. Neurologists and neuropsychologists who work with patients having this problem agree that some remedies are acceptable, some unacceptable and others uncertain. Going to bed in random fashion with no set routine is bad. Drinking alcohol to sedate oneself backfires, and causes the person to bolt awake in the middle of the night. Smoking or drinking coffee right before bed will keep you awake. Eating a big meal or eating sweets just  before bed will do the same. Napping during the day will also keep you awake. Regular exercise during the day, a glass of warm milk or a warm bath all seem to help people fall gently to sleep. Keeping your room not too hot and not too cold helps. Keeping the mind on pleasant thoughts or images, to block out anxiety, helps. What about Melatonin? This is a human hormone produced by the pineal gland in the brain and is a breakdown product of serotonin. For people who have a true shortage of this hormone, Melatonin in pill form from the health food store may help, but anyone trying this remedy should be aware that no studies exist on the long term adverse effects of taking it. Further the Melatonin sold in pills may be impure, mislabeled or sold in unknown concentrations, which makes dose-response impossible to measure. Anyone contemplating taking a sleep medication, anti-depressant or Melatonin, should discuss it with the neurologist treating their brain injury.

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Nicotine and the Brain

Why do people smoke? The nicotine delivered by cigarette smoke causes decrease of tension, a sensation of pleasure and an increase of concentration and memory helpful to performing work. These effects relate to the release of certain neurotransmitters in the brain on arrival of nicotine, such as opioids and dopamine. The problem with getting your nicotine from cigarette smoke is that the tars in the smoke cause fatal lung cancers and heart disease. Not  surprisingly the people who have the hardest time quitting the habit are people with a genetic flaw in dopamine transport, people who are very reliant on an outside stimulant for internal release of dopamine (the reward chemical.  In the Jan. 1999 issue of Health Psychology a medical psychologist at Georgetown, Caryn Lerman, published a stud showing that persons with a certain dopamine transporter gene were less likely to start smoking and more likely to quit smoking than persons lacking the gene. How is RJ Reynolds handling all the negative publicity about smoking? The 6/28/99 edition of the Wall Street Journal reports that RJ Reynolds has decided not to get into the nicotine patch business to help smokers quit (which would undermine its existing product sales), but has decided to plan for the future (when fewer people will smoke) by developing medical applications for nicotine as a pharmaceutical.  Solid clinical research has shown that smokers are less likely to get Alzheimers or Parkinsons than non-smokers and, if they do get it, tend to develop it later in life in less severe form. No one knows why this is so, but Alzheimers patients have much fewer nicotinic receptors in their brains than other people and smokers have more. The new unit of RJ Reynolds (called Targacept for "Target" and "Receptors") will compete head on with established drug companies to develop and market nicotinic drug compounds for such diseases as Alzheimers, Parkinsons, schizophrenia, depression, ADHD, Tourettes and chronic pain.

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fMRI Maps Math and Attention Circuits

Using bi-lingual college students as subjects neuro-scientist Stanislas Dehaene of NIH and cognitive psychologist Elizabeth Spelke of MIT ascertained the existence of two separate brain circuits for mathematical operations. They found an intuitive non-verbal sense of such things as relative size, relative proportion and approximation of quantities in both parietal lobes. They found a language based capacity for precise calculations in the left frontal lobe in the vicinity of Broca's area which articulates speech. In making this discovery they used superfast imaging of  brain activity (fMRI) while students made different kinds of math calculations, precise and approximate. This was reported in the May 1999 issue of Science. The authors state that many other animals have a non-verbal sense of quantity, but humans have taken math to a higher level because they synergistically use this capacity with the capacity for precise calculation using language. This knowledge may be of use now, or someday, to neuropsychologists trying to find a connection between brain injury and lost math ability, and trying to compensate for the loss.

