Prolonged impairment in activities of daily living due to postdural puncture headache after diagnostic lumbar puncture.

To assess the incidence of postdural puncture headache and its effects on patients' activities of daily living, we interviewed 325 adult patients subjected to a diagnostic lumbar puncture during a 1-year period. Two hundred and eighteen (67%) of the subjects replied to the questionnaire; 41 (19%) of these were diagnosed as having suffered a postdural puncture headache. Impairment of the activities of daily living persisting for 1 week or more was experienced by 16 (7%) of the subjects.

Neurological recovery after liver transplantation: a prospective study of 22 patients.

A group of 22 liver transplantation patients were examined pre- and postoperatively using clinical neurological, neurophysiological and neuroradiological methods. After the operation improvement was observed in neurological symptoms, and in neuropsychological and neurophysiological test results. Our study shows that liver recipients have a high prevalence of nervous system dysfunction and that successful transplantation is followed by significant improvement.

Encephalopathy and neuropathy in end-stage liver disease before and after liver transplantation.

The nervous system involvement of 8 patients with end-stage liver disease was evaluated by means of clinical neurological, neuropsychological, neurophysiological and neuroradiological investigation before and 6-12 months after a successful liver transplantation. Preoperatively, all subjects (7 women, 1 man; mean age 40 years, range 30-54 years) exhibited decreased muscle strength and 2 patients manifested clinical signs of polyneuropathy. In neuropsychological tests, slight visuoconstructive apraxia, and disturbances of verbal memory and cognitive function were observed. Magnetic resonance imaging (MRI) revealed cerebral lesions in two patients. After transplantation, muscle strength reverted to normal in all patients, polyneuropathy improved and in all but 2 patients recovery of neuropsychological functioning was observed. Clinical signs of encephalopathy had disappeared. All patients were emotionally better adjusted after transplantation. Four subjects showed new, albeit mild changes in neurophysiological and neuropsychological tests postoperatively. We conclude that the majority of neurological impairment disappeared after liver transplantation. We want to stress that evaluation of neurological sequelae of liver transplantation needs to be based on assessments both before and after liver transplantation.

Effects of exercise and ethanol ingestion on platelet thromboxane release in healthy men.

We studied the effects of repeated bicycle exercises and ethanol ingestion (1.5 g/kg) on platelet aggregation and thromboxane (TxB2) release in 10 healthy male volunteers. After a bicycle exercise performed in the morning, the adenosine diphosphate (ADP)-induced platelet aggregation and the aggregation-associated thromboxane release were found to be decreased in fasting men. In contrast, after ingestion of fruit juice and a second exercise at noon, platelet aggregation and thromboxane release were increased. These latter changes were negligible when ethanol was ingested together with fruit juice. A third exercise, performed in the evening, again caused a decrease in the aggregation and associated thromboxane release during the control session, but provoked an increase during the ethanol session. Exercise increased the urinary excretion of 2,3-dinor-6-keto-PGF1 alpha. Changes in the plasma arachidonic acid (AA) concentration probably influenced the platelet thromboxane release. The results suggest that both physical exercise and ingestion of ethanol in fruit juice influence the ADP-stimulated platelet thromboxane release.

Influence of improved drinking habits on brain atrophy and cognitive performance in alcoholic patients: a 5-year follow-up study.

In the period 1977-1979, a sample of consecutively admitted alcoholic in-patients was studied with CT scan of the brain and neuropsychological tests. A subsample of 52 patients met the following criteria: age less than 46 years, no history of severe head injury or focal signs of traumatic brain damage, and no history of liver disease, drug abuse, or long-lasting anticonvulsant therapy. However, 72% of the patients showed brain atrophy and 49% intellectual impairment as compared to 16% and 13%, respectively, in an age-matched sample of men from the general population. Five years later, after excluding patients with head trauma, serious alcoholic liver disease and drug abuse, 37 patients were reinvestigated. Sixteen patients were abstinent or had greatly improved drinking habits during the 5-year follow-up period and 21 were still drinking. Alcohol abstinence was found to be associated with a regress of cortical atrophy and central atrophy as assessed by the width of the 3rd ventricle. However, the recovery was not complete as compared with the prevalence of atrophy in the sample from the general population. Among the patients a significant improvement in one cognitive test and a trend to improvement in some other tests associated with improved drinking habits was observed. Regression of central atrophy as assessed by a decreased diameter of the 3rd ventricle was associated with improvement in the very same cognitive tests. The results suggest that both atrophy of the brain and cognitive ability can improve in alcoholics who give up drinking.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of vitamin E therapy on ethanol-induced changes in platelet aggregation, thromboxane formation, factor VIII levels and serum lipids.

A transient increase in platelet thromboxane formation has been observed in non-alcoholics during acute ethanol intoxication and in alcoholics shortly after ethanol withdrawal. Whether these effects are related to the generation of free radicals and lipid peroxidation was investigated by using vitamin E as a free radical scavenger and inhibitor of lipid peroxide formation. The results demonstrate that a high dose of vitamin E (1800 IU) taken daily by non-alcoholic men slightly (P less than 0.05) decreases aggregation-associated platelet thromboxane formation during ethanol oxidation. Likewise, vitamin E prevents the ethanol-induced increase (P less than 0.01) in factor VIII coagulant activity. These observations suggest that the enhancement of platelet thromboxane formation and factor VIII coagulant activity by acute ethanol ingestion may be related to stimulated lipid peroxidation. By contrast, similar effects of vitamin E were not found in alcoholics shortly after ethanol withdrawal suggesting other mechanisms for their platelet hyperreactivity.

