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)

Eight vaccinated dogs suddenly developed progressive ataxia, paresis or paralysis of short duration. A histopathological examination revealed a non-suppurative meningoencephalitis suggestive of a viral infection, and immunohistochemical examination confirmed the presence of canine distemper virus antigen in five of the dogs. Distemper had not been suspected from the clinical examination of the dogs.
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PMID:Canine distemper infection associated with acute nervous signs in dogs. 159 46

Four cases of gaze paresis occurred in association with viral disease. In three cases the viral prodrome preceded the oculomotor disturbance. In one, gaze palsy was followed several days later by a viral syndrome. One had isolated bilateral horizontal ophthalmoplegia; another patient had motility disturbance with blepharoptosis and peripheral areflexia. Two patients had clinical evidence of brain-stem involvement: unilateral gaze paresis and gaze-evoked nystagmus in one and Parinaud's syndrome in the other. No accompanying long-tract signs or changes in mental status were present in any case. Recovery was complete in all four patients.
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PMID:Gaze palsy associated with viral syndrome. 403 36

To evaluate the hypothesis of CNS involvement in Bell's palsy, the auditory brain stem responses (ABR) of 31 patients were studied. In nine of these patients ABR abnormalities were found. None of these patients showed evidence of dysfunction of the cochlear nerve. Six of the patients who had abnormal ABR were retested after they recovered from the facial paresis. Five of these patients showed persistent ABR abnormality, and one showed a normalization of the ABR. These results may be consistent with an injury at the brain stem level in some patients with Bell's palsy. The possible causative agent of a reactivation of a herpes simplex virus infection is discussed.
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PMID:Auditory brain stem response abnormalities in patients with Bell's palsy. 641 90

A 61-year old man with a history of arterial hypertension suffered a left HZO, and was treated with acyclovir. Three weeks later he suddenly developed moderate left hemiparesis particularly of the leg, severe paresis of the right leg, aphasia and somnolence. Treated with IV acyclovir and high-dose corticosteroids deterioration of the right hemiparesis was apparent. Serological and CSF-studies showed acute varicella-zoster virus infection with intrathecal antibody synthesis (antibody specificity index 2.7). On the third day CT scan revealed infarctions in the territory of both anterior cerebral arteries, at the fifth day additionally left striatocapsular infarction. Selective carotid arteriogram showed bilateral occlusions of anterior cerebral arteries in their proximal segment. With a mean delay of seven weeks granulomatous vasculitis is a rare complication of HZO, leading commonly to ischemic infarctions in the region of the middle cerebral artery. Trigeminovascular connections are the probable pathway of virus-transmission from the trigeminal nerve to ipsilateral branches of the circle of Willis. Because of the presumed pathogenesis immediate therapy with high-dose corticosteroids and acyclovir is justified.
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PMID:[Granulomatous vasculitis of the CNS as a complication of herpes zoster ophthalmicus]. 852 86

Usually dysphonia is the result of a functional disorder of the larynx. It can also result from paresis or paralysis of a hemilarynx. Four patients, men aged 57, 41, 42 and 18 years, had a neurological cause of paralysis of a hemilarynx. Processes responsible for this kind of pathology can appear at three different levels: central, nuclear and peripheral. Each of the four patients had a disorder at the peripheral level: two had a tumour, in one the vagus nerve was severed during lobectomy for squamous cell carcinoma (iatrogenic), and in the last one an upper respiratory viral infection was the probable cause. Other causes of these peripheral lesions are toxicological, traumatic or idiopathic. When dysphonia does not improve within three weeks, inspection of the larynx and palpation of the neck, including examination of the aspect and mobility of the vocal folds by an otorhinolaryngologist should be performed. If paresis of a hemilarynx is seen, an orientation examination of the cranial nerves and selective additional examination is necessary, as paresis of a hemilarynx is a symptom, not a diagnosis.
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PMID:[The immobile vocal cord]. 985 73

West Nile (WN) virus infection is a mosquito-borne flavivirosis endemic in Africa and Asia. Clinical disease is usually rare and mild and only in a few cases the infection causes encephalomyelitis in horses, fever and meningoencephalitis in man. We report here the clinical and pathological findings in an epidemic of the disease involving 14 horses from Tuscany, Italy. All cases were observed from August to October 1998. Affected horses showed ataxia, weakness paresis of the hindlimbs and, in 6 cases, there was paraparesis progressing to tetraplegia and recumbency within 2 to 9 days. Eight animals recovered without any important consequences. Serological investigations revealed positivity to WN virus in all the 14 horses and the agent was isolated from the cerebellum and spinal cord of an affected horse. Postmortem examination was carried out on 6 horses. The neuropathological pattern was that of a mild to moderate, nonsuppurative polioencephalomyelitis with constant involvement of the ventral horns of the thoracic and lumbar spinal cord, where focal gliosis and haemorrhage were also apparent in some cases. Differential diagnoses with other equine viral encephalomyelitides are discussed. Climatological and environmental characteristics of the geographic area in which the outbreaks occurred suggest the existence of suitable conditions for the development of the disease. This is the first report of WN virus equine encephalomyelitis in Italy.
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PMID:Clinical and neuropathological features of West Nile virus equine encephalomyelitis in Italy. 1066 82

Herpes zoster (HZ) is essentially a viral disease of the posterior root ganglia and sensory nerve fibers, which presents clinically with vesicular eruption of the skin, radicular pain and sensory changes in the distribution of the affected ganglion. However, motor involvement can be seen as well. If classic cutaneous lesions are present, HZ-related motor paresis is easily diagnosed. Otherwise, the diagnosis may be suspicious, especially if the weakness occurs before the cutaneous lesions have appeared, or weeks after they have subsided. We present a patient with HZ-related motor paresis due to radiculopathy in the cervical segments whose motor symptoms and signs appear as major clinical features.
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PMID:Zoster paresis. 1283 88

Psychogenic dysphonia refers to loss of voice where there is insufficient structural or neurological pathology to account for the nature and severity of the dysphonia, and where loss of volitional control over phonation seems to be related to psychological processes such as anxiety, depression, conversion reaction, or personality disorder. Such dysphonias may often develop post-viral infection with laryngitis, and generally in close proximity to emotionally or psychologically taxing experiences, where "conflict over speaking out" is an issue. In more rare instances, severe and persistent psychogenic dysphonia may develop under innocuous or unrelated circumstances, but over time, it may be traced back to traumatic stress experiences that occurred many months or years prior to the onset of the voice disorder. In such cases, the qualitative nature of the traumatic experience may be reflected in the way the psychogenic voice disorder presents. The possible relationship between psychogenic dysphonia and earlier traumatic stress experience is discussed, and the reportedly low prevalence of conversion reaction (4% to 5%) as the basis for psychogenic dysphonia is challenged. Two cases are presented to illustrate the issues raised: the first, a young woman who was sexually assaulted and chose to "keep her secret," and the second, a 52-year-old woman who developed a psychogenic dysphonia following a second, modified thyroplasty for a unilateral vocal fold paresis.
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PMID:Psychogenic voice disorders and traumatic stress experience: a discussion paper with two case reports. 1451 54

The tickborne encephalitis (TBE) serocomplex of flaviviruses consists primarily of viruses that cause neurologic disease; these viruses include Omsk hemorrhagic fever virus (OHFV), a virus that is genetically related to other TBE serocomplex viruses but that circulates in an ecologically distinct niche and causes markedly different human disease. The objective of this study was to examine a potential small-animal model for OHFV and to compare the pathology of infection with that of the neurotropic tickborne flavivirus, Powassan virus (POWV). POWV-infected BALB/c mice demonstrated typical arboviral encephalitis, characterized by paresis and paralysis before death, and viral infection of the cerebrum, characterized by inflammation and necrosis. In contrast, lethal OHFV infection did not cause paralysis or significant infection of the cerebrum but showed marked involvement of the cerebellum. Distinct pathological results in the spleens suggest that the immune response in OHFV-infected mice is different from that in POWV-infected mice. This study demonstrates a clear pathological difference between OHFV-infected mice and POWV-infected mice and supports the use of the BALB/c mouse as a disease model for OHFV.
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PMID:An animal model for the tickborne flavivirus--Omsk hemorrhagic fever virus. 1559 10

Saimiriine herpesvirus 1 (SaHV-1), an alphaherpesvirus enzootic in squirrel monkeys, is genetically related to monkey B virus and human herpes simplex virus (HSV). To study the temporal progression of viral spread and associated lesions, Balb/c mice were inoculated epidermally by scarification with a green fluorescent protein (GFP)-expressing recombinant strain of SaHV-1 and killed sequentially. Pinpoint ulcerative lesions in the inoculated epidermis progressed over a few days to unilateral or bilateral hindlimb paresis or paralysis, urinary and faecal incontinence, abdominal distension, hunched posture and eventual depression warranting euthanasia. Viral replication was present within epidermal keratinocytes, neurons of the dorsal root ganglia and thoracolumbar spinal cord, regional autonomic ganglia, lower urinary tract epithelium and colonic myenteric plexuses, as indicated by histological lesions and GFP expression. Almost all mice inoculated with 10(5) or 10(6) plaque-forming units (PFU) of SaHV-1 developed rapidly progressive disease. Two of eight mice given 10(4)PFU developed disease, but no mice receiving less than 10(4)PFU gave evidence of infection. Mice that showed no clinical signs also failed to develop an antiviral IgG response, indicating absence of active viral infection. For SaHV-1 inoculated epidermally, the ID(50), CNSD(50) and LD(50) values were identical (10(4.38)), indicating that successful infection by this route invariably resulted in lethal CNS (central nervous system) disease. Consistently severe disease in all infected animals, with regionally extensive distribution of viral replication, constituted a marked difference from the disease produced by intramuscular inoculation.
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PMID:Temporal progression of viral replication and gross and histological lesions in Balb/c mice inoculated epidermally with Saimiriine herpesvirus 1 (SaHV-1). 1596 89


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