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The findings on computed tomography (CT) and neuropathological examinations were correlated in 87 autopsied cases of cerebrovascular disease with regard to the seize and location of lesions, experience of reviewers, and improvement in CT quality. Small infarctions less than 5 mm were very difficult to detect accurately on CT. This was largely because of the limitations in the efficiency of the CT scanner. Accurate diagnosis of medium sized infarctions was also often difficult. This was mainly due to the anatomical location of lesions, the confluence of deep and widened sulci, periventricular white matter, and structures in the posterior fossa. Large infections could be visualized easily on CT, except in their early periods or in cases with hemorrhagic infarctions. The improved accuracy of CT diagnosis for small and medium sized infarctions could not be attained by the experience of reviewers, but was only possible by instrumental improvement of CT quality.

Flunarizine hydrochloride (FZ), a calcium entry blockade, has been used nationwide in Japan as a cerebral active vasodilator since October, 1984. The present paper reports 31 cases of FZ-induced Parkinsonism, depression and akathisia, referred to our hospital between October 1986 and September 1988. Out of the 31 patients, four including two with Parkinson's disease and one each with progressive supranuclear palsy and olivopontocerebellar atrophy showed worsening of their parkinsonian symptoms within a few months after FZ administration. The remaining 27 patients (7 males and 20 females) newly developed Parkinsonism after treatment with FZ. Symptoms appeared one week to two years (mean: 6.1 months) after starting FZ of a daily dose of 10 mg. FZ had been used in 6 patients for cerebrovascular episodes confirmed by clinical history or brain CT, and in the remainder, for dizziness, light-headedness, hypertension, amnesia or hypochondric neurotic complaints. Akinesia and bradykinesia progressed rather rapidly after onset, and patients became unambulatory within several months. Symptoms had worsened, and L-dopa, anticholinergic drugs, and bromocriptine had been ineffective until FZ was discontinued. Their Parkinsonism was characterized by marked akinesia, bradykinesia, and moderate rigidity. Masked face was seen in most of them. Tremor was absent at rest, and induced in 12 patients by posture and/or action. Sixteen patients were accompanied by depression, and five, by akathisia. Improvement began several weeks after withdrawal of FZ, and most patients recovered almost completely within a few months although mild rigidity and bradykinesia remained in some.(ABSTRACT TRUNCATED AT 250 WORDS)

For the prevention of recurrent embolic stroke, 23 elderly patients with non-valvular atrial fibrillation (NVAF) were treated with oral anticoagulants (warfarin) during a mean period of 3.8 years. Only one patient suffered recurrent embolism, and another had acute myocardial infarction. There was no cerebral haemorrhage during the treatment. In an untreated control group (from an autopsy series), recurrent embolic strokes occurred in 18 of 70 NVAF patients (26%) during a mean period of 1.3 years. Long-term anticoagulant therapy appears to be effective in the prevention of recurrent embolic stroke in elderly patients with NVAF.

An autopsy case is reported which revealed not only clinical and neuropathological features of progressive supranuclear palsy, but also the presence of large numbers of Lewy bodies in the brain stem nuclei and cerebral cortex. This case seems to be progressive supranuclear palsy with Lewy bodies distributed as in Parkinson's disease. Such case has not been previously reported.

The effects of nucleotides on the Ca2+-gated cation channel in sarcoplasmic reticulum (SR) vesicles were studied by measuring choline influx. The choline influx was measured by following the change in scattered light intensity using the stopped flow technique. ATP enhanced the Ca2+-induced choline influx. The activation followed a single-site titration curve with a dissociation constant of 1.0 +/- 0.5 mM, independent of the Ca2+ concentration. ATP seems to increase the pore radius or number of channels without affecting the gating mechanism of the Ca2+-gated cation channel. ADP, AMP, and adenine enhanced the choline transport in a manner similar to ATP, but cAMP, ITP, UTP, CTP, and GTP did not. The apparent dissociation constants and the maximal activations were as follows: ATP 1.0 mM, 28-fold; ADP 0.9 mM, 18-fold; AMP 0.6 mM, 7-fold, and adenine 0.4 mM, 4-fold. Adenine and AMP behaved as a competitive inhibitor for the activation by ATP. These results are consistent with the Ca2+-induced Ca2+ release observed in skinned muscle fiber and isolated SR.

