Considerations in the prophylactic treatment of transient ischemic attack or ischemic stroke in the carotid artery territory

This non-randomized study surveys the prophylactic treatment of 154 patients after transient ischemic attack or ischemic stroke in the carotid artery territory. Clinical presentation and etiologies were compared on the basis of the proposed prophylactic treatment. A surgical intervention or a long-lasting anticoagulation was restricted to only 30 patients (20%) due especially to the gravity of the ischemic cerebral lesions, general deterioration, and the advanced age of most of the patients. The purpose is to emphasize the "down-to-earth" situation in current medical care of non-selected patients as distinguished from the strictly selected patients of randomized studies. More importance should be done to open studies which better reflect the daily medical reality

Magnetic resonance imaging with gadolinium contrast agent in small deep (lacunar) cerebral infarcts.

OBJECTIVE--To assess gadolinium-diethylenetriamine-pentaacetic acid (Gd-DTPA) contrast-enhanced magnetic resonance (MR) imaging as an index of recent symptomatic small deep cerebral infarcts (SDCIs). DESIGN--Prospective case series. SETTINGS--Primary-care center. PATIENTS--Thirty-one consecutive patients presenting with the clinical diagnosis of SDCI in the territory of the perforators of the internal carotid artery or the vertebrobasilar system and confirmed by MR imaging. INTERVENTION--Rapid intravenous infusion of Gd-DTPA 5 to 10 minutes prior to acquisition of T1-weighted images. MAIN OUTCOME MEASURES--Precise clinicotopographic correlation on MR scans. RESULTS--Non-contrast-enhanced MR imaging allowed precise clinicotopographic correlation in five (38%) of 13 patients with SDCI symptoms in the internal carotid artery territory. After Gd-DTPA administration, precise clinicotopographic correlation improved in 11 (85%) of 13 patients. In five patients, precise correlation was possible only after Gd-DTPA enhancement. Nonenhanced MR imaging allowed precise clinicotopographic correlation in 15 (83%) of 18 patients with SDCI symptoms in the vertebrobasilar territory. After Gd-DTPA administration, we could establish precise clinicotopographic correlation in all patients with SDCIs in the vertebrobasilar territory. In three patients, precise correlation was possible only after Gd-DTPA contrast enhancement. In seven (23%) of 31 patients, Gd-DTPA failed to enhance symptomatic lesion: in five patients MR scans were performed early (less than 7 days) and in two patients later in the course (greater than 7 days). CONCLUSIONS--Although Gd-DTPA administration is unlikely to improve the sensitivity of MR images in visualizing SDCIs, it significantly improves the rate of precise clinicoanatomic correlation. All enhancing lesions showed precise clinicotopographic correlation. Enhancement may be absent in the acute phase (less than 7 days)

"Hyperneglect", a sequential hemispheric stroke syndrome.

We studied 8 patients with stroke and hemineglect, who presented with a transient active orientation and explorative behavior, turning head, eyes, and trunk in the opposite direction to any stimuli given in the neglected hemispace, as if repelled. This peculiar active behavior increased on repetitive stimulation, with the patient turning over by more than 180 degrees, with extreme rotation and opisthotonos-like extension of the axial muscles, as if looking for something behind him, his pillow or his bed. This behavior fluctuated during the day and vanished after a few days. We coined the term "hyperneglect" for this behavior, postulating a higher degree in the neglecting behavior or an additional field of hemineglect in the non neglected hemispace, or the release of repellent active behavior from parietal origin by the acute lesion. On CT, five patients showed two sequential uni- or bilateral hemispheric strokes of different ages on CT, while two patients had a large, unilateral infarct associated with hypertensive leukoencephalopathy and contralateral brain edema respectively. This behavioral syndrome seems to be associated with an acute stroke involving the frontal or parietal lobes and a previous lesion in the same or the opposite hemisphere

Infarcts in the territory of the deep perforators from the carotid system

We studied risk factors and presumed causes of infarct in 100 consecutive patients with a first stroke, who had an appropriate CT-proven infarct in the territory of the deep perforators from the carotid system (ITDPCS). The infarct involved the territory of the lenticulostriate arteries in 65 cases, the anterior choroidal artery in 23 cases, watershed zones between these two territories in four cases, and another territory in eight cases. In 42% of the patients, we felt the cause of the infarct to be small-artery disease. In 36%, at least one source of embolism was present (in 27% from the internal carotid artery, in 17% from the heart), either with (25%) or without (10%) associated hypertension (HT) and diabetes mellitus (DM). Other possible less common etiologies included migraine, syphilitic angiitis, and systemic diseases. We have confirmed that HT or DM are the most common etiologic factors of ITDPCS. However, large-artery disease and cardioembolism may be more important than previously assumed

Infarcts in the territory of lenticulostriate branches from the middle cerebral artery. Etiological factors and clinical features in 65 cases

We studied 65 consecutive patients with a first stroke who had an appropriate CT-proven small infarct in the territory of the lateral (61 patients), medial (3 patients) or both lateral and medial lenticulostriate arteries (1 patient) from the middle cerebral artery. While more than 75% of these patients were either hypertensive or diabetic (having at least one cause for small-artery disease), embolic sources were encountered in 35%, either from large vessels (28%), and/or from the heart (15%). Other causes (angiitis, migraine) were found in only 9%. The neurologic deficit was purely motor in more than 50% of the patients (in half of them with neuropsychological dysfunctions), a sensori-motor deficit was present in 30% (in half of them with neuropsychological dysfunctions), and only 20% had ataxic hemiparesis. No one had pure sensory stroke. None of the classical lacunar syndrome or the modality of sensory, motor or ataxic deficits were specific for any topographic subdivision of LS territory, but there was a tendency for clinical features to be linked with the involved basal ganglia and the topography of pathways in the internal capsule as delineated by anatomical studies. Pure motor deficits were associated with infarcts in the medial and posterior part of LS territory, visual field deficits and hemineglect always corresponded to posteriorly situated infarcts. Neuropsychological deficits were common in infarcts in the anterior and posterior subdivisions of LS territory, with a major effect of the size of infarct. Sensory deficits were not correlated with any location in LS territory, probably because thalamo-efferent fibres have a more diffuse course through the internal capsule

Chiasmal apoplexy: haemorrhage from a cavernous malformation in the optic chiasm.

We present a patient who experienced sudden onset of orbital headache, visual loss and bitemporal visual field defect. MRI of the optic chiasm suggested a diagnosis of haemorrhage and hence a vascular malformation. Pterional craniotomy revealed an intrachiasmatic haematoma with a cavernous angioma. The malformation was totally excised and vision improved after surgery. The syndrome of chiasmal apoplexy is discussed

Encephalite "benigne" du tronc cerebral. [Benign encephalitis of the brain stem]

Seven cases of an encephalitic brainstem syndrome are reported. All had an initial flu-like phase, with a febrile state. Then, all had eye movements disturbances and ataxia. Six had a variable dysfunction of other cranial nerves, five had dysmetria of limbs and three had pyramidal signs. In all, the topographic diagnosis was based on clinical, neurophysiological (electromyography, evoked potentials) and neuroradiological (swelled brainstem on CT scan) findings. Analysis of cerebro-spinal fluid revealed pleocytosis (mean; 165 cells/ml), without profile indicative of multiple sclerosis. Serologic tests for Adenovirus or Echovirus were positive in three cases. All recovered spontaneously. With a mean follow-up of three years there was no relapse and the clinical examination remained normal. These seven cases had, after exclusion of other brainstem syndromes, a Bickerstaff's encephalitis. Previous reports are discussed and a post-infectious origin is proposed to this benign syndrome