Brain damage in relation to psychiatric disability after head injury.
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Adult↗
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[Computerized tomography in post-traumatic cerebral lesions (author's transl)].
A review of 108 cases of cranial injury, dating back for more than three months, and having had computerized tomography examinations, revealed 96 abnormalities in the results. These included overall, 65 times, and localized, 20 times, ventricular dilatations, generalized atrophy 27 times, porencephaly 27 times, enlargement of the sylvian fossa 28 times, chronic subdural hematomas 8 times, intracranial calcification 3 times, meningiomas 3 times, and a cerebral abscess in 1 patient. The computerized tomography results were normal in 12 patients. Very good correlations were found between clinical and computerized tomography results in patients with psychic disturbances and disorders of the higher centers. They were variable in cases of epilepsy and neurological deficiency states. The greatest number of normal results was found in so-called subjective syndromes.
Brain Diseases↗
Surgical pathology of drug-resistant partial epilepsy. A 10-year-experience with a series of 327 consecutive resections.
Herein we reviewed the histopathological findings in 327 consecutive surgical specimens from patients with pharmaco-resistant epilepsy (PRE). Three major pathological groups (78.3% of all cases) were identified: Ammon's horn sclerosis (85 cases as an isolated lesion plus 18 as one part of a dual pathology), tumors (94 cases), and malformations (77 cases). Tumors, often associated with cortical dysplasias (CDs), were all of low histological grade and included 61 dysembryoplastic neuroepithelial tumors (DNTs), 29 gangliogliomas, and 4 pleomorphic xanthoastrocytomas (PXAs). Among the malformations were observed 52 CDs, 13 cavernomas, 8 cortical tubers, and 4 cysts. The remaining findings consisted of 16 scars (mostly post-traumatic) and 4 Rasmussen's encephalitis. Fifty-one (15.6%) specimens contained non-specific changes, and histological samples from 215 patients with presurgical implantation of electrodes revealed iatrogenic changes. All these figures are in agreement with the most recent and comparable series, and confirm the high incidence of DNTs that appear clearly as the most common tumoral entity in PRE. Our data also support the hypothesis of a close histogenetic relationship between DNT, ganglioglioma, and PXA, with a putative common origin from pluripotential progenitor CD34 positive cells of the subpial granular layer. As for CDs, our study confirms the clinical relevance of two main subtypes: severe CD (or Taylor's type CD) with neuronal cytomegaly and balloon cells, and non-Taylor's type CDs with a better outcome. Eventually, this series demonstrates that most patients have significant histopathological lesions, among which, aspects that are relevant to the diagnostic surgical pathologist are highlighted [published with a complete image database on CD-Rom].
Adolescent↗
[Clinical and social fate of craniocerebral injuries in young adults].
After looking 15 years back, the authors based two detailed observations of young adult cranio-cerebral injured taken amongst a group of 30 others who had been the subject of a medical doctorate thesis. From then on, the authors drew notions of semeiology, concerning the subjects becoming aware of their body before being injured, when waking up from coma and during the phasis of after effects. They mean to suggest to consider the notions of "normal person" and of pre-traumatic mind, of "present person" and of traumatic mind, and of "future person" and of post-traumatic mind. They attempted to write a comparative essay with the cerebral and physical disable of early youth. By way of conclusion, they briefly studied the attitudes of the clinical, familial and social relations and of the medical and legal consequences of these attitudes.
Adaptation, Psychological↗
[Rare and atypical forms of migraine].
There are three categories of rare forms of migraine headache. Atypical aura can raise difficult diagnostic questions due to their clinical expression (visual or sensorial illusions and hallucinations), their mode of onset (sudden aura, developing in less than 4 minute), their duration (prolonged aura lasting more than 60 minutes), and the lack of an accompanying headache. Differential diagnostics include partial epilepsy or AIT, requiring careful search for the underlying cause. Rare migraine syndromes are separate clinical entities, most of which are recognized by the International Headache Society (IHS). These syndromes include basilar migraine, familial hemiplegic migraine, ophthalmoplegic migraine and the exceptional retinal migraine. Confusional migraine, usually observed in children, is no individualized by the IHS but can be included here. For secondary migraines there is a triggering factor leading to migraine in patients with no history of migraine previously. These include post-traumatic migraine and cervical migraine as well as migraine occurring with epileptic seizures and rare symptomatic migraine headache disclosing a general disease or an intracranial neurological lesion.
Humans↗
The use of tiagabine augmentation for treatment-resistant anxiety disorders: a case series.
Tiagabine is currently approved by the Food and Drug Administration for use in treating certain forms of epilepsy. Like other anticonvulsant agents, tiagabine has been explored for use as a mood stabilizer and in panic disorder. This article presents a case series of five patients who were prescribed tiagabine for treatment-resistant anxiety.
Adult↗
[Rare and atypical forms of migraine].
