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Biomedical subjects

M Hillbom

Publications and source records attributed to M Hillbom.

At least 73 records · Page 4Linked to original sources
PubMed1986

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.

Adult↗
PubMed1986

The significance of cerebrospinal fluid routine screening for neurosyphilis.

From 1980 to 1985 the cerebrospinal fluid microhaemagglutination assay for Treponema pallidum antibodies (MHA:TP-CSF) was routinely examined from 10 386 consecutive CSF samples of more than 10,000 patients admitted to a large neurological unit in Helsinki. Twenty one patients were considered to have neurosyphilis on the basis of clinical, serological and CSF findings. The MHA:TP-CSF test was positive in 14 patients, in 4 patients the result was undefined, and in 3 patients negative. No false-positive results were obtained. Ten of the patients had no previous history of syphilis demonstrating the value of this type of routine screening, and in only 2 of these patients the diagnosis was suspected by clinicians before the CSF examination. The serum MHA:TP was positive in all examined 18 neurosyphilis patients indicating its value for the routine screening method instead of the CSF examination.

Adult↗
PubMed1986

Contribution of traumatic head injury to neuropsychological deficits in alcoholics.

The contribution of head injuries to neuropsychological deficits was studied in 157 recently detoxified alcoholics and 400 control subjects consisting of age-stratified randomly selected men and women from the same geographical area as the alcoholics. Head injuries had occurred in 41% and 22% of the male and female alcoholics, but only in 15% and 6% of the male and female control subjects. One third of the injured subjects in both groups had been admitted to hospital for treatment of the acute injury. The neuropsychological test results of alcoholics were significantly inferior to those of control subjects. Unexpectedly, alcoholics with head injuries not identified at hospital were significantly inferior in several Halstead-Reitan subtests when compared with uninjured alcoholics with a similar duration of alcoholism and abstinence. By contrast, control subjects who had sustained a head injury not identified at hospital did not show signs of intellectual impairment when compared with uninjured controls. We conclude that traumatic brain injuries that may cause significant intellectual impairment may easily remain unrecognised in alcoholics.

Adult↗
PubMed1985

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.

Adult↗
PubMed1984

Prognosis of alcoholic peripheral neuropathy.

Ten male alcoholics aged 38-72 years with clear clinical and electroneurographical signs of peripheral neuropathy were re-examined three to five years later. Conduction velocities, latencies and nerve action potential amplitudes were measured from median, peroneal and sural nerves on both occasions and the results were compared with age-matched reference values from 80 healthy men. Seven of the alcoholics showed normal or nearly normal scores in electroneurographical and clinical examination and they had all managed to stop drinking alcohol. The results suggest that the prognosis of alcoholic peripheral neuropathy is good and independent of age provided that intake of alcohol is discontinued and other causes of neuropathy (malignancy, diabetes, nerve trauma) are carefully excluded.

Adult↗
PubMed1983

Cardiovascular effects of acetaldehyde accumulation after ethanol ingestion: their modification by beta-adrenergic blockade and alcohol dehydrogenase inhibition.

Left ventricular function was examined by echocardiography and systolic time intervals in nine healthy male volunteers, who ingested ethanol 0.35 g/kg 4 hr after a 50-mg peroral dose of calcium cyanamide, an aldehyde dehydrogenase inhibitor. Accumulation of acetaldehyde in blood was accompanied by marked increases in heart rate (53%) and cardiac output (78%) as well as by decreases in diastolic arterial blood pressure (19%) and peripheral vascular resistance (46%). Ejection fraction and maximum circumferential fibre shortening velocity increased by 25 and 47%, respectively; the preejection period/ejection time ratio decreased by 31%. 4-Methylpyrazole, an alcohol dehydrogenase inhibitor, efficiently reduced blood acetaldehyde levels when injected intravenously (7 mg/kg) at the height of the reaction. It was as effective as intravenous propranolol (0.1 mg/kg) in attenuating the hyperdynamic circulation and stabilized arterial blood pressure better than propranolol. We conclude that even a very mild alcohol intoxication (30-50 mg/100 ml) causes a marked enhancement of cardiac function, in addition to vasodilation, in subjects with impaired acetaldehyde oxidation. These changes are reversed by preventing acetaldehyde formation through alcohol dehydrogenase inhibition.

Acetaldehyde↗
PubMed1983

Can ethanol intoxication affect hemocoagulation to increase the risk of brain infarction in young adults?