Meanwhile at the Medical College of Wisconsin, a team of reseachers led by Edgard DeYoe, a professor of cellular biology and neurobiology, used fMRI to map rapid shifting of attention in frontal lobe circuits. While volunteers stared at a stationary grid pattern, and new visual objects were introduced, the researchers were able to watch and track different areas of the frontal lobes light up on the brain imaging display. News of the discovery was released in May 1999. While Dr. DeYoe is primarily interested in using his maps to understand what has gone wrong with the brain in ADHD (attention deficit disorder), the technique and the data may be useful to persons with brain injuries, many of whom sustain contusions and/or diffuse shearing lesions to the frontal lobes with loss of capacity for multi-tasking, inability to ignore distractions and other features of executive function disorder.

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Self-Managing Chronic Pain

Although chronic pain management programs have sprung up in many communities, they are very expensive and very hard to get into. Program directors screen for adequate insurance coverage and for any psychological condition (e.g. addiction) or medical condition, which studies identify as a risk factor in not achieving successful completion of the program. Getting paid and getting insurance companies to select a particular program depends upon showing a consistently high rate of good patient outcomes, so program intake is slanted towards those patients most likely to show improvement, rather than the hard cases.

If a person with a brain or spinal cord injury who has CPD (chronic pain disorder) cannot get into a decent chronic pain management program because of lack of money, lack of insurance or rejection by the program director, is there a way to manage one's own pain? The answer is a qualified yes. While self-management cannot address all the problems associated with CPD, self-management is surely better than no management. Furthermore, since a portion of the suffering from CPD has to do with the psychological response of the individual to living with chronic pain, self-management makes sense, because one's attitude is at least partly under one's own control, and can be changed without the necessity for professional, outside intervention.

Dana S. DeBoskey, Phd has written an excellent book entitled "Pain: Making Life Liveable," which is a blueprint for self-management of CPD, written in simple, non-technical terms and full of points to reflect on along with suggestions, exercises and goals for positive attitudinal change. The book is a slim and inexpensive, soft-cover volume available from HDI Publishers P.O. Box 131401 Houston, Texas 77219. This book and other self-help titles for persons living with a brain or spinal cord injury can be ordered from HDI by phone at (800) 321-7037 or by fax at (713) 956-2288. Recently there has been a lot of interest in the use of magnets to ease pain flareups as an alternative to narcotic analgesics like Vicodin, which make people drowsy and have a potential for addiction. One double-blind randomized study with real and placebo magnets has been done. The result was that pain patients who applied the real  magnets for 45 minutes obtained substantial pain relief as opposed to the placebo group which received very little or  none. The power of the magnets was the equivalent of two refrigerator magnets. No one has quite been able to explain the effectiveness of magnets in temporary relief of acute somatic pain. The theory of local increase in blood flow did not check out, because the magnets caused no increase in red skin color. The theory that the magnets affected the hemoglobin was rejected because the iron in hemoglobin does not react to magnets. One possibility is electro-magnetism, which might block pain signals by changing the flow of electric current in the nerve cells acting as pain fibers, but this is just speculation. Since there is no known harm in using magnets, why not try it?
                                                   

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In a recent issue of Brain Injury it was reported that electric stimulation of the median nerve in the arm of coma patients showed significant success in shortening the duration of coma as compared with a control group. The median nerve is wired directly to the ARAS (ascending reticular activating system) in the brain stem, which awakens the cortex by sending norepinephrine to the thalmus. The authors postulate that stimulation of the median nerve produces stimulation of the ARAS which in turn raises the arousal level of the cortex above the coma threshold. They state that median nerve stimulation cannot be regarded as a "cure" for coma based on this one study, but they believe this novel method of coma therapy holds great promise.
                                            

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Pitfalls of Medicating Apathy

A common sequelae of frontal lobe injury is apathy or loss of ability to spontaneously initiate activity. Persons with this executive function disorder symptom cannot set themselves in motion, and need constant reminders from others to do just about anything, even eat a meal.  In the January 1999 edition of Brain Injury, it was reported that administration of the drug Amantadine, which stimulates extra release and utilization of dopamine, helped a female patient with bilateral front lobe injury overcome her apathy. However, the higher dosage required to achieve this led to the opposite problem of agitation, impulsivity and aggression. Lowering the dose stopped the side effects, but she became apathetic again. Fine tuning the dosage to obtain the benefit while avoiding undesirable side effects is no easy matter, as this report shows. The authors recommend further trials of amantadine and other dopamine agonists such as bromocriptine and sinemet in hopes of finding the right balance of meds.

