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A 68-year-old woman with a history of mild hypertension developed a toxic encephalopathy following myelography with metrizamide. Concomitant with the symptoms of vomiting, headache, muscle twitching, and hallucinations was a sudden and marked increase in arterial pressure. Treatment with parenteral vasodilators caused a partial, but transient lowering of the blood pressure. The mental status abnormalities were resolved by treatment with parenteral lorazempam and, subsequently, the blood pressure returned to the premyelography levels. This report demonstrates that metrizamide can induce a severe, accelerated form of hypertension.
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PMID:Accelerated hypertension associated with the central nervous system toxicity of metrizamide. 394 59

We describe a renal allograft recipient with cat-scratch disease in whom refractory hypotension, severe metabolic acidosis, pulmonary infiltrates, and encephalopathy developed. The patient first presented with a history of cat bites and scratches, fever, headache, and arthralgias. Four weeks later, the clinical presentation of septic shock suddenly developed in the patient. Cat-scratch disease was documented clinically and by finding delicate pleomorphic bacilli in Warthin-Starry silver stains of biopsy specimens taken from the primary inoculation site and regional lymph node. The administration of intravenous sulfamethoxazole and trimethoprim, erythromycin lactobionate, and tobramycin sulfate therapy correlated with recovery. Although cat-scratch disease is usually a benign, self-limited illness, this article illustrates its systemic nature, its potential for devastating complications in the immunocompromised host, and its possible response to vigorous antibiotic therapy.
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PMID:Life-threatening cat-scratch disease in an immunocompromised host. 394 99

Two patients had clinical findings of encephalopathy that progressed in 4 to 5 months. One patient had headache, fatigue, lethargy, hemiparesis, and a seizure. The second patient had only forgetfulness, confusion, and lethargy without focal signs. Herpes simplex virus was grown from brain biopsy in the first patient and from CSF in the second patient. These cases suggest that herpes simplex virus caused the encephalitis and that it should be considered in the differential diagnosis of chronic encephalopathy.
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PMID:Chronic encephalitis possibly due to herpes simplex virus: two cases. 403 28

The neurologic manifestations of Legionnaires' disease were reviewed in this paper. Nine (42.9%) of 21 patients seen at this institution had neurologic abnormalities during acute infection, comparable to 52% of patients found in the literature. Abnormal mentation was most common, occurring in all our patients and in 29.6% of patients in the literature. Encephalopathy disproportionate to metabolic disturbances varied from mild confusion to coma, was not associated with increased mortality, and tended to resolve with acute illness although some patients reported persistent memory defects. Rarely did these changes in mentation precede the development of pulmonary infiltrates. Headache occurred in two (22.2%) of our patients and in 28.7% of those in the literature. Headache, noted in many febrile illnesses, is common but nonspecific in Legionnaires' disease. Other neurologic abnormalities including cerebellar dysfunction and focal deficits were relatively infrequent and tended to persist beyond resolution of clinical infection. In some cases these neurologic derangements may have occurred coincidentally with Legionnaires' disease. Diagnostic evaluations and autopsies were frequently normal, nonspecific, or revealing of pathology unrelated to infection. Only two patients had evidence of direct invasion of the central nervous system by Legionella, and the cause of encephalopathy and neurologic abnormalities in most cases remains unclear. Patients with neurologic abnormalities and Legionnaires' disease deserve full evaluation to exclude other entities. Only encephalopathy appears to be a characteristic manifestation of Legionnaires' disease.
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PMID:Neurologic manifestations of Legionnaires' disease. 608 42

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

In a comparative randomized double-blind study, 73 patients underwent myelography using iopamidol (36 patients) or metrizamide (37 patients) as contrast medium. The overall diagnostic adequacy of iopamidol myelography was found to be comparable to that of metrizamide myelography. The incidence of examinations graded as superior (64%) or adequate (36%) with iopamidol was equivalent to that with metrizamide (57% superior, 43% adequate). Adverse reactions after iopamidol myelography were fewer, less severe, and generally of shorter duration than those associated with metrizamide. In the iopamidol group, adverse reactions occurred in nine (25%) patients, all of whom experienced mild or moderate headache, one with nausea, vomiting, and fatigue. In the metrizamide group, adverse reactions occurred in 17 (46%) patients, all of whom experienced mild or moderate headache, six with nausea and vomiting and four with back and leg pain. Of nine individuals who underwent myelography using 300 mg 1/ml metrizamide injected via lateral C1-C2 puncture, three experienced a toxic encephalopathy with confusion, dysphasia, headache, nausea, and vomiting, and a fourth individual suffered severe nausea, vomiting, fever, and irregular pulse. Encephalopathy was not observed in any of the 11 patients in whom myelography was performed via lateral C1-C2 puncture with a similar concentration of iopamidol. No seizures were encountered, and no clinically significant changes in laboratory studies were observed with either contrast medium.
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PMID:Iopamidol and metrizamide for myelography: prospective double-blind clinical trial. 638 81