The rare forms of migraine should be studied so that they can be recognized, thereby avoiding diagnostic errors and unnecessary complementary investigations. These rare forms can be divided into three categories: 1) atypical auras, characterized by the following: their semiology (visual or sensory illusions or hallucinations); their manner of onset (sudden onset of aura, with development of migraine in under four minutes); their duration (aura prolonged for between 60 minutes and seven days); aura with absence of accompanying cephalgia. This form of migraine could be confused with a case of partial epilepsy or AIT and raises a problem of differential diagnosis requiring an etiological investigation to ensure correct diagnosis; 2) clinical forms which are for the most part recognized by the International Headache Society's (IHS) classification, i.e., basilar artery migraine, familial hemiplegic migraine, ophthalmoplegic migraine and the rare occurrence of retinal migraine. Confusional migraine, a disorder which is mainly encountered in childhood, has not been categorized by the IHS but may be part of the symptomatology of the above-described forms; and 3) secondary migraines, in which a triggering mechanism causes migraine attacks to appear in a subject who was not previously affected by this disorder. This category covers post-traumatic migraine, migraine of cervical origin, the co-morbidity of migraine and epileptic seizures, and rare cases of symptomatic migraine which are indicative of underlying general disease or an intracranial lesion, i.e., a tumor or arteriovenous malformation.
Craniocerebral Trauma↗
[Post-traumatic arteriovenous communication of the renal pedicle producing severe hypertension (author's transl)].
Post-traumatic arteriovenous communications of the renal pedicle with the inferior vena cava, the kidney remaining in position, are rare. The present case, to our knowledge, is the fifth in the world literature (Cohen et al., Rex et al., McAlhany et al., Sechas et al.). The diagnosis was made, first by the clinical signs of murmur and thrill, furthermore, by the characteristic finding of diastolic hypertension and by cardiac hypertrophy, and the diagnosis was confirmed by angiography. Treatment was surgical, in an attempt to save the kidney by means of reconstruction of the vessels of the renal pedicle. Finally, as the renal lesions were not reversible and as the state of the patient was aggravated by epilepsy, nephrectomy was carried out during a second operation. One should note the fall in arterial blood pressure during the first postoperative period.
Angiography↗
Benign post-traumatic encephalopathy in young people and its relation to migraine.
Thirteen children and adolescents between ages 4 and 19 years developed transient nonconvulsive neurological symptoms and signs within a few hours apparently trivial head injuries. Some became quite seriously ill, but all made rapid and complete recoveries. Some of these young people are known to have suffered from migraine before and/or after this episode, and in all but one of the others a family history of migraine was elicited. With these patients are compared five younger children who developed epileptic fits after equally slight trauma. A diagnosis of migraine should be considered in children who develop delayed impairment of consciousness after head trauma, with or without convulsive phenomena or focal neurological deficits, and in whom specialized investigations reveal no sign of a mass lesion or of intracranial hemorrhage.
Adolescent↗
[Initial epileptic crisis after the age of 60: etiology, clinical aspects and EEG].
We reviewed retrospectively a series of 100 inpatients with onset of epileptic seizure after the age of 60. All of them were investigated by EEG and 96 by CT scan. The most frequent cause of seizure was previous stroke, with 25 cerebral infarcts and 5 hemorrhages. Neoplastic lesions were present in 18 cases, with glioma (high grade), meningioma and metastases in the same proportion. Other etiologies included toxico-metabolic (18 cases), post-traumatic (9 cases), cerebral atrophy (4 cases) and miscellaneous (14 cases). The causes of seizure remained unknown in 7 patients, of whom 6 had focal signs in either clinical examination or EEG. Focal seizures (with or without secondary generalization) accounted for 65% of all cases and generalized seizures for 35%. The EEG was normal in 12 patients and abnormal in 88, with diffuse slowing in 55 patients and focal signs in 70 (some patients had both diffuse slowing and focal signs). Fourteen patients presented status epilepticus. Ten died during hospitalization. We conclude that epileptic seizure with onset after age 60 is nearly always symptomatic, and neuroradiologic investigations are necessary in the search for cerebral lesions. In our study, the prevalence of "idiopathic epilepsy" is lower than previously described.
Aged↗
The late neurological, psychological, and social aspects of severe traumatic coma.
Thirty patients who had survived a heavy head trauma and a post-traumatic coma, lasting for more than one week, were investigated 8 to 14 years after the trauma. The patients have been followed up from a social, psychological, and neurological point of view. Fifty per cent of these patients are considered to be well rehabilitated. All the investigated patients showed slight to severe reduction in mental capacity. Eighty per cent of the patients had neurological defects which were not as important with respect to social rehabilitation as was the mental capacity reduction.
Accidents, Traffic↗
Diphenylhydantoin-induced hepatic necrosis. A case study.
