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Biomedical subjects

B Hindfelt

Publications and source records attributed to B Hindfelt.

At least 73 records · Page 4Linked to original sources

On cerebral infarction in childhood and adolescence.

This report is based on a retrospective analysis of clinical and angiographic findings in 14 children and adolescents suffering from cerebral infarction. They were all examined during the acute stage and selective angiography was performed within a day or two of the stroke. Pathogenesis is discussed and focuses particularly on the occurrence of segmental arteritis from unknown (infectious?) aetiology.

Adolescent↗

Motor nerve conduction velocity in experimental portal-systemic shunting. Preliminary communication.

The influence of portal-systemic shunting on motor nerve conduction velocity (MCV) was analyzed in rats with portacaval shunts. At 3 and 8 weeks after the shunting there was a marked but transient fall in MCV. At 16 weeks the MCV had almost normalized, despite sustained portal-systemic shunting. The results favour hepatocellular failure as the more important pathophysiological mechanism in hepatic neuropathy.

Animals↗

The crossed extensor hallucis response in neurological disorders; an electromyographic analysis.

The electromyographic activity in several leg muscles during the elicitation of "the crossed up-going toe sign" (CUT) was studied in patients and compared with that obtained in connection with the Babinski sign and in normal subjects. The results indicate that the patterns of activation and the responsible pathways are different for the CUT and Babinski signs. The difference between the normal subjects and the CUT positive patient is a matter of quantitative difference of coactivation of distal leg muscles during the test procedure rather than a change of reflex patterns.

Adult↗

The prognosis of ischemic stroke in young adults.

The report provides prognostic information on 60 patients (aged 16 to 40 years) with ischemic stroke. Immediate mortality from stroke is low and long-term mortality is due to other causes than cerebrovascular disease. The recovery from neurological deficits is good except for patients with occlusions of the internal carotic artery or the proximal parts of the middle cerebral artery. Reinfarction is rare (about 0.5 per cent annually) and other late neurological complications do not seriously affect long-term prognosis. More than 80 per cent of the patients will be able to resume work on a full or part-time basis.

Adolescent↗

Brain infarction in young adults (with particular reference to pathogenesis).

Sixty-four young adults (aged 16 to 40 years) with ischemic stroke were analyzed in retrospect with regard to possible pathogenetic mechanisms. In older patients various predisposing factors emerge (arterial hypertension, hyperlipidemia etc.) which are rare among younger age groups. In patients lacking predisposing causes the stroke incidence exhibits a seasonal variation. It is suggested that infection may be important for the development of ischemic stroke.

Adolescent↗

Brain proteins in hepatic encephalopathy.

Brain proteins were analyzed in supra- and infratentorial structures of 6 patients dying from liver failure. An equal number of patients, lacking any evidence of liver disease or neurological disorder, served as controls. The results were related to regional light microscopic findings. Hepatic coma was associated with a marked reduction of soluble brain proteins, particularly in areas of grey matter. The protein loss is probably neuronal and may be secondary to abnormalities in glial function. Implications for the pathogenesis of hepatic encephalopathy are discussed.

Adult↗

Effect of acute ammonia intoxication on cerebral metabolism in rats with portacaval shunts.

Rats were made chronically hyperammonemic by portal-systemic shunting and, 8 wk later, were subjected to acute ammonia intoxication by the intraperitoneal injection of 5.2 mmol/kg of ammonium acetate. In free-ranging animals, ammonia treatment induced a brief period of precoma (10-15 min) that progressed into deep, anesthetic coma lasting for several hours and was associated with a high mortality. In paralyzed, artificially ventilated animals that were lightly anesthetized with nitrous oxide, acute ammonia intoxication caused major disturbances of cerebral carbohydrate, amino acid, and energy metabolism that correlated in time with the change in functional state. At 10 min after injection (precoma), the concentrations of most glycolytic intermediates were increased, as was the lactate/pyruvate ratio. Citrate declined, despite a twofold rise in pyruvate, suggesting that the conversion of pyruvate to citrate had been impaired. Concentrations of phosphocreatine, and of the putative neurotransmitters, glutamate and aspartate, declined during precoma, but the concentrations of the adenine nucleotides in the cerebral hemispheres, cerebellum, and brain stem remained within normal limits. At 60 min after injection (coma), ATP declined in all regions of brain; the reduction in total high-energy phosphates was most notable in the brain stem. The findings indicate that cerebral dysfunction in chronic, relapsing ammonia intoxication is not due to primary energy failure. Rather, it is suggested that ammonia-induced depletion of glutamic and aspartic acids, and inhibition of the malate-asparate hydrogen shuttle are the dominant neurochemical lesions.

Adenosine Diphosphate↗

The prognostic significance of subfebrility and fever in ischaemic cerebral infarction.