The clinical versus radiological diagnosis of alcoholic cerebellar degeneration.

We report the clinical characteristics of 65 patients with alcoholic cerebellar degeneration as verified by computerized tomography of the brain. Thirty-two patients (49%) had clear clinical signs of the disease such as broad-based staggering gait, impaired heel-to-toe walking, terminal oscillations in heel-knee test and slow (3/s) leg tremor. These signs were virtually absent in 33 patients (51%) who, nevertheless, had radiological signs of cerebellar degeneration. Traumatic brain injuries were more frequent in those patients who had both clinical and radiological signs of alcoholic cerebellar degeneration. Furthermore, this group showed longer periods of heavy drinking, more severe cerebral atrophy and more profound neuropsychological impairment than a control group of 92 alcoholics with neither clinical nor radiological signs of cerebellar disease. We conclude that careful clinical neurological examination is needed to diagnose alcoholic cerebellar degeneration which is apparently a more common disease than first realized. Subclinical cases can be diagnosed with the help of computerized tomography of the brain.

Mortality from ischaemic heart disease among patients using anticonvulsive drugs: a case-control study.

Patients who use phenytoin and some other anticonvulsive drugs have been shown to have raised concentrations of plasma high density lipoprotein. As this lipoprotein is known to be inversely associated with the incidence of ischaemic heart disease the causes of death of all patients with epilepsy known to be taking anticonvulsive drugs who died during 1978-80 were studied. Of 1399 deaths of anticonvulsant users, 258 (18.4%) were caused by ischaemic heart disease. This was significantly less (p less than 0.001) than the 382 deaths from ischaemic heart disease (27.3%) observed among paired controls matched for sex, age, and date of death. The total cardiovascular mortality was also lower among patients with epilepsy than among controls (p less than 0.02) despite there being more deaths due to cerebrovascular disease among patients. The difference in mortality from ischaemic heart disease was significant for both sexes and was not accounted for by excess deaths due to any other single cause. Users of phenytoin, carbamazepine, and barbiturates (alone or in combination) showed 29% less mortality due to ischaemic heart disease than respective controls (p less than 0.001).

Platelet thromboxane formation and bleeding time is influenced by ethanol withdrawal but not by cigarette smoking.

Platelet count, mean volume, aggregation and associated thromboxane (TXB2) formation, circulating platelet aggregates and bleeding time were examined in 19 noncirrhotic male alcoholic cigarette smokers for four weeks following cessation of prolonged heavy drinking, and in 24 nonalcoholic healthy male volunteers (10 smokers and 14 nonsmokers). The alcoholics showed a 9-fold increase (p less than 0.001) in ADP-stimulated platelet thromboxane formation one to two weeks after ethanol withdrawal. The effect was transient and coincided with a significant (p less than 0.01) shortening of skin bleeding time and a slight increase in circulating platelet aggregates suggesting proneness to thrombosis. No differences were seen between the smoking and nonsmoking healthy volunteers. We conclude that the recovery phase after prolonged heavy drinking is characterized by a transient increase in platelet reactivity which may lead to increased spontaneous formation of circulating platelet aggregates and shortening of bleeding time.

Effects of ethanol on platelet function.

To obtain evidence for an ethanol mediated disruption of hemostasis we compared the effects of acute and chronic ethanol ingestion on platelet reactivity. Since ADP may be important for hemostasis in vivo it was used to induce platelet aggregation in platelet-rich plasma. Thromboxane B2 (TXB2) formed during the aggregation was measured by radioimmunoassay. Ethanol (1.5 g/kg) given to 8 healthy non-alcoholic male volunteers increased platelet reactivity to ADP and the associated TXB2 formation rose from 289 +/- 60 (mean +/- SE) to 984 +/- 263 fmol/10(7) platelets (p less than 0.025). The effects lasted for as long as ethanol was present in blood. In 13 non-cirrhotic male alcoholics the withdrawal of ethanol caused a 4-fold increase in TXB2 formation within one week but the basal levels before ethanol withdrawal were the same as in controls. These findings are discussed in relation to the higher risk of brain infarction seen in alcoholics and even associated with binge drinking. Further studies are needed to establish the effects of ethanol on prostacyclin formation.

Outcome of surgical treatment of 110 patients with transient ischemic attack.

