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.

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.

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.

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.

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.