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J Meulstee

Publications and source records attributed to J Meulstee.

34 records · Page 2Linked to original sources
PubMed1995

Electrodiagnostic criteria for polyneuropathy and demyelination: application in 135 patients with Guillain-Barré syndrome. Dutch Guillain-Barré Study Group.

Since the development of effective but expensive therapeutic strategies for the treatment of Guillain-Barré syndrome, early confirmation of the diagnosis has become very important. Electrodiagnostic criteria were developed for the discrimination of polyneuropathy and in particular for demyelination. The sensitivity and specificity of these criteria were determined in 135 patients with Guillain-Barré syndrome in an early stage of the disease, along with 45 healthy volunteers. The algorithms used to develop our criteria consisted of sets of selected electrodiagnostic variables, each of them relevant to the detection of polyneuropathy. Each set was applied on all of three consecutive electrodiagnostic examinations within one month of disease onset. Application of the best set resulted in 85% of patients with Guillain-Barré syndrome fulfilling the criteria for polyneuropathy at the first examination (mean time interval six days of disease onset), whereas none of the healthy volunteers fulfilled the criteria (sensitivity 85%, specificity 100%). The set of criteria for the detection of demyelination was fulfilled by 60% during the first examination (by 66% and 72% during the second and third examination). Application of criteria for demyelinating polyneuropathy as defined by others resulted in substantially lowered incidence (3%-46%). It is concluded that these criteria for the electrodiagnostic delineation of polyneuropathy are the most sensitive to date, with respect to the early confirmation of the diagnosis of Guillain-Barré syndrome.

Adult↗
PubMed1994

Lowered motor conduction velocity of the peroneal nerve after inversion trauma.

To analyze the effect of inversion trauma on peroneal nerve function, motor conduction velocity was measured in 22 patients. In the injured leg, 4-8 d post trauma motor nerve conduction velocity in the knee-caput fibulae segment of the superficial peroneal nerve was significantly smaller when compared with the contralateral leg and the control group. Five weeks post trauma these values were normal again. For three segments of the deep peroneal nerve, the motor conduction velocity was significantly reduced, 4-8 d post trauma, when compared with the control group. In the caput-ankle and knee-ankle segment, motor conduction velocity was still significantly lowered 5 wk post trauma. Lowered amplitudes of the Compound Motor Action Potentials of the extensor digitorum brevis muscle were found 4-8 d post trauma. No correlation was found between motor nerve conduction velocities and subjective clinical tests (anterior drawer sign and (manually performed) talar tilt test). The results of this study support the hypothesis that inversion trauma is frequently accompanied by lesions of the peroneal nerve. Motor conduction velocity measurements can be a valuable tool in assessing more objectively functional instability of the ankle joint induced by inversion trauma.

Adolescent↗
PubMed1991

Axonal damage in Guillain-Barré syndrome.

In Guillain-Barré syndrome patients, severe axonal degeneration occasionally occurs, often resulting in permanent functional deficit. In order to assess the development of axonal degeneration, we followed a consecutive series of 42 patients longitudinally using clinical and neurophysiological methods. Eight patients were considered to have severe axonal degeneration: in these patients denervation potentials were eventually found and at least 1 nerve proved inexcitable, and clinical recovery was slow and incomplete. Five of these 8 patients initially showed a pronounced generalized conduction block, the physiological hallmark of demyelination, before signs of axonal degeneration developed. In the remaining three patients, the first evaluation revealed low amplitudes with only modest conduction block; this is consistent with predominantly distal demyelination, but might, alternatively, be explained by primary axonal degeneration. Caution is necessary in using distal CMAP parameters for prognostic purposes, because the distal CMAP may be relatively spared in the early phase of the disease despite severe axonal degeneration later.

Action Potentials↗
PubMed1991

In vivo effects of sera from Guillain-Barré subgroups: an electrophysiological and histological study on rat nerves.