Between 1980 and 1982, 227 consecutive patients with transient ischemic attack (TIA) or ischemic brain infarction (IBI) were evaluated as possible candidates for carotid surgery in the Department of Neurology, University of Helsinki. One hundred and ten patients (mean age 58, range 41-72 years) were selected for surgery; 82 of them had had TIA and 28 IBI as the presenting symptom. After a total of 128 operations (84 unilateral and 18 bilateral endarterectomies, and 8 arterial reconstructions), 16 patients (14.5%) developed neurological deficits. In 7 patients (6.4%), the deficit was severe and 4 of them (3.6%) died within the first four days after surgery. Ten patients had occlusion of the contralateral internal carotid artery and/or severe hypertension. Five of them suffered ischemic brain infarction after the operation and two died. Operation on an occluded internal carotid artery in 7 patients was complicated by hemiparesis in two patients, one of whom died. Patients with surgical complications more often had severe hypertension (p less than .001), total occlusion of the contralateral internal carotid artery, (n.s.) and severe angiographic changes (n.s.) compared with patients without complications. During the follow-up the annual rate for IBI was 3.3% and for acute myocardial infarction (AMI) 4.4%. Vascular death occurred with a frequency of 1.7% per year. The results emphasize that patients with TIA or IBI should be carefully evaluated before recommending surgical treatment for prevention of threatened stroke. Patients with severe risk factors may fare better on medical treatment than with surgical intervention.

Visual and spectral EEG analysis in the evaluation of the outcome in patients with ischemic brain infarction.

Serial EEGs were recorded in 15 patients with acute cerebral infarctions in order to study clinical and prognostic correlations. The EEG was recorded within 48 h from the first symptoms and thereafter weekly for 4 weeks. The EEGs were analyzed both visually and with a computerized spectral analysis. Eight of the patients recovered fully and seven had permanent neurological deficits. On admission, 87% of the patients had an abnormal EEG by visual analysis. The spectral parameters correlated well with visual findings, especially the delta and alpha bands. The spectral analysis was superior to visual in predicting the correct laterality of the lesion. It showed the correct side of the lesion in 87%, while the visual did it in only 54% of the cases. The first EEG records reliably predicted the outcome of the patients. The degree of background abnormality was most important in visual EEG analysis. In spectral analysis, parameters from single derivations were superior to the average of all derivations. A high proportion of delta or low proportion of alpha power were reliable indicators of poor outcome.

Increase of low serum concentrations of high-density lipoprotein (HDL) cholesterol in TIA-patients treated with phenytoin.

Serum high density lipoprotein (HDL) cholesterol and other lipoproteins were measured in 27 TIA-patients with a mean age of 49 +/- 10 years before and during phenytoin therapy. The pretreatment concentrations of HDL-cholesterol (mmol/l, mean +/- SD) were lower (p less than 0.001) in male (1.03 +/- 0.25) and in female patients (1.15 +/- 0.44) than in healthy male (1.28 +/- 0.34) and female controls (1.52 +/- 0.31) respectively. After one month's phenytoin therapy HDL cholesterol concentrations reached normal levels (men 1.33 +/- 0.38, women 1.61 +/- 0.27) and after 9 months of therapy even surpassed them (men 1.47 +/- 0.27, p less than 0.05; women 1.91 +/- 0.33, p less than 0.01). Percent increase of HDL cholesterol after 9 months of therapy was 42 +/- 25 in men and 68 +/- 46 in women. There was a positive correlation (r = 0.43, p less than 0.05) between serum phenytoin level and increase of HDL cholesterol. HDL/LDL cholesterol ratio increased (p less than 0.01) also during 9 months of therapy (men from 0.26 +/- 0.05 to 0.36 +/- 0.10, women from 0.26 +/- 0.07 to 0.43 +/- 0.13) and showed a positive correlation (r = 0.91, p less than 0.001) with increase of serum HDL cholesterol. The HDL cholesterol levels achieved have been maintained with a mean serum phenytoin level of 5.6 +/- 3.6 mg/l. Phenytoin induced increase in serum HDL levels should not yet be equated with protection against atherosclerosis.

Outcome of 314 patients with transient ischemic attacks.

Between 1967 and 1976, 314 patients with transient ischemic attack (TIA) were evaluated and treated. Follow-up has been from 2.8 to 13.2 years (mean 7.8). As of 1979, 55 of the patients had succumbed to cardiovascular disease (28), cerebrovascular disease (9), malignancy (10), and other causes (8). During the follow-up period, 15 patients suffered brain infarction (4.8% under the risk) while 40 had myocardial infarction (12.7%) under the risk). Brain infarction occurred as often in patients with carotid TIA as in those with vertebral-basilar TIA, and was more common in patients under anticoagulation therapy than in those without it (p less than 0.05). Arterial hypertension, heart disease, peripheral arterial disease and diabetes did not increase the risk of brain infarction, but all (except diabetes) increased the risk of myocardial infarction. Combination of TIA with arterial hypertension, heat disease, or peripheral arterial disease increased the mortality (p less than 0.001). A life table analysis of surviving 1, 5, and 10 years gave probabilities of 99 and 100%, 89 and 91%, and 60 and 75% for males and females respectively. In the case of normotensive and hypertensive patients, a life table analysis of chances of surviving 1, 5, and 10 years gave probabilities of 100 and 95%. 94 and 80%, and 76 and 49% in both groups respectively. The result clearly emphasize treating of arterial hypertension, and demonstrate that TIA is not only a warning sign of impending stroke but also that of myocardial infarction.