                                                    
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A New Anti-Depressant

Pharmacia & Upjohn have submitted a new anti-depressant called Reboxetine to the FDA for review. SSRIs like Prozac and Zoloft work by blocking re-uptake of serotonin, which lightens and brightens the heavy, dark and bleak mood state of depression in which the glass is always seen as half empty. Reboxetine works by blocking the breakdown of norepinephrine at the synaptic junction. Increasing the supply of norepi will presumably boost energy, drive, vitality and motivation. It is well known that TBI may spare IQ while robbing the survivor of the capacity to initiate and complete activities, leaving her in a state of apathy and indifference. This is called executive function disorder which is distinct from feeling sad, worthless, etc. In the past, neurologists tried amphetamines to boost lost "get up and go." One problem with amphetamines is addiction. They also disrupt the normal sleep-wake cycle. Readers of New & Noteworthy are encouraged to find out more about Reboxetine from their neurologists, the FDA or Upjohn. Studies conducted so far indicate it boosts energy but is not addictive.
                                            

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Anti-Depressants and Cognition

Neuropsychologists say that depression so lowers cognitive peformance on standard tests (e.g Wechsler Adult Intelligence Scale) that they may postpone testing until admininstration of anti-depressants, participation in psychotherapy, or both, have lessened the patient's depression. Is this a coincidental assocation or a causal assocation? What is the mechanism behind the relationship between cognitive sharpness and depression? A psychological explanation is that people who are depressed are pre-occupied, less attentive to their surroundings and feel tired and depleted. Is there a bio-chemical or neurobiological explanation for the blunting of intellligence by depression? In the January 15, 1999 edition of the Journal of Neuroscience, it was reported that chronic administration of anti-depressants to rats was found to significantly raise the level of certain enzymes in the nucleus accumbens, an area of the brain associated with the presence or absence of  craving, as well as feelings of "emotional reward" such as pleasure or joy. These particular enzymes play a key role in the the encoding of short term memory and its conversion to long term memory by the hippocampus.  Thus a depressed person has less of a supply of the brain enzymes she needs for the hippocampal activity necessary to build long term memory and achieve new learning. Depression and poor short termy memory with deficits in new learning are very common after a TBI. Standard treatment of the depression involves anti-depressant medication. Persons with TBI who reject the idea of taking anti-depressants  because they think such drugs are only for "crazy people" should be aware that anti-depressants may boost their replenish the enzymes  they need to boost flagging short term memory function. Further, depression is not craziness. It is a mood disorder directly caused by brain trauma and also results from conscious awareness of being disabled. It is not a sign of weakness and should not be viewed as a stigma. One note of caution. Many clinicians who prescribe the anti-depressant trazadone, find it helps people sleep, but - unlike other anti-depressants, appears to diminish short term memory, sometimes rather dramatically. This brings to mind the oft repeated dictum that brain functions are so complex there are no one-to-one relationships between specific neurotransmitters and specific acts of cognition.

                                                       
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Off-Label Prescriptions

Because of the rigors of the approval process, the FDA invariably approves new prescription drugs for just one purpose (e.g. headache relief). Very frequently physicians will entertain a hunch that the drug may be effective in treating other conditions (e.g. depression) for which the RX drug has not been formally tested, studied and approved by the FDA, and this is called off-label prescribing. This kind of prescribing is legal, but amounts to experimentation. A recent decision by a Superior Court in Philadephia, PA, entitled Southard v. Temple University Hospital held that orthopaedic surgeon who implanted bone screws in a spinal fusion procedure for which they had not yet received FDA approval, had a legal duty to inform their patients before they made their decision to have the surgery. The privilege of off-label prescribing allows physicians to use their creativity and intuition, and can be of major benefit to suffering patients. However, it is important that patients (or their decision makers if they are under conservatorship) have the information first that this type of prescribing lacks FDA approval and carries certain unknowns. This is fair and appropriate. Persons with TBI should check with their physician whether the prescription is for an approved or off-label use and what risks they may be incurring in trying the medicine for their condition. Prudent self-protection means being informed of all relevant considerations in taking a medication, and this is  one of them.

