Early neurological deterioration following thrombolysis for minor stroke with isolated internal carotid artery occlusion.

BACKGROUND AND PURPOSE: Better understanding the incidence, predictors and mechanisms of early neurological deterioration (END) following intravenous thrombolysis (IVT) for acute stroke with mild symptoms and isolated internal carotid artery occlusion (iICAo) may inform therapeutic decisions. METHODS: From a multicenter retrospective database, we extracted all patients with both National Institutes of Health Stroke Scale (NIHSS) score <6 and iICAo (i.e. not involving the Willis circle) on admission imaging, intended for IVT alone. END was defined as ≥4 NIHSS points increase within 24 h. END and no-END patients were compared for (i) pre-treatment clinical and imaging variables and (ii) occurrence of intracranial occlusion, carotid recanalization and parenchymal hemorrhage on follow-up imaging. RESULTS: Seventy-four patients were included, amongst whom 22 (30%) patients experienced END. Amongst pre-treatment variables, suprabulbar carotid occlusion was the only admission predictor of END following stepwise variable selection (odds ratio = 4.0, 95% confidence interval: 1.3-12.2; P = 0.015). On follow-up imaging, there was no instance of parenchymal hemorrhage, but an intracranial occlusion was now present in 76% vs. 0% of END and no-END patients, respectively (P < 0.001), and there was a trend toward higher carotid recanalization rate in END patients (29% vs. 9%, P = 0.07). As compared to no-END, END was strongly associated with a poor 3-month outcome. CONCLUSIONS: Early neurological deterioration is a frequent and highly deleterious event after IVT for minor stroke with iICAo, and is of thromboembolic origin in three out of four patients. The strong association with iICAo site-largely a function of underlying stroke etiology-may point to a different response of the thrombus to IVT. These findings suggest END may be preventable in this setting.

[Brain magnetic resonance imaging and neuropathology of cortical laminar necrosis]. / Nécrose laminaire corticale: aspects en imagerie par résonance magnétique et étude anatomoclinique.

INTRODUCTION: The most frequent acute and sub-acute complications of chronic alcoholism are delirium tremens, hepatic encephalopathy and Gayet-Wernicke encephalopathy. Morel laminar sclerosis is a rare and less known complication, often reported with Marchiafava-Bignami disease. CASE REPORT: A 57-year-old alcoholic man presented delirium after surgery. Anterograde and retrograde amnesia as well as wrong recognitions appeared progressively and one generalized seizure occurred. He then developed mutism and became bedridden. Magnetic resonance imaging (MRI) showed high-intensity bilateral temporoparietal signals from white matter on T2-weighted images and high-intensity signals from the parietal cortex on T1-weighted images. The patient died four months after the onset of the delirium. Post-mortem examination of the brain showed cortical laminar necrosis with Alzheimer Type II gliosis but without demyelinisation of the corpus callosum. CONCLUSION: Cortical laminar necrosis with chronic ethylism is usually called Morel's laminar sclerosis. Nevertheless, histology is not typical of this diagnosis, because of necrosis especially of the second (and not the third) layer of the cortex, and because of the absence of lesion of the corpus callosum. MRI data are of interest here because they were rarely reported in cases of Morel's laminar sclerosis.

[Idiopathic chronic dysautonomia: when should the diagnosis be made?]. / Dysautonomie chronique idiopathique: quand porter le diagnostic?

INTRODUCTION: Chronic autonomic disorders may complicate a wide range of conditions which can be divided into secondary, due to specific diseases, and primary, in which no cause has been determined. CASE REPORT: We report the case of a 43-year-old woman, who presented a chronic autonomic failure, which had begun by symptomatic orthostatic hypotension. Progressively, syncopes became daily, causing considerable discomfort associated with other signs of sympathic dysfunction: unilateral Horner's syndrome, diarrhea and hypohidrosis. The autonomic involvement was confirmed by study of the cardiovascular responses to tilt-up and electrophysiological autonomic testing. Etiologic search for a chronic acquired neuropathy (diabetes, amyloidis, paraneoplastic) or an inherited neuropathy was not conclusive. After five years, dysautonomic symptoms increased, but remained isolated. The physical examination did not show other clinical abnormalities such as cerebellar, pyramidal or extrapyramidal failure in favor of a multiple system atrophy or Parkinson's disease. All these data suggest the diagnosis of a primary autonomic failure. CONCLUSION: The diagnosis of primary autonomic failure is difficult to make because it requires that all the investigations in search of an etiology are negative and a long follow-up to be sure that dysautonomic symptoms persist isolated after many years of progression.

[Multiple strokes after chickenpox primo-infection in an adult]. / Accidents vasculaires cérébraux multiples et primo-infection varicelleuse chez un adulte.

INTRODUCTION: Chickenpox is considered as a high risk factor for developing stroke in childhood, but descriptions in adult are exceptional (only three cases reported, to our knowledge). CASE REPORT: A 37-year-old man presented with a chickenpox eruption, followed by a right parietal and a left occipital infarcts, associated with multiple lacunae. There was no coagulation disorder, no hypertension or cardiovascular disorder. Cerebral angiography showed an irregular narrowing of the right internal parietal artery and vascular defects in right parietal and left occipital areas. The diagnosis of VZV-related vasculitis was evoked. White cell count, serology and VZV PCR were negative in the cerebrospinal fluid. Clinical improvement was observed after treatment by corticosteroids and aciclovir. CONCLUSION: Chickenpox is a rare cause of cerebral vasculitis. Involvement of both medium and small vessels was present here, contrary to other adult case reports in the literature. Hematogenous dissemination of the virus responsible for cerebral vasculitis seems to be the most probable pathophysiological mechanism.