Myopathies are not an unusual complication of drug therapy. The major symptoms in drug-induced myopathies are proximal muscle weakness, increased muscle enzyme levels, electromyographic changes and histological lesions. Some drug-induced myopathies are associated with neuropathy. Drug-induced myopathies can be classified according to the presence or absence of muscular pain and associated neuropathy. Among painless myopathies, we can distinguish myopathies without neuropathy (corticosteroids), myopathies with neuropathy (colchicine, chloroquine and hydroxychloroquine) and myasthenic syndromes (D-penicillamine, antibiotics, beta-blockers). Among painful myopathies, the classification is similar: painful myopathies may or may not be associated with neuropathies. Painful myopathies include polymyositis (D-penicillamine, cimetidine, zidovudine) and other myopathies without polymyositis (clofibrate, statines, cyclosporin). Among the painful neuromyopathies, eosinophilia-myalgia syndrome is a recently described disorder associated with the use of L-tryptophan. Combinations of drugs (for example, a fibrate and a statine or cyclosporin and colchicine) can induce severe myopathies. If such drugs are used together a vigorous surveillance to detect any sign of myopathy is warranted. Instead of classifying drug-induced myopathies according to clinical features, a histological classification can be proposed. Many drugs can induce vacuolar myopathy (colchicine, chloroquine, amiodarone, cyclosporin, drugs causing hypokalaemia and lipid-lowering agents), some others cause a mitochondrial myopathy (zidovudine) or a necrotizing myopathy as seen with vincristine. Overall, several criteria for reporting drug-induced myopathy can be recommended: lack of pre-existent muscular symptoms, a free period between the beginning of the treatment and the appearance of symptoms, lack of another cause accounting for the myopathy, and complete or incomplete resolution after withdrawal of the treatment. Rechallenge of the treatment is not advisable because of the risk of a serious relapse. The exact mechanisms by which drugs cause myopathies are unknown. Some cases may be due to metabolic changes, whereas others may be immune mediated. Nevertheless, the aspect these conditions have in common is the regression of the myopathy with the discontinuation of the drug.

Drug-induced myopathies

Ranitidine was first marketed in 1981; since then many patients have been treated such that much experience has been accumulated on the safety of this histamine H2-receptor antagonist in the treatment of gastroduodenal disease. A wide array of ranitidine-associated side effects has been described, but infrequently. As so much information is now available, the aim of this review is to assess the weight of evidence for a causal link between ranitidine and the reported side effects.

Side effects of ranitidine.

Magnetic resonance imaging (MRI) is more sensitive than computerized tomography in the detection of many intracerebral lesions; however, the significance of some MRI findings may be unclear. Over four years, nine patients, aged 40-79 years, have been encountered whose initial MRI scans were negative or had minimal abnormalities and soon thereafter had high grade glioma. Initial MRI was performed in eight patients for new-onset seizures and one patient for a focal deficit. MRI was negative in four of the patients and mildly abnormal in five of the patients (small areas of increased T2 and/or minimal enhancement). The initial diagnoses usually included inconclusive differentials of stroke and infection with neoplasm less frequently considered. Radiographic progression leading to the diagnosis of high grade glioma became evident on repeat MRI in 1-8 months with six patients showing progression within three months. All patients underwent surgery and had histologic diagnosis of glioma. Although MRI is quite sensitive, four of the initial scans were negative with reasonable quality studies. Conversely, in five of the initial scans, the tumors were detected when so small that the radiographic findings were not typically diagnostic. Glioma must be considered as a possible cause of initial seizures or new neurologic deficits in adults with normal or minimally abnormal MRI. In this group, seizures were the overwhelming hallmark of presentation. In such a clinical situation, close follow-up with short interval repeat MRI should be performed.

Early MRI findings in High Grade Glioma

Guanfacine and secondary mania in children.

OBJECTIVE AND IMPORTANCE: Neuroma of the 11th nerve disclosed by subarachnoid bleeding is a very rare condition. Clinical diagnosis is almost impossible, but previous episodes of muscle spasm and mild signs of subarachnoid hemorrhage with a hematoma in the cisterna magna should suggest magnetic resonance imaging as well as angiography. CLINICAL PRESENTATION: We present a case of an 11th nerve neuroma disclosed by subarachnoid bleeding. Previous episodes of muscle spasm and neck pain treated with nonsteroid anti-inflammatory drugs had been overlooked, preventing the neuroma from being diagnosed at that time. The computed tomographic scan showed an intracisternal hematoma spreading into the subarachnoid space. The hematoma appeared heterogeneous on the magnetic resonance image, and a tumor mass growing into the cisterna magna against the brain stem was also revealed. INTERVENTION: The tumor was totally removed by a suboccipital craniectomy and C1 laminectomy. It originated from the spinal root of the 11th nerve, from which it was able to be dissected without damage to the nerve. CONCLUSION: To our knowledge, this is the first reported case of an 11 th nerve neuroma disclosed by a subarachnoid hemorrhage. Furthermore, this is the seventh documented case of an 11th nerve neuroma developing in the cisterna magna. We emphasize the importance of a high index of suspicion for the rare instances of hematic density limited to the cisterna magna, especially if associated with recurring episodes of localized neck pain and muscle spasm treated with nonsteroid anti-inflammatory drugs.

Neuroma of the spinal accessory nerve disclosed by a subarachnoid hemorrhage: case report.

Mania-like episodes associated with ranitidine.

Toxicité musculaire du fénofibrate

Muscular toxicity caused by fenofibrate

Gliomes d'évolution aiguë et scanner négatif. A propos de trois observations.

Papular mucinosis recurrent comas benign dysglobulinemia

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