                                                     
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Kids of Parents with a TBI

In April 1999 Childhood Trends, Inc., a non-profit Washington, D.C. group concerned with the well being of children, issued a report stating that one-eighth of parents in this country have significant (partially disabling) health problems which may have serious adverse psychological consequences for their children. A child raised by a parent who suffers from chronic depression, pain or fatigue, is forced to deal with a parent who removes herself emotionally and physically, and may view this as rejection by the parent. A parent who suffers from reduced frustration tolerance, heightened irritability and poor short term memory, may repeatedly yell and scream at her child and not remember doing it.  This is hurtful and confusing to the child, because she sees and feels the inconsistency in her parent's behavior and moods, but the parent acts as if everything is OK. What can be done? Education, awareness and counselilng are critical. A good MFCC (marriage, family and child counselor) with experience in the dynamics of parental brain injury in the family can be of immeasurable help. The treating neuropsychologist should address the issue and make the referral.

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Telephonic Monitoring

Following post-acute rehabilitation, some persons with a TBI end up living alone, at least some of the time, out of personal choice (e.g. to assert their independence), for economic reasons or out of necessity. How can worried family members check up on them to make sure they are OK without being irritating? For just $1.00 a day a company called TelAssure has a computer call a designated person twice daily. If she doesn't answer, the computer notifies selected family or friends. Caring Technologies of Bethesda, Maryland, is marketing a new product called iPERS (Intelligent Personal Emergency Response System) which consists of a small device on a strap worn on the chest. If the person falls or stops breathing, the device contacts 911. Such a device could be life saving for someone with post-traumatic epileptic seizures with black outs. Crozer-Keystone Health System of Springfield, PA, has redesigned the web TV box to contain a camera which transmits images of the viewer to family, social workers or health care providers. Medicaid has approved telemedicine hookups of this nature for at-home seniors in some parts of the country. Case managers, physiatrists and TBI advocates should try for approval of the same devices for  persons with a TBI.
                                                         
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Migraines and Triptans

Migraine is a common sequelae of closed head trauma, which may cause headache and disability longer than cognitive disruption, irritability and other symptoms associated with TBI. Bringing migraine under control through prophylactic medication (to prevent onset) and abortive medication (to stop headache already in progress) is essential. Biofeedback (for self-regulation of stress), nerve block injections to trigger points at the base of the head, neck or trapezius, and avoidance of known migraine triggers may help, but does not substitute for medication.  Today the family of 5-HT receptor agonists known as the triptans are among the best known and most effective migraine drugs of the abortive type. Anti-convulsant medications like Depakote are effective in preventing headache. SSRI medications like Sertraline are highly effective in reducing depression, but when tested as migraine peventers in persons with depression and migraine, they have shown little promise. The best known of the triptans is sumatriptan (imitrex), which has worked well for my clients. Newer triptans have come out with new benefits. Amerge (naratriptan) can tackle even stronger migraine headaches than Imitrex. Maxalt (rizatriptan) is extremely well tolerated by migraine sufferers who experience nausea, because it comes in a tiny pill which dissolves quickly under the tongue and does not require a glass of water. A recent study showed that Maxalt is absorbed twice as fast into the bloodstream than aspirin, tylenol or non-steroidal anti-inflammatories like Ibuprofen. Migraine appears to slow digestion in the GI tract, but this slowing is bypassed by Maxalt. How do these medications work?   A new study in Journal of Neuroscience (5/1/99) shows how Imitrex works. The trigeminal nerve is a large cranial nerve in the head with 3 sensory branches about the eyes, cheek and jaw. Once the trigger (e.g. bright light) activates trigeminal ganglion neurons, they release CGRP (calcitonin gene-related peptide). This sets off rapid expansion (dilatation) of the diameter of blood vessels in the head, degeneration of mast cells and release of inflammatory substances such as substance P and neurokinin. These substances signal the trigeminal to relase more CGRP in a feedback loop which can make a head squeezing migraine last up to 72 hours. The study showed that Imitrex causes the trigeminal ganglion neurons to hold extra calcium ions over a prolonged period of time, which blocks potassium-stimulated CGRP release. Thus Imitrex interferes with the increased phosphatase activity involved in the inflammation process. Administration of Imitrex rapidly reduces the level of CGRP back to normal (basal) levels with shrinkage of blood vessel diameter and reduction in headache severity and duration.
                                                            
