Alcohol consumption and stroke incidence in male smokers.

BACKGROUND: Studies on alcohol consumption and incidences of stroke subtypes have suggested distinct dose-response relationships. Blood pressure and HDL cholesterol mediate the effect of alcohol on coronary heart disease, but similar evidence on cerebrovascular diseases is not available. METHODS AND RESULTS: We studied the risk of stroke in 26 556 male cigarette smokers 50 to 69 years of age without history of stroke. The men were categorized as nondrinkers, light (60 g/d) drinkers. A total of 960 men suffered from incident stroke: 83 with subarachnoid and 95 with intracerebral hemorrhage, 733 with cerebral infarction, and 49 with unspecified stroke. The adjusted relative risk of subarachnoid hemorrhage was 1.0 in light drinkers, 1.3 in moderate drinkers, and 1.6 in heavy drinkers compared with nondrinkers. The respective relative risks of intracerebral hemorrhage were 0.8, 0.6, and 1.8; of cerebral infarction, 0.9, 1.2, and 1.5. Systolic blood pressure attenuated the effect of alcohol consumption in all subtypes of stroke, whereas HDL cholesterol strengthened the effect of alcohol in subarachnoid hemorrhage and cerebral infarction but attenuated the effect in intracerebral hemorrhage. CONCLUSIONS: Alcohol consumption may have a distinct dose-response relationship within each stroke subtype-linear in subarachnoid hemorrhage, U-shaped in intracerebral hemorrhage, and J-shaped in cerebral infarction-but further studies are warranted. Systolic blood pressure and HDL cholesterol seem to mediate the effect of alcohol on stroke incidence, but evidently additional mechanisms are involved.

Vitamin E and beta carotene supplementation in high risk for stroke: a subgroup analysis of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study.

CONTEXT: High serum or dietary levels of vitamin E and beta carotene appear to be associated with lower risk of stroke, but studies regarding their supplementation have not supported their use in stroke prevention. OBJECTIVE: To determine if vitamin E (dl-alpha tocopherol) and beta carotene supplementations could be used in prevention of stroke in men at high risk for hemorrhagic or ischemic events. DESIGN: Population-based, randomized, double-blind, placebo-controlled, 2 x 2 factorial design trial (the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study), conducted from April 1985 through April 30, 1993, with median follow-up of 6 years. INTERVENTIONS: Alpha tocopherol, 50 mg; beta carotene, 20 mg; both; or placebo. PARTICIPANTS: From the total male population aged 50 through 69 years in southwestern Finland (n = 290,406), 29,133 male smokers were randomized to 1 of 4 treatment regimens. We excluded 614 men because of previous stroke at baseline, leaving 28, 519. MAIN OUTCOME MEASURES: Incident and fatal subarachnoid and intracerebral hemorrhage, cerebral infarction, and unspecified stroke. RESULTS: Stroke occurred in a total of 1057 men: 85 had subarachnoid and 112 had intracerebral hemorrhage, 807 had cerebral infarction, and 53 had unspecified stroke. Within 90 days from onset, 160 men died of stroke. Vitamin E supplementation increased the risk of subarachnoid hemorrhage (relative risk [RR], 2.45; 95% confidence interval [CI], 1.08-5.55) and decreased risk of cerebral infarction (RR, 0.70; 95% CI, 0.55-0.89) in hypertensive men but had no effect among normotensive men. Furthermore, it decreased the risk of cerebral infarction, without elevating the risk of subarachnoid hemorrhage, among hypertensive men with concurrent diabetes (RR, 0.33; 95% CI, 0.14-0.78). Beta carotene supplementation appeared to increase the risk of intracerebral hemorrhage and modestly decrease that of cerebral infarction among men with greater alcohol consumption. CONCLUSION: Vitamin E supplementation may prevent ischemic stroke in high-risk hypertensive patients, but further studies are needed. Arch Neurol. 2000;57:1503-1509

Comparison between the effects of pindolol and propranolol on essential tremor.

The effects of 120 mg propranolol and 15 mg pindolol daily on positional tremor of 24 patients with benign essential tremor were analyzed with a double-blind crossover trial and electrical tremor recording. Compared with the placebo effect, tremor amplitude was smaller under propranolol and larger under pindolol, whereas the frequency did not change.

Effect of propranolol on essential tremor.

The investigators tested the effect of 120 mg propranolol daily on 21 patients with essential tremor using a double-blind cross-over method and electrical recording of tremor amplitude and frequency. The patients varied in age between 15 and 60 years and had a mean tremor frequency of 10 cps. Propranolol had no effect on the tremor frequency but reduced the amplutide in 15 of the patients. Propranolol was most effective in older patients and in those with slow tremor frequencies.

Diurnal blood pressure variations and onset of subarachnoid haemorrhage: a population-based study.