The prognostic influence of subfebrility and fever during the first week after an ischaemic cerebral stroke was analysed retrospectively in 110 patients with varying neurological disabilities. The results indicate that fever, and even subfebrility, carry a bad prognosis with respect to residual symptoms. It is concluded that fever and subfebrility, irrespective of their genesis, should be intensely combated during the early stages of an ischaemic stroke.

Adult↗

The electrocardiogram in young adults with ischaemic stroke.

Electrocardiograms in young adults with ischaemic stroke were analysed for abnormalities within 24 h after the onset of symptoms. Fifteen patients out of 44 had some ECG abnormality, mainly ST-T changes, sinus tachycardia and minor disturbances of intraventricular conductance. In most cases the ECG abnormality could be attributed to some extracerebral cause. It is concluded that ischaemic brain lesion per se never, or very rarely, affects the electrocardiogram.

Adolescent↗

The significance of a crossed extensor hallucis response in neurologic disorders: a comparison with the Babinski sign.

The significance of a crossed extensor hallucis response on active flexion of the hip was analysed in various neurological disorders. It is concluded that this sign, not formerly described, is a pathological reflex or synkinesia. In the cooperative patient the crossed extensor response is a more sensitive indicator of a minor disturbance within the cortico-spinal motor pathways than the Babinski sign. With lesions above the foramen magnum a crossed extensor hallucis response is observed more frequently than the Babinski sign.

Adolescent↗

Electrocardiographic findings in motor neurone disease.

The electrocardiogram was analyzed in 31 patients with motor neurone disease. ECG abnormalities were encountered in 27 of the patients. The dominating ECG changes consisted of ST-T wave changes and supraventricular arrhythmias. The underlying mechanisms are discussed in relation to the neurological symptomatology.

Adult↗

The electrocardiogram in infratentorial infarcts.

Sixty-nine patients with infratentorial infarcts were studied with respect to associated electrocardiographic (ECG) abnormalities. ECG changes were encountered in about 70% of the patients, the most frequent abnormalities being arrhythmias, conduction disturbances and ST-T changes. No relationship was found between the localization of the brain-stem lesion and the accompanying ECG pattern. It is concluded that ischaemic lesions within the central nervous system do not per se affect the ECG and that associated ECG changes are merely coincidental, reflecting the same basic vascular disease.

Adult↗

The distribution of ammonia between extracellular and intracellular compartments of the rat brain.

1. The distribution of ammonia between extra-and intra-cellular compartments of the brain was evaluated in anaesthetized rats exposed to sustained hyperammonaemia and superimposed acute hypo- or hyper-capnia. 2. It is concluded that the concentration gradient for ammonia between arterial plasma and cerebro-spinal fluid (CSF) cannot be explained by pH-dependent non-ionic diffusion of ammonia. A continuous uptake by the brain tissue of ammonia from the CSF is postulated and possible mechanisms are discussed.

Ammonia↗

Whole-brain blood flow and oxygen metabolism in the rat after halothane anesthesia.

A recent modification of the Kety-Schmidt wash-out technique for 133xenon was used to measure whole-brain blood flow (CBF) and oxygen consumption (CMRO2) 1 to 4 hours after termination of halothane anesthesia in 15 Wistar rats. In this 3-hour experimental period, mean CBF and CMRO2 were reduced to 29 and 43% of control values, respectively. CBF and CMRO2 determined at the beginning and end of the experimental period were not significantly different from each other. Cerebral venous O2 tension was significantly higher than in the control group, supporting recent suggestions of a primary, intrinsic effect of halothane on the homeostatic control of this variable. It is concluded that halothane is not useful for cerebral metabolic studies in the rat.

Anesthesia, General↗

Whole-brain blood flow and oxygen metabolism in the rat during nitrous oxide anesthesia.

The Kety-Schmidt washout technique has been modified to measure whole-brain blood flow and metabolism in the rat. During nitrous oxide anesthesia, 14 rats exhaled (133)Xe, and continuous and simultaneous arterial and cerebral venous samples were drawn from a femoral artery and the transverse sinus of the brain. Extracerebral contamination of the venous sample was minimal, and equilibration of (133)Xe in brain tissue and blood was obtained after 10-24 min of inhalation. Cerebral blood flow was calculated from the total activity of the mechanically integrated arterial and venous samples according to the principle of Scheinberg and Stead. At a mean Paco2 of 40 mmHg, CBF averaged 98 +/- 6 (SEM) ml/100 g-min and CMRO2 averaged 5.4 +/- 0.7 (SEM) ml/100 g-min. CBF changed 2.4% with each millimeter Hg change of Paco2 while CMRO2 changed only insignificantly. The values obtained for CBF are higher than reported for man and large laboratory animals bur reflect the proportionately greater amount of gray matter in the rat brain.

Anesthesia, Inhalation↗