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Estrogen and Memory

A new study in the Journal of Neuroscience (5/1/99) indicates that women begin losing short term memory capacity after menopause, because cyclic release of high doses of estrogen are needed to preserve the vigor of neurons in the hippocampus, the inner temporal lobe area where working memories are encoded for long term storage. Chronic low dose hormone replacement therapy did not stop progressive loss of dendritic spines in hippocampal neurons, because only cyclic bursts of large quantities of estrogen works.

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Bicycle Helmets
The Consumer Product Safety Commission just announced the recall of 5,800 helmets made by Bell Sports, Inc. of San Jose (the Rhythm, the Bellistic and the Qualifier) for loose chin strap rivets, which allegedly could cause the strap to pull off and the helmet to come off in a fall. Parents of children who ride bikes should always make sure their child is wearing a helmet and that the rivets are tight. Parents should also make sure the helmet fits snugly and is sufficiently low in front to protect the forehead where the frontal lobes are located. Bicycle accidents without helmet use continue to be the leading cause of TBI in children.
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Prosthetic Memory
Neuropsychologist Neil Hersh of San Mateo has developed a prosthetic memory system for persons who cannot remember when to take specific action without external prompting, such as take medication, visit the doctor, prepare a meal, and the like. Each client gets a beeper with a very loud beep which will go off at times predesignated on Dr. Hersh's computerized schedule at his office. The schedule can be reprogammed by the client as his routines change. For those interested contact Dr. Hersh at neilhersh@prodigy.com

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Brain Implant
Neurosurgeon Roy Bakay of Emory has successfully implanted a device in the brain of one stroke patient and one ALS patient, which permitted them to move a cursor on a lap top computer to language based icons merely by willing the cursor to move. The device (a tiny sensor in a glass case) was inserted in the motor cortex where it picked up movement commands and sent them to receiver in the skin and an amplifier in the scalp. The device was invented by Dr. Phillip Kennedy who worked with scientists at Emory University and the Georgia Institute of Technology in Atlanta. With practice, and some mechanical fine tuning of the device, both patients achieved success in establishing limited communication of words and phrases. Both patients were paralyzed and unable to speak or move their limbs. This device has the potential to end isolation and "open up whole new worlds" for patients with aphasia and/or paralysis.

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Brain Death
A recent article in Cerebrum (Dana Press) distinguished between: (1) lack of cortical function (conscious thought) with an intact brain stem which would keep the patient alive in a biologic sense without the need for mechanical means since the heart would beat and the lungs respire on their own; (2) intact cortical function without brain stem function, in which a person having conscious thought would need mechanical means to keep him alive; and (3) total, irreversible cessation of cortical and brain stem function in which mechanical means would be necessary to keep the patient alive in a biologic sense but where the patient would never have conscious thoughts, perceptions or memories. It was category #3 that the author stated would be acceptable on ethical and religious as well as legal and medical grounds, as a standard criterion for brain death, which would permit "pulling the plug" and harvesting organs for donation.

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Credit Card Abuse
The Wall Street Journal reports that competition among credit card vendors has led some unscrupulous companies to target persons with diminished mental capacity, including persons with TBI. Impulsive spending by a TBI survivor with a credit card can, and does, lead to insolvency and bankruptcy. Hence the parents, spouses and guardians of persons with TBI are advised to exercise vigilance in screening credit card applications in the mail, preventing or limiting use of credit   cards, monitoring credit card charge statements and the like.

