Rolandic type cerebral palsy in children as a pattern of hypoxic-ischemic injury in the full-term neonate.

Magnetic resonance images (MRIs) of the brains of 11 patients aged from 1 week to 12 years with a distinctive type of cerebral palsy were selected based on distribution of cerebral lesions, which were restricted to bilateral perirolandic cortical and subcortical regions, including frequent symmetric involvement of basal ganglia and ventrolateral nucleus of thalami. Retrospectively, the perinatal history and clinical features were reviewed to correlate clinical data with this distinctive pattern of brain injury. Clinically affected neonates had an encephalopathy associated with a severe perinatal asphyxial event. Older children with cerebral palsy survived a similar perinatal course and demonstrated spastic quadriparesis with bulbar or pseudobulbar involvement, lack of verbal speech and variable delays in cognitive development. The distribution of hypoxic-ischemic lesions involving bilateral perirolandic regions, basal ganglia, and thalami, appears to correlate with increased metabolic areas of primary myelination in full-term neonates, but not with arterial border zones nor a single cerebral artery distribution. Myelination is a critical process in maturing brain associated with marked increase in tissue respiration and thus greater susceptibility to oxygen deprivation. It is believed that the extent of hypoxic-ischemic brain injury is determined principally by brain maturity and regional metabolic rates at time of insult and this correlates with active myelination in full-term neonates. This study confirms previous data from neuropathologic literature and recent reports of neuroimaging studies of asphyxiated neonates. In addition, retrospective analysis of the clinical data enables recognition of a type of cerebral palsy that might be the hallmark of hypoxic-ischemic injury in term neonates.

Magnetic resonance angiography demonstrates vascular healing of carotid and vertebral artery dissections.

BACKGROUND AND PURPOSE: Dissection of the carotid and vertebral arteries is most accurately diagnosed with conventional angiography. MR techniques are sensitive for detecting the abnormalities associated with dissection but may lack specificity. We hypothesized that MR may be useful for serial monitoring of dissection and may therefore guide therapy. METHODS: All patients with angiographically proven carotid and/or vertebral artery dissection from July 1994 to June 1996 were followed for a median duration of 10.5 months. Of these 29 patients (44 vessels), 18 were concurrently evaluated with MR, and a target group of 9 patients (17 vessels) was prospectively followed with MR at 3-month intervals. RESULTS: In the 18 patients with both imaging studies at baseline, angiography revealed 30 dissected vessels while MR detected 27 (90%). In the target group of 9 patients, initial MR identified 15 of the 17 dissections diagnosed with angiography. Serial MR revealed complete healing in 5 vessels, improvement in 6 vessels, no change in 4 vessels, and worsening in 2 vessels. The radiographic features most likely to resolve were stenosis and mural hematoma, while occlusion and luminal irregularity tended to persist. Late ischemic events occurred in 2 patients, both with persistent MR evidence of dissection, one while subtherapeutic on warfarin therapy and the other occurring 1 week after warfarin was discontinued. CONCLUSIONS: MR is a reliable noninvasive method for following the vascular response to treatment and may guide the course of a clinical trial comparing medical therapies for carotid and vertebral artery dissection.

Anterior choroidal artery aneurysm and stroke.

We report the unique combination of a mid anterior choroidal artery (AChA) aneurysm and ischemic stroke presenting as a movement disorder in a young man. The mechanism for stroke in the AChA territory may either reflect a cause or an effect of aneurysm formation. We provide evidence for both arguments and speculate on the anatomic basis for the initial presentation of hemibody spasm.

Rheumatoid nodulosis of the meninges.

Rheumatoid nodulosis of the brain and leptomeninges has been reported only rarely, usually in patients with severe rheumatoid arthritis (RA). We describe the occurrence of leptomeningeal rheumatoid nodulosis occurring in a patient with nondeforming RA occurring in the setting of methotrexate therapy.

Impaired retention of visual discriminated escape training produced by subseizure amygdala stimulation.

These experiments examined the effects on memory of posttrial, subseizure, electrical stimulation of the amygdala. Rats were trained in a visual discriminated avoidance Y-maze. Each animal received 6 tirals on the training day. Retention, tested the following day, was measured both by the number of correct choices on the first 6 retraining trials and by the number of trials to a criterion of 5 of 6 correct choices. If administered 2 min, 1 h, or 4 h, but not 10 h, after training, bilateral amygdala stimulation significantly impaired retention as measured 24 h after training. In a second experiment, rats received unilateral amygdala stimulation in order to examine better the anatomical localization of effective stimulation sites. The unilateral stimulation was administered either 2 min, 10 min, 1 h, or 4 h after training. The behavioral procedures were the same as those used in the first experiment. For animals stimulated 2 min after training, the optimal stimulation region was one which extended rostrally from the ventrolateral portion of the basomedial nucleus to the dorsomedial region of the amygdala near the stria terminalis and nucleus centralis. For animals stimulated after a 10 min training-treatment interval, this amygdala region was not an effective stimulation site. However, in these animals, stimulation of the basolateral nucleus impaired later retention. Unilateral, posttraining amygdala stimulation administered 1 or 4 h after training did not appear to produce retention deficits. The findings of these experiments thus indicate that posttrial unilateral or bilateral amygdala stimulation impairs retention of discriminated avoidance training. Furthermore, the specific amygdala site at which posttrial stimulation impairs later retention varies with the training-treatment interval.