Brain injury, traumatic

Although traumatic brain injury (TBI) is not, in and of itself, a psychiatric illness, it nonetheless warrants attention in our discussion of psychiatric medicines for two important reasons. First, it is not unusual for TBI to produce psychiatric symptoms severe enough to require pharmacological treatment. Second, treatment with psychiatric medicines after TBI often raises clinical concerns that are unique to these patients. More specifically, an injured brain is often especially vulnerable to medication side effects. Thus, the medical axiom first, do no harm is particularly important when treating TBI patients and must be considered when deciding whether to use psychiatric medicines, and if so, what medicines to use, and at what doses. 

Approximately 2 million people suffer head injuries each year in the United States alone. Of these, nearly 500,000 will be hospitalized and nearly 100,000 will suffer 

Principles of Psychopharmacology for Mental Health Professionals By Jeffrey E. Kelsey, D. Jeffrey Newport, and Charles B. Nemeroff Copyright 2006 John Wiley Sons, Inc. 

By definition, most patients who suffer a serious TBI present to an emergency room in the immediate aftermath of the traumatic event. However, patients may also be brought to medical attention days or even weeks after an apparently mild head injury when the symptoms are delayed or so subtle that they initially escaped detection. In some instances, patients may even visit a clinic unaware that their psychiatric symptoms are attributable to a remote head injury. One extreme example is so-called dementia pugilistica that occurs after years of repeated minor TBIs over the course of a boxer s career. 

The third factor to influence the likelihood of psychiatric complications after TBI is the patient s health prior to the injury. Elderly patients, those with preexisting 

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Neurological diseases Huntington s disease (A), amylotrophic lateral sclerosis (A,I), Parkinson s disease (A), traumatic brain injury (A,I), glaucoma (A)... 

ChEI treatments have been expanded also to include other dementias and CNS disorders, e.g. delirium, traumatic brain injuries and memory impairments, as well as myasthenia gravis, glaucoma and parasite infections. 

Traumatic brain injury is the most common cause of death in subjects under the age of 40, and an important risk factor for AD. Loss of hippocampal cells and depletion of ACh and of muscarinic receptors can be attenuated in injured experimental animals, improve blood perfusion in ischemic areas and increase cholinergic transmission in cortex and hippocampus the same mechanism invoked for treatment of VD. 

Tokutomi T, Mayagi T, Morimoto K, Kanikaya T, Shigemori M. Effect of h3fpothermia on serum electrolyte, inflammation, coagulation, and nutritional parameters in patients with severe traumatic brain injury. Neurocrit Care 2004 1(2) 171-182. 

Thomas SH, Orf J, Wedel SK, Conn AK. Hyperventilation in traumatic brain injury patients inconsistency between consensus guidelines and clinical practice. J Trauma 2002(l) 52 47-52. 

No role for corticosteroids in cerebrovascular accidents or traumatic brain injury based on the available literature. 

TBI Total-body irradiation, traumatic brain injury yr Year... 

Bayir, H. et al. (2005) Enhanced oxidative stress in iNOS-deficient mice after traumatic brain injury support for a neuroprotective role of iNOS. Journal of Cerebral Blood Flow el Metabolism, 25 (6), 673-684. 

Hypothermia improves imbalances of TXA2 and PGI2 after traumatic brain injury in humans (Aibiki et al., 2000). 

Marion D, Puccio A, Wisniewski S, Kochanek P, Dixon C, et al. 2002. Effect of hyperventilation on extracellular concentrations of glutamate, lactate, pyruvate, and local cerebral blood flow in patients with severe traumatic brain injury. Grit Care Med 30(12) 2619-2625. 

Panter S, Faden A. 1992. Pretreatment with NMDA antagonists limits release of excitatory amino acids following traumatic brain injury. Neurosci Lett 136(2) 165-168. 

Sarrafeadeh AS, Kiening KL, CaUsen TA, Unterberg AW. 2003. Metabolic changes during impending and manifest cerebral hypoxia in traumatic brain injury. Br J Neurosurg 17(4) 340-346. 

Gibson JB, Maxwell RA, Schweitzer JB, et al. Resuscitation from severe hemorrhagic shock after traumatic brain injury using saline, shed blood, or a blood substitute. Shock 2002 17 234. 

PolyADP-ribosylation has been reported to play a role in traumatic brain injury (TBI), excitotoxic, and oxidative injury. In the mitochondria after TBI, PARPs are activated and poIyADP-ribosylate multiple proteins involved in electron transfer. Since the ribosylation of these proteins shuts down electron transport, cells are sent into an apoptotic state. This gives insight into mitochondrial-based brain injuries and diseases. 

Traumatic Dementias. Traumatic brain injury can also result in dementia. This can result from a single massive head injury such as in a motorcycle accident or a gunshot wound. Repeated small head injuries can also cause dementia. The best example is dementia pugilistica, the dementia observed in professional boxers after many years and many prizefights. 

TABLE 12.1. Medication Strategies for Traumatic Brain injury Syndromes... 

Glenn MB. A differential diagnostic approach to the pharmacological treatment of cognitive, behavioral, and affective disorders after traumatic brain injury. J Head Trauma Rehabil 2002 17(4) 273-283. 

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