Biomedical subjects

J De Reuck

Publications and source records attributed to J De Reuck.

At least 91 records · Page 5Linked to original sources

PubMed1994

New findings and symptomatic treatment for neurolathyrism, a motor neuron disease occurring in north west Bangladesh.

Neurolathyrism is a form of spastic paraparesis caused by the neuroexcitatory amino acid 3-N-oxalyl-L-2,3-diaminopropanoic acid (beta-ODAP) present in the seeds and foliage of Lathyrus sativus. The disease is irreversible and usually nonprogressive. Tolperisone HCl, a centrally acting muscle relaxant, has been shown to reduce significantly the spasticity in neurolathyrism patients. Sporadic occurrence of HTLV-1 infection (0.9%) and of osteolathyrism was found among the neurolathyrism patients. Osteolathyrism is linked to the consumption of the green shoots of Lathyrus sativus.

Bangladesh↗

PubMed1994

A double-blind study of neurotropin in patients with acute ischemic stroke.

Neurotropin was found to reduce brain oedema in an experimental model of brain infarction in the guinea-pig. A randomized double-blind controlled trial with Neurotropin was performed in 220 patients admitted within 24 h after an acute ischemic stroke. 35 of the neurotropin and 41 of the placebo-randomized patients had to be excluded. 10 included patients in the neurotropin and 13 in the placebo-treated group died within the study period of 15 days. A better clinical outcome was observed in the 65 included surviving neurotropin compared with the 56 placebo-treated patients. The size of the infarct and of the oedema zones was significantly more decreased on CT scans from Day 11 compared with Day 3 after stroke in the neurotropin than in the placebo treated group. Neurotropin is helpful in treating brain oedema, related to acute ischemic stroke.

Aged↗

PubMed1994

Long-term video-EEG monitoring revisited. The value of interictal and ictal video-EEG recording, a follow-up study.

Between October 1990 and November 1992, 100 patients were monitored at the University of Gent Epilepsy Monitoring Unit. Sixty-three patients were referred for refractory epilepsy, 38 of whom were entered in the epilepsy surgery protocol. Thirty-seven patients were evaluated for the diagnosis of attacks of uncertain origin. Average duration of monitoring was 3.5 days (2-15 days). Prolonged interictal EEG was recorded in all patients. Ictal EEG was obtained in 63 patients; the average number of recorded episodes was 3 (1-15). Pre-monitoring tentative seizure diagnosis was available in 81 patients, 59 of whom had clinical attacks. Premonitoring diagnosis was confirmed in 31 patients and revised in 28 patients. As a result of the monitoring session, anticonvulsant medication was started in 10 patients, changed in 47, stopped in 5 and left unchanged in 23 patients. Twelve patients underwent surgery. Average follow-up after monitoring was 17 months (4-30 months). Four patients were lost to follow-up; 2 patients died of an underlying disease. In the nonsurgical group (85 patients), 60 patients became seizure-free or experienced significant reduction in seizure frequency. Outcome was unrelated to the availability of ictal recording. While prolonged interictal EEG monitoring is mandatory in the successful management of patients with refractory epilepsy, ictal video-EEG monitoring is very helpful but not indispensable, except in patients enrolled for epilepsy surgery or suspected of having pseudoseizures.

Adolescent↗

PubMed1994

Comparison of cerebral haemodynamic and oxygen metabolic changes due to cavernous angiomas and arteriovenous malformations of the brain. A positron emission tomography study.

The cerebral haemodynamic and metabolic changes due to cavernous angiomas in three patients and to arteriovenous malformations in four patients were compared by positron emission tomography, using the steady state technique with 15O. In the brains with a cavernous angioma no important changes in blood flow were observed. Only a decreased oxygen consumption was present in the cortex supplied by the arterial branches of the angioma, most probably related to neuronal deafferentation. In the four cases of arteriovenous malformation cerebral blood flow was significantly increased in the territory of the feeding vessels of the angioma. In the two huge ones the oxygen extraction rate was increased in the other vascular areas remote from the supply territory of the angioma, indicating chronic ischaemia. The present study confirms that chronic vascular steal phenomena can occur in large arteriovenous malformations, while cavernous angiomas do not induce important haemodynamic changes.

