[Good prognosis of brain infarction in young adults].
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Biomedical subjects
Publications and source records attributed to B Hindfelt.
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A 44-year-old man suffered from recurrent episodes of unconsciousness, without any other concomitant manifestations. After routine workup, EEG and CT had proven nondiagnostic, prolonged Holter monitoring revealed a single episode of asystole, lasting 7.6 seconds. A pacemaker was inserted but did not abolish his episodic syncope. Subsequently, long-term EEG recording revealed epileptiform activity with independent foci in both temporal lobes. Antiepileptic treatment relieved the patient of his symptoms. This case illustrates the intimate relationship between the heart and the brain that sometimes lies behind syncope.
Twenty-five consecutive patients with idiopathic spasmodic torticollis (IST) were investigated with computerized tomography (CT) or magnetic resonance imaging (MRI) of the brain. In only six patients (24%) did CT or MRI reveal brain pathology (focal cortical atrophy and lacunary infarcts). No consistent pathological pattern was detected. Consequently, CT and MRI of the brain provides little diagnostic information in this disorder.
Prognostic information is provided for 74 young adults (age 16-40 yrs, mean age at stroke 29.5 yrs), who suffered from ischemic stroke and survived the first month after the stroke. The patients were followed for 13-26 yrs; in total for 1190 yrs after their stroke. At follow-up 12 of the patients were dead, mostly from severe underlying disease that was complicated by ischemic stroke. In 3 cases death was unrelated to cerebrovascular disease. Among the surviving 62 patients, 7 had experienced recurrent ischemic events (3 reinfarctions, 4 TIA:s). These 7 patients all had risk factors for cerebrovascular complications already at the time of their primary stroke. It is concluded that the long-term prognosis for ischemic stroke in the young adult is favourable. The recovery from neurological deficits is usually good (exceptions are occlusions within the internal carotid and middle cerebral arteries), the risk for recurrence is low (1.1-1.2% annually), and the social prognosis with respect to working capacity and family relation is fair.
Cluster headache is considered a clinically distinct entity with no underlying gross pathology. However, in rare cases this kind of headache may be mimicked by an arteriovenous malformation. A 49-year-old male is described who had severe bouts of unilateral headache resembling those of cluster headache. The usual accompanying autonomic manifestations were minor and the headache attacks were prolonged. Treatment with ergotamine tartrate and pizotifen failed. A large ipsilateral arteriovenous malformation was diagnosed. Prospectively, true clustering of the headache attacks could not be documented.
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Irrespective of their mechanism of action, which so far has not been clarified, calcium channel blockers (CCBs) have a documented prophylactic effect on classical and common migraine, as well as on cluster headache. The drugs may reduce migraine prodromes, the frequency of migraine attacks, and also decrease the severity and possibly the duration of these attacks. Notably, their optimum effect is often seen after more than 2 months of treatment. Side effects seem to be few and mild. Whether or not there are differences in therapeutic efficacy between different CCBs is presently unclear. As comparisons with other alternatives of treatment are sparse, the place of CCBs in migraine therapy remains to be established.
Experimental portal-systemic shunting is accompanied by a reduction of the soluble brain proteins. Isoelectric focusing does not indicate any selective decrease of one particular protein or group of proteins. The reduction persists with sustained shunting. The interference with brain protein metabolism is compatible with a grossly normal behavior, alterness and locomotion.
Brainstem hematoma is generally considered a very rare condition with a grave prognosis. This report presents two patients with extensive brainstem hematomas who both recovered without major sequele. A brainstem hematoma is often impossible to differentiate from an infarction despite angiographic and cerebrospinal fluid examinations, but is readily disclosed by computerized tomography. It is suggested that the seriousness of the prognosis in brainstem hematoma may earlier have been exaggerated as there may have been a tendency to classify cases exhibiting a good recovery as infarcts, while the diagnosis hematoma was reserved for cases verified at autopsy.
In three families with hereditary ataxia, where the inheritance pattern was autosomal and dominant, HLA antigens were determined in 25 members. In two of the families, HLA linkage of disease was suggested, whereas in the third family, the data did not directly support this concept, since two recombinational events between the postulated locus for disease and the HLA region had to be assumed. However, with this assumption, our data are compatible with those of one family described recently (Jackson et al. 1977) implying the presence on the sixth chromosome, outside the HLA region, of a locus that determines the development of spino cerebellar ataxia (SCA). Further tests with definition of enzyme markers will have to be performed before conclusions as to HLA linkage of a postulated SCA gene can be made.
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.
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.
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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.
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.
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.
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.
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.