Eclampsia occurring more than 48 hours postpartum has been observed in an unusual number of patients. From August 1977 to November 1982 at E. H. Crump Women's Hospital and Perinatal Center (Memphis), there were 132 documented cases of eclampsia, of which 36 (27%) occurred postpartum. Seventeen (47%) of these occurred more than 48 hours postpartum. Preeclampsia was diagnosed before the onset of convulsions in 12 patients, all of whom received intravenous magnesium sulfate postpartum. The mean duration of postdelivery magnesium sulfate therapy was 32 hours (range 24 to 72 hours). Headaches and visual disturbances were reported by all 17 patients before onset of convulsions. Physical and laboratory findings immediately after the convulsions were consistent with eclampsia. Treatment consisted primarily of intravenous magnesium sulfate. Neurologic consultation was obtained to rule out a neurologic disorder, and metabolic studies were also done. Electroencephalograms were done on 15 patients; eight of them showed patterns consistent with encephalopathy.
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PMID:Late postpartum eclampsia: an update. 664 9

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

Lyme disease, caused by a tick-transmitted spirochete, typically begins with a unique skin lesion, erythema chronicum migrans. Of 314 patients with this skin lesion, almost half developed multiple annular secondary lesions; some patients had evanescent red blotches or circles, malar or urticarial rash, conjunctivitis, periorbital edema, or diffuse erythema. Skin manifestations were often accompanied by malaise and fatigue, headache, fever and chills, generalized achiness, and regional lymphadenopathy. In addition, patients sometimes had evidence of meningeal irritation, mild encephalopathy, migratory musculoskeletal pain, hepatitis, generalized lymphadenopathy and splenomegaly, sore throat, nonproductive cough, or testicular swelling. These signs and symptoms were typically intermittent and changing during a period of several weeks. The commonest nonspecific laboratory abnormalities were a high sedimentation rate, an elevated serum IgM level, or an increased aspartate transaminase level. Early Lyme disease can be diagnosed by its dermatologic manifestations, rapidly changing system involvement, and if necessary, by serologic testing.
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PMID:The early clinical manifestations of Lyme disease. 685 26

A short review is given of the pharmacokinetic characteristics and side effects of the nitroimidazoles: metronidazole, tinidazole and ornidazole. The drugs are well absorbed from the gastrointestinal tract, maximum plasma levels generally being obtained 1 to 4 h after oral intake. Metronidazole has been shown to be absorbed after rectal administration; vaginal absorption is documented for all three drugs. The nitroimidazoles are widely distributed in the body, cross the placenta and appear in breast milk. Therapeutically effective concentrations of e.g. metronidazole have been demonstrated in e.g. the central nervous system, middle ear discharges, bile, peritoneal fluid, and fluids and tissues of the female genital tract. The binding to plasma proteins is less than 20%. Available data suggest that the elimination half-lives of these drugs differ, being 7-8 h for metronidazole, about 12 h for tinidazole and 14-15 h for ornidazole. Both metronidazole and ornidazole, but not tinidazole, seem to be extensively metabolized before elimination. The nature and frequency of adverse reactions to this drug include encephalopathy in a few patients treated with doses between 5 and 10 g daily as an adjunct to radiotherapy, and peripheral neuropathy observed in patients treated for prolonged periods with high doses. Among the common side effects of the nitroimidazoles are symptoms from the gastrointestinal tract such as nausea, anorexia, vomiting and metallic or bitter taste. Dizziness, ataxia and headache have been reported. When given together with alcohol, a disulfiram-like intolerance reaction can be obtained.
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PMID:Pharmacokinetics of nitroimidazoles. Spectrum of adverse reactions. 694 57


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