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Biomedical subjects

C H van der Meyden

Publications and source records attributed to C H van der Meyden.

13 recordsLinked to original sources

Significance of cerebrospinal fluid adenosine deaminase isoenzymes in tuberculous (TB) meningitis.

Adenosine deaminase (ADA) exists as two isoenzymes, ADA(1) and ADA(2). It appears that the ADA(2) isoenzyme originates mainly from monocytes and macrophages. In tuberculous pleural effusions most of the ADA activity consists of ADA(2). The aim of this prospective study was to analyse ADA isoenzymes in the CSF of patients with meningitis to investigate whether the expected rise of the ADA(2) isoenzyme would occur in tuberculous meningitis. ADA isoenzyme analysis was performed on the CSF of 15 patients with tuberculous and 11 patients with bacterial meningitis by an automated kinetic enzyme coupled assay in the presence and absence of a specific ADA inhibitor. The ratio of ADA(2)/ADA(Total) was > 0.8 in 14/15 patients with tuberculous meningitis. In bacterial meningitis the ratio was > or =0.8 in 10/11 patients. The ADA(2) isoenzyme is the major contributor to increased ADA activity in the CSF of patients with tuberculous meningitis, probably reflecting the monocyte-macrophage origin of the ADA.

Adenosine Deaminase↗

X linked severe mental retardation, craniofacial dysmorphology, epilepsy, ophthalmoplegia, and cerebellar atrophy in a large South African kindred is localised to Xq24-q27.

To date over 150 X linked mental retardation (XLMR) conditions have been documented. We describe a five generation South African family with XLMR, comprising 16 affected males and 10 carrier females. The clinical features common to the 16 males included profound mental retardation (100%), mutism despite apparently normal hearing (100%), grand mal epilepsy (87.5%), and limited life expectancy (68.8%). Of the four affected males examined, all had mild craniofacial dysmorphology and three were noted to have bilateral ophthalmoplegia and truncal ataxia. Three of 10 obligate female carriers had mild mental retardation. Cerebellar and brain stem atrophy was shown by cranial imaging and postmortem examination. Linkage analysis shows the gene to be located between markers DXS424 (Xq24) and DXS548 (Xq27.3), with a maximum two point lod score of 3.10.

Abnormalities, Multiple↗

A prospective study of Glasgow Coma Scale (GCS), age, CSF-neutrophil count, and CSF-protein and glucose levels as prognostic indicators in 100 adult patients with meningitis.

BACKGROUND: The Glasgow coma scale (GCS) is an objective measurement of a patient's level of consciousness and has prognostic implications in traumatic head injuries. Morbidity and mortality of patients with meningitis have been related amongst others to level of consciousness, hypoglycorrhachia, extremes of age, and high CSF protein values. In this prospective study of 100 patients the correlation between the GCS, age, CSF-neutrophil count and CSF-glucose and protein levels and the eventual outcome of the patients was assessed. METHODS: In 100 consecutive patients with meningitis (bacterial, viral, tuberculous, cryptococcal and other) the GCS, age, CSF-neutrophil count and CSF-protein and glucose levels were determined at admission. After treatment the outcome of the patient was assigned to one of four categories: healthy, minor and severe neurological deficits and death. RESULTS: From a non-parametric one-way analysis of variance it was found that with respect to mean GCS-values significant differences were present among the outcome categories (P < 0.0001). The outcome categories did not differ significantly with respect to age, CSF-neutrophil count or CSF-glucose level, but did differ significantly with respect to the CSF-protein level (P < 0.0025). Additionally, 88% of patients with a GCS value of > 12 had a good neurological outcome, while 88% of those with a GCS value of < or = 8 had a poor outcome. CONCLUSION: A good correlation between both the GCS and CSF-protein level at admission and the outcome of patients with meningitis was found, with the GCS value being a better prognostic indicator than high CSF protein levels.

Adolescent↗

Gadolinium ring enhancement and mass effect in acute disseminated encephalomyelitis.