A patient with post-traumatic seizure disorder developed lymphadenopathy, exfoliative dermatitis, and hepatic failure while on diphenylhydantoin therapy and died in hepatic coma. Autopsy disclosed massive hepatic necrosis. The clinical and pathological pictures are similar to the six previously reported cases of diphenylhydantoin-induced hepatic necrosis, with the exception of the time of onset of hepatic failure, which is explained. The cause of such hepatotoxicity is unknown, although hypersensitivity is postulated. It appears that studies of liver function in patients receiving diphenylhydantion are indicated to assess the true indicence of hepatocellular injury.
Adult↗
Decreased plasma protein binding of valproate in patients with acute head trauma.
1. One hundred and ten plasma samples were obtained from 50 patients treated with valproate for prophylaxis of post-traumatic head injuries. The samples were selected to include a wide range of albumin concentrations and were assayed for free and total valproate concentrations. Valproate binding parameters were determined from the Scatchard equation for one binding site using reweighted least squares analysis. 2. Plasma albumin concentrations were measured in 130 patients with head trauma. They started to decrease immediately after trauma, reaching a minimum at 5-7 days of approximately 24% of baseline value and did not return to normal until 1 month. 3. The free fraction of valproate varied six to seven-fold as albumin concentration ranged from 1.5 to 4.8 g 100 ml-1 (218-696 mumol l-1). The mean association constant for binding (Ka) was 0.008 mumol l(-1) and the mean number of binding sites (N) was 2.0. There values were similar to those reported for valproate in otherwise healthy patients with epilepsy. 4. Because of saturable protein binding of valproate, hypoalbuminaemia may necessitate the monitoring of free valproate concentrations to avoid toxicity when valproate is used in patients with acute head injury.
Acute Disease↗
The role of N-methyl-D-aspartate (NMDA) receptor-mediated neurotransmission in the pathophysiology and therapeutics of psychiatric syndromes.
The study of excitatory amino acids (EAAs) has recently resulted in new and fundamental concepts in neuroscience. This progress has led to a growing awareness of the crucial role that brain EAAs systems play in a variety of physiological and pathological processes. The N-methyl-D-aspartate (NMDA) receptor, presently the most well understood subtype of EAAs receptors, has been implicated in crucial physiological processes such as synaptogenesis, learning and memory. Dysfunctions of NMDA receptors seem to play a crucial role in the neurobiology of disorders such as Parkinson's disease, Alzheimer's disease, epilepsy and ischemic stroke. This paper is a review of emerging data indicating that alterations of NMDA receptor function may be pivotal to the pathophysiology of four common psychiatric syndromes: schizophrenia, major depression, posttraumatic stress disorder, and alcoholism. Special emphasis is placed on the current state of development of pharmacological strategies aiming at the modulation of NMDA receptor-mediated neurotransmission in these disorders.
Alcoholism↗
A prospective study of children with head injuries: I. Design and methods.
The main unresolved issues with respect to the psychological sequelae of brain damage in childhood are noted, and the previous studies of children suffering head injury are critically reviewed. A new prospective study is described. Three groups of children were studied: (a) 31 children with "severe" head injuries resulting in a post-traumatic amnesia of at least 7 days; (b) an individually matched control group of 28 children with hospital-treated orthopaedic injuries; and (c) 29 children with "mild" head injuries resulting in a post-traumatic amnesia exceeding 1 hour but less than 1 week. The children were studied as soon as possible after the accident and then again 4 months, 1 year, and 2 1/4 years after the injury. The parents were interviewed, using systematic and standardized interview techniques; both parents and teachers completed behavioural questionnaires; and the children were seen for individual psychological testing the WISC, the Neale Analysis of Reading Ability and a battery of tests of more specific cognitive functions. At the final follow-up, the severe head injury group (but not the other 2 groups) received a systematic neurological examination and the school teacher who knew the child best was personally interviewed. The findings are given on physical handicap, neurological abnormality, school placement and psychiatric referrals. All types of disabilities were both more frequent and more persistent in the children with severe head injuries.
Amnesia↗
Anti-epileptic drugs for preventing seizures following acute traumatic brain injury.
