Tamotsu Shinohara

Three-dimensional mapping of local cerebral perfusion in alcoholic encephalopathy with and without Wernicke-Korsakoff syndrome

Seventeen severe chronic alcoholic patients with and without Wernicke-Korsakoff syndrome (WKS) were examined prospectively after being treated by withdrawal from alcohol. The WKS patients also received thiamine supplements. Three-dimensional measurements of local cerebral blood flow (LCBF) and local partition coefficients (LΛ) were made utilizing xenon contrast computed tomography (Xe CT-CBF). Results were displayed as color-coded brain maps before and after treatment and these were correlated with neurological and cognitive examinations. Before treatment chronic alcoholics without WKS (n = 10) showed diffuse reductions of LCBF values throughout all gray matter including hypothalamus, vicinity of nucleus basalis of Meynert, thalamus, and basal ganglia. Similar, but more severe, reductions were seen in patients with WKS (n = 7), however, white matter perfusion was also reduced. In WKS, most prominent reductions of LCBF were also seen in hypothalamus and basal forebrain nuclei but thalamus, basal ganglia, and limbic systems were severely reduced. After treatment, both groups with alcoholic encephalopathy showed marked clinical improvement and cerebral perfusion was restored toward normal. Chronic alcohol abuse, in the absence of thiamine deficiency, reduces CBF by direct neurotoxic effects. If thiamine deficiency is also present, more severe and localized hemodynamic reductions are superimposed.

Enhanced erythrocyte aggregability in occlusive cerebrovascular disease.

We measured the rate of erythrocyte aggregation using our whole-blood aggregometer in 80 patients with occlusive cerebrovascular disease during the acute and chronic phases. We compared the data with values for 38 age-matched healthy controls. Mean +/- SD erythrocyte aggregability of the patients during both the acute phase (0.145 +/- 0.21/sec, n = 35) and the chronic phase (0.139 +/- 0.21/sec, n = 45) was higher than that in the controls (0.123 +/- 0.21/sec, n = 38; p less than 0.01). Erythrocyte aggregability was positively correlated with the plasma concentration of globulin and fibrinogen and inversely correlated with the albumin:globulin ratio. However, these correlations did not necessarily exclude the possibility that some unknown substance(s) released from ischemic tissue might enhance erythrocyte aggregability.

Bilateral hemispheric reduction of cerebral blood volume and blood flow immediately after experimental cerebral hemorrhage in cats.

Acute cerebral circulatory changes following experimental cerebral hemorrhage were investigated in eight cats. The cerebral hemorrhage was produced in the right basal ganglia by introducing arterial blood via a thin catheter, using the systemic arterial blood pressure of the cat as a driving force. Local cerebral blood volume was measured continuously in the bilateral parietotemporal cortexes employing photoelectric apparatuses. Carbon black dilution curves were recorded from the regions, and the mean transit time of blood was calculated. Local cerebral blood flow was estimated from mean transit time and cerebral blood volume. Intracranial pressure was monitored continuously in the right parietal epidural space. Five minutes after cerebral hemorrhage, intracranial pressure increased by 24.0 +/- 6.1 mm Hg, while mean arterial blood pressure increased by only 2.9 +/- 2.0 mm Hg. Cerebral blood volume decreased by 1.60 +/- 0.24 vol% in the hemorrhagic and 1.14 +/- 0.30 vol% in the nonhemorrhagic hemisphere. Cerebral blood flow decreased by 30.0 +/- 4.5 ml/100 g brain/min in the hemorrhagic (initially 64.5 +/- 13.6) and by 30.3 +/- 7.5 ml/100 g brain/min in the nonhemorrhagic (initially 60.9 +/- 6.9) hemisphere. Increased intracranial pressure appeared to be the main cause of the observed cerebral blood volume/flow reduction shortly after experimental hemorrhage in the basal ganglia. Several other factors and mechanisms involved are discussed.

