Hitoshi Kurabayashi

Delayed Manifestation and Slow Progression of Cerebral Infarction Caused by Polycythemia Rubra Vera

Background:Polycythemia rubra vera is often found after the manifestation of cerebral infarction, though the pathogenesis is still controversial. We present a case of cerebral infarction secondary to polycythemia rubra vera, which presented a slow expansion on magnetic resonance imaging despite severe hemiplegia. This case suggests a possible mechanism for development of cerebral infarction in polycythemia rubra vera. Methods:This case report was conducted in a university hospital. Magnetic resonance imaging and diffusion-weighted imaging were performed to assess the evolution of infarction, and the total blood volume and cerebral blood flow were determined with the use of isotopes, 51Cr and 99mTc, respectively. Phlebotomy was performed, but intervention was not applicable. The manual muscle test and sensory disturbance were assessed by the same physiotherapist throughout the clinical course. Results:A 64-year-old male patient with polycythemia rubra vera had a cerebral infarction. A subtle change was observed on CT scan on the third day after the onset of infarction, and a small signal was demonstrated on magnetic resonance imaging on the fourth day. The cerebral infarction expanded slowly in size and reached a maximum on day 24. A diagnosis of cerebral infarction secondary to polycythemia rubra vera was made, and treatment by phlebotomy, hydration, and hydroxyurea was begun. Though the hemiplegia remained, he became ambulatory with a brace, as do patients with atherosclerotic infarction. Conclusions:It is suggested that the delayed manifestation and slow expansion of cerebral infarction caused by elevated hematocrit might be derived from a pathogenesis different from atherosclerotic infarction.

Is insulin resistance related to recurrence of stroke or incident of ischemic heart disease in patients with stroke? A preliminary report.

Insulin resistance promotes atherosclerosis and has been recognized as an important risk factor for both stroke and ischemic heart disease (IHD). However, the precise relationship between insulin resistance and ischemic stroke recurrence or development of IHD is uncertain. The aim of this study was to investigate the relationship of insulin resistance to ischemic stroke recurrence or IHD in patients with a history of stroke. A total of 32 patients poststroke with hypertriglyceridemia but without a history of diabetes mellitus were asked whether they had experienced stroke recurrence or IHD after discharge. We found that 4 of 32 patients experienced recurrence. Three of these 4 patients had insulin resistance. We classified the subjects into two groups: one group with stroke recurrence and the other group without. We then compared the insulin profiles between these two groups. Although there was no significant relationship between recurrence and insulin resistance, fasting glucose level was higher in patients with recurrence than without. Insulin-resistant patients with recurrence had significantly lower levels of plasma insulin at 120 minutes in the oral glucose tolerance test compared with those without recurrence. This study suggests that insulin resistance in combination with decreased insulin secretion may be associated with ischemic stroke recurrence or IHD.

Insulin resistance in patients with stroke is related to visceral fat obesity and adipocytokines.

Insulin resistance is associated with hyperglycemia and dyslipidemia and promotes atherosclerosis. Although insulin resistance is associated with adipocytokines, little is known about the association in patients with stroke without diabetes mellitus. The aim of the current study was to examine the relationship among insulin resistance, visceral fat area, and adipocytokines in patients with stroke. This study design was cross-sectional in a university hospital. We studied 60 patients with stroke and no history of diabetes mellitus who had hyperglycemia or hypertriglyceridemia or reduced fasting plasma high-density lipoprotein cholesterol. We measured insulin resistance, the plasma level of tumor necrosis factor (TNF)-alpha, adiponectin, and the visceral fat area. Insulin resistance was defined by the homeostasis model assessment and the level of insulin at 120 minutes after consuming oral glucose. We classified two groups (insulin sensitive or insulin resistant). In all, 21 of 60 patients (35.0%) had insulin resistance and 35 (58.3%) had hyperinsulinemia. Compared with insulin-sensitive patients with stroke (n = 18), insulin-resistant patients with stroke (n = 21) had significantly wider visceral fat areas and a high level of plasma TNF-alpha. The plasma level of adiponectin in insulin-resistant patients with stroke was similar to that in insulin-sensitive patients. Insulin-resistant patients with stroke in this study had a large amount of visceral fat and increased levels of TNF-alpha. We recommend that obese patients with stroke should be examined for insulin resistance to reduce the risk of the development of atherosclerosis.

Clinical improvements in higher brain function and rapid functional recovery in a case of cerebellar hemorrhage treated by neurocognitive rehabilitation

Cerebellar stroke rarely causes disorders of higher brain function such as cognitive deficits and emotional dysfunction; hence, the prognosis of these patients is uncertain. We report the case of a 34-year-old patient with cerebellar hemorrhage due to arteriovenous malformation causing higher brain dysfunction who was able to return to full-time employment after neurocognitive rehabilitation. Cerebellar stroke caused by nonatherosclerotic diseases or diaschisis may lead to cognitive deficits but these symptoms can be reversed by appropriate therapy. It is important to assess higher brain function in cerebellar stroke patients and to tailor neurocognitive rehabilitation programs appropriately to promote functional recovery.