Traumatic brain injury treatment

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. 

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. 

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. 

Lea P. M. and Faden A. I. (2001). Traumatic brain injury developmental differences in glutamate receptor response and the impact on treatment. Ment. Retard. Dev. Disabil. Res. Rev. 7 235-248. 

New research on the antioxidative properties of creatine shows that the supplement may have even therapeutic properties beyond the treatment of musculoskeletal disease and injury. A 2000 study in Annals of Neurology reported that creatine had a protective effect against traumatic brain injury (TBI) in animal studies, reducing brain damage in mice and rats by up to 50%. 

Several animal models suggest that the time to initiate cooling following TBI is brief. Some rat models suggest that the therapeutic window for treatment with hypothermia is approx 25 min (41,42). These data would seem quite discouraging, as most traumatic brain injury patients do not arrive at the hospital and receive complete evaluation until significantly more time has elapsed. Even with rapid transporta-... 

Marion D. W., Penrod L. E., Kelsey S. F., etal. (1997) Treatment of traumatic brain injury with moderate hypothermia. N. Engl. J. Med. 336,540-546. 

Resurgence of Hypothermia as a Treatment for Brain Injury. The Effects of Hypothermia and Hyperthermia in Global Cerebral Ischemia. Mild Hypothermia in Experimental Focal Cerebral Ischemia. Hypothermic Protection in Traumatic Brain Injury. Postischemic Hypothermia Provides Long-Term Neuroprotection in Rodents. Combination Therapy With Hypothermia and Pharmaceuticals for the T reatment of Acute Cerebral Ischemia. Intraoperative and Intensive Care Management of the Patient Undergoing Mild Hypothermia. Management of Traumatic Brain Injury With Moderate Hypothermia. Hypothermia Clinical Experience in Stroke Patients. Hypothermia Therapy Future Directions in Research and Clinical Practice. Index. 

Stroke is a global health problem affecting approximately 750,000 people annually in the United States alone and ranks as the third leading cause of death and the most common cause of disability in most developed countries. Traumatic brain injury (TBI) accounts for an estimated 34% of all injury-related deaths in the United States. Stroke and TBI can produce both focal and widespread damage to the brain, which can yield acute and chronic impairments of sensory, motor, and cognitive functions. Because of their enormous medical and socioeconomic impact, a tremendous research investment is being made in the treatment and prevention of stroke and TBI. 

Fink, himself a member of the 1978 and 1990 APA ECT task forces, for decades argued and demonstrated scientifically that ECT s therapeutic effect is produced by brain dysfunction and damage. He pointed out in his 1979 textbook that patients become more compliant and acquiescent with treatment (p. 139). He connected the so-called improvement with denial, disorientation (p. 165), and other signs of traumatic brain injury and an organic brain syndrome. This is a direct confirmation of the brain-disabling treatment and the use of iatrogenic denial in authoritarian psychiatry. 

Mauler F, Horvath E, de Vry J, Jaeger R, Schwarz T, Sandmann S, Weinz C, Heinig R, Boettcher M (2003) BAY 38-7271 a novel highly selective and highly potent cannabinoid receptor agonist for the treatment of traumatic brain injury. CNS Drug Rev 9 343-358... 

---