BACKGROUND: Seizure activity in the early post-traumatic period following head injury may cause secondary brain damage as a result of increased metabolic demands, raised intracranial pressure and excess neurotransmitter release. OBJECTIVES: To determine the effects of prophylactic anti-epileptic agents for acute traumatic head injury. SEARCH STRATEGY: We searched the Cochrane Injuries Group trials register, Medline and the databases of the Cochrane Stroke Group and Cochrane Epilepsy Group. We also contacted pharmaceutical companies who manufacture anti-epileptic agents, the National Institute of Neurological Disorders and Stroke, Epilepsy Division, and the National Institute of Health, United States. SELECTION CRITERIA: All randomised trials of anti-epileptic agents, in which study participants had a clinically defined acute traumatic head injury of any severity. Trials in which the intervention was started more than eight weeks after injury were excluded. DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data and assessed the quality of the trials. Relative risks and 95% confidence intervals were calculated for each trial on an intention to treat basis, which included pre-drug loading exclusions. As long as statistical heterogeneity did not exist, for dichotomous data, summary relative risks and 95% confidence intervals were calculated using a fixed effects model. Where the source of heterogeneity could obviously be related to allocation concealment, drug type, or drug dose, we stratified the analyses on that dimension. MAIN RESULTS: We identified 10 eligible randomised controlled trials, including 2036 participants. Data are currently unavailable for four unpublished trials, representing 631 participants. For the remaining trials, the pooled relative risk (RR) for early seizure prevention was 0.34 (95% confidence interval 0.21 to 0.54); based on this estimate, for every 100 patients treated, 10 would be kept seizure free in the first week. Seizure control in the acute phase was not accompanied by a reduction in mortality (RR=1.15; 95% confidence interval 0.89 to 1. 51), a reduction in death and neurological disability (RR = 1.49; 95% confidence interval 1.06 to 2.08 for carbamazepine and RR= 0.96; 95% confidence interval 0.72 to 1.26 for phenytoin) or a reduction in late seizures (pooled RR =1.28; 95% confidence interval 0.90 to 1. 81). The pooled relative risk for skin rashes was 1.57 (95% confidence interval 0.57 to 39.88). REVIEWER'S CONCLUSIONS: Prophylactic anti-epileptics are effective in reducing early seizures, but there is no evidence that treatment with prophylactic anti-epileptics reduces the occurrence of late seizures, or has any effect on death and neurological disability. Insufficient evidence is available to establish the net benefit of prophylactic treatment at any time after injury.
Anticonvulsants↗
Impaired K(+) homeostasis and altered electrophysiological properties of post-traumatic hippocampal glia.
Traumatic brain injury (TBI) can be associated with memory impairment, cognitive deficits, or seizures, all of which can reflect altered hippocampal function. Whereas previous studies have focused on the involvement of neuronal loss in post-traumatic hippocampus, there has been relatively little understanding of changes in ionic homeostasis, failure of which can result in neuronal hyperexcitability and abnormal synchronization. Because glia play a crucial role in the homeostasis of the brain microenvironment, we investigated the effects of TBI on rat hippocampal glia. Using a fluid percussion injury (FPI) model and patch-clamp recordings from hippocampal slices, we have found impaired glial physiology 2 d after FPI. Electrophysiologically, we observed reduction in transient outward and inward K(+) currents. To assess the functional consequences of these glial changes, field potentials and extracellular K(+) activity were recorded in area CA3 during antidromic stimulation. An abnormal extracellular K(+) accumulation was observed in the post-traumatic hippocampal slices, accompanied by the appearance of CA3 afterdischarges. After pharmacological blockade of excitatory synapses and of K(+) inward currents, uninjured slices showed the same altered K(+) accumulation in the absence of abnormal neuronal activity. We suggest that TBI causes loss of K(+) conductance in hippocampal glia that results in the failure of glial K(+) homeostasis, which in turn promotes abnormal neuronal function. These findings provide a new potential mechanistic link between traumatic brain injury and subsequent development of disorders such as memory loss, cognitive decline, seizures, and epilepsy.
Animals↗
The usefulness of EEG, exogenous evoked potentials, and cognitive evoked potentials in the acute stage of post-anoxic and post-traumatic coma.
Three-modality evoked potentials (TMEPs) have been used for several years in association with the EEG as a diagnostic and prognostic tool in acute anoxic or traumatic coma. Cognitive EPs have been recently introduced. EEG and cognitive EPs provide functional assessment of the cerebral cortex. TMEP parameters can be described by two indices: the index of global cortical function (IGCF) and the index of brainstem conduction (IBSC). Although it remains a unique tool for epilepsy assessment, the value of EEG is largely limited by its high sensitivity to the electrical environmental noise, its dependence on sedative drugs, and its inability to test the brainstem. Major TMEP alterations (absence of cortical activities more than 24 hours after the onset of post-anoxic coma, major pontine involvement in head trauma) are associated in all cases with an ominous prognosis (death or vegetative state). However, even if mild TMEP changes are associated with a good prognosis in 65% (post-anoxic coma) to 90% (head trauma) of cases, some patients never recover despite exogenous TMEPs that are only mildly altered in the acute stage. Thus, cognitive EPs can usefully complement exogenous EPs as a prognostic tool in coma. Indeed, even if the absence of cognitive EPs in comatose patients does not have any prognostic value, their presence implies a very high (more than 90%) probability of consciousness recovery. The major technical challenge for the future will be the development of reliable tools for continuous EEG and TMEP monitoring.
Acute Disease↗