Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is the first report of brachial plexus inflammation associated with clinical herpes zoster paresis. A 78-year-old female with a 3-week history of herpes zoster of the C4, C5, and C6 dermatomes developed left upper arm monoplegia. She died from an acute myocardial infarction. Post-mortem provided a rare opportunity to study the neuropathology of herpes zoster motor involvement. Histology of the brachial plexus showed extensive lymphocytic infiltration, myelin breakdown, and preservation of axons without vasculitis. The cervical spinal cord showed perivascular lymphocytic cuffing and no anterior horn necrosis. We suggest, the brachial plexus inflammation was a distal extension of a dorsal ganglionitis. Brachial plexus neuritis may be a direct cause of reversible upper limb paresis in herpes zoster. We demonstrate the motor neuropathy is an inflammatory demyelinative process consistent with the recovery observed in a number of patients. We postulate post-herpetic neuralgia may be related to an ongoing inflammatory process.
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PMID:Herpes zoster brachial plexus neuritis. 910 Nov 5

Myeloencephalopathy is an uncommon manifestation of equine herpesvirus 1 (EHV-1), but it can cause devastating losses during outbreaks on individual farms. Clinical signs of neurologic disease reflect a diffuse multifocal hemorrhagic myeloencephalopathy secondary to vasculitis and thrombosis. Sudden onset and early stabilization of signs, including ataxia, paresis, and urinary incontinence; involvement of multiple horses on the premises; and recent history of fever, abortion, or viral respiratory disease in the affected horse or herdmates are typical features, although there is considerable variation between outbreaks in epidemiologic and clinical findings. Prevention is difficult because many asymptomatic horses are infected latently with EHV-1 myeloencephalopathy and because vaccines do not confer protection against neurologic manifestations of infection. This article reviews the pathogenesis, pathology, clinical manifestations, diagnosis, and treatment of EHV-1 myeloencephalopathy and discusses prevention and control of equine herpesviral infections in the context of their epidemiology.
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PMID:Equine herpesvirus 1 myeloencephalopathy. 910 43

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74

We report our clinical experience in managing a 59-year-old Italian male with Churg-Strauss syndrome (CSS) whose first clinical manifestation was a persistent dysphonia; the patient worked as a mechanic. Video-laryngostroboscopic examination revealed paresis of the right vocal fold with a reduction in adduction together with incomplete glottal closure. Spectrographic and spirometric tests both showed abnormal changes. Laryngeal electromyography revealed neurogenic damage of the right thyroarytenoid and crycoarytenoid muscles. Due to the appearance of typical signs of systemic involvement of CSS as a necrotizing vasculitis, the patient was admitted to the Rheumatology Unit of the University of Pisa. Histologic analysis of a skin lesion on the patient's foot confirmed the diagnosis. Treatment with 6-methylprednisolone quickly brought remission from systemic and laryngeal symptoms, as well as improvement in the results of video-laryngostroboscopic, spectrographic and laryngeal myographic tests.
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PMID:Neuro-laryngeal involvement in Churg-Strauss syndrome. 969 26

Neurologic manifestations are present in about 10-20 percent of patients with trichinosis. They could be a serious diagnostic problem in the absence of corresponding epidemiological data and typical symptoms and signs of the disease. In untreated patients the mortality rate is about 50%. Several pathogenic mechanisms are responsible for the neurological complications in trichinosis: obstruction of brain blood vessels by larvae, cysts or granulomas, toxic vasculitis with secondary thrombosis and haemorrhages, granulomatous inflammation of the brain parenchyma and allergic reaction. Neurotrichinosis is manifested with clinical symptoms and signs of meningitis, encephalitis, polyradiculoneuritis, poliomyelitis, myastenia gravis, paresis and paralysis, with the clinical picture of systemic disease of the connective tissue involving the nervous system and, extremely rare, as a sinus thrombosis. Thus, the broad spectrum of neurological lesions in trichinosis is, probably, the results of the fact that Trichinella spiralis larvae, during haematogenic dissemination has no special affinity for particular parts of the nervous system. We present five patients with encephalitis and focal cerebral lesions in trichinosis. In one patient the neurologic manifestations were the only sign of the disease. We believe that all pathogenic mechanisms mentioned above, were involved in the onset of neurological manifestations in our patients. The diagnosis of the disease was based on the clinical picture, epidemiological data, microscopic identification of larvae in the muscular tissue, the presence of antibodies against Trichinella spiralis in cerebrospinal fluid (with preserved blood brain barrier) and in serum confirmed by IIF method, computerised tomography and magnetic resonance imaging of the brain, eosinophilia in the peripheral blood picture. One patient died, and in the remaining patients the course of the disease was favourable; they were discharged from the hospital with minimal neurologic sequelae.
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PMID:[Neurologic manifestations in trichinosis]. 986 83