Levodopa-induced local cerebral blood flow changes in Parkinson's disease and related disorders

Local cerebral blood flow (CBF) in the steady state and after intravenous administration of levodopa (1 mg/kg) was measured by xenon-enhanced computed tomography in patients with Parkinsons disease (PD, n = 16), progressive supranuclear palsy (PSP, n = 6), olivopontocerebellar atrophy (OPCA, n = 5), and arteriosclerotic parkinsonism (AP, n = 7). Three patterns of local CBF changes following levodopa were observed: (1) diffuse CBF increases, especially in striatum and thalamus, as found in patients with PD; (2) no significant changes in CBF, as in patients with OPCA and AP; and (3) CBF reductions in basal ganglia and thalamus, as seen in patients with PSP. The CBF increases after levodopa in PD may be secondary to metabolic activation of the nigrostriatal dopaminergic system. The poor CBF responses in patients with OPCA, AP, and PSP appeared to reflect degeneration of the dopaminergic neurons and dopamine receptors to various degrees. The CBF increases, especially in striatum and thalamus, tended to be greater (not significant) among responders to oral levodopa therapy. Levodopa-induced CBF measurements may be useful for the differential diagnosis of parkinsonian syndromes of various etiologies, but are not necessarily sufficient for predicting outcomes of long-term levodopa therapy.

Cerebral microcirculatory changes during and following transient ventricular tachycardia in cats

Although reduced cerebral perfusion is believed to be the cause of syncope due to cardiac arrhythmias, investigations on the cerebral microcirculation during cardiac arrhythmias have been rare. We therefore studied the effects of transient ventricular tachycardia on the local cerebral blood volume and blood flow. Experimental ventricular tachycardia was induced in cats by electrically stimulating the ventricle of the heart at a rate of 300/min for 1 min. Using our photoelectric method, the local cerebral blood volume, mean transit time of blood, and cerebral blood flow in the parieto-temporal region were measured during and for 3 h after ventricular tachycardia. Transient ventricular tachycardia of as short as 1 min caused cerebral ischemia with a blood flow reduction of approximately 30%. This was considered to be due to reduced blood pressure plus transient autonomic dysfunction, or dysautoregulation, during the ventricular tachycardia. Mild and transient reactive hyperemia occurred immediately after termination of the dysrhythmia, but continuous reductions of cerebral blood flow were observed thereafter for 3 h. This delayed hypoperfusion is attributable to either vasoconstriction of the large resistance vessels or changes in the hemorheological properties of the blood caused by cerebral ischemia. Ventricular tachycardia of the type reported has significant and long-lasting effects on the cerebral microcirculation.

RBC Aggregation Is Not a Primary Factor for Microvascular Stasis on Temporary Complete Ischemia of the Feline Brain

Vascular dementia could be triggered by cerebral ischemia, in which micro-circulatory stasis and subsequent impairment of microcirculation may constitute the cardinal events. The possibility that aggregation of red blood cells (RBC) might contribute to the stasis and no-reflow has been suggested for many years, since the viscosity of blood in a sluggish flow or stasis is predicted to increase from the hemorrheological viewpoint. We examined the effect of RBC aggregation in the leptomeningeal vessels and parenchymal microvasculature on reflow after a brief, complete interruption of flow through the brain tissue produced by cardiac arrest.

Diffusion of Oxygen and Hydrogen Gas is Faster Through a Layer of Suspended Cultured C6 Cells than Through the Medium

The gas diffusion in the living cerebral cortex has been reported by Gotoh et al. to be faster than that in the dead cortex (Gotoh, Tazaki and Meyer, 1961). This was attributed by them to a mixing effect due to the vasomotor action of the microvasculature in the tissue, by which gas molecules could be transported to far distant areas. The present study examined whether or not such a facilitated process persisted even in a cell suspension where the microcirculation was deprived.

