Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient appeared to be in coma following pneumococcal meningitis, an intracerebral haemorrhage, and a cardiac arrest. Late in the course of his illness neurophysiological investigations confirmed a proposal that he also had a fulminant acute demyelinating polyneuropathy which, for a period of five days, rendered the patient completely unresponsive. The patient recovered and is now working without any disability.
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PMID:The differentiation of peripheral effector neuron failure from acute brain stem dysfunction in a critically ill patient. 131 83

Lyme neuroborreliosis is one of the chronic manifestations of Lyme disease and is caused by the neurotropic spirochete, Borrelia burgdorferi. Two of the three stages of Lyme disease potentially involve the central nervous system: a second stage that may manifest as meningitis, cranial neuritis, or radiculoneuritis; and a third stage, or chronic neuroborreliosis, with parenchymal involvement. The tertiary stage may mimic many conditions, including multiple sclerosis, polyneuropathy, viral encephalitis, brain tumor, vasculitis, encephalopathy, psychiatric illness, and myelopathy. We report a 10-year-old child with signs, symptoms, and radiological manifestations of intracranial mass lesions, without previously recognized manifestations of Lyme disease. This proved to be Lyme neuroborreliosis, documented by histological and serological examination, which responded well to antibiotic therapy. The need to establish a tissue diagnosis of intracranial mass lesions is emphasized, and the utility of a computed tomographic-guided stereotactic system for this purpose is discussed.
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PMID:Lyme neuroborreliosis manifesting as an intracranial mass lesion. 158 93

We have measured levels of soluble interleukin-2 receptor (sIL-2R) and soluble CD8 (sCD8) in serum and cerebrospinal fluid (CSF) of 127 human immunodeficiency virus (HIV)-seropositive and 51 HIV-seronegative individuals. Serum levels of sIL-2R and sCD8 were higher in HIV+ than in HIV- individuals. HIV+ individuals were grouped by neurological status: asymptomatic, abnormal on neuropsychological screening, HIV-related meningitis, inflammatory demyelinating polyneuropathy, opportunistic central nervous system (CNS) infections and HIV-related dementia, myelopathy or sensory neuropathy. Serum levels of sIL-2R and sCD8 were higher in all HIV+ categories compared to HIV- individuals. Patients with HIV-related meningitis had higher levels of sIL-2R and sCD8 than asymptomatic HIV+ individuals, and inflammatory polyneuropathy patients had higher levels of sCD8. CSF levels of sCD8 were higher in all categories of HIV+ than in HIV- individuals. Patients with HIV-related meningitis, inflammatory neuropathy and opportunistic infections had higher levels than asymptomatic individuals. Examination of the time course showed that serum and CSF levels of sIL-2R and sCD8 increased to very high levels during acute HIV infections. Serum levels then declined over several months to relatively stable elevated levels. By 1-2 years after HIV infection sIL-2R was relatively low in CSF, while sCD8 remained elevated with a gradual decrease over the subsequent years of follow-up.
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PMID:Soluble interleukin-2 receptor and soluble CD8 in serum and cerebrospinal fluid during human immunodeficiency virus-associated neurologic disease. 211 34

A 54 year-old male patient developed acute cranial polyneuropathy including prominent facial diplegia and radicular++-neuritis. He was proven to have lymphocytic pleocytosis, and elevated serum Borrelia burgdorferi antibody to X800 (normal; less than X200). A diagnosis of typical early neuro-borreliosis was made after these clinical and laboratory findings. This case is the first neuro-borreliosis showing the triad of neurological manifestations (meningitis, cranial neuritis, radicular++-neuritis) in Japan. It is concluded that neuro-borreliosis should be considered to be a cause of acute cranial polyneuropathy, particularly of facial diplegia, even if the patient has no apparent history of a tick bite.
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PMID:[A case of cranial polyneuropathy presenting with prominent facial diplegia, elevated serum Borrelia burgdorferi antibody and lymphocytic pleocytosis]. 224 36