OBJECTIVES: To analyse the association between time of onset of subarachnoid haemorrhage and diurnal blood pressure variations of ambulant normo- and hypertensive subjects. DESIGN: Retrospective, population-based study. SETTING: The population (246,000) of the Health Care District of Central Finland. PATIENTS: During 1980-1987 a total of 332 subjects in the study population had their first subarachnoid haemorrhage. The hour of onset could be obtained for 287 patients, and these form the basis of the present study. RESULTS: The onset of subarachnoid haemorrhage occurred significantly more often during the waking hours than during the night. The correlation between the hourly numbers of patients suffering a haemorrhage and the corresponding mean systolic and diastolic blood pressure values of ambulant normo- and hypertensive subjects was highly significant (r = 0.88, P < 0.001). The results were similar when the 224 patients with proved aneurysmal bleed were analysed separately (r = 0.79-0.85, P < 0.001). CONCLUSIONS: The diurnal blood pressure variations of ambulant normo- and hypertensive subjects, especially the transient blood pressure peaks reaching much higher levels of pressure during the waking hours than during the night, may be crucial in determining the time of rupture of a critically weakened aneurysm wall.

Serum cortisol and outcome of ischemic brain infarction.

The predictive value of serum cortisol level on the prognosis in acute brain infarction of the carotid circulation territory was studied in 101 patients younger than 70 years. The levels of 7 a.m. and 7 p.m. serum cortisol were measured initially and at 1 week. All patients underwent a computed cerebral tomography (CT) within 2 days of the onset of symptoms, and a second CT 3 weeks or 3 month later. Serum cortisol values predicted the stroke outcome. Both the 7 a.m. and the 7 p.m. values in the initial and 1-week samples correlated positively with the severity of hemiparesis on the corresponding days. The 7 p.m. values predicted better than the 7 a.m. values the functional outcome and case fatality during the 3 month follow-up. Initially and at 1 week, the median 7 p.m. serum cortisol values were statistically significantly higher in those with frontally extending infarcts than in those with non-frontal infarcts. Both 7 a.m. fasting blood glucose and glycosylated hemoglobin (HbA1c) measurements were taken within 3 days of the onset in 95 cases. The patients were diagnosed to have prestroke normoglycemia (n = 73) and hyperglycemia (n = 22) on the basis of the HbA1c level. A highly significant (P = 0.0001) correlation was demonstrated between the initial 7 p.m. cortisol and 7 a.m. fasting blood glucose values in those with prestroke normoglycemia, suggesting that hyperglycemia during the acute phase of stroke is a stress response.

Blood glucose, glycosylated haemoglobin, and outcome of ischemic brain infarction.

From August 1987 through December 1989 all consecutive conscious patients younger than 70 years with a recent (less than 48 h) brain infarction of the carotid territory were prospectively included in the study. Blood samples for fasting blood glucose and glycosylated haemoglobin (HbA1c) were taken after a median delay of 23 h of the onset of symptoms. The severity of hemiparesis was assessed on admission, at 1 week, 3 weeks, and 3 months. The functional outcome was assessed at 3 months. Computed cerebral tomography was performed on admission, and later on at 3 weeks or 3 months. The brain infarct volume was measured from the CTs. The patients were diagnosed to have prestroke normoglycemia (n = 76) and prestroke hyperglycemia (n = 23) on basis of the HbA1c level. The case fatality rate, severity of hemiparesis, functional outcome, and infarct size did not differ between these 2 groups. On the other hand, fasting blood glucose level of the non-diabetics correlated strongly with the severity of hemiparesis and predicted stroke outcome. A statistically significant correlation was observed between blood glucose values and the volumes of cortical infarcts in non-diabetics. Because prestroke blood glucose level, in contrast to post-stroke blood glucose level, did not have any predictive value concerning stroke outcome it is concluded that high fasting blood glucose values after stroke reflect a stress response to a more severe ischemic brain lesion.

Chronic subdural hematoma in adults. Influence of patient's age on symptoms, signs, and thickness of hematoma.

The relationship of age to clinical and pathological findings was analyzed in 109 adult patients operated on because of chronic subdural hematoma. A well-formed membrane on the inner and outer surface of the hematoma was used as the criterion for chronicity of the hematoma. Younger patients had more evidence of increased intracranial pressure; older patients had more evidence of mental deterioration and pyramidal tract lesions. The interval from trauma to operation was shorter in the young patients. The thickness of the hematoma as measured from angiograms increased with the age of the patient. The cause of this difference is discussed.

Smoking and intervertebral disc degeneration.

Cigarette smokers have an increased risk of low back pain which may be caused by disc degeneration and spinal instability, for example. Ischemia, apoptosis, faulty synthesis of disc macromolecules, and an imbalance between disc matrix proteinases and their inhibitors may be involved in the pathogenesis of disc degeneration. Along with degeneration, the primary avascular disc turns vascular. There is some evidence that disc degeneration of cigarette smokers is of more severe degree than that of non-smokers.Cigarette-smoking increases serum proteolytic activity by releasing proteolytic enzymes from neutrophils in alveolar capillaries, and by inhibiting the activity of alpha-1-antiprotease, the most potent protease inhibitor. We hypothesize that the high serum proteolytic activity of cigarette-smokers gets access to a previously degenerated neovascularized disc and speeds up the degerative process. The increased proteolytic activity may also weaken the spinal ligaments resulting in spinal instability. These processes may explain the increased risk of low back pain of cigarette smokers.