Disease relevance of Craniocerebral Trauma

• Concentration of 3', 5' cyclic adenosine monophosphate in ventricular cerebrospinal fluid of patients with prolonged coma after head trauma or intracranial hemorrhage [1].
• Brain injury, as occurs in stroke or head trauma, induces a dramatic increase in levels of tumor necrosis factor-alpha (TNF), but its role in brain injury response is unknown [2].
• High rates of epilepsy have been observed after cranial surgery in patients with meningioma, aneurysm, and head injury with or without intracranial clots, and routine prophylaxis with phenytoin would seem to be indicated in such patients [3].
• Obsessive-compulsive disorder (OCD) has been linked to altered neurological function following head trauma, encephalitis, abnormal birth events, and Gilles de la Tourette's syndrome [4].
• Hyponatremia responsive to fludrocortisone acetate in elderly patients after head injury [5].

Psychiatry related information on Craniocerebral Trauma

• We present a practical set of guidelines for assessing competency in patients with cognitive deficits due to neurologic disorders such as stroke, head injury, Alzheimer disease, and multi-infarct dementia [6].
• Here, we studied the ATP1A2 FHM2 gene in a young girl with episodes of both very severe and transient neurological symptoms that were triggered by mild head trauma as well as permanent mental retardation [7].
• The NMDAR2B subunit is the focus of increasing interest as a therapeutic target in a wide range of CNS pathologies, including acute and chronic pain, stroke and head trauma, drug-induced dyskinesias, and dementias [8].
• Ascorbic acid (vitamin C) has been suggested to protect cerebral tissue in a variety of pathophysiological situations such as head trauma, ischemia or Alzheimer's disease [9].
• The importance of this technique in nuclear medicine today should not be overlooked, particularly in cerebrovascular diseases, dementias, epilepsy, head injury, malignant brain tumors, movement disorders, obsessive-compulsive disorder, Gilles de la Tourette's syndrome, schizophrenia, depression, panic disorder, and drug abuse [10].

High impact information on Craniocerebral Trauma

• METHODS: In the first phase of the study, we recorded clinical findings in 520 consecutive patients with minor head injury who had a normal score on the Glasgow Coma Scale and normal findings on a brief neurologic examination; the patients then underwent CT [11].
• Phenytoin exerts a beneficial effect by reducing seizures only during the first week after severe head injury [12].
• The delayed development of recurring seizures is a common consequence of traumatic head injury; the cause of such epilepsy is unknown [13].
• Apolipoprotein E epsilon 4 allele is associated with deposition of amyloid beta-protein following head injury [14].
• Isoflurane demonstrated some advantages over midazolam, and ketamine had a more favorable hemodynamic profile than fentanyl in patients with head injuries [15].

Chemical compound and disease context of Craniocerebral Trauma

• To study further the effectiveness of phenytoin (Dilantin) in preventing post-traumatic seizures, we randomly assigned 404 eligible patients with serious head trauma to treatment with phenytoin (n = 208) or placebo (n = 196) for one year in a double-blind fashion [12].
• Effects of pegorgotein on neurologic outcome of patients with severe head injury. A multicenter, randomized controlled trial [16].
• Phencyclidine abuse mimicking head injury [17].
• Decrease in glutamate in the jugular vein after head injury [18].
• Propofol use in head-injury patients [19].

Biological context of Craniocerebral Trauma

• In 1975 and 1976 190 head injury patients died after admission to 19 general hospitals in Mersey Region or after transfer to the regional department of neurosciences [20].
• CONCLUSIONS: Mild childhood head injury may play a role in the expression of schizophrenia in families with a strong genetic predisposition [21].
• Indeed, peptide-based caspase inhibitors prevent neuronal loss in animal models of head injury and stroke suggesting that these compounds may be the forerunners of non-peptide small molecules that halt apoptosis processes implicated in these neurodegenerative disorders [22].
• Mutation S218L in the Ca(V)2.1 alpha(1) subunit of P/Q-type Ca(2+) channels produces a severe clinical phenotype in which typical attacks of familial hemiplegic migraine (FHM) triggered by minor head trauma are followed, after a lucid interval, by deep (even fatal) coma and long lasting severe cerebral edema [23].
• The joint effects of head injury and APOE genotype were evaluated in a subsample of 942 probands and 327 controls (spouses and siblings) [24].

Anatomical context of Craniocerebral Trauma

• More people who die from head injuries than non-head-injured controls have deposits of amyloid beta-protein in the cerebral cortex, with amyloid beta-protein deposits present predominantly in patients with the APOE epsilon4 allele [25].
• We conclude that IL-1-dependent pathways project from the striatum to the cortex via the hypothalamus and lead to cortical injury, and that these may contribute to a number of human neurological conditions including stroke and head trauma [26].
• Fetal hippocampal grafting paradigms are of considerable significance because of their potential to treat neurological disorders affecting primarily hippocampus, including temporal lobe epilepsy, cerebral ischemia, stroke, and head injury [27].
• Some patients with central nervous system infections, acute demyelinating disease, certain drug overdoses, head trauma, and complex migraine also had elevations of serum and CSF CK-BB isoenzyme [28].
• Gram-negative bacillary meningitis (typically caused by E. coli, K. pneumoniae, P. aeruginosa, A. calcoaceticus, and others) has been associated with head trauma, neurosurgical operations, pathologic anastomosis with nasal cavity, and CSF rhinorrhea, as well as with impaired host defenses [29].

Gene context of Craniocerebral Trauma

• We report a prospective clinical study to test the hypothesis that patients with APOE epsilon4 have a worse clinical outcome 6 months after head injury than those without APOE epsilon4 [25].
• A "paradoxical" response of GH to TRH was observed on the day after the head trauma (basal vs. peak, p = .002) but not on day 16 [30].
• An elevated serum level of vWf may suggest endothelial activation in severe head injury [31].
• The levels of serum TM and vWf appear to be good indicators of the cerebral endothelial injury and of endothelial activation in severe head injury [31].
• Regarding severity and outcome, BDNF levels showed a sharp peak after head injury, but the only significant association was between NGF expression in the CSF and a good outcome versus a poor outcome ( p=0.007) [32].

Analytical, diagnostic and therapeutic context of Craniocerebral Trauma

• Glutamate antagonists are in human clinical trials aiming to demonstrate limitation of neuronal injury after head trauma, which consists of both rapid and slowly progressing neurodegeneration [33].
• RESULTS: Mx and Sx correlated with CPP (r = -.34, P = < .002; r = -.2, P = NS. respectively), with ICP (r = .46, P < .0001; r = .34, P < .003, respectively), with admission Glasgow Coma Scale score (r = -.34, P < .0025; r = -.38, P < .0008, respectively), and with outcome after head injury (r = .41, P < .0002; r = .48, P < .00009, respectively) [34].
• The sample consisted of 106 consecutive patients with accidental injuries (mean Injury Severity Score = 21.9, mean Glasgow Coma Scale score = 14.4) admitted to the intensive care unit of a University Hospital. Patients with severe head injuries, suicide attempters, and victims of physical assault were excluded [35].
• GEE logistic regression was used to examine the joint effects of APOE genotype and head injury on the odds of AD in probands and a control group comprised of unaffected siblings and spouses [24].
• Positron emission tomography scans of patients with head injuries often show discrete areas of increased 18F-fluorodeoxyglucose uptake ("hot spots") when performed hours to days after the initial ictus [36].

References