A 9-year-old boy presented with a subacute history of optic neuritis followed by brainstem involvement, with fever and a lymphocytic pleocytosis in the cerebrospinal fluid. Gadolinium-enhancing ring lesions were demonstrated in the white matter of the cerebrum, brain-stem and cerebellum on day 17 of the illness, all appearing simultaneously as part of a monophasic illness. A parietal lesion exerted mass effect. Needling and biopsy yielded no evidence of a pyogenic lesion, tumour or tuberculosis and showed vasculitis. There was insufficient material for myelin staining. Dexamethasone therapy lead to rapid improvement of the radiological lesions: MRI and CT on day 34 of the illness showed complete clearing of the lesions except for residual abnormality at the biopsy site.

Acute Disease↗

Encephalitis and chorioretinitis associated with neurotropic African horsesickness virus infection in laboratory workers. Part I. Clinical and neurological observations.

Four laboratory workers from the same vaccine-packing facility developed at different times over an 8-year period an illness characterised by encephalitis (in 3 workers) and uveochorioretinitis (in 4). Low complement fixation titres were detected in all 4 patients to African horsesickness (AHS) virus and enzyme immunoassay and plaque reduction neutralising tests were positive, the latter against both serotypes 1 and 6. Five of 15 laboratory workers from the same facility who were healthy on clinical and ophthalmological examination showed positive plaque reduction neutralising tests but none to both serotypes 1 and 6. It is postulated that the encephalitis with the predominant temporal lobe involvement was caused by an airborne transnasal route of infection of the neurotropic AHS virus released in dried powder form, secondary to the accidental breaking of vaccine bottles. This is possibly the first report of subclinical and probable clinical neurotropic AHS infection in man.

Adolescent↗

Encephalitis and chorioretinitis associated with neurotropic African horsesickness virus infection in laboratory workers. Part II. Ophthalmological findings.

Four laboratory workers developed uveitis-chorioretinitis, associated with encephalitis in 3 cases. The retinitis was characterised by haemorrhages and areas of retinal oedema, most marked over the posterior polar regions, and was associated with exudative retinal detachments. The lesions progressed over weeks and showed a severe retinal arterial vasculopathy with arteriolar narrowing, ghost vessel formation and the development of optic atrophy. The picture in 2 of the patients resembled that of the acute retinal necrosis syndrome (ARN). Antibodies to African horsesickness (AHS) virus were detected. The serology for AHS virus was positive in all 4 patients as well as in 5 of 15 laboratory workers from the same facility who were clinically and ophthalmologically normal. This is to our knowledge the first description of subclinical and probable clinical neurotropic AHS virus infection in man. AHS is a hitherto-unrecognised possible cause of viral retinitis and the ARN syndrome.

Adolescent↗

Encephalitis and chorioretinitis associated with neurotropic African horsesickness virus infection in laboratory workers. Part IV. Experimental infection of the vervet monkey (Cercopithecus pygerythrus).

Neurotropic vaccine strains of African horsesickness (AHS) virus types 1 and 6 were implicated as the possible aetiological agents in 4 cases of encephalitis and uveochorioretinitis in laboratory workers accidentally exposed to the freeze-dried vaccine preparations of the virus. To date, AHS virus has not been known to infect man. To ascertain whether or not primates were susceptible to infection with AHS virus, vervet monkeys (Cercopithecus pygerythrus) were inoculated, either transnasally or intraconjunctivally, with vaccine strains of AHS virus types 1 and 6. The course of infection was monitored using parameters such as behavioural changes, febrile reaction, cerebrospinal fluid pleocytosis, serology, magnetic resonance imaging and autopsy. Encephalitis, manifested by varying degrees of fever, behavioural changes and pleocytosis, but no chorioretinitis was detected in all 6 transnasally infected monkeys. This was confirmed by autopsy, where a meningo-encephalitis affecting the medial temporal lobe but no lesions in the eyes was demonstrated. Neither virus appeared to infect the animals after intraconjunctival inoculation. These findings support the theory that the patients were infected by the inhalation of freeze-dried vaccine preparations. The pathogenesis of the eye lesions, however, remains uncertain.

African Horse Sickness↗

Effects of clobazam and clonazepam on saccadic eye movements and other parameters of psychomotor performance.