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ID Cards

TPN, Inc. has created an ID card for survivors of TBI with simple language descriptions of symptoms/deficits to help others understand their situation in emergency situations or during a period of interrupted communication due to stress, aphasia, etc. TPN invites you to request an ID card by mailing a legal-sized stamped and self-addressed envelope to TPN, Inc. Attn: ID Cards P.O. Box 1859 Cumming, Georgia 30128-1859. If anyone does order one, please let me know if it is helpful or not helpful to you.

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Handheld Computers

To compensate for deficits in memory, organization and retrieval of useful, everyday information, some survivors of TBI have used a written paper notebook or calendar. A more sophisticated approach has been to use a tiny, palm-sized computer such as the PalmPilot (a product of a 3M Corp. subsidiary) which electronically stores address information and calendar dates. Now there is a computer the size of a credit card called the Rex which weighs just 1.4 ounces and fits in a shirt pocket or business card case. It can store up to 2,500 items of information, such as to-do lists, and can display them on a tiny screen in sharp, clear print. The higher capacity model costs $159 and the lower capacity, which stores 750 items of info, costs $129. To use the Rex you must buy a $40 cradle which lets the Rex interface with a desk top PC or a mobile laptop computer, and this connection is necessary for you to input data into the Rex, something you cannot do directly at this time. If anyone buys the Rex and has comments pro, con or both, please e-mail your comments to me at hhyman@headinjurylaw.com.

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Creatine Risks to Atheletes

The FDA has just put out a warning that prolonged ingestion of creatine at the high doses recommended on the containers may be responsible for deaths and seizures suffered by college wrestlers. Creatine is a popular protein ingested by athletes and body builders to make themselves work harder and stronger when lifting and to accelerate buildup of muscle mass. Unfortunately it appears that too much use of this protein may be neuro-toxic at least to some individuals, and at this time no one knows what a safe dose would be for any particular individual. Accordingly strong caution should be exercised by anyone who uses creatine or contemplates using it. Nutritional literature indicates that drinking a shot of espresso before exercise can increase the efficiency and power of the work-out, and to my knowledge the only adverse side-effect of espresso is sour stomach or jitteriness in some people. Personally I love espresso and drink it a lot without problems.

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Court Appointed Guardians

Recent reports indicate that some Court Appointed guardians and conservators of persons with TBI have fallen prey to temptation and begun converting funds for their own use - to buy cars, paintings, jewelry, real estate, etc. Family members of persons with TBI must remember that Courts have insufficient staff and resources to carefully monitor the honesty of all appointed guardians all the time. Family members should carefully investigate anyone whom the Court nominates to serve as a guardian, and thereafter keep in good contact with the guardian and ask for frequent accountings. This will tend to prevent or at least uncover any financial abuses.

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Soccer Head Injuries

The Journal of Head Trauma Rehabilitation (Vol 13 Issue 2) reports that cumulative closed head trauma from heading a soccer ball is associated with deficits in memory, cognition and motor control similar to what is seen in boxers. It is recommended that soccer players rely less on heading than other means of blocking or passing, and that soccer plays who do head the ball must learn and master proper techniques of bracing their necks. Apparently the news that repeated heading of a soccer ball could cause mild brain injury was greeted with total surprise by coaches and players. There needs to be much better information for coaches and players alike, and the quicker the better.

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Herbal Remedies

People taking anti-depressants (e.g. Zoloft, Prozac or Paxil) who are interested in trying a natural remedy alternative (e.g. tyrosine or St. John's Wort) sometimes pursue a "don't ask don't tell" approach - meaning they do not tell their treating internist or psychiatrist that they are seeing a homeopath and do not tell their homeopath they are taking prescription medications. The result can be disastrous even fatal, because unmonitored mixing of prescription and powerful herbal medicines may wreck havoc with blood pressure, kidney function, liver function, etc. Concerns over being branded as a flake or weirdo by ones doctor must be subordinated to maintaining good health. Furthermore, mainstream doctors are not as uptight as they are portrayed and they need to be educated by their own patients as to herbal remedies which can safely supplement, enhance or replace everyday drugs.

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Mandatory Helmets for Skiiers?

