Endovascular management of the traumatic cerebral aneurysms associated with traumatic carotid cavernous fistulas. (57/230)

BACKGROUND AND PURPOSE: Simultaneous traumatic carotid-cavernous fistulas(TCCFs) and traumatic cerebral aneurysms (TCAs) of the internal carotid artery (ICA) are rare. We describe the pitfalls of detecting a TCA before TCCF occlusion and the endovascular management of the TCA and TCCF. METHODS: Over 12 years, 156 patients with TCCFs were treated at our institute. In four men (mean age, 34 years), associated TCAs were detected before (n = 1) or after (n = 3) endovascular occlusion of the TCCFs. Causes for the missed detection of the TCA before TCCF occlusion were masking by a parent artery and fistula drains (n = 1), steal phenomenon (n = 1), and a latent period (n = 1). The TCAs were in the supraclinoid ICA (n = 3) or the paraophthalmic artery (n = 1). Three TCAs were treated with the endosaccular placement of electrodetachable coils. RESULTS: Two TCCFs and associated TCAs were successfully occluded with preservation of the ICA. The paraophthalmic TCA was treated with coil occlusion of the TCA and TCCF. Spontaneous fatal rupture of the TCA occurred in one patient after subtotal TCCF occlusion. No notable procedure-related complication was observed in the other three patients. CONCLUSION: TCAs may be difficult to detect before treatment of the TCCF because it may be overlooked, a latent period may occur, flow may be shunted, or they may be masked by a nearby parent artery or fistula drains. As soon as a TCA is found, endovascular management should be initiated promptly.  (+info)

Dynamic changes in N-methyl-D-aspartate receptors after closed head injury in mice: Implications for treatment of neurological and cognitive deficits. (58/230)

Traumatic brain injury is a leading cause of mortality and morbidity among young people. For the last couple of decades, it was believed that excess stimulation of brain receptors for the excitatory neurotransmitter glutamate was a major cause of delayed neuronal death after head injury, and several major clinical trials in severely head injured patients used blockers of the glutamate N-methyl-D-aspartate (NMDA) receptor. All of these trials failed to show efficacy. Using a mouse model of traumatic brain injury and quantitative autoradiography of the activity-dependent NMDA receptor antagonist MK801, we show that hyperactivation of glutamate NMDA receptors after injury is short-lived (<1 h) and is followed by a profound and long-lasting (> or =7 days) loss of function. Furthermore, stimulation of NMDA receptors by NMDA 24 and 48 h postinjury produced a significant attenuation of neurological deficits (blocked by coadministration of MK801) and restored cognitive performance 14 days postinjury. These results provide the underlying mechanism for the well known but heretofore unexplained short therapeutic window of glutamate antagonists after brain injury and support a pharmacological intervention with a relatively long (> or =24 h) time window easily attainable for treatment of human accidental head injury.  (+info)

Cerebral perfusion pressure management of severe diffuse head injury: effect on brain compliance and intracranial pressure. (59/230)

BACKGROUND: Cerebral perfusion pressure management (CPPM) is an accepted modality of treatment of severe diffuse head injury (SDHI). However, CPPM has the potential to cause transcapillary exudation in the presence of a disrupted blood brain barrier and can lead to further increase of intracranial pressure (ICP) and worsening of compliance. AIMS: This study attempts to evaluate the effect of both transient and prolonged changes in cerebral perfusion pressure (CPP) on ICP and cerebral compliance as measured by the Pressure Volume Index (PVI), and to correlate changes in PVI with outcome at 12 months using the Glasgow Outcome Score. SETTINGS AND DESIGN: Prospective study in a neurosurgical ICU. MATERIAL AND METHODS: Twenty-seven SDHI patients managed using standard protocol to maintain CPP above 70 mmHg. Mean arterial pressure (MAP), ICP and CPP were monitored every half-hour. Daily monitoring of the PVI and ICP was done before, and after the induced elevation of MAP using IV Dopamine infusion. The relationship between CPP, MAP, ICP, PVI and outcome was evaluated. STATISTICAL ANALYSIS USED: The paired and independent samples T-test, and the Pearson correlation coefficient. RESULTS: CPPM rarely leads to progressive rise in ICP. Maintaining CPP above 70mmHg does not influence ICP or PVI. Transient elevations in CPP above 70mmHg may produce a small rise in ICP. Trend of change in PVI influenced outcome despite similar ICP and CPP. CONCLUSION: Elevating the CPP above 70mmHg does not either reduce the ICP or worsen the compliance. Monitoring changes in compliance should form an integral part of CPPM.  (+info)