Adult↗

PubMed1994

Electromyography in relation to end-plate acetylcholinesterase in rats poisoned by different organophosphates.

Organophosphate (OP) poisoning produces various forms of acute, subacute, or delayed neurotoxicity. We investigated in vivo the relationship between clinical, histochemical and electromyographic (EMG) parameters in rats at various stages of poisoning by paraoxon or fenthion. Paraoxon is acutely toxic, whereas fenthion produces more sustained AChE inhibition. Fenthion has been involved in a subacute type of OP-related neurotoxicity in patients, the so-called intermediate syndrome. The animals underwent serial EMGs, with single and repetitive nerve stimulation, and concomitant contralateral muscle biopsies to determine the end-plate acetylcholinesterase (AChE) activity. Repetitive activity (RA) after single nerve stimulation and decrements on repetitive nerve stimulation (RNS) were the major EMG findings in either type of poisoning, occurring in the initial and later stages of the poisoning, respectively. RA was highly correlated to fasciculations in acute, but not in prolonged intoxication. Amplitude decrements provoked by RNS occurred only in weak rats with severe end-plate AChE inhibition. The smallest amplitude occurred either at the second response with gradual improvement in the subsequent responses (decrement-increment phenomenon), or the amplitude decrease progressed up to the last response (decrement phenomenon). The decrement-increment phenomenon preceded the decrement phenomenon and occurred at a slightly less severe degree of AChE inhibition. Various types of impairment of neuromuscular transmission coexist, probably to a different extent at distinct stages of anticholinesterase poisoning.

Animals↗

PubMed1994

Acute and subacute organophosphate poisoning in the rat.

The intermediate syndrome in organophosphate poisoning is clinically characterized by weakness in the territory of cranial nerves, weakness of respiratory, neck and proximal limb muscles, and depressed deep tendon reflexes. It occurs between the acute cholinergic crisis and the usual onset of organophosphate-induced delayed neurotoxicity. The weakness has been ascribed to muscle fiber necrosis. Fenthion has been the most common cause. This study assesses the occurrence of the necrotizing myopathy in rats in relation to the clinical course and the acetylcholinesterase (AChE) inhibition after poisoning with organophosphates representative for each of the major types of organophosphate-related neurotoxicity. Marked differences are noted in the duration of cholinergic symptoms and of AChE inhibition after either paraoxon and mipafox, or fenthion poisoning. The necrotizing myopathy begins shortly after the initial decline in AChE activity with all organophosphates studied. Maximal muscle involvement occurs within the first 2 days of the poisoning with all organophosphates studied. The myopathy is not aggravated by a further decline in AChE activity in fenthion poisoning. Our data argues against the monophasic necrotizing myopathy being the cause of the intermediate syndrome, and is suggestive of persistent AChE inhibition being involved.

Animals↗

PubMed1993

A positron emission tomography study of patients with acute carbon monoxide poisoning treated by hyperbaric oxygen.

Seven patients with an acute and severe carbon monoxide intoxication were treated with hyperbaric oxygen and underwent a positron emission tomographic examination 2-5 days after the acute event. Although the final clinical outcome was good in all patients, ischaemic changes were observed. Three patients with temporary sequelae after hyperbaric oxygen treatment showed the most severe changes, mainly in striatum and thalamus. Although positron emission tomographic examination cannot predict the final outcome, it can show the regions at risk for development of late complications following carbon monoxide poisoning.

Adult↗

PubMed1993

Pure sensory stroke revealing a complex malformation of extra- and intracranial cerebral arteries.

Pure sensory strokes (PSS) are usually due to thalamic lacunar infarcts. We report a case of PSS in a 34-year-old female suffering from migraine who complained of sudden isolated left-sided paresthesia involving face, upper and lower limbs. We found a complex vascular abnormality associating internal carotid artery occlusion, posterior cerebral artery agenesia, aneurysm at the posterior face of the carotid siphon and angiomatous rete at the top of the basilar artery. The acquired origin of the carotid artery occlusion by possible neonatal dissection is probable since this patient has a permeable carotid canal on CT scan.

Adult↗

PubMed1992

Positron emission tomography study of the human hypothalamus during normal ageing and in ischemic and degenerative disorders.