Recent skiing deaths of celebrities from closed head injuries has lead to a call for mandatory helmets for skiers. Those calling for helmets point out that it is universal practice for bike riders, motorcycle riders and horse riders to wear protective helmets, so why not skiers too? Not everyone agrees. Opponents say high speed crashes will kill the skier no matter what, even from fractured necks. This is not a good argument, since Olympic downhill skiers wear helmets and do survive very high speed crashes with tremendous impacts. Herman Maier is a great example. He wore a helmet, and got up to win 2 gold medals after a crash which might have killed him. The helmets worn by Olympic skiers do not prevent them from seeing the slopes or skiing with maximum speed, power and grace. Motorcycle riders in California are now launching an all-out challenge to force the repeal of recently enacted legislation requiring that they wear helmets. They are focusing the debate on individual freedom, but ignoring statistics showing a drop in severe head injury, death, disability and hospital and medical costs related to highway accidents involving motorcyclists due to passage of this law.

The opportunity to use our roads is not an unconditional right, but a privilege which may be legally taken away. Traffic laws in all 50 states make speeding, reckless driving and drunk driving illegal. So why should operating a motorcycle without a helmet at speeds fast enough to cause death, permanent vegetative coma or severe life-long disability be legal, especially when you consider that tax dollars build, maintain and repair the roads and it is our tax dollars which end up paying for hospital, medical and other care for helmetless riders who wipe out. TBI is not just a personal tragedy but a huge socio-economic burden on the community, and if simple, inexpensive means can be taken to prevent it with minimal sacrifice of personal choice, why should we not act as a community?

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New Location for National Brain Injury Association

The National Brain Injury Association, Inc. has moved from its old location on Massachusetts Ave. in Washington, D.C. to a brand new building at 105 N. Alfred Street, Alexandria, VA 22314 (703) 236-6000. Their new fax number is 703-236-6001 and their website address is: http://www.biausa.org . Congratulations to the BIA, George Zitnay (former President of BIA) and to all the persons whose financial contributions made this possible.

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Toy Guide for Differently-Abled Kids

Pediatric brain injuries associated with use or innocent, foreseeable misuse of toys. Every year America's children receive a staggering 1.6 billion new toys. Every year there are 165,000 injuries and a few dozen deaths. More than half of all deaths come from choking. The Consumer Product Safety Commission tries to identify toys which cause a choking hazard and requires manufacturers to use a warning label for children aged 3-5. Other hazards include burns from toy ovens, hearing loss from toys which simulate firecrackers or involve a blast of compressed air and eye injuries from dart guns and bottle rockets. How can you find out about toy hazards? The CPSC maintains a consumer hotline at 1-800-638-2772. Press releases can be obtained on demand via fax at 301-504-0051 or by browsing the CPSC website at www.cpsc.gov. Another source of information is the website at www.kidsource.com which lists toy recalls.

Children with central nervous system injuries or disorders who may be at risk from playing with toys designed for completely able-bodied kids can obtain toys with special safety features. Toys-R-Us publishes a Toy Guide for Differently-Abled Kids in association with the National Parent Network on Disabilities and National Lekotek Center. To request a copy write to Toys "R" Us, Guide for Differently-Abled Kids P.O. Box 4422, River Edge, New Jersey 07661-9894 or inquire at your local store.

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Apathy Widespead Among Those with TBI

A recent survey has shown that apathy is more widespread among survivors of TBI than depression and may create an even greater obstacle to successful return to work, successful psychotherapy or successful re-integration into the community. Families of survivors who detect apathy in their injured member, should bring this to the attention of their loved one's treating physician. The survey showed that apathy was more likely to afflict the young TBI survivors than the older one's, but no age group was immune.

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Donepezil Boosts Short Term Memory

Anecdotal information now suggests that use of the prescription drug Donepezil can be helpful in alleviating the functional severity of short term memory impairment following TBI. The postulated mechanism is blocking the breakdown of AcH (acetylcholine) leaving more in the central nervous system for short term memory processing. Three week trials on a two patients showed good enhancement of short term memory akin to what is sometimes seen with Alzheimer's patients who take the drug. However, the authors of the study caution that the sample size was far too low to permit any solid, scientific conclusions at this time.

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