Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histoplasma meningitis (HM) has been reported to occur primarily in association with disseminated histoplasmosis (DH). We report a case of histoplasma meningitis occurring in a patient with common variable hypogammaglobulinemia (CVH) in which no manifestations of DH were observed. L. L., a 66-year-old Caucasian male, clerical worker, developed occasional episodes of dizziness and tinnitus in mid-1971. During 1972, increasing frequency of these episodes and gradually progressive confusion were noted. In January 1973, vomiting, forther confusion, obnubilation, and a left central facial paresis developed and he was hospitalized. Physical examination revealed no pulmonary abnormalities, lymphadenopathy or hepatosplenomegaly. Over the ensuing 6-week evaluation, there was occasional fever to 38.5 degrees C. Chest roentgenogram was normal. Cerebral angiography suggested a mass in the left cerebellar hemisphere. EEG was diffusely slow. Multiple CSF examinations revealed: Glucose 7-18 mg/with a normal blood glucose, protein 109-256 mg/and cells 66-140 (95 + % mononuclear). Histoplasma capsulatum was cultured from CSF but not from sputum, urine, blood or bone marrow. Skin tests for PPD, histoplasmosis, coccidiodomycosis, blastomycosis, mumps, dinitrochlorobenzene and streptokinase-streptodornase were negative then and 6 months later. Histoplasma serum antibody was absent. Immunoglobulin analysis revealed IgG 430 mg %, IgA 46 mg %, and IgM 35 mg %, which with the history and skin test results suggested CVH. Treatment with 2.51 gm of amphotericin B given intravenously over a 3-month period resulted in complete reversal of all neurologic signs and clearing of the confusion. The remission has been maintained for two years. This case represents a primary infection of the CNS by histoplasma. The relationship between the HM and the CVH will be discussed.
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PMID:Histoplasma meningitis with common variable hypogammaglobulinemia. 61 43

This is a case report of the 2nd oldest patient reported in the literature with transverse myelitis after mumps, and the 1st with magnetic resonance imaging (MRI) correlation. He is a 38-year-old Chinese man presenting with bilateral lower limb weakness and numbness, and urinary retention starting 3 weeks after an attack of mumps parotitis. Clinically, there was mild lower limb paresis, absent plantar responses and reduced pain sensation below the umbilicus. MRI revealed cord swelling and increased T2 signal from T7 to T11. Cerebrospinal fluid showed 23 cells/mm3 and 55 mg protein/dl. He received a 5-day course of intravenous methylprednisolone 0.5 g/d. The sensory and motor deficits improved over 2 weeks; urinary symptoms improved over the next year. Transverse myelitis following mumps is recognizable clinically and radiologically, and potentially responsive to methylprednisolone.
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PMID:Transverse myelitis following mumps in an adult -- a case report with MRI correlation. 940 4

A number of nonpolioviruses have been implicated as the probable etiologic agents of paralytic illness clinically resembling poliomyelitis, including certain immunotypes of Coxsackie group A, Coxsackie group B, and ECHO viruses, and the viruses of mumps, herpes simplex and arthropod-borne encephalitides. A number of well documented cases provide evidence that some of these viruses may on occasion be the causative agents of severe, even fatal, myelitis, bulbomyelitis or encephalomyelitis, but they have been associated much more frequently with cases of "poliomyelitis" in which there has been slight to moderate paresis. In the aggregate, various "nonpolioviruses" have been encountered in approximately 10 per cent of the patients with clinical poliomyelitis studied, but it is uncertain how many of these cases may represent coincidental infections not causally related to the current illness.
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PMID:Nonpolioviruses and paralytic disease. 1446 69

We report a case of mumps deafness with acute vestibular symptoms secondary to both retrolabyrinthine and inner ear dysfunction. To our knowledge, no such case has been reported elsewhere. The patient was a 6-year-old girl in whom mumps deafness was initially diagnosed. Two days after onset of the hearing impairment, severe vertigo developed. Neurotologic examinations revealed spontaneous right-beating nystagmus, left canal paresis, absence of vestibular-evoked myogenic potentials in the left ear, and absence of responses to a left galvanic body sway test (GBST). The vertigo resolved 7 days after onset. However, the left hearing impairment progressed to complete deafness. Six months later, left canal paresis was still present, but bilateral GBST responses were normal, suggesting that retrolabyrinthine vestibular function had been restored. Mumps virus may affect retrolabyrinthine function as well as the inner ear.
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PMID:Mumps virus may damage the vestibular nerve as well as the inner ear. 1856 98

A 58-year-old man was admitted to our hospital with fever, vomiting and disturbance of consciousness after common cold-like symptoms for 2 days. Physical examination showed high fever, moderate hypertension and tachycardia. There were no superficial lymph nodes swelling nor skin rashes. Cerebrospinal fluid (CSF) examination revealed increased protein level (467 mg/dl) and pleocytosis (508 cells/mm3), but no glucose was detected. CSF smear test detected the pneumococcus. Intravenous cefotaxime was administered along with intravenous immunoglobulins and steroid pulse therapy. However, DIC developed, so FOY therapy was started. With these treatments, level of consciousness gradually improved and he became able to eat. At 11th days after the onset, the patient suddenly developed left facial palsy and paresis of the left arm. Head T2-weighted magnetic resonance imaging demonstrated tumor-like hyperintensity signal lesions (28 x 16.6 mm) with ring enhancements in the right frontal lobe. Acute disseminated encephalomyelitis (ADEM) was diagnosed based on MRI and CSF findings, and then additional corticosteroid pulse therapy was administered twice. Herpes simplex virus and herpes zoster virus DNA in the CSF were undetectable by PCR. After 6 days of treatment with corticosteroid pulse therapy, left facial palsy and paresis of the left arm gradually improved and MRI showed the disappearance of tumor-like hyperintense signals. Although ADEM usually develops as a complication after viral infection such as measles, rubella, mumps and herpes zoster, this case suggests that ADEM complication should be considered even after pneumococcal meningoencephalitis.
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PMID:[A case of acute disseminated encephalomyelitis (ADEM) following treatment for pneumococcal meningoencephalitis]. 1934 73

We report a 38-year-old man with vaccine associated paralytic poliomyelitis (VAPP) which showed unusual biphasic worsening. The patient developed mild paresis of left upper and right lower extremities, five weeks after the oral poliovirus vaccination of patient's son and two weeks after the intramuscular injection of mumps/varicella vaccine in the left triceps muscle for himself. Needle electromyography (EMG) of his left arm and right leg was not remarkable, and the weakness recovered almost completely in three weeks. However, four weeks after the needle EMG, severe weakness and muscle atrophy of the four extremities, accentuated at the left arm and right leg, developed again. Cervical MRI showed gadolinium-enhanced, T(2) high-signal intensity area in the left C4-C6 anterior horn, most prominent at the height of C5 spine. Significant elevation of serum anti-poliomyelitis type 2 neutralizing antibody confirmed the diagnosis of VAPP. Immunomodulatory treatment, intravenous immunoglobulin (IVIg), did not improve weakness. We consider that the second clinical worsening of this patient was provoked by the needle EMG performed just after the first exacerbation, which injured the skeletal muscles and might have enhanced the retrograde transport of poliovirus via neural pathway.
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PMID:[Vaccine-associated paralytic poliomyelitis showing biphasic motor paresis]. 2306 24