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Cerebrospinal Fluid Examination (cerebrospinal + fluid_examination)
Selected AbstractsAcyclovir-induced neuropsychosis successfully recovered after immediate hemodialysis in an end-stage renal disease patientINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 8 2007Hung-Hsu Yang MD A 70-year-old man developed herpes zoster over the right L5,S2 region for 3 days and was admitted for acyclovir therapy. He had a medical history of rectal cancer status post-colostomy and end-stage renal disease undergoing thrice weekly hemodialysis. Without a prior loading dose, acyclovir 500 mg (7.7 mg/kg) daily was given intravenously in two divided doses. On the third dosage, the patient became confused and agitated and developed insomnia. Within the following 24 h, delirium, visual and auditory hallucinations, disorientation to place and time, as well as impaired recent memory occurred. At the same time, a transient low grade fever (38 °C) was noted but resolved spontaneously after ice pillow (Fig. 1). Figure 1. The clinical and treatment course of the patient The etiology was vigorously explored. He had no history of any neurological or psychiatric disorders. Drug history was reviewed, but no other medications besides acyclovir were currently being used. Physical examination revealed neither meningeal signs nor focal neurological deficits. Serum blood urea nitrogen, glucose, and electrolytes were within normal limits except for an elevated creatinine level at 6.2 and 5.7 mg/dl (before and after neuropsychotic symptoms, respectively). Complete blood count with differentiation was also unremarkable. Cerebrospinal fluid examination was not possible as the patient's family refused the lumbar puncture. Moreover, an electroencephalograph study and head computed tomography scan disclosed no abnormalities. Acyclovir-induced neurotoxicity was suspected. Therefore, acyclovir was discontinued. Subsequently, serum acyclovir and CMMG were checked by enzyme-linked immunosorbent assay. Serum acyclovir level was 1.6 mg/l (normal therapeutic level, 0.12,10.8 mg/l) and CMMG level was 5 mg/l. Emergent hemodialysis (4-h/session) was given; the neuropsychotic symptoms, including agitation, delirium, and visual and auditory hallucinations, greatly abated after the second session. The patient fully recovered after three consecutive days of hemodialysis; the serum was rechecked and revealed that the acyclovir level was below 0.5 mg/l and the CMMG level was undetectable. At the same time, his herpetic skin lesions resolved well. [source] Chronic inflammatory demyelinating polyneuropathy associated with tumor necrosis factor-, antagonistsMUSCLE AND NERVE, Issue 5 2010Amer Alshekhlee MD Abstract Biologic therapy with tumor necrosis factor (TNF)-, antagonists for rheumatoid arthritis has been well established. We describe two patients with rheumatoid arthritis who developed chronic inflammatory demyelinating polyneuropathy (CIDP) during their course of therapy with TNF-, antagonists. A 45-year-old woman and a 49-year-old man, both with a history of rheumatoid arthritis, were treated with etanercept and infliximab, respectively. Clinical signs of peripheral neuropathy developed 2 weeks and 12 months after the initiation of TNF-, antagonists. Electrodiagnostic studies at variable points during the disease course showed signs of acquired demyelination consistent with CIDP. Cerebrospinal fluid examination showed albuminocytologic dissociation (total protein concentration 118 mg/dl and 152 mg/dl, respectively). Both patients failed to improve after discontinuation of the offending agent, and they responded poorly to corticosteroids. However, there was clinical and electrophysiologic recovery after initiation of intravenous immunoglobulin (IVIg) therapy. CIDP may occur early or late during the treatment course with TNF-, antagonists. IVIg may reverse and stabilize the inflammatory process. Muscle Nerve 41: 742,747, 2010 [source] Homonymous hemianopia in a pug with necrotising meningoencephalitisJOURNAL OF SMALL ANIMAL PRACTICE, Issue 4 2000W. A. Beltran A 24-month-old female pug, which had previously been treated for visual hemifield loss, was referred with generalised seizures and other neurological disorders. A diagnosis of necrotising meningoencephalitis was suggested from the clinical signs together with the results of computed tomography and cerebrospinal fluid examination. This was confirmed seven months later by histological examination of the brain following euthanasia. Typical histopathological lesions of the disease were found in various areas of both cerebral hemispheres, including the visual striated cortex of the right cerebrum. [source] Acute myeloid leukemia, the 3q21q26 syndrome and diabetes insipidus: A case presentationASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY, Issue 2 2010Cameron CURLEY Abstract Diabetes insipidus (DI) is a rare presenting complication of acute myeloid leukaemia (AML). Typically, the combination of DI and AML is associated with structural abnormalities of the neurohypophysis. We present a case of AML and DI presenting without any abnormalities of the neurohypophysis on radiological scanning and with normal cerebrospinal fluid examination. The AML karyotype at presentation was characterized by the presence of a t(3; 3)(q21; q26) translocation and monosomy 7. After treatment with induction chemotherapy, the patient achieved a complete remission and his DI resolved. At subsequent AML relapse, characterized by a complex karyotype without the t(3; 3)(q21; q26) translocation or monosomy 7, DI did not recur. Our case provides clinical support to the hypothesis that the t(3; 3)(q21; q26) translocation and/or monosomy 7 in AML may directly result in dysregulation of transcription factors resulting in development of DI in AML patients. [source] | ||||||||||