Subacute disseminated histoplasmosis is an uncommon entity. Typical neuro-ophthalmologic manifestations are usually secondary to histoplasmomas or encephalitis. A 45-year-old man noted blurred vision while receiving empiric antituberculosis therapy for fever and diffuse granulomatous disease of unknown origin. Vertical-gaze palsy, right horizontal-gaze paresis, and mild right optic neuropathy were found on neuro-ophthalmologic examination. Further questioning revealed a history of frequent contact with fighting cocks from South America. Magnetic resonance images were consistent with multiple hemorrhagic infarcts, areas of inflammation, or both, and cerebral angiography showed changes consistent with vasculitis. A previously obtained biopsy specimen from the duodenum was restained and found to be positive for fungal elements. Serum antigen titers for Histoplasma capsulatum demonstrated evidence of active infection. This case is a rare example of a supranuclear ocular motility disturbance and optic neuropathy secondary to an occlusive vascular process in a patient with subacute disseminated histoplasmosis.
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PMID:Disseminated histoplasmosis causing reversible gaze palsy and optic neuropathy. 1038 Jan 38

On November, 1997, a 15-year-old boy visited our hospital because of headache, fever and arthralgia. He was treated with 5 mg/day of prednisolone thereafter. On October 21, 1998, he was admitted because of remittent fever and multiple arthralgia and diagnosis of juvenile rheumatoid arthritis (JRA) was made. He was also found to have hypertension of 210/110 mmHg, and soon developed ptosis of the eye, facial paresis and perceptive deafness of the right side. Cerebrospinal fluid showed protein of 98 mg/dl and mildly elevated IgG, IgA and IgM levels with normal cell count. Brain MRI examination revealed multiple cerebral lesions in the frontal, parietal and cerebellar areas on the right, whose cause was thought to be vasculitis. Renal angiography demonstrated a right renal artery stenosis, compatible with renovascular hypertension. He was treated with 60 mg of prednisolone per day, which brought about a satisfactory improvement of the above rheumatic and neurologic signs. On November 17, 1998, he received a follow-up study of MRI, which failed to show any cerebral lesions, supporting the effectiveness of prednisolone. An angiotensin converting enzyme inhibitor successfully normalized hypertension and renin activity in serum, although renal blood flow did not increase.
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PMID:[A case with juvenile rheumatoid arthritis who developed cerebral vasculitis and venovascular hypertension]. 1121 60

An axonal sensory neuropathy is a frequent complication in the course of HIV infection; more than 30% of all HIV-infected individuals will develop a polyneuropathy. Low CD4 cell counts and high HIV RNA loads increase the risk. This neuropathy causes pain, paresthesias and burning sensations and/or numbness in the feet, which sometimes occurs in the hands as well. Neurological examination reveals sensory deficits in a stocking and glove distribution and depressed or absent ankle reflexes, without severe paresis. The cause of the sensory neuropathy is unknown. Either the HIV infection or certain other infections, for example cytomegalovirus, may play a role in the pathogenesis; vasculitis may be a process associated with this. Some antiretroviral drugs within the nucleoside analogue group cause a neuropathy but the pathogenesis of this remains unclear. Amitriptyline, tramadol and carbamazepine can be used for symptomatic treatment. The efficacy of lamotrigine and gabapentin has yet to be confirmed.
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PMID:[Sensory neuropathy in HIV infection: pathogenesis and therapy]. 1133 55

A rare case of primary angiitis of the central nervous system (PACNS) is reported with its clinical and magnetic resonance imaging (MRI) features. A 20-year-old girl presented with headache, projectile vomiting, unsteadiness of gait and urgency of micturition. She had left seventh nerve upper motor neuron type paresis, increased tone in all four limbs, exaggerated deep tendon reflexes, cerebellar signs, and papilloedema. Cerebrospinal fluid showed lymphocytosis with elevated protein and normal glucose level. Cerebral computerised tomographic scan and MRI showed bilateral diffuse asymmetric supra- and infra-tentorial lesions (predominantly in the supratentorial and left cerebrum). On MRI, the lesions were hyperintense on T2, and proton density-weighted images and hypointense on T1-weighted images. Based on the clinical findings of raised intracranial tension and MRI features, initial diagnoses of gliomatosis cerebrii, tuberculous meningitis, primary central nervous system lymphoma and chronic viral encephalitis were considered. PACNS was not included in the initial differentials and, an open brain biopsy was advised which established the definitive diagnosis.
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PMID:Primary angiitis of the central nervous system: an ante-mortem diagnosis. 1143 55

Subacute motor neuropathy involving bulbar nerves is an unusual complication of hyperthyroidism. Clinical and neurophysiologic follow-up of such patients has been rarely reported. We describe a 41-year-old Colombian patient who developed respiratory failure associated with motor neuropathy and severe weight loss. The major clinical features included diffuse amyotrophy, bilateral facial paresis, and fasciculations, suggesting motor neuropathy. Electromyography confirmed the presence of axonal neuropathy, with predominant motor involvement. Goiter with hypervascularization was noticed, associated with pure T3 hyperthyroidism (T3l=26 pg/ml; N<3.8). The patient was given carbimazole which induced a severe skin vasculitis 10 days later. Carbimazole was stopped and replaced by propylthiouracile, which also induced vasculitis with secondary cardiac failure. Total thyroidectomy was then performed. General status improved rapidly as well as motor deficit, amyotrophy and pyramidal syndrome. Electromyographic abnormalities improved significantly within 3 months. This observation demonstrates that hyperthyroidism can produce motor axonal neuropathy, curable with radical surgery.
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PMID:[Subacute motor neuropathy induced by T3 hyperthyroidism]. 1473 39


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