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Biomedical subjects

G K van Wijngaarden

Publications and source records attributed to G K van Wijngaarden.

At least 19 recordsLinked to original sources
PubMed1991

[The late whiplash syndrome; reality or fiction?].

To answer the question whether there are clinical arguments for organic lesions in patients with persistent complaints after whiplash-injuries, 200 patients referred for assessment by insurance companies and legal institutions, were investigated 2 years or more after the injury. There were 89 males and 111 females. Pain in neck, head and arms persisted in 195 patients. Dizziness persisted in 60 patients. Vestibular investigation revealed abnormalities in 48 of them and in 9 patients without dizziness. As these vestibular findings can not be understood from a neurological point of view, further research as to their significance is needed. Asthenopia was present in 3 cases and psychic disturbances in 27. Of 100 patients 87 regarded themselves as more or less severely invalidated. It is concluded that this investigation shows no evidence for organic lesions in these patients. This does not mean however that the complaints should be considered unjustified.

Adolescent↗
PubMed1985

Rhabdomyolysis and concomitant neurological lesions after intravenous heroin abuse.

Seven cases of rhabdomyolysis in heroin addicts are presented. All patients showed concomitant neurological symptoms suggesting mononeuropathy, incomplete plexus lesions or myelopathy. In most cases rhabdomyolysis occurred without preceding trauma to the muscles (for example tissue compression or coma). Five patients had a history of recently resumed heroin abuse after prolonged abstinence. An allergic or toxic reaction to heroin or adulterants seems to be more likely than trauma in the pathogenesis of these complications. Severe rhabdomyolysis can occur without visible muscular swelling. Routine screening of creatine kinase is recommended in heroin addicts with neurological complications, as rhabdomyolysis may lead to fatal renal failure and may easily fail to be diagnosed.

Acute Kidney Injury↗
PubMed1983

Follow-up study of a myopathy with loosely coupled mitochondria.

This communication deals with a clinical, histological, histochemical and biochemical follow-up study of a boy with an ameliorating myopathy with loosely coupled mitochondria who was studied earlier. In the course of about 15 years the clinical condition of the patient improved greatly. In a biopsy of skeletal muscle the same pathological features were found as before, but the pathological changes were much less severe. In contrast to earlier findings, the majority of the fibres with a loosely coupled state of the mitochondria belonged to the anaerobic type II fibres.

Adenosine Triphosphatases↗
PubMed1982

Leucoencephalopathy after inhaling "heroin" pyrolysate.

47 patients with spongiform leucoencephalopathy but no other consistent abnormalities, except brown pigmentation of the alveolar macrophages in the lungs, are described. 11 patients have died. Epidemiological studies indicate at the cause of the illness the inhalatory use of poisoned heroin vapours (pyrolysate). The heroin is primarily sold on the black market in Amsterdam. The Netherlands. Over 170 suspect heroin samples were collected for analysis of the possible poisonous factor. Although suspect, none of the samples could be unambiguously related to the observed illness. Chemical, toxicological, and histopathological investigations have not so far revealed the nature of the poisonous factor, but several neurotoxic agents that are known to cause comparable leucoencephalopathies have been ruled out. This appears to be the first manifestation of the poisonous potential of the unknown causative factor.

Adolescent↗
PubMed1982

Epsilon-aminocaproic acid myopathy. Report of a case and literature review.

A case of acute necrotic myopathy due to epsilon-aminocaproic acid (EACA) is described and compared with similar cases in the literature. This myopathy has only been noted after prolonged administration of the drug. The pathogenesis of this necrotic myopathy remains unclear, but our finds did not support a muscular vasculitis or an autoimmune reaction. Systematic preventive measures in patients with prolonged EACA therapy are proposed.

Adult↗
PubMed1979

Familial carnitine deficiency. A fatal case and subclinical state in a sister.

A 15-year-old girl with a large accumulation of lipid in the muscle fibers, was suffering from systemic carnitine deficiency. She died in acidosis. The blood carnitine level was normal. At necropsy, carnitine levels were low in skeletal muscles and heart, whilst a normal level was found in the liver. Carnitine palmitoyltransferase II and palmitoyl-CoA synthetase activities were increased, whereas carnitine acetyltransferase, glycerol-3-phosphate dehydrogenase (FAD) and succinate dehydrogenase were decreased. Investigation of blood and skeletal muscle of the family members revealed marked abnormalities in a 7-year old sister who had only minor neurological symptoms. Histochemical investigation revealed abnormal accumulations of lipid between the myofibrils. Carnitine was decreased in her skeletal muscle and blood. Muscular carnitine palmitoyltransferase II and palmitoyl-CoA synthetase were again increased in activity while glycerol-3-phosphate dehydrogenase (FAD) was decreased. The activities of succinate dehydrogenase, carnitine palmitoyltransferase I and glycerol-3-phosphate dehydrogenase (NAD+) were normal. The unexpected normal carnitine level in blood and liver of the deceased patient was attributed to muscle wasting, which was confirmed by the very high blood level of creatine phosphokinase. This fatal case indicates that the fasting condition must be avoided in persons with carnitine deficiency. In crises, glucose supply is necessary since gluconeogenesis may be blocked.

Adenosine Triphosphatases↗
PubMed1977

Familial focal loss of cross striations.

Two patients, a brother and sister, both suffering from congenital generalized muscle weakness with a progressive course are reported. Muscle biopsy revealed areas with loss of cross striations in the muscle fibers, electronmicroscopically presenting complete disorganization of the myofibrils with streaming of the Z discs and absence of mitochondria. Vesicular nuclei with prominent nucleoli were present in these areas. There was a type I fiber predominance in both cases. The mean diameter of the type I muscle fibers in one of the cases was too small. Motor endplate alterations in this patient gave no evidence of denervation but were suggestive of a delayed development of motor nerves.

Adolescent↗
PubMed1976

Changes in motor innervation and histochemical pattern of muscle fibers in some congenital myopathies.

Changes in motor innervation were compared with histologic and histochemical pattern of muscle fibers in three biopsies of central core disease, four biopsies of nemaline myopathy, one biopsy of myotubular myopathy, and three biopsies of mitochondrial myopathy. Evidence of collateral reinnervation was obtained only in one biopsy from central core disease. In other biopsies, no structural or ultrastructural abnormality of axis cylinders, myelin, or myoneural junction suggesting denervation were observed. The only relevant change found in centronuclear myopathy and to a lesser extent in nemaline myopathy was an unusual smallness and simplication of motor endings, suggesting delayed or impaired maturation. Muscle fibers strongly reactive for both adenosinetriphosphatase and nicotinamide-adenine dinucleotide diaphorase, observed in central core disease and mitochondrial myopathy, were not associated with increased terminal innervation ratio.

Adolescent↗
PubMed1972

Rare muscle diseases.

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Adenosine Triphosphatases↗