Cortical Subarachnoid Hemorrhage Research Articles

Subarachnoid hemolysate produces DNA fragmentation in a pattern similar to apoptosis in mouse brain

Stroke and traumatic brain/spinal cord injuries are often associated with hemorrhage. Despite the relative frequency of hemorrhage in the central nervous system (CNS), little is known about what role blood and hemoglobin (Hb) play in mediating cellular injury. Since Hb and hemolysate have been associated with generation of oxidative stress and cell injury, we examined whether apoptosis was present after cortical exposure to subarachnoid hemolysate. Subarachnoid hemorrhage (SAH) was induced in CD-1 mice ( n=25) by injection of 50 μl of autologous hemolysate over the right parietal cortex. Saline-injected mice ( n=13) were used as controls. Subjects were sacrificed at 24 h. Transcardiac perfusion fixation was performed on a subgroup of hemolysate- ( n=15) and saline-injected ( n=9) animals. Sections were stained for DNA fragmentation using the terminal deoxyuridine nick end-labeling (TUNEL) method and also immunostained for the hemeoxygenase-1 (HO-1) protein to assess blood distribution. In the remaining animals ( n=6 SAH, n=4 saline), DNA was extracted and precipitated from 40 mg of tissue and subjected to electrophoresis on a 1.5% agarose gel. DNA fragmentation was evident on TUNEL staining in 10/15 subjects injected with hemolysate as compared to 0/9 subjects injected with saline ( p<0.01, Fisher exact test). TUNEL-positive cells were most abundant closest to the site of cortical SAH, as evidenced by HO-1 immunoreactivity. TUNEL-positive cells were also seen remotely in the hippocampus and basal forebrain. The presence of apoptosis was suggested by DNA laddering on electrophoresis in the hemolysate-injected subjects (4/6 animals). No laddering was evident in saline-injected subjects ( n=4). These results provide evidence that the presence of subarachnoid blood products is associated with DNA fragmentation and apoptotic cell death.

Epileptic seizures in subcortical vascular encephalopathy

Cerebrovascular disease is one of the most common causes of epilepsy in the elderly. Most of the studies published relate to cortical infarction, subarachnoid, and intracranial hemorrhage, whereas the incidence of epilepsy from subcortical ischemia, i.e. deep lacunar infarctions and diffuse white matter lesions, is obscure. Therefore, we prospectively examined 18 patients with the precisely defined diagnosis of subcortical vascular encephalopathy (SVE), who were admitted to our hospital due to epileptic seizures (group A), and compared them to a similarly selected group matched for age, sex, risk factors, and neurological deficits with an equivalent severity of SVE but without seizures (group B). Subcortical lacunar infarctions were significantly more frequent in group A than group B ( 15 18 versus 4 18 , p < 0.001), whereas neither the extension, degree, distribution of periventricular white matter changes, nor the presence of internal hydrocephalus, focal or diffuse cortical atrophy showed any statistical significance. However, a temporal constant theta or delta EEG focus was present in 10 18 patients in group A but only in 1 18 patients from group B (p ⩽ 0.005). 10 18 patients developed epilepsy with further seizures during follow-up. The association of SVE, multiple subcortical lacunas, and temporal EEG abnormalities are suggestive for an increased risk for epileptic seizures, which is particularly important for the treatment of patients with SVE if uncertain paroxysmal episodes occur, e.g. transient ischemic attacks, seizures, or cardiac syncope.