A study comparing SPECT with CT and MRI after closed head injury. (60/230)

After closed head injury nineteen patients had single photon emission tomography (SPECT) using the lipophilic tracer 99m-Technetium hexamethyl-propylene-amineoxime (HMPAO) to compare the defects shown by CT and MRI. SPECT showed more focal cerebral lesions than either CT or MRI alone or in combination. Most lesions shown by SPECT were not shown by CT or MRI in the corresponding anatomical regions. The most severely disabled patients showed the highest number of SPECT lesions (average four per patient) and the lowest (mean, SE) cerebral blood flow (718, 69 ml/min) compared with the less disabled patients (two per patient and 1058, 51 ml/min, p less than 0.05). There was a correlation between the Glasgow Outcome Scale grade and the global cerebral blood flow (r 0.74, p less than 0.05). The perfusion defects may correlate with clinical signs that were not explained by CT or MRI findings. SPECT may complement the clinical evaluation in the assessment of outcome after head injury.  (+info)

Differential responses in three thalamic nuclei in moderately disabled, severely disabled and vegetative patients after blunt head injury. (61/230)

In vivo imaging techniques have indicated for many years that there is loss of white matter after human traumatic brain injury (TBI) and that the loss is inversely related to cognitive outcome. However, correlated, quantitative evidence for loss of neurons from either the cerebral cortex or the diencephalon is largely lacking. There is some evidence in models of TBI that neuronal loss occurs within the thalamus, but no systematic studies of such loss have been undertaken in the thalamus of humans after blunt head injury. We have undertaken a stereological analysis of changes in numbers of neurons within the dorsomedial, ventral posterior and lateral posterior thalamic nuclei in patients assessed by the Glasgow Outcome Scale as moderately disabled (n = 9), severely disabled (n = 12) and vegetative (n = 10) head-injured patients who survived between 6 h and 3 years, and controls (n = 9). In histological sections at the level of the lateral geniculate body, the cross-sectional area of each nucleus and the number and the mean size of neurons within each nucleus was quantified. A statistically significant loss of cross-sectional area and number of neurons occurred in the dorsomedial nucleus in moderately disabled, and both the dorsomedial and ventral posterior thalamic nuclei in severely disabled and vegetative head-injured patients. However, there was no change in neuronal cell size. In the lateral posterior nucleus, despite a reduction in mean cell size, there was not a significant change in either nuclear area or number of neurons in cases of moderately disabled, severely disabled or vegetative patients. We posit, although detailed neuropsychological outcome for the patients included within this study was not available, that neuronal loss in the dorsomedial thalamus in moderately and severely disabled and vegetative patients may be the structural basis for the clinical assessment in the Glasgow Outcome Scale. In severely disabled and vegetative patients, loss of neurons from the ventral posterior thalamic nucleus may also reflect loss of response to afferent stimuli.  (+info)

Serial evaluation of diffusion tensor brain fiber tracking in a patient with severe diffuse axonal injury. (62/230)

Serial evaluation of diffusion tensor brain fiber tracking was performed in a 27-year-old female patient with diffuse axonal injury after a traffic accident. Although the result of brain fiber tracking was not necessarily parallel to her clinical symptoms, it may have predicted the neurologic prognosis.  (+info)

Cognitive remediation in schizophrenia: should we attempt it? (63/230)

Subtle cognitive deficits persist in schizophrenia even after active periods of psychosis subside. Even though early attempts to ameliorate cognitive impairments were relatively successful, the endeavor was abandoned nearly 30 years ago. We contrast this state of affairs with that of closed-head injury, in which less well-designed and less successful attempts to treat similar impairments have been greeted with much enthusiasm. Objections to cognitive remediation in schizophrenia are evaluated and the attempt is encouraged.  (+info)

Cognitive remediation in schizophrenia: proceed ... with caution! (64/230)

The apparent neglect of neuropsychologic deficits in schizophrenia as the basis for therapeutic intervention, together with only isolated attempts at remediating them, probably reflect the nature of impairments, the functional significance of which is uncertain. A critique of the limitations inherent in the appealing cognitive remediation of the closed-head injured is followed by positive suggestions for the restructuring of cognitive schema that appear to underlie schizophrenic disability in social and vocational functioning.  (+info)