Reversible Verbal and Visual Memory Deficits after Left Retrosplenial Infarction

The retrosplenial cortex is a cytoarchitecturally distinct brain structure located in the posterior cingulate gyrus and bordering the splenium, precuneus, and calcarine fissure. Functional imaging suggests that the retrosplenium is involved in memory, visuospatial processing, proprioception, and emotion.We report on a patient who developed reversible verbal and visual memory deficits following a stroke. Neuropsychological testing revealed both anterograde and retrograde memory deficits in verbal and visual modalities. Brain diffusion-weighted and T2-weighted magnetic resonance imaging (MRI) demonstrated an acute infarction of the left retrosplenium.     

White matter hyperintensity determines ischemic stroke severity in symptomatic carotid artery stenosis

Neurological Sciences - The aim of this study is to investigate the influence of white matter hyperintensity (WMH) on stroke severity and prognosis in patients with symptomatic carotid artery...     

Ischemic Stroke in Takayasu's Arteritis: Lesion Patterns and Possible Mechanisms

Background and Purpose

The purpose of the present study was to use brain magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) to identify the mechanism of stroke in patients with Takayasu''s arteritis (TA).

Methods

Among a retrospective cohort of 190 TA patients, 21 (3 males and 18 females) with a mean age of 39.9 years (range 15-68 years) who had acute cerebral infarctions were included in lesion pattern analyses. The patients'' characteristics were reviewed, and infarction patterns and the degree of cerebral artery stenosis were evaluated. Ischemic lesions were categorized into five subgroups: cortical border-zone, internal border-zone, large lobar, large deep, and small subcortical infarctions.

Results

In total, 21 ischemic stroke events with relevant ischemic lesions on MRI were observed. The frequencies of the lesion types were as follows: large lobar (n=7, 33.3%), cortical border zone (n=6, 28.6%), internal border zone (n=1, 4.8%), small cortical (n=0, 0%), and large deep (n=7, 33.3%). MRA revealed that 11 patients had intracranial artery stenosis.

Conclusions

Hemodynamic compromise in large-artery stenosis and thromboembolic mechanisms play significant roles in ischemic stroke associated with TA.     

Expression of the type 1 and type 2 receptors for tumor necrosis factor after traumatic spinal cord injury in adult rats

Posttraumatic inflammation has been implicated in secondary tissue damage after spinal cord injury (SCI). Tumor necrosis factor-alpha (TNF-alpha) is a key inflammatory mediator that is increasingly expressed after SCI. The effect of TNF-alpha is mediated through its receptors TNFR1 (p55) and TNFR2 (p75). However, whether these two receptors are expressed after SCI has not been demonstrated. In the present study, the temporo-spatial expression of TNFR1 and TNFR2 was examined in rats that had received a 10 g impact injury dropped at a height of 12.5 mm using the New York University impact device. In sham operates, no detectable TNFR1 or TNFR2 immunoreactivity (IR) was observed. In contused spinal cord, TNFR1 protein expression and immunoreactivity (IR) were detected as early as 15 min postinjury, reached its peak at 8 h, and declined markedly after 1 and 3 days postinjury. The temporal pattern of TNFR2 expression was similar to that of TNFR1 but its expression peaked at 4 h postinjury. During peak expression, TNFR1- and TNFR2-IR were most intense at the site of injury and decreased gradually from the injury epicenter. TNFR1- and TNFR2-positive cells included neurons, astrocytes, and oligodendrocytes. Methylprednisolone (MP), a synthetic glucocorticoid, partially inhibited the injury-induced expression of TNFR1 and TNFR2, an effect which could be reversed by RU486, an antagonist of glucocorticoid receptors. We suggest that the expression of TNFR1 and TNFR2 after SCI may contribute to posttraumatic inflammatory responses of TNF-alpha.