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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CNS manifestations appear in one of 1,000 patients with Mycoplasma pneumoniae-associated infections. Encephalitis is the most frequent manifestation, but cases of meningitis, myelitis, and polyradiculitis, as well as many other symptoms (e.g., coma, ataxia, psychosis, and stroke), have been reported. The onset of these manifestations is usually acute, with lowered consciousness, convulsions, pareses, and other neurological signs. Severe, even fatal, cases are known. The pathophysiology of CNS manifestations is unknown. To our knowledge, M. pneumoniae has never been isolated from brain tissue, but instead it has been recovered from CSF specimens in at least seven cases. Besides direct invasion of M. pneumoniae into the brain, neurotoxic or autoimmune reaction within the brain tissue is suspected. At neuropathological examination, edema, demyelination, and microthrombi have been described. Improved diagnostic methods may reveal the pathophysiology of CNS manifestations associated with M. pneumoniae infection.
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PMID:CNS manifestations associated with Mycoplasma pneumoniae infections: summary of cases at the University of Helsinki and review. 839 38

A 15 year-old boy developed meningoencephalitis two weeks after onset of a respiratory tract infection caused by Mycoplasma pneumoniae. Central nervous complications are seen in 2-7% of patients hospitalized for M pneumoniae infection. Meningoencephalitis, meningitis, ataxia, polyradiculitis, psychosis and a few cases of apoplexy have been reported. In clinical practice one should be aware of M pneumoniae in the differential diagnosis of patients with suspected microbiologically induced central nervous complications. The pathogenetic aspects and prognosis are briefly discussed.
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PMID:[Meningoencephalitis after Mycoplasma pneumoniae infection]. 846 13

Eight years of case histories of patients with positive serum tests for Borrelia burgdorferi (Bb) are reviewed with the aims of analyzing the neurological manifestations involved and of assessing the value of serology in the diagnosis of neuroborreliosis (NB) in our clinical setting. Of the 105 cases with neurological manifestations that could be examined, 25 patients (24%) with other infections, neoplasms or other diseases had false positive serologies. Forty-one patients (39%) met the criteria for NB diagnosis: 26 had lymphocytic meningitis, 13 had polyradiculitis and 20 had cranial neuropathy. Spinal fluid cultures were positive in 43% of the patients on whom the test was performed, and all patients in this group who were treated with antibiotics improved. The other 39 patients (37%) had only neurological manifestations, which were not typical of NB (peripheral neuropathy, stroke, demyelinating disease, dementia or myelopathy), but for which no other etiology could be demonstrated. Spinal fluid serology was positive in 16% of those cases studied and none of those treated only with antibiotics improved. Among patients with both neurological manifestations and Bb positive serology, there were many false positives and cases with signs that were of dubious relation to infection by Bb; therefore, the prevalence of cases consistent with NB is low [corrected].
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PMID:[Neurological manifestations in patients with sera positive for Borrelia burgdorferi]. 930

Extrapulmonary manifestations of Mycoplasma pneumoniae are well described, including a subset of central nervous system (CNS)-associated syndromes. In pediatric populations, frequencies of CNS sequelae occur in 0.1% to 7% of patients. Neurologic illness associated with M. pneumoniae, such as meningitis, encephalitis, polyradiculitis, Guillain-Barre, and stroke have been reported; however, the incidence of M. pneumoniae-associated organic brain syndrome is rare. We present the case of a 20-year-old midshipman with acute psychosis following resolution of M. pneumoniae pneumonia and review 6 other adult cases found in the literature. M. pneumoniae remains one of the most common causes of respiratory illnesses in the military recruit setting and therefore should always be suspected as an organic cause of mental status changes in young persons such as recruits, cadets, and midshipmen particularly with antecedent respiratory illnesses.
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PMID:Psychosis following mycoplasma pneumonia. 1978 Mar 79

Stroke-induced immunodepression (SIDS) is an essential cause of poststroke infections. Pharmacological inhibition of SIDS appears promising in preventing life-threatening infections in stroke patients. However, SIDS might represent an adaptive mechanism preventing autoreactive immune responses after stroke. To address this, we used myelin oligodendrocyte glycoprotein (MOG) T-cell receptor transgenic (2D2) mice where >80% of peripheral CD4(+) T cells express a functional receptor for MOG. We investigated in a murine model of middle cerebral artery occlusion the effect of blocking SIDS by inhibiting body's main stress axes, the sympathetic nervous system (SNS) with propranolol and the hypothalamic-pituitary-adrenal axis (HPA) with mifepristone. Blockade of both stress axes robustly reduced infarct volumes, decreased infection rate, and increased long-term survival of 2D2 and C57BL/6J wild-type mice. Despite these protective effects, blockade of SIDS increased CNS antigen-specific Type1 T helper cell (Th1) responses in the brains of 2D2 mice 14 d after middle cerebral artery occlusion. One month after experimental stroke, 2D2 mice developed signs of polyradiculitis, which were diminished by SIDS blockade. Adoptive transfer of CD4(+) T cells, isolated from 2D2 mice, into lymphocyte-deficient Rag-1KO mice did not reveal differences between SIDS blockade and vehicle treatment in functional long-term outcome after stroke. In conclusion, inhibiting SIDS by pharmacological blockade of body's stress axes increases autoreactive CNS antigen-specific T-cell responses in the brain but does not worsen functional long-term outcome after experimental stroke, even in a mouse model where CNS antigen-specific autoreactive T-cell responses are boosted.
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PMID:Blocking stroke-induced immunodeficiency increases CNS antigen-specific autoreactivity but does not worsen functional outcome after experimental stroke. 2599 66