Cerebral Hemodynamics in Patients with Periventricular White-Matter Lesions on Brain Imaging

Periventricular or deep white-matter lesions on brain imaging, so-called leukoaraiosis [8], have been frequently observed in elderly subjects with or without dementia. They are associated with age, increased systolic blood pressure, motor and reflex deficits, and with deficits in cognitive function [1,19]. Recently these changes have attracted the attention of clinicians and pathologists in relation to Binswanger’s disease [3,6,12,17,18] or senile dementia [15]. The pathological significance of these changes are, however, still in dispute. Hachinski and his coworkers [8,19,20] concluded from their studies that white-matter changes were associated with intellectual impairment and sometimes with vascular disease. On the other hand, Leys et al. [14] reported that periventricular and white-matter hyperintensities on magnetic resonance imaging (MRI) were frequent incidental findings in the elderly and did not significantly differ between patients with Alzheimer’s disease and healthy controls. In order to clarify the underlying pathophysiological mechanism of these changes, we investigated cerebral hemodynamics in patients with periventricular white-matter lesions on brain imaging and correlated the data with severity of white-matter changes, mental function, and other clinical findings.

The Mechanical Filtration Coefficient (Lp) of the Cell Membrane of Cultured Glioma Cells (C6)

The mechanical filtration coefficient (Lp) of the membrane of cultured glioma cells was determined from the rate of swelling of the cells. The swelling was induced by exposing the cells to distilled water. Assuming that cells swell in a symmetrical manner, Lp was 2.2 x 10(-8) cm/s.mmHg, or 1.7 x 10(-4) microns/s.cmH2O when calculated from changes of the cell diameter.

Cerebral hemodynamics in patients with "Moyamoya Disease" compared with those in patients with atherosclerotic occlusion of the major cerebral arterial trunk.

Xe enhanced CT法を用いて, ウィリス動脈輪閉塞症11例 (22側), および動脈硬化性脳主幹動脈閉塞症8例 (内頚動脈閉塞症2例, 中大脳動脈閉塞症2例, 中大脳動脈領域梗塞4例) の安静時局所脳血流量および局所CO2反応性を測定した.動脈硬化性主幹動脈閉塞症では, 閉塞側の前頭葉皮質, 側頭葉皮質, 被殼, 尾状核の局所脳血流量, CO2反応性は, 非閉塞側の同部位に比し有意に低下していた.ウィリス動脈輪閉塞症の局所脳血流量は, 後頭葉皮質以外の部位で, 動脈硬化性主幹動脈閉塞症の閉塞側に比し有意に高値を示した.また, 局所CO2反応性は, 被殼, 尾状核の基底核部で, 動脈硬化性主幹動脈閉塞症の閉塞側に比し有意に高値であった.すなわち, ウィリス動脈輪閉塞症と動脈硬化性主幹動脈閉塞症では, 脳循環動態に明かな相異を認めた.これは, ともに脳主幹動脈が閉塞する疾患でありながら, 側副血行路の発達が異なることに起因すると考えられた.1.Xe enhanced CT法を用いて, ウィリス動脈輪閉塞症11例, および動脈硬化性脳主幹動脈閉塞症8例の安静時局所脳血流量および局所CO2反応性を測定した.2.動脈硬化性主幹動脈閉塞症において, 非閉塞側半球の平均脳血流量はCO2負荷により有意に増加したが, 閉塞側半球の平均脳血流量は有意には増加しなかった.3.動脈硬化性主幹動脈閉塞症では, 閉塞側の内頚動脈潅流領域の局所脳血流量, 局所CO2反応性は非閉塞側の同部位に比し, 有意に低値であった.4.ウィリス動脈輪閉塞症では, 動脈硬化性主幹動脈閉塞症の閉塞側に比し, 内頚動脈潅流領域の安静時局所脳血流が有意に高値であった.5.ウィリス動脈輪閉塞症の局所CO2反応性は, 基底核部において, 動脈硬化性主幹動脈閉塞症の閉塞側に比し有意に高値であった.6.以上の結果は, ウィリス動脈輪閉塞症において, 脳底部モヤモヤ血管を中心とした側副血行路の発達が良好なためと考えられた.