Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Direct intracerebral administration of glial cell line-derived neurotrophic factor (GDNF) is neuroprotective against ischemia-induced cerebral injury. Utilizing viral vectors to deliver and express therapeutic genes presents an opportunity to produce GDNF within localized regions of an evolving infarct. We investigated whether a herpes simplex virus (HSV) amplicon-based vector encoding GDNF (HSVgdnf) would protect neurons against ischemic injury. In primary cortical cultures HSVgdnf reduced oxidant-induced injury compared to the control vector HSVlac. To test protective effects in vivo, HSVgdnf or HSVlac was injected into the cerebral cortex 4 days prior to, or 3 days, after a 60-min unilateral occlusion of the middle cerebral artery. Control stroke animals developed bradykinesia and motor asymmetry; pretreatment with HSVgdnf significantly reduced such motor deficits. Animals receiving HSVlac or HSVgdnf after the ischemic insult did not exhibit any behavioral improvement. Histological analyses performed 1 month after stroke revealed a reduction in ischemic tissue loss in rats pretreated with HSVgdnf. Similarly, these animals exhibited less immunostaining for glial fibrillary acidic protein and the apoptotic marker caspase-3. Taken together, our data indicate that HSVgdnf pretreatment provides protection against cerebral ischemia and supports the utilization of the HSV amplicon for therapeutic delivery of trophic factors to the CNS.
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PMID:HSV amplicon delivery of glial cell line-derived neurotrophic factor is neuroprotective against ischemic injury. 1295 87

A woman, aged 27 years, developed acute headache and fever followed by tremor, rigidity, and bradykinesia. Masked face, drooling saliva, monotonous voice, and dysphagia were observed. She was totally bedridden during the worst period because of marked generalized rigidity and bradykinesia. There was no neurological disturbance other than parkinsonism. Several herpetic vesicles were noticed at the left angle of her mouth. The cerebrospinal fluid revealed a mononuclear pleocytosis with a normal concentration of sugar and protein. The antibody test for Type I herpes simplex virus was positive in the serum but negative in the cerebrospinal fluid. Brain CT and EEG were normal. However, MRI study showed markedly increased signals in the bilateral substantia nigra on T2-weighted, proton density, and in gradient recall acquisition imagings. Those abnormal findings had almost disappeared in a follow-up MRI study 2 months later. Her parkinsonian symptoms were substantially resolved by the time. However, PET scans, performed 8 months later, disclosed: (1) mild reduction of fluorodopa uptake; and (2) increased raclopride binding, predominantly in the putamen. These findings suggest a subclinical nigrostriatal dopaminergic deficit and a relative excess of the D2 receptors, with a pattern similar to that found in typical idiopathic parkinsonism.
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PMID:Isolated involvement of substantia nigra in acute transient parkinsonism: MRI and PET observations. 1859 Oct 4

Herpes simplex encephalitis (HSE) is the most frequent cause of sporadic fatal encephalitis in the Western world. Definitive diagnosis by viral PCR of cerebrospinal fluid (CSF) and treatment with aciclovir have improved the prognosis significantly. Nevertheless, the condition is rare and presents with non-specific symptoms that can easily be mistaken for systemic infection or non-infective encephalopathy. We report a case of HSE which was not recognised by four separate doctors, leading to substantial delay in diagnosis and treatment. Our patient presented with fever, headaches, altered behaviour and generalised bradykinesia. This was initially diagnosed as otitis interna (labyrinthitis) and, subsequently, an ischaemic stroke. There was a delay of 10 days in the initiation of aciclovir from symptom onset. MRI and CSF PCR confirmed herpes simplex virus type-1 (HSV-1) infection. The patient improved on aciclovir, but is disabled with word-finding difficulties and cognitive slowing.
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PMID:Diagnostic delay in a case of herpes simplex encephalitis. 2168 59

Toxoplasmosis encephalitis in patients with human immunodeficiency virus may progress rapidly with a potentially fatal outcome. Less common neurological symptoms associated with this are Parkinsonism, focal dystonia, rubral tremor and hemichorea-hemiballismus syndrome. A 58 year old woman suddenly lost consciousness and was admitted to the emergency service. Her medical history was unremarkable, except for frequent headaches in the last year, recurrent herpes simplex skin lesions and an episode of urticaria. A computer tomography scan showed supra and infra-tentorial lesions on suggestive of cerebral toxoplasmosis. Both Toxoplasma gondii and HIV tests were positive. In the intensive care unit, antiparasitic and antiretroviral drugs were administered, and she recovered from the coma after six weeks but presented with tetraparesis, diplopia, and depression. The LCD4 count increased from 7 to 128/mm3. The neurological lesions slowly resolved over the next two months, although postural instability, rigidity, bradykinesia and predominantly left side tremor persisted. Mild improvement was achieved after the administration of levodopa. Associated Parkinsonian syndrome in HIV patients is a rare condition, explained by the location of the brain and basal ganglia lesions, and by the observed effect of Toxoplasma gondii which increases dopamine metabolism in neural cells. Early HIV diagnostic and treatment are necessary to prevent neurological disability.
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PMID:Parkinsonian Syndrome and Toxoplasmic Encephalitis. 2996 44