Serum from 20 patients with Guillain-Barré syndrome (GBS), 10 healthy controls and 10 patients with recent cytomegalovirus, Epstein-Barr virus, or Campylobacter jejuni/coli infections was injected into rat sciatic nerve. The 20 GBS patients consisted of 2 groups of 10 patients with different electrophysiological and clinical disease patterns. The main aim of the study was to investigate possible differences in humoral (auto)-immunity between these subgroups. We found no statistically significant differences in electrophysiological or histological parameters between nerves injected with sera from the 2 GBS groups. The sera of the GBS groups caused significantly more compound muscle action potential reduction at 3 to 5 days postinjection than the healthy control sera. No significant difference in nerve conduction was found between nerves injected with GBS serum and serum of patients with proven infections without GBS. Histological analysis of the same nerves that were studied electrophysiologically showed no significant differences in demyelination or other histological parameters between patients and controls at 5 days postinjection. Based on the findings in this study that sera of GBS groups with important differences in disease pattern and sera of patients with proven infection but without GBS show similar in vivo effects on rat nerves, we suggest it may be more likely that these effects are caused by aspecific serum factors associated with immune-system activation, especially by precedent infections, than by specific disease-related factors such as anti-myelin antibodies.

Action Potentials↗
PubMed1990

High-dose intravenous immunoglobulin treatment in chronic inflammatory demyelinating polyneuropathy: a double-blind, placebo-controlled, crossover study.

We discontinued high-dose intravenous immunoglobulin treatment (IVIg) in 7 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) who seemed to have responded to IVIg. After discontinuation of treatment, all 7 patients deteriorated. We then randomized the patients to IVIg or placebo (albumin) treatment in a double-blind crossover study. The clinical condition of all patients improved after IVIg and did not improve after placebo treatment. The mean time lapse from the end of the trial treatment to the occurrence of deterioration was 6.4 weeks after treatment with IVIg and 1.3 weeks after treatment with placebo. This selected group of patients with CIDP had a beneficial response to IVIg.

Adult↗
PubMed1989

Landau-Kleffner syndrome: a case study with a fourteen-year follow-up.

In a 14-year follow-up the improvement of language functions and the decrease of EEG abnormalities are described in a girl with the Landau-Kleffner syndrome. In this case, the results of subsequent EEG recordings do not permit conclusions about the course of the aphasia. Disappearance of focal spike and waves, bilateral paroxysms and slow background activity lack synchronicity with improvement of language. Finally, subtle language deficits were still present 14 years after the onset of the aphasia; the lastly recorded EEG showed mild abnormalities.

Aphasia↗
PubMed1989

Reliability of the diagnosis of a first seizure.

We studied the interrater variability among three neurologists of the diagnosis of a seizure in 100 patients evaluated for a possible "first seizure." We found that use of simple descriptive diagnostic criteria and discussion among the neurologists themselves improved the diagnostic agreement.

Adolescent↗
PubMed1988

Patterns of conduction failure in the Guillain-Barré syndrome.

Within the limits of the Guillain-Barré syndrome, the pattern of clinical deficit is variable. Motor deficit may begin proximally or distally in the extremities and sensory deficit is sometimes, but not always present. Longitudinal studies were performed in 13 patients, starting during the progressive phase. The severity of the clinical deficit was related to the amplitude of the compound muscle action potentials (CMAPs) and sensory nerve action potentials (SNAPs). Two patterns were detected, but could only be reliably distinguished during the progressive phase of the disease. (1) A length-dependent reduction of the CMAP, i.e., a progressive decrease of the CMAP on moving the stimulating electrode to more proximal stimulation sites. This could often be attributed to conduction block. In this pattern (Group A), the sensory potentials were spared with only 1 exception. These patients had motor involvement without sensory deficit and the myotatic reflexes could be preserved up to MRC grade 3 paresis. (2) A simple reduction of the CMAP, i.e., the amplitude decreased during clinical deterioration, but during a single investigation remained similar for stimulation at all levels of the nerve. In this pattern (Group B), motor and sensory fibres were similarly involved. These patients showed both motor and sensory deficit and early myotatic areflexia. The second pattern might be explained by an immunological mechanism with a predilection for those regions of the peripheral nervous system where the blood-nerve barrier is naturally deficient. In the first pattern the discrepancy between the involvement of motor and sensory fibres raises new questions, the solution of which might be of importance for the understanding of the Guillain-Barré syndrome.

Action Potentials↗
PubMed1988

Guillain-Barré syndrome: a model of random conduction block.

In the Guillain-Barré syndrome clinical deficit is caused by failure of conduction in nerve fibres. Immunological mechanisms are generally held responsible, but the mechanism has not yet been elucidated. A recent longitudinal analysis of the distribution of lesions along the nerve trunks suggested two main patterns. In one of them, motor conduction block dispersed over the length of the nerve trunk was found, whereas sensory fibres were usually spared. For further pathogenetic studies of this subgroup, it is important to know whether conduction block occurs randomly or at preferred sites. As a tool to establish this, a model for conduction block is presented, based on a random distribution of lesions in the peripheral nerves. It is applicable to compound muscle action potentials (CMAP) obtained in routine EMG studies. Comparison of predicted and measured CMAPs in a first group of seven Guillain-Barré patients with evidence of conduction block supports the concept of a random distribution of lesions in this subgroup.

Electric Stimulation↗
PubMed1988

Treatment of Guillain-Barré syndrome with high-dose gammaglobulin.

Intravenous gammaglobulin (IVGG) can improve the clinical course of several immune-mediated diseases. We report the first results of such treatment in eight patients with severe Guillain-Barré syndrome (GBS). We observed that IVGG was beneficial in at least some of the patients with severe GBS. These results should be confirmed in a randomized trial.

Adult↗
PubMed1980

Olfactory disturbances in Parkinsonism.

Disturbance of smell should be regarded as a common symptom of Parkinson's disease. It often presents as a precursor of the motor disability. The common underlying cause might be the deficiency of catecholamines in the brain of Parkinson patients, especially in the mesolimbic projection areas.

Discrimination Learning↗
PubMedDate not supplied

Flumazenil therapy for hepatic encephalopathy. A double-blind cross over study.

OBJECTIVES AND METHODS: Thirty-one patients with acute or chronic liver disease were included in the study to investigate the effect of flumazenil on hepatic encephalopathy. After screening for recent benzodiazepine use or non-hepatic causes of encephalopathy, 18 patients entered a double-blind cross-over study. The 13 remaining patients, most of them with renal failure or recent use of benzodiazepines, were given flumazenil in an open study. In the controlled study, flumazenil (1.0 mg) or placebo was given in a single injection on two separate days to study the immediate effect; half the patients received a continuous infusion of flumazenil (0.25 mg/h) or placebo for two 3-day periods to study a potential steady state effect. In the open study, a single bolus of flumazenil (1.0 mg) was given. RESULTS: In the controlled study, fifteen minutes after bolus injection, the clinical grade of hepatic encephalopathy decreased in 6 patients after injection of flumazenil, whereas a decrease was found in 2 after the placebo (P = 0.06). However, the EEG grade did not change in any of the patients, and the changes in the mean dominant frequency as measured by spectral analysis did not differ between flumazenil and the placebo. Furthermore, patients on flumazenil did not differ significantly from those on placebo during the infusion period. Subgroup analysis of underlying liver disease and the causes of encephalopathy revealed a trend for clinical improvement only in the patients with chronic liver disease, but without significant changes in the mean dominant frequency. In the open study, the clinical grade of encephalopathy decreased in 3 patients and, in contrast to the controlled study, the EEG also improved in 2 patients and the mean dominant frequency increased significantly. Responders had previously used benzodiazepines. CONCLUSION: Our study does not support a major therapeutic effect of flumazenil on hepatic encephalopathy.

Adolescent↗