We studied the effects of acute ethanol intoxication on platelet function, coagulation factors, and fibrinolytic activity in 12 healthy men. During the ethanol session, 10 of the 12 developed a transient decrease in fibrinolytic activity. Ethanol ingestion increased factor VIII coagulant activity. VIII-related antigen, and VIII-ristocetin cofactor. The highest levels were detected 16 hours after beginning ethanol ingestion (p less than 0.001), and the bleeding time decreased at 12 hours (p less than 0.01). Ethanol had no effects on platelet count, beta-thromboglobulin, antithrombin III, ethanol gelation, or fibrin/fibrinogen degradation products. Decreased fibrinolytic activity, increased factor VIII complex, and shortened bleeding time may explain why ethanol intoxication increases susceptibility to cerebral thrombosis.

Adult↗
PubMed1982

Effects of ethanol intoxication and hangover on plasma levels of thromboxane B2 and 6-keto-prostaglandin F1 alpha and on thromboxane B2 formation by platelets in man.

We detected a significant decrease in plasma thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) levels together with a significant increase in plasma 6-keto-PGF1 alpha/TXB2 ratio in young healthy non-alcoholic male volunteers after acute ingestion of ethanol (1.5 g/kg). Paradoxically, during ethanol intoxication and the following hangover a significant increase in ADP-induced formation of TXB2 by the platelet rich plasma could be observed, which suggests that ethanol intoxication via some unknown mechanism sensitized platelets to produce TXB2. Whether these observations contribute to the increased risks of subarachnoid haemorrhage or ischaemic brain infarction among occasional heavy drinkers recently described by us remains to be proved.

Adenosine Diphosphate↗
PubMed1982

New cases of neurosyphilis in Finland.

A more than tenfold increase in the annual incidence of infectious syphilis occurred in Finland during the 60s. Since then about 4 cases per 100 000 per year have been reported to the Central Medical Board. During the 70s, 39 new cases of neurosyphilis, verified by clinical and serological examinations, were recorded. At least 14 of these patients were primarily infected after 1955. The data suggest that new cases of neurosyphilis may turn up in the near future and indicate that intensified epidemiological control is still needed.

Adult↗
PubMed1982

Drinking habits and peripheral alcoholic neuropathy.

Drinking habits of 156 consecutive polyneuropathic and 106 consecutive pressure palsy patients were evaluated in retrospect. Respectively, 46 patients (30%) had alcohol polyneuropathy and 32 (30%) got pressure neuropathy while being drunk and these patients were analyzed in more detail. Most of the patients with alcoholic neuropathies were men, those with polyneuropathy being older than those having pressure palsies. Pressure neuropathy coincided with alcoholic polyneuropathy in 13 patients (28%). Other medical complication of heavy alcohol drinking (i.e. liver diseases, seizures and cerebellar signs) were seen in 54% of the patients with polyneuropathy and in 6% of the patients with pressure palsies. Heavy drinking prolonged the disability due to pressure palsy. The present study confirms the significant role of alcohol abuse in etiology of peripheral neuropathies. Heavy drinking seems to worsen the prognosis of these neuropathies.

Adult↗
PubMed1982

Alcohol intoxication: a risk factor for primary subarachnoid hemorrhage.

We studied 172 consecutively presenting patients (88 men and 84 women; aged 15 to 55) with primary subarachnoid hemorrhage (SAH) verified by hemorrhagic CSF or at autopsy. In 37 (22%) of the patients, the onset of symptoms was preceded within 24 hours by alcohol intoxication. Alcohol intoxication preceding SAH was two to three times as common in men and two to thirteen times as common in women as alcohol intoxication in the general Finnish population of the same age and sex. Thirty-two (19%) of the patients were heavy drinkers. Heavy drinking was twice as common in men and seven times as common in women as heavy drinking in the general Finnish population of the same age and sex. Both occasional ethanol intoxication and regular heavy drinking seem to carry an increased risk of SAH.

Adolescent↗
PubMed1982

Possible cardiovascular hazards of the alcohol-calcium carbimide interaction.

Healthy volunteers taking ethanol after pretreatment with calcium carbimide, a drug commonly used in treatment of alcoholism, were studied by echocardiography. Marked facial flushing and accumulation of acetaldehyde after ethanol were accompanied by circulatory acceleration corresponding in magnitude to at least moderate physical exercise. The heart rate (+/- SD) rose from 58 +/- 6 to 107 +/- 11 beats/min (p less than .001) the cardiac output from 4.1 +/- 0.6 to 9.4 +/- 1.1 L/min (p less than .001), and the ejection fraction from 70 +/- 3 to 89 +/- 2% (p less than .001). The systolic blood pressure rose initially from 121 +/- 6 to 143 +/- 5 mmHg (p less than .001). The diastolic blood pressure declined from 80 +/- 0 to 51 +/- 13 mmHg (p less than .01), and the estimated peripheral resistance to one-third of its preethanol level (p less than .001). These marked cardiovascular changes suggest that the ethanol-calcium carbimide interaction can be hazardous to alcoholics with ischaemic or other forms of myocardial diseases.

Acetaldehyde↗