Allegation of Faking Depression in Litigation can be Disproven

Research published in October 2012 by a team at Mt. Sinai Medical Center led by Georgia Hodes Phd shows that real depression is related to and co-occurs with a measurable spike in the protein IL-6 produced by the immune system. In litigation over TBI claims the plaintiff is frequently depressed and the defense is either that the depression pre-existed the TBI (but was never diagnosed) or that the plaintiff is faking bad (i.e. pretending to be depressed to collect money he doesn’t deserve). Based on this published research if a plaintiff developed severe depression consequent to a TBI and his blood shows elevated IL-6 it will be easier to show that his depression is organic. In the rare case where the plaintiff had his blood tested shortly prior to the TBI and his IL-6 was measured as normal, you would have a strong pre vs. post incident contrast.

Zolpidem Wakes Some Patients From Persistent Coma

TBI and other conditions can put a person in a deep coma for years on end. This condition is called PVS which is short for “persistent vegetative state.” In a number of highly publicized incidents use of the drug Zolpidem (sold under the names Ambien, Ambien CR and Stilknox) has woken people up enabling them to sit up and speak after being in a PVS for years. Zolpidem is typically used to help people with insomnia get to sleep. It works by binding to the receptors for GABA, an inhibitory neurotransmitter. It has long been established that sleep and coma are different, and that coma is not a form of sleep. So how does Zolpidem wake people up from coma? We don’t know at this point. But the utterly remarkable success of Zolpidem in some cases has led people to call it the Lazarus drug.

Relationship of Sleep and Memory Disorders From TBI

Consequent to TBI some people suffer damage to an area of the brain called the Suprachiasmatic Nucleus or SCN. The SCN is about the size of a grain of rice and sits above the spot in the brain where the two sides of the optic nerve cross. It controls the 24 hour biological rhythym of sleep in humans and other mammals. Traumatic damage to the SCN disrupts normal sleep patterns and can also impair normal memory formation. This may be due to the fact that people need to sleep and dream a certain amount of time each night to form lasting memories. The function of the hippocampus (the brain organ of memory encoding) and the SCN are related. They share a certain number of genes in common. The matter is still under investigation.

Manage Pathological Laughing and Crying From TBI

One consquence of TBI known as the “psuedobulbar affect” or PBA is uncontrollable, inappropriate fits of laughter, crying or both. Jonathan Fellus, MD of Seacaucus, New Jersey, is an expert on the treatment of PBA. He recommends trying behavioral strategies first. For example, when you feel an episode coming you can try to relax, breathe, and distract yourself. If behavioral strategies do not work, then he recommends taking a medication called NUEDEXRA which can eliminate or decrease symptoms of PBA.

Human Growth Hormone Deficiency May Play a Role in Mild TBI Problems

Dr. Adriana G. Ioachimescu of Emory University, Atlanta presented a paper in September 2012 at the annual meeting of the Endocrine Society concerning the possible role of human growth hormone (HGH) deficiency in causing some problems for TBI suvivors. The subjects of her pilot study were 20 men (mean age, 34 years) with mild TBI resulting from military combat which had been sustained an average of 44 months earlier. Dr. Ioachimescu observed that all of the subjects had normal thyroid status and cortisol production, but 5 of them (25%) had a deficiency in their production of HGH.

While all 20 subjects with mild TBI performed similarly on measures of memory, learning, and simple and complex attention, the 5 subjects with deficient HGH did worse on tests of executive dysfunction, especially those relating to measures of inhibitory control and self-monitoring. The GH deficient soldiers show greater levels of depression and lower quality of life than the others even though they did not have a higher incidence of PTSD.

Was the deficiency of HGH present before the 5 veterans sustained their mild TBI or did it result from the MTBI? Either way the presence of deficient HGH in a person with MTBI appears to produce a worse outcome with regard to some executive functions and depressed mood. This suggests the possibility that treating MTBI survivors with poor executive function and/or depression using HGH may improve their condition. Futher research is needed.

Adult Stem Cell Therapy for TBI Still on the Horizon

In the Jan.-Feb 2009 issue of Disease Models & Mechanisms Dr. Peter A. Walker and colleagues summarized what we know so far about the use of progenitor cell therapies for traumatic brain injury. Due to evidence in rats that transplanation of embryonic stem cells grow tumors in the post-TBI brain and strict limits on the use of such cells, researchers have focused on adult stem cells. These cells congregate in certain areas of the adult human body, especially the bone marrow, the subventricular zone of the brain, the umbilicial cord and adipose (fat) tissue. There is preliminary evidence at this time that infusion of pluripotent adult stem cells into the brain post-TBI can protect damaged cells by supplying intact genetic material, producing neurotrophic growth factors, and by reducing inflammation.

Much more clinical experimentation needs to be done, but researchers are hopeful that one day adult stem cells will become part of the acute treatment for TBI. Right now there is little physicians can due in the acute stage except monitor intracranial pressure; reduce IC pressure with drugs, shunts or both; and increase cerebral blood perfusion with drugs.

One Cortisone Shot May Prevent PTSD

PTSD (post-traumatic stress disorder) can co-occur with TBI from the same event or occur on its own. Either way PTSD can cause serious emotional suffering and disability from work. A recent study on PTSD prevention by Joseph Zohar, M.D., of Tel Aviv University and Hagit Cohen, Ph.D., from Ben-Gurion University showed that traumatized patients who received a single injection of cortisone within a few hours of the event were more than 60% less likely to develop PTSD.

The researchers said the current prevention therapy using diazepine tranquilizers like Valium or Xanax to calm the traumatized patient down has not worked. They speculate the reason is that diazepines block the release of cortisol (which is made from cortisone). Why would blocking cortisol increase the likelihood of PTSD?

Cortisol increases blood sugar which reduces memory formation. Diabetics (who have high blood sugar) have poor cognitive function including poor memory. It may be that giving a shot of cortisone increases the material needed for cortisol synthesis which raises blood sugar and reduces memory of the event. Whatever the reason, the two researchers have been given a grant to continue studying the underlying mechanism(s).

Statin Drug use before TBI Improves Survival and Outcome

In the October 2011 issue of the journal Trauma epidemiologist Eric B. Schneider, Ph.D., of the Johns Hopkins University School of Medicine reported that older patients who happened to have been taking cholesterol-lowering statin drugs when admitted to the hospital with serious head injuries were 76% more likely to survive than those not taking the drugs, according to results of a Johns Hopkins study. Those taking statins also had a 13%greater likelihood of achieving good, functional recovery after one year.

Dr. Schneider suspects these effects are due to the anti-inflammatory properties of statin drugs which would prevent masses of white cells from moving into areas of traumatized brain tissue and killing them. He plans to do a clinical trial that would involve giving statins to in the ICU to seriously brain injured patients who had not previously taken statins.

Can A New Blood Test Diagnose TBI In The Field?

A study published by Dr. Linda Papa of Orlando, Florida, on November 10, 2011 in the Annals of Emergency Medicine found that patients with TBI had a significantly higher amount of an acidic protein in their blood than those without TBI. The protein at issue is called glial fibrillary acidic protein (GFAP). Dr. Papa said the test, which must be done within four hours after the injury, may be used someday in the field to diagnose TBI in wounded soldiers. She also said the test could help determine which patients with head trauma need or don’t need a head CT scan at a hospital.

The Concussion Crisis

Science writers Linda Carroll and David Rosner have just published an important book called “The Concussion Crisis: Anatomy of a Silent Epidemic” to dispel the myth that a concussion is not really serious and does not involve actual damage to the human brain that can produce long term symptoms with subjective misery and (in some cases) objective disability from employment.