The acquired immunodeficiency syndrome (AIDS) is caused by human immunodeficiency virus (HIV) and characterized by disorders of the nervous system in addition to opportunistic infection and cancer. Centers for Disease Control (CDC) recommend the classification system consisting of four major groups. Group I is patients with acute HIV infection, and Group II is asymptomatic carriers. Group III is those with persistent generalized lymphadenopathy (PGL). Group IV includes five subgroups: IVA with constitutional disease, IVB with neurologic disease, IVC with secondary infectious diseases, IVD with secondary cancers and IVE with other conditions. The nervous system disorders are classified into two types: one is produced by HIV itself and not directly related to immunodeficiency, and the other caused by opportunistic infectious agents and cancers. The former is further divided into two kinds: atypical aseptic meningitis and acute inflammatory demyelinating polyneuropathy (AIDP) occur mainly in Group I and II, whereas HIV encephalopathy, distal symmetric polyneuropathy (DSPN) and vacuolar myelopathy in Group III and IV. Group I or II patients have no apparent medical problems. Therefore, when neurologists see patients with risk factors for HIV infection presenting with atypical meningitis or AIDP, it is of utmost importance to have a high index of suspicion and to look for evidence of HIV infection.
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PMID:[Disorders of the nervous system associated with the acquired immunodeficiency syndrome (AIDS)-clinical approach]. 263 Jan 48

The peripheral and central nervous systems are commonly affected in patients with acquired immunodeficiency syndrome (AIDS). Primary infection with human immunodeficiency virus (HIV) can cause an acute encephalitis, meningitis, or an acute polyneuropathy. Spinal cord involvement can result in a progressive spastic paraparesis. Many patients develop dementia which can be severely debilitating. Sensory neuropathies can also occur late in the course.
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PMID:The neurologic manifestations of primary HIV infection. 265 95

Data concerning 292 neurologic complications of AIDS were supplied by ten Departments of Neurology of Spanish hospitals. The period of study was from june 1984 to june 1988. The most frequent complications were: Toxoplasmosis of the CNS (28%), subacute encephalopathy (17%), distal polyneuropathy (8%), tuberculous meningitis (7.5%) and cryptococcal infection of the CNS (6.5%). The most important risk factors for AIDS in this series were intravenous drug addiction (77%) and homosexuality in males (12%). The overall mortality among the reported complications was 54.7%. The main causes of mortality were toxoplasmosis (32% of the fatalities), subacute encephalopathy (19%), and progressive multifocal leukoencephalopathy (8%). These data are compared to those obtained from other European and American series.
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PMID:[Neurologic complications of AIDS. Panoramic view based on a multicenter hospital study]. 270 Feb 95

Primary manifestations of HIV infection may present as a mononucleosis-like syndrome. Cases have also been reported where it presents with symptoms of encephalitis, meningitis or acute polyneuropathy. When no cause is found for such clinical symptoms, they should suggest the possibility of primary HIV infection even in a patient who is not at risk. HIV antibody will appear in the following weeks and serum studies should be done within the three months that follow. The patient should then be warned that he is contagious. Short term prognostic is usually good. But long term progosis remains uncertain.
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PMID:[Acute symptomatology in HIV virus primo-infection. 2 cases]. 295 Apr 84

An unexplained peripheral neuropathy was observed in five patients with positive serology for LAV/HTLV III. Three of them presented with polyneuropathy, one with chronic meningitis and oculomotor palsies, and one with a mononeuropathy. CSF was abnormal in 5/5, with elevated protein content (0.4-4 g/l) and abnormal cell count (29-65/mm3). Intrathecal production of LAV-specific IgG was demonstrated in 3/4 cases. Electromyographic examination showed reduced nerve conduction velocity in 4/5. Neuromuscular biopsy revealed microvasculitis with mononuclