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Biomedical subjects

J De Bleecker

Publications and source records attributed to J De Bleecker.

At least 19 recordsLinked to original sources
PubMed2003

A pure sensorimotor stroke due to cervical vertebral artery occlusion.

We reviewed the case history of a 45 year-old women, who presented a pure right sensorimotor stroke, due to a left paramedial medullary infarct as result of a left cervical vertebral artery occlusion. The unusual location of the infarct could be explained by the combination of an anatomical variant of the left branch of the anterior spinal artery and the presence of a deep cervical artery, issued from the costo-cervical trunck. This collateral circulation allowed that the lateral and upper medulla was not infarcted.

Angiography↗
PubMed2001

Differential regional cerebral uptake of (18)F-fluoro-2-deoxy-D-glucose in Alzheimer's disease and frontotemporal dementia at initial diagnosis.

In this paper, the cerebral uptake of (18)F-fluoro-2-deoxy-D-glucose (FDG) was studied in a relatively small group of patients suffering from either clinically diagnosed Alzheimer's disease (AD) or frontotemporal dementia during the initial differential diagnostic workup. The image analysis was done visually and semiquantitatively using three different reference regions. Visual analysis confirmed earlier literature findings on the distribution of decreased FDG uptake and demonstrated prevalent asymmetric patterns in both groups. Only semiquantitative analysis using the sensorimotor cortex as a reference region confirmed the visual findings. Moreover, there were no differences in medial temporal lobe activities between both groups, and there was no correlation of medial temporal lobe activity with dementia severity. In the AD group, a correlation of parietal FDG uptake with MMSE scores was found.

Adult↗
PubMed2001

Blue native polyacrylamide gel electrophoresis: a powerful tool in diagnosis of oxidative phosphorylation defects.

Catalytic activity of oxidative phosphorylation complexes is maintained following separation by Blue Native polyacrylamide gel electrophoresis (BN-PAGE). In BN-PAGE gels, using histochemical staining methods, we have demonstrated enzymatic activity of the complexes I, II, IV, and V in heart and skeletal muscle, liver, and cultured skin fibroblasts. The combination of BN-PAGE and catalytic staining can be successfully applied for detection of complex deficiencies. Tissues from 18 patients with deficiency in the oxidative phosphorylation as detected by spectrophotometric assay were used (10 patients complex IV, three patients complex I, one patient complex II, one patient complex I+III, three patients complex I+IV). The gene defect was located in nuclear DNA in five patients and mitochondrial DNA in one patient. In samples from patients with a severe deficiency, almost complete absence of the corresponding enzyme band is observed after catalytic staining in the gel. In patients with known partial deficiency, a milder decrease of the corresponding enzyme band is demonstrated. The amount of protein in complexes I, V, and III can easily be evaluated in samples from heart and skeletal muscle after separation by BN-PAGE using silver or Coomassie staining. The protein amount in complex IV is difficult to visualize by silver staining but easier by the Coomassie technique. In samples from liver and cultured skin fibroblasts, evaluation of protein amount is more difficult due to high background staining. In these tissues, immunoblotting can be done after BN-PAGE and subsequent transfer to a nitrocellulose membrane.

Adolescent↗
PubMed2000

Cobalt-55 positron emission tomography in late-onset epileptic seizures after thrombo-embolic middle cerebral artery infarction.

The pathogenesis of late-onset epileptic seizures after thrombo-embolic cerebral infarction is poorly understood. Our previous positron emission tomographic (PET) studies with 15O have demonstrated that post-apoplectic epilepsy is associated with more severe brain ischemia, but we were unable to determine if this was the cause or the consequence of the seizures. Using cobalt-55 (55Co) as PET tracer we can now distinguish recurrent, recent infarction in patients with a previous old infarct in the same vascular territory. In seven out of twelve patients with post-apoplectic seizures an increased uptake of 55Co was observed in the border area and in two of them also within the old infarct core. In the control group, composed of eight seizure-free patients with also an old infarct involving the cortical territory of the middle cerebral artery, no increase in 55Co uptake was observed on PET examination. The present study indicates that in a significant number of patients late-onset epilepsy is the clinical expression of recurrent strokes, occurring in the same vascular territory.

Aged↗
PubMed2000

Successful immunoglobulin treatment in a patient with neuromyotonia.

Neuromyotonia is characterized by spontaneous and continuous muscle fibre activity leading to muscle cramps, pseudomyotonia, myokymia and weakness. Electromyographic recordings show typical findings. An auto-immune mechanism has been suggested in at least a subset of patients. Various therapies have been tried with different outcome. A patient with neuromyotonia responding well to high-dose immunoglobulin treatment is presented.

Autoimmunity↗
PubMed1999

Cobalt-55 positron emission tomography in recurrent ischaemic stroke.

The present study investigates if Cobalt-55 (55Co) positron emission tomography (PET) allows us to distinguish and detect recent, recurrent strokes in patients who had already suffered a previous infarct in the same vascular territory. Fourteen patients with recurrent strokes underwent a 55Co PET scan of the brain. Recently infarcted areas, less than 2 months old, had a high 55Co uptake ratio, whereas infarcts of 6 months to 1 year had an uptake ratio comparable to normal brain tissue. In infarcts older than 2 years the 55Co uptake ratio was decreased compared to the control values. The evolution in 55Co uptake ratios with time can be explained by the dynamics of the inflammatory response within the infarct core. 55Co PET allows to demonstrate stroke recurrence and suggests that single photon emission tomography, using 57Co as the tracer, could be a more easy alternative to be used in routine neurological practice.

Adult↗
PubMed1999

Leptomeningeal metastases from ethmoid sinus adenocarcinoma: clinico-radiological correlation.

A patient with sinonasal adenocarcinoma is presented with leptomeningeal metastases affecting multiple cranial nerves and spinal nerve roots. Head and neck cancer is known to be an extremely rare source for leptomeningeal metastatic spread. The cranial nerves, the spinal cord and roots and the cerebral hemispheres can be affected in case of leptomeningeal metastatic spread. Examination of the CSF is the hallmark of the diagnosis if leptomeningeal metastatic spread is suspected, but this case illustrates that the combination of specific clinical features on one hand and specific lesions on the Gd-enhanced T1-weighted MRI study on the other hand is reliable enough to make a presumed diagnosis if the CSF analysis remains negative. We suggest that in our patient direct leptomeningeal spread occurred through the cribriform plate to the CSF, followed by further spread in a gravity dependent way.

Adenocarcinoma↗
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

Intermediate syndrome in organophosphorus poisoning: a prospective study.

OBJECTIVES: To estimate the frequency of the intermediate syndrome in organophosphorus-poisoned patients, and examine its relationship to cholinesterase inhibition and electromyographic findings. Muscle biopsies were available in some patients. DESIGN: A 3-yr prospective study. SETTING: University teaching hospital intensive care unit. PATIENTS: Consecutive patients with acute organophosphorus poisoning (n = 19). MEASUREMENTS AND MAIN RESULTS: We determined the frequency of the intermediate syndrome in poisonings with various organophosphates, duration of (acetyl) cholinesterase inhibition and metabolite excretion, evolution of alterations on repetitive nerve stimulation, type and frequency of muscle lesions. A total of eight of 19 patients developed an intermediate syndrome. In some patients, short relapses of muscarinic symptoms superimposed on the intermediate syndrome. Agents such as methylparathion, fenthion, and dimethoate carry a high risk, but we also noted a prolonged intermediate syndrome in an ethyl-parathion-poisoned patient. Prolonged and severe cholinesterase inhibition occurred during the intermediate syndrome in all patients, and metabolite excretion was prolonged. As the intermediate syndrome evolved, repetitive nerve stimulation initially demonstrated decrement, then increment, and finally, normal responses. Necrotic fibers were noted in muscle biopsies, but these fibers were too sparse to explain severe muscle weakness and were similar in patients with and without the intermediate syndrome. No patients developed delayed neuropathy. CONCLUSIONS: The intermediate syndrome is not rare. Although it is more likely to occur with some organophosphates, it is not confined to a few distinct compounds. This syndrome coincides with prolonged cholinesterase inhibition, and is not due to muscle fiber necrosis. When viewed together, the clinical and electromyographic features are best explained by combined pre- and postsynaptic dysfunction of neuromuscular transmission. The intermediate syndrome is not related to an incipient delayed neuropathy.

Acute Disease↗
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

The intermediate syndrome in organophosphate poisoning: presentation of a case and review of the literature.

A dimethoate-poisoned woman gradually developed a moderately severe cholinergic crisis that was readily treated by atropine. After being symptom-free for nearly two days, she suffered from sudden life-threatening respiratory paresis and weakness of the facial, extraocular, neck flexor and proximal limb muscles. Muscarinic symptoms were absent. Cholinesterase inhibition was severe, and EMG revealed marked decrements at low rates of repetitive nerve stimulation, and increments at a high rate. The clinical course was compatible with the Intermediate Syndrome. This syndrome seems due to persistent cholinesterase inhibition presumably leading to combined pre- and postsynaptic impairment of neuromuscular transmission. Inadequate pralidoxime therapy is proposed but not established as contributory. Prolonged monitoring of respiratory function in patients poisoned by particular organophosphate agents is mandatory.

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↗