We report the clinical and neuropathological findings in an autopsy case of progressive dementia, Parkinsonism, pseudobulbar palsy and supranuclear ophthalmoplegia. Since 70 years old, this hypertensive patient developed forgetfulness, unsteady gait and festination. These symptoms rapidly worsened and he was admitted in October 1983, at age 71. He had severe dementia and showed stiff face. Voluntary vertical movement of the eyes was severely disturbed, but reflex vertical movement by the doll's head eye maneuver was not affected. Muscle tone in the limbs increased slightly, and deep tendon reflexes were hyperactive in jaw and the upper extremities. Babinski sign was negative bilaterally. Sensation and coordination remained normal. Although he was not paretic or ataxic, his movements were very slow. He could not stand by himself and easily fell backward. These clinical features resembled those of progressive supranuclear palsy except for severe dementia and rapid progression. Brain CT scan revealed marked dilatation of the lateral ventricles, prominent periventicular lucency and atrophy of brainstem and cerebral cortex. Treatment with levodopa slightly improved his movement, but difficulty in swallowing worsened increasingly. He died of hypoglycemic coma and aspiration pneumonia in September 1984, about two years after the initial symptoms. General autopsy showed severe pneumonia and atrophy of the liver. The brain weighed 1,210g. Atherosclerotic change in the cerebral arteries were mild. Coronal sections of the cerebral hemispheres revealed diffuse ischemic change and multiple small infarctions in the bilateral cerebral white matter. Cortical atrophy was observed in the cerebral hemispheres. The basal ganglia, thalamus, and pons showed status lacunaris. Atrophy of midbrain and depigmentation of the substantia nigra were observed macroscopically.

The relationship between the indicence of cerebral infarction and the hematocrit was studied using 432 consecutive autopsied patients with the average age of 77.1 years. The incidence of cerebral infraction was higher in patients with hematocrit values of more than 46%, (the average in younger adult subjects). The increase in the frequency of cerebral infarction with high hematocrit values was more conspicuous in patients with severe cerebral atherosclerosis than in those with slight cerebral atherosclerosis. High blood pressure per se did not influence the relationship between the hematocrit value and the incidence of cerebral infarction. With hematocrit values of more than 41%, cerebral infarction occurred more frequently in patients over 78 years of age than in the younger patients, but the difference was not significant statistically. High hematocrit values are associated with a higher risk of cerebral infarction in deep subcortical structures of the brain than for cartical infarctions. The pathogenetic and preventive implications of these results are discussed in the light of blood rheology.

A 73-year-old woman had progressive right hemiparesis, aphasia, and focal motor seizures. EEG showed periodic discharges on the left. She died 8 weeks after onset. At autopsy, there was marked spongiform change, neuronal loss, and severe proliferation of astrocytes predominantly on the left and most prominently in the insular and centroparietal cortex. The changes were consistent with Creutzfeldt-Jakob disease (CJD), but pathology was slight or absent on the right side. This case appears as the first report of what might be called unilateral CJD. Such a condition should be included within the differential diagnosis of progressive unilateral cerebral disorders.

A clinicopathologic study was made of 45 elderly persons whose autopsied brains showed the pathologic changes of progressive subcortical vascular encephalopathy (Binswanger type). Progressive subcortical vascular encephalopathy (PSVE) was observed in 3.8 per cent of all autopsied brains of elderly persons and in 6.7 per cent of the brains of those with cerebrovascular diseases. White matter lesions were graded from I to III (slight to severe). Small infarcts in the basal ganglia, thalamus, and pons were common, but the cerebral cortex was usually preserved. Neuropsychiatric symptoms included dementia, urinary incontinence, hemiplegia, pseudobulbar palsy, psychosis, parkinsonism, and mutism. In thge Grade III group there was a high incidence of pseudobulbar palsy, parkinsonism, and mutism. Pathologic study showed marked cerebral arteriosclerosis in almost all cases. Angionecrosis was observed in 60 to 80 per cent. Fibrotic and stenotic changes of the blood vessels in the deep white matter were also noted, particularly in 90 per cent of the Grade III cases. A suggested explanation for the pathogenesis of PSVE is based on the effects of various complications such as hypertension, cardiac disease and malnutrition which may play an important role in PSVE when they occur in elderly persons with a history of long-standing hypertension, marked cerebral arteriosclerosis, and arteriolar changes in the cerebral white matter.

A 77-year-old man suffered intermittent hemiconvulsions of unknown etiology on the left side for a period of about 5 weeks. At the autopsy, there was marked neuronal loss, severe proliferation of astrocytes and spongiform changes in the right cerebral cortex. The cerebral white matter showed loosening with astroglial proliferation in areas on the same side. These neuropathological changes were slight or absent in the left cerebral hemisphere. Histopathological changes were similar to those seen in unilateral Creutzfeldt-Jakob disease (CJD). Although unilateral CJD can not be ruled out, these unilateral hemispheric changes might be induced by intermittent hemiconvulsions.