Regional blood flow and oxygen metabolism were determined by positron emission tomography, using the steady state technique with 15O, in the hypothalamus and in the whole brain of fifty two normal persons and patients suffering from cerebral ischemia and degenerative dementia. During normal ageing regional blood flow and oxygen consumption appeared to increase slightly in the hypothalamus and to decrease in the whole brain in 24 persons. In the young age group the hypothalamus was more protected against ischemia than in the elderly group. In the aged group with cerebral ischemia and degenerative dementia regional blood flow and oxygen consumption were decreased in the hypothalamus to the same extent as in the whole brain.

Adult↗

PubMed1992

Brain abscess after esophageal dilatation for stenosis.

The case is presented of a 28-year-old female with a brain abscess after esophageal dilatation for stricture, secondary to an acute necrotizing esophagitis. Other causes of brain abscess were excluded. To our knowledge this is the first documented case of brain abscess after dilatation for esophageal stricture in adult life. Some reports in the pediatric literature have been published previously.

Adult↗

PubMed1992

Transoesophageal echo-Doppler in patients suspected of a cardiac source of peripheral emboli.

The initial results of a controlled and partly blinded study aimed at evaluating the accuracy of transoesophageal echo-Doppler in detecting cardiac sources of peripheral emboli are reported. A total of 120 consecutive patients suspected of acute embolic events were entered. After completion of all investigations, the patients were classified into three groups: patients who had definitely not suffered an embolic event (controls; n = 56); patients in whom the differentiation between local thrombosis, embolic event originating from a diseased infarct-related artery or embolic event from a cardiac source was not possible (questionable cases; n = 24) and patients in whom a cardiac source of a definite embolic event was highly suspected (cardiac emboli; n = 40). Isolated interatrial septum anomaly and mitral valve prolapse were as frequent in the control group as in the embolism group. Transoesophageal echo-Doppler had a sensitivity of 83% and a specificity of 86% in correctly assigning a patient to the cardiac embolism group or to the control group. The positive and negative predictive values were 80% and 87% respectively. It is concluded that transoesophageal echo-Doppler is highly sensitive but is also specific in demonstrating cardiac sources of peripheral emboli.

Adult↗

PubMed1992

Unusual CT and MRI findings in palatal myoclonus.

A 23-year-old man suffered from palatal myoclonus for 2 years. It had appeared one week after a minor head trauma. MRI and basal cisternography revealed a localized atrophy of the left paramedian part of the medulla, encroached upon the left vertebral artery. Clonazepam treatment was beneficial. This particular case is discussed in relation to etiopathogenesis and other causes of palatal myoclonus.

Adult↗

PubMed1992

Intermediate syndrome due to prolonged parathion poisoning.

A parathion-poisoned patient with prolonged cholinesterase inhibition due to impaired hepatic metabolism and urinary excretion is reported. An intermediate syndrome characterized by respiratory paresis, weakness in the territory of several motor cranial nerves and of proximal limb and neck flexor muscles, persisted for 3 weeks. During this whole period, cholinesterase remained markedly reduced. Serial EMGs with repetitive nerve stimulation pointed to a combined pre- and postsynaptic disorder of neuromuscular transmission. Electron microscopy of an intercostal muscle biopsy showed focal degeneration at the poorly branched postsynaptic folds, and was considered to be nonspecific.

Acetylcholinesterase↗

PubMed1992

Does the severity of leukoaraiosis contribute to senile dementia? A comparative computerized and positron emission tomographic study.

The present study evaluates the origin, severity and location of leukoaraiosis in senile dementia and in normal ageing. The regional white-matter lucency scores, determined on computed-tomographic scan of the brain, are compared to the regional blood flow, oxygen extraction rate and oxygen consumption, determined by the [15O] steady-state technique with positron emission tomography. Thirty patients, classified according to the presence or absence of leukoaraiosis and their mental status, are examined. The occurrence and severity of dementia appear to be mainly correlated to decreased blood flow and oxygen metabolism in the frontal, temporal and parietal cerebral cortex. Leukoaraiosis in demented and nondemented patients is associated with lowered blood flow in the frontal and parietal white matter. The regional lucency score is increased, and blood flow and oxygen consumption decreased in the frontal white matter of severely demented patients. Frontal leukoaraiosis contributes to dementia and is probably of ischemic origin, while parietal and occipital leukoaraiosis is due to wallerian degeneration.

Aged↗

PubMed1992

Significance of white matter lucencies in posthypoxic-ischemic encephalopathy: comparison of clinical status and of computed and positron emission tomographic findings.

The clinical status and the computed and positron tomographic findings were compared in 10 patients with sequelae of hypoxic-ischemic encephalopathy after cardiopulmonary arrest and successful resuscitation. Conscious patients with moderate neuropsychiatric deficits had no significant computed tomography (CT) scan changes and normal values of regional cerebral blood flow and oxygen consumption, while patients in vegetative state had definite cerebral atrophy on CT scan and a severe and widespread decrease of regional cerebral blood flow and oxygen consumption. This decrease was even more pronounced in vegetative patients with the worst neurological score and with CT scans demonstrating additional diffuse white matter lucencies and hypodensities in the basal ganglia. In this group of patients increased regional oxygen extraction rates mainly in the white matter indicated the occurrence of delayed ischemic changes. The positron emission tomography and CT findings correlated well with the degree of posthypoxic-ischemic damage and the clinical status of the studied subjects.

Adult↗

PubMed1992

Prolonged toxicity with intermediate syndrome after combined parathion and methyl parathion poisoning.

A prolonged type of organophosphate toxicity, previously characterized as the Intermediate Syndrome, has been recognized in 6 out of 7 prospectively studied patients poisoned by insecticide containing parathion and methyl parathion in equal proportions. The clinical characteristics included respiratory paresis, weakness in the territories of several motor cranial nerves, neck flexors and proximal limb muscles, and depressed tendon reflexes, all lasting for several days or weeks. Electromyography in the early stages disclosed diverse types of impaired neuromuscular transmission. EMG normalization preceded clinical recovery. Severe plasma butyrylcholinesterase and erythrocyte acetylcholinesterase inhibition persisted along with the occurrence of Intermediate Syndrome-related symptoms. We conclude that combined parathion and methyl parathion poisoning is more likely to induce Intermediate Syndrome than parathion poisoning alone. The mechanisms underlying this difference remain obscure. The Intermediate Syndrome shows clinical and electromyographic hallmarks of combined postsynaptic impairment of neuromuscular transmission.

Adult↗

PubMed1991

Postsynaptic neuromuscular dysfunction in organophosphate induced intermediate syndrome.

A 65-year-old Caucasian female developed an intermediate syndrome seven days after an acute cholinergic crisis, caused by the ingestion of fenthion. Cholinesterase activity in the blood, plasma and red cells was monitored daily by the method according to Nenner and serial serum fenthion levels were measured by capillary gas chromatography. Electromyographic studies showed fade on tetanic stimulation by means of surface electrodes at 20 Hz of the left M. abductor digiti quinti at day 7, which could no longer be observed at day 19. Fade on low-frequency stimulation and post-tetanic facilitation were both absent. A biopsy of the N. suralis was normal. A biopsy of the M. tibialis anterior revealed a limited rhabdomyolysis with a very weak staining for cholinesterase. It is hypothesized that the pathophysiologic process underlying the syndrome is the result of a time-confined phenomenon, which includes both changes in the postsynaptic structures by a desensitization process and a gradually restoring ratio of acetylcholine to acetylcholinesterase. This hypothesis is suggested by the similarity in the EMG-findings of this patient and those in myasthenia gravis, which is known to be characterized by a postsynaptic transmission defect.

Acetylcholinesterase↗

PubMed1991

Persisting chloroquine-induced myasthenia?

A middle-age woman had intermittently had chloroquine as an antimalarial agent for 21 years. Although she had discontinued the drug for more than 10 years due to occurrence of a retinopathy, mild ocular myasthenic symptoms persisted. Cardiac conduction disturbances were detected as well. A quadriceps muscle biopsy revealed mild neurogenic changes and interstitial lymphorrhages. The decremental response after repetitive stimulation was reversed by edrophonium administration. The history suggests that the persisting myasthenia might have been caused by chloroquine intake.

Chloroquine↗