Suicide after traumatic brain injury: a population study. (1/39)

OBJECTIVES: To determine the rates of suicide among patients who have had a traumatic brain injury. METHODS: From a Danish population register of admissions to hospital covering the years 1979-93 patients were selected who had had either a concussion (n=126 114), a cranial fracture (n=7560), or a cerebral contusion or traumatic intracranial haemorrhage (n=11 766). All cases of deaths by the end of the study period were identified. RESULTS: In the three diagnostic groups there had been 750 (0.59%), 46 (0.61%), and 99 (0.84%) cases of suicide respectively. Standardised mortality ratios, stratified by sex and age, showed that the incidence of suicide among the three diagnostic groups was increased relative to the general population (3.0, 2.7, and 4.1 respectively). In all diagnosis groups the ratios were higher for females than for males, and lower for patients injured before the age of 21 or after the age of 60. The presence of a codiagnosis relating to substance misuse was associated with increased suicide rates in all diagnosis groups. There was a tendency, among patients with cerebral contusions or traumatic intracranial haemorrhages, for suicide risk to increase with duration of stay in hospital. Cox regression analyses for proportional hazards confirmed that there was a significantly greater risk of suicide among patients with cerebral contusions or traumatic intracranial haemorrhages than among patients with concussion or cranial fractures (hazard ratios=1.42 and 1.50 respectively). There was, however, no evidence of a specific risk period for suicide after injury. CONCLUSION: The increased risk of suicide among patients who had a mild traumatic brain injury may result from concomitant risk factors such as psychiatric conditions and psychosocial disadvantage. The greater risk among the more serious cases implicates additionally the physical, psychological, and social consequences of the injuries as directly contributing to the suicides.  (+info)

The structural basis of moderate disability after traumatic brain damage. (2/39)

The objective was to discover the nature of brain damage in survivors of head injury who are left with moderate disability. Macroscopic and microscopic examination was carried out on the brains of 20 persons who had died long after a head injury that had been treated in a neurosurgical unit. All had become independent but had various disabilities (moderate disability on the Glasgow outcome scale) Most deaths had been sudden, which had led to their referral from forensic pathologists. Post-traumatic epilepsy was a feature in 75%. An intracranial haematoma had been evacuated in 75%, and in 11 of the 15 with epilepsy. Diffuse axonal injury was found in six patients, five of the mildest type (grade 1) and one of grade 2. No patient had diffuse thalamic damage but one had a small focal ischaemic lesion in the thalamus. No patient had severe ischaemic brain damage, but three had moderate lesions which were bilateral in only one. No patient had severe cortical contusions. In conclusion, the dominant lesion was focal damage from an evacuated intracranial haematoma. Severe diffuse damage was not found, with diffuse axonal injury only mild and thalamic damage in only one patient.  (+info)

Giant cell glioblastoma manifesting as traumatic intracerebral hemorrhage--case report. (3/39)

A 33-year-old male presented with intracerebral hemorrhage in the left temporoparietal region after a traffic accident. Ten months later, the traumatic hemorrhage was found to originate in an underlying giant cell glioblastoma. Our case indicates that non-traumatic underlying pathologies, such as vasculopathies, coagulopathies, or tumors, should be considered in the differential diagnoses of intracerebral hemorrhage occurring in unusual locations after traumatic accidents.  (+info)

Magnetization transfer MR imaging in patients with posttraumatic epilepsy. (4/39)

BACKGROUND AND PURPOSE: Intractable epilepsy is a well-recognized complication following head trauma, and many factors have been implicated in its pathogenesis. This study was performed to determine the severity of tissue damage after severe head injury as assessed with magnetization transfer (MT) MR imaging and the relationship of this damage with seizure intractability. METHODS: Forty-four patients, 13 without seizures (disease controls) and 31 with seizures, underwent T1-weighted MT MR imaging 1-10 years after head trauma. Phase-corrected gradient-echo (GRE) imaging was also performed in all patients to look for the presence of hemosiderin. All patients were evaluated for the presence of an MT abnormality beyond an abnormality seen on T2-weighted images, an MT abnormality within a T2 abnormality, and hemosiderin deposition. RESULTS: Patients with an MT abnormality beyond a T2 abnormality had a significantly higher intractability of seizures compared with those with an MT abnormality within a T2 abnormality (P <.05). In addition, the mere presence of hemosiderin deposit was not associated with seizure intractability; however, gliosis around the hemosiderin as seen on T1-weighted MT images was associated with seizure intractability. CONCLUSIONS: T1-weighted MT imaging may be of value in predicting the intractability of the seizure in delayed posttraumatic epilepsy.  (+info)

