ABSTRACT
Sulindac (Clinoril), a nonsteroidal anti-inflammatory agent, has few reported neurologic toxic effects, all of which have been associated with systemic disease. To our knowledge, we describe the first reported case of isolated paresthesia and peripheral neuropathy, without systemic involvement, secondary to sulindac administration. A healthy, 30-year-old man, exposed to sulindac on two separate occasions, had an incapacitating isolated idential sensory neuropathy. The onset and duration of symptoms correlated directly to drug ingestion. This hypersensitivity response cannot be explained pathophysiologically by any mechanism. Repeated exposure and rechallenge of the subject to sulindac was deemed too dangerous, and precludes exact method to establish mechanisms to explain this transient, reproducible, idiosyncratic, adverse drug reaction.
Subject(s)
Drug Hypersensitivity/etiology , Indenes/adverse effects , Paresthesia/chemically induced , Peripheral Nervous System Diseases/chemically induced , Sulindac/adverse effects , Adult , Humans , Male , Pain/drug therapyABSTRACT
Eleven patients met rigid criteria for having both polymyositis and systemic lupus erythematosus (SLE). The patients differed little in clinical features when compared with patients who had SLE and polymyositis in a previously reported series. The overall mortality rate of 18% and the finding that 56% of survivors were asymptomatic at latest follow-up (average four years) suggest that the prognosis for this subgroup of patients may be more favorable than that for patients with rheumatoid arthritis and scleroderma complicated by polymyositis and may be comparable to the prognosis of the overall group of patients with polymyositis.
Subject(s)
Lupus Erythematosus, Systemic/complications , Muscular Diseases/complications , Adolescent , Adult , Biopsy , Electromyography , Female , Follow-Up Studies , Humans , Lupus Erythematosus, Systemic/pathology , Middle Aged , Muscles/pathology , Muscular Diseases/pathologyABSTRACT
The effect of anticoagulation on lesions caused by cerebral emboli of different types was studied in 57 dogs. The resultant arterial and parenchymal lesions were assessed by pathologic and angiographic studies. Embolization with emboli that caused little or no inflammatory response in the artery (12 dogs) was not associated with hemorrhagic infarcts or with subdural or subarachnoid hemorrhage; furthermore, treatment with anticoagulants (9 dogs) did not change the character of the lesions. Embolization with emboli that caused arteritis, that is, bacterial contamination or presence of lead chromate in the embolus (21 dogs), was associated with hemorrhagic infarcts, focal subarachnoid hemorrhage, and increased incidence of acute subdural hemorrhage. Treatment with anticoagulants (16 dogs) was associated with a further increase in the incidence of subdural hemorrhage.
Subject(s)
Anticoagulants/adverse effects , Bacterial Infections/drug therapy , Cerebral Hemorrhage/chemically induced , Intracranial Embolism and Thrombosis/drug therapy , Animals , Anticoagulants/therapeutic use , Brain/pathology , Cerebral Hemorrhage/complications , Disease Models, Animal , Dogs , Hematoma, Subdural/chemically induced , Intracranial Embolism and Thrombosis/complications , Intracranial Embolism and Thrombosis/pathology , Subarachnoid Hemorrhage/chemically inducedABSTRACT
In order to study the effects of septic embolism on the brain, silicone rubber emboli of various types were injected into the carotid arteries of 35 dogs. Pathologic and angiographic studies were performed to assess the resultant arterial and parenchymal lesions. Pure silicone rubber emboli (14 dogs) produced occasional intra-arterial thrombosis but no arteritis. Sterile and bacterially contaminated emboli containing a lead-chromate pigment (similar to those used in previous studies of septic embolism) (11 dogs) and pure silicone rubber emboli with transversely oriented canals (10 dogs), after brief placement in a bacterial suspension, were associated with intense inflammatory arteritis. This was accompanied by focal meningitis, subarachnoid hemorrhage, thrombosis, and cerebritis of the underlying cortex. The findings resembled those found in mycotic aneurysm. Aneurysmal dilatation was observed in one postmortem angiogram. In previous models of mycotic aneurysm, the inflammation attributed to bacterial contamination was probably due to the lead-chromate pigment used.
Subject(s)
Arteritis/etiology , Cerebral Arterial Diseases/etiology , Intracranial Embolism and Thrombosis/complications , Animals , Arteritis/pathology , Brain/pathology , Cerebral Arterial Diseases/pathology , Disease Models, Animal , Dogs , Enterococcus faecalis , Intracranial Aneurysm/pathology , Intracranial Embolism and Thrombosis/pathology , Silicone Elastomers , Staphylococcal Infections/etiology , Streptococcal Infections/etiology , Subarachnoid Hemorrhage/pathologyABSTRACT
We performed electromyography on the vastus lateralis muscle in 36 normal subjects and in 18 patients with inflammatory myopathy using a specially constructed dual electrode. This permitted simultaneous recording of a motor unit from a single fiber (SF) and standard sized electrode surface. We then correlated parameters of the SF potential (jitter, blocking, fiber density and duration) and the motor unit potential (MUP) (number of phases, duration) for different sites within the same individual. The mean values for the above parameters were correlated between individuals, and the group means were compared for the control and the inflammatory myopathy group.
