ABSTRACT
CASE: Non-convulsive status epilepticus (NCSE) is among the differential diagnoses of decreased consciousness, but often presents a diagnostic challenge. A 65-year-old woman was admitted to our emergency department with bradylalia. No abnormal finding was detected by computed tomography or magnetic resonance imaging. Subsequently, acquired arterial spin-labeling images showed hyperperfusion in the right hemisphere. OUTCOME: After the examination, the patient began experiencing left hemifacial seizures, which were relieved by diazepam; however, she was still agitated. Ictal confusion due to NCSE was suspected. Electroencephalography revealed periodic, generalized epileptiform activities with brief seizures of facial muscles by intermittent photic stimulation. Another supportive case of NCSE detected by arterial spin-labeling from a 56-year-old right-handed man has also been presented. CONCLUSION: Arterial spin-labeling magnetic resonance perfusion imaging provides valuable information regarding cerebral perfusion status in NCSE patients in emergency/acute settings.
ABSTRACT
BACKGROUND AND PURPOSE: Thrombin is activated in the cerebrospinal fluid (CSF) after a subarachnoid hemorrhage (SAH). However, the relationship between thrombin and cerebral vasospasm has not yet been fully established. The aim of this study was to investigate the possibility of thrombin as a causative factor for cerebral vasospasm and to delineate the signal transduction mechanism that results in thrombin-inducing sustained vasoconstriction in cerebral vasospasm. METHODS: In the SAH group, SAH was simulated by the 2-hemorrhage rabbit model. In the treatment group, antithrombin III (AT-III) was injected into the cisterna magna just before production of the SAH. CSF samples were obtained serially to measure d-dimer with latex photometric immunoassay. On day 4, the basilar artery was excised after perfusion-fixation. The degree of cerebral vasospasm was evaluated by measuring the cross-sectional area of each basilar arterial lumen, and the expression of mitogen-activated protein kinase (MAPK) in the vascular wall was examined with an immunohistochemical technique. RESULTS: In the treatment group, the value of d-dimer on day 4 was 0.83+/-0.07 microg/mL, which was statistically significantly lower than that in the nontreated SAH group (2.49+/-0.09 microg/mL, P<0.01). The cross-sectional area of the arterial lumen in the treatment group was 3.67x10(5)+/-1.58x10(4) square pixels, which was statistically significantly larger than that in the nontreated SAH group (2.60x10(5)+/-2.29x10(4) square pixels; P<0.01). MAPK was detected diffusely in the vascular smooth muscle cell layer in the nontreated SAH group, but it was absent in the treatment group. CONCLUSIONS: Inhibition of thrombin activity leads to amelioration of cerebral vasospasm and suppression of MAPK diphosphorylation. This suggests that thrombin and its related signal transduction, including the MAPK cascade, appear to play an important role in the pathogenesis of cerebral vasospasm after SAH.