Acute fatal haemorrhage during percutaneous dilatational tracheostomy. (5/39)

Percutaneous dilatational tracheostomy (PDT) is associated with a number of life-threatening complications. We present a case of massive and fatal arterial haemorrhage that occurred in the intensive care unit during an elective PDT on an 86-year-old woman following earlier evacuation of a traumatic subdural haematoma. An avulsed right subclavian artery was found at post mortem. Previous thyroid surgery and aberrant arterial anatomy contributed to the fatal outcome.  (+info)

Low doses of dexamethasone decrease brain water content of collagenase-induced cerebral hematoma. (6/39)

Different doses of dexamethasone were evaluated for the treatment of cerebral trauma using a rat model of cerebral hematoma induced by intracerebral (IC) stereotaxic injections of collagenase. Control animals received an intracerebral collagenase injection followed by intraperitoneal (IP) saline injection. Sham operated animals received saline only (IC, IP). Forty-eight hours following the surgeries, the brains were removed from the euthanized animals. Cerebral hemispheres were separated and the 4 coronal sections (antero-posterior plane) were weighed. Each slice was dried for 24 h (100 degrees C) and weighed again to establish brain water content. In hematoma-induced saline treated rats, significant differences in brain water content were observed when compared to sham operated animals. Rats treated with 1 mg/kg dexamethasone had a significant brain water content decrease; however, no significant differences were observed with higher doses of dexamethasone. In conclusion, low doses of dexamethasone seem to be beneficial for the treatment of cerebral trauma.  (+info)

Diffuse axonal injury associated with chronic traumatic brain injury: evidence from T2*-weighted gradient-echo imaging at 3 T. (7/39)

BACKGROUND AND PURPOSE: Diffuse axonal injury is frequently accompanied by tissue tear hemorrhages. We examined whether high field strength T2*-weighted gradient-echo imaging performed during the chronic stage of traumatic brain injury may have advantages in the evaluation of diffuse axonal injury as compared with T1- and T2-weighted MR imaging. METHODS: Prospective MR imaging of 66 patients (age range, 17-57 years) was performed using a 3-T system 3 to 292 months (median, 23.5 months) after traumatic brain injury. T1-, T2-, T2*-hypointense and T2-hyperintense foci of 1- to 15-mm diameter were registered in 10 brain regions by two readers separately. Foci that appeared hypointense both on the T1- and T2- and/or on the T2*-weighted images were defined as traumatic microbleeds. RESULTS: For 46 (69.7%) of the patients, T2*-weighted gradient-echo imaging revealed traumatic microbleeds. Hyperintense foci were observed on the T2-weighted images of only 15 (22.7%) patients. T2*-weighted imaging showed significantly more traumatic microbleeds (P =.000) than did T1- and T2-weighted imaging. Interobserver agreement was strong (kappa = 0.79, tau = 0.749, P =.000). For 14 (21.2%) of the patients, T2*-weighted gradient-echo imaging revealed traumatic microbleeds in the corpus callosum, whereas for only two (3%), hyperintense callosal lesions were seen on the T2-weighted images. Although a significant correlation existed between the total amount and callosal appearance of traumatic microbleeds and Glasgow Coma Scale scores (P =.000), no correlation existed with extended Glasgow Outcome Scale scores. CONCLUSION: T2*-weighted gradient-echo imaging at high field strength is a useful tool for the evaluation of diffuse axonal injury during the chronic stage of traumatic brain injury. Diffuse axonal injury-related brain lesions are mainly hemorrhagic. The relevance of diffuse axonal injury for long-term clinical outcome is uncertain.  (+info)

Endovascular management of intracranial pial arterio-venous fistulas. (8/39)

From 1996-2002 we treated 5 consecutive cases of pial fistula. There were 3 patients with a single hole-single channel pial fistula and two patients had a complex pial fistula. Three patients presented with intracerebral hematoma and had a focal neurological deficit. One patient presented with history of seizures and 1 patient had headache. The results of the treatment were analyzed both clinically and angiographically. The follow-up period ranged from 6 months to 6 years. All fistulas were treated with concentrated glue. The glue cast included the distal part of the feeding artery, A-V connection and the proximal part of the vein. Post-embolisation angiography showed complete occlusion of two single-hole fistulas and one complex pial A-V fistula and near total occlusion of one single-hole and one complex pial A-V fistula. Four patients had excellent clinical outcome. One patient with single-hole fistula had a hemorrhagic venous infarct resulting in transient hemiparesis.  (+info)