The effects of two benzodiazepine anticonvulsants clobazam (20 mg) and clonazepam (2 mg) in a variety of psychomotor performance tests were compared in a placebo controlled double-blind acute oral dose study in ten healthy volunteers. Assessments included critical flicker fusion (CFF) threshold, the Sternberg memory scanning and choice reaction time (CRT), peak saccadic velocity (PSV) and visual analogue scales, all previously shown to be sensitive to the effects of benzodiazepines. Clobazam did not significantly impair saccadic eye movements, CFF threshold, Sternberg memory scanning and CRT compared to placebo. Clonazepam significantly lowered PSV, reduced the CFF threshold, slowed the Sternberg CRT and decreased an alertness factor in the visual analogue scales compared to placebo. Clonazepam significantly increased memory scanning time compared to clobazam. Clobazam was remarkably free of cognitive and psychomotor side-effects.

Adult↗

Auditory brainstem evoked potentials in leprosy.

An electrophysiological study of conduction in the auditory nerve and brainstem auditory pathways using the brainstem auditory evoked potential was undertaken in a group of 47 leprosy patients. There were no statistically significant differences between mean conduction times (interpeak latencies) in the leprosy and the control groups. Abnormal interpeak latencies were encountered in 3 leprosy patients, 1 of whom had a positive serological test for syphilis. In the remaining 2 patients, caudal pathway dysfunction (I-III interpeak latency abnormality) was indicated but specific auditory nerve involvement (an abnormally prolonged I-II interpeak latency) was not demonstrated. An explanation for these findings, other than the patients' disease, was not apparent.

Adolescent↗

Myotonic dystrophy. Part I. A genealogical study in the northern Transvaal.

Myotonic dystrophy is a disabling multisystem disorder which appears to be more common in South Africa than is generally recognized. Twenty white kindreds with the disease were studied; of these 4 large kindreds had a common ancestry. Genealogical data for 1 527 individuals were acquired. The minimum prevalence of myotonic dystrophy in the northern Transvaal was found to be 14,3/100 000 of the population. Recognition of the disorder is important since some of its complications are preventable and others potentially treatable.

Female↗

IgA in epileptics receiving anticonvulsant therapy.

Epilepsy is a common disorder and requires long-term drug treatment. Epileptics on anticonvulsant therapy have often been reported to have a depressed immune system, especially an IgA deficiency. An association with clinical manifestations has not yet been clearly explored. So far investigations have been performed in Whites only. The objectives of this study were to assess if there is a racial difference in the immune response to anticonvulsants between Blacks and Whites and to establish the clinical significance of the IgA deficiency. Our results showed normal IgA values in Black and White epileptics on anticonvulsant therapy. This implies, at least at the present stage, that patients do not require immunological monitoring or protective measurements. Further studies including the determination of secretory IgA might help to explain the discrepancy between our findings and the literature and should provide deeper insight into the correlation between potential immune disturbances and clinical implications.

Adult↗

Effect of acute doses of controlled-release carbamazepine on clinical, psychomotor, electrophysiological, and cognitive parameters of brain function.

The neurotoxic effect of acute doses of carbamazepine controlled-release (CBZ-CR) divitabs (800, 1,200, and 1,600 mg) was assessed on clinical, psychomotor, electrophysiological, and cognitive parameters of brain function in 10 healthy volunteers in a double-blind, randomised, placebo-controlled, phase I study. Significant changes compared to placebo were demonstrated for the clinical scales, ataxia (AT), convergence of the near-point (CNP), peak saccadic velocity (PSV), critical flicker fusion (CFF), spectral analysis of the EEG, and brainstem auditory evoked potential (BAEP) tests. Digit repetition, digit symbol substitution, Sternberg memory scanning time, Sternberg choice reaction time, saccadic latency, and saccadic accuracy showed important negative findings. Significant clinical tolerance to side effects developed within 20 to 33 h after CBZ-CR dosage during a period in which the mean CBZ blood levels remained virtually unchanged. CBZ-CR, 800, 1,200, and 1,600 mg yielded low, medium, and high therapeutic blood levels, respectively, for +10 to +33 h after dosage without the development of severe clinical side effects.

Adult↗