BACKGROUND AND PURPOSE: The present study was carried out to investigate transient arteriolar vasospasm following reperfusion in the gerbil as an ischemic model and relationship between vasospasm and the changes of morphologic, physiologic and regional blood flow. METHODS: The transient arteriolar vasospasm was observed under the microscope. All gerbils were perfusion fixed and ischemic neuronal damage was checked in the CA1 subfield of the dorsal hippocampus. Metabolic parameters were serially measured during the occlusion and after recirculation, and cerebral blood flow was measured with a laser Doppler flowmetry. RESULTS: 1. Among the 18 gerbils with BCAO(bilateral carotid artery occlusion) for 2 minutes, 8 gerbils showed vasospasm after reopening, namely post-ischemic vasospasm, and 10 gerbils did not show vasospasm. 2. In all animals, metabolic parameters showed decreased PaCO2 and high pH just after the occlusion but increased PaCO2 and lowered pH following the recirculation. BCAO caused marked increase in systemic blood pressure but it returned to preischemic levels following the recirculation. 3. In all animals, BCAO caused marked decrease of cerebral blood flow compared to preischemic levels immediately following the occlusion but it returned to preischemic levels following the recirculation. And it took some longer the onset and duration of the transient increase in blood volume after reopening in the animals with vasospasm than those without vasospasm. 4. There was no morphological neuronal damage in the hippocampal CA1 subfield, at 1, 3, 7 days following 2-minute ischemic insult. CONCLUSION: The present study confirmed that BCAO in gerbils resulted in forebrain ischemia caused transient cortical vasospasm in the gerbil. But there was no close relationship between vasospasm and the changes of morphologic, physiologic and regional blood flow.
Animals ; Blood Pressure ; Blood Volume ; Brain Ischemia* ; Brain* ; Carotid Arteries* ; Cerebral Cortex* ; Gerbillinae* ; Hippocampus ; Hydrogen-Ion Concentration ; Ischemia ; Laser-Doppler Flowmetry ; Microcirculation* ; Neurons ; Perfusion ; Prosencephalon ; Regional Blood Flow ; Reperfusion

Seizure induced transient brain CT or MRI abnormalities following status epilepticus have previously been reported. However, focal transient imaging abnormalities involving hippocampus or mesial temporal lobe as a consequence of seizure are rare findings. We report 2 patients with transient mesial temporal abnormalities on MRI associated with partial seizure of temporal lobe origin. A 59-year-old man with a 4-month history of occasional epigastric rising sensation had developed frequent olfactory hallucination 7 days prior to presentation. On brain MRI, T2 signal was increased in the right mesial temporal region, and the lesion showed mild mass effects and partial enhancement after gadolinium injection. Interictal spikes were noted from right nasopharyngeal electrode, but there was no clinical or electrical evidence of status epilepticus during prolonged scalp/sphenoidal EEG monitoring. His seizures were successfully controlled by phenytoin. T2 high signal was markedly decreased and prior enhancement was no longer seen on brain MRI done 5 weeks later. A 33-year old woman with a 6 month history of occasional vacant staring and oral automatism with amnesia complained progressive memory impairment. Right amygdala and hippocampal head was enlarged and showed T2 high signal without contrast enhancement. EEG with sphenoidal electrodes showed right sphenoidal spikes. Her seizures were controlled by carbamazepine and brain MRI became unremarkable 6 weeks later. Suggested mechanisms and significance of the transient imaging abnormalities following seizures will be briefly reviewed.
Adult ; Amnesia ; Amygdala ; Automatism ; Brain ; Carbamazepine ; Electrodes ; Electroencephalography ; Female ; Gadolinium ; Hallucinations ; Head ; Hippocampus ; Humans ; Magnetic Resonance Imaging ; Memory ; Middle Aged ; Phenytoin ; Seizures* ; Sensation ; Status Epilepticus ; Temporal Lobe*

BACKGROUND: Microalbuminuria predicts cardiovascular events in diabetic and non-diabetic patients. But, few studies have addressed the relationship between microalbuminuria and cerebral infarction. We determined the incidence of microalbuminuria in non-diabetic subjects with cerebral infarction and investigated the relationship between urinary albumin excretion and risk factors of the stroke. METHODS: Urinary albumin excretion rate, 24 hours blood pressure monitoring, fasting serum lipid profiles, fibrinogen, fasting glucose, insulin and c-peptide were evaluated in 50 non-diabetic patients with acute cerebral infarction and matched 48 controls. RESULTS: Microalbuminuria was detected in 23 of 50(46%) patients with acute cerebral infarction and 4 of 48(8%) control subjects. Hypertension was present in 13 of 23(57%) microalbuminuric patients and 9 of 27(33%) non-microalbuminuric patients. In the microalbuminuric patients with cerebral infarction, diastolic blood pressure and fasting glucose were significantly greater than the control group. But, no difference in systolic blood pressure, lipid level, fibrinogen, fasting insulin and c-peptide level. CONCLUSIONS: The prevalence of microalbuminuria in patients with cerebral infarction was higher than controls and it was associated with increased diastolic blood pressure(DBP) and fasting blood glucose(FBS). Therefore, microalbuminuria is associated with thrombogenic cerebral infarction and it was partly mediated by DBP and FBS.
Blood Pressure ; Blood Pressure Monitors ; C-Peptide ; Cerebral Infarction ; Fasting ; Fibrinogen ; Glucose ; Humans ; Hypertension ; Incidence ; Insulin ; Prevalence ; Risk Factors ; Stroke

The typical attacks of hypokalemic periodic paralysis come on during sleep or at late night. The patients usually awaken to find mild or severe weakness of the limbs and the attacks evolve over minutes to several hours. Once established, the weakness lasts a few several hours in most cases. However, our two patients due to the hypokalemia of renal tubular acidosis showed more prolonged, progressive courses of flaccid, hyporeflexic motor weakness. Especially one patient also showed slowed motor nerve conduction velocities which were normalized after potassium correction of one day. So we initially mistook the motor weakness for Guillian Barre Syndrome.
Acidosis, Renal Tubular* ; Extremities ; Guillain-Barre Syndrome* ; Humans ; Hypokalemia ; Hypokalemic Periodic Paralysis ; Neural Conduction ; Potassium

The typical attacks of hypokalemic periodic paralysis come on during sleep or at late night. The patients usually awaken to find mild or severe weakness of the limbs and the attacks evolve over minutes to several hours. Once established, the weakness lasts a few several hours in most cases. However, our two patients due to the hypokalemia of renal tubular acidosis showed more prolonged, progressive courses of flaccid, hyporeflexic motor weakness. Especially one patient also showed slowed motor nerve conduction velocities which were normalized after potassium correction of one day. So we initially mistook the motor weakness for Guillian Barre Syndrome.
Acidosis, Renal Tubular* ; Extremities ; Guillain-Barre Syndrome* ; Humans ; Hypokalemia ; Hypokalemic Periodic Paralysis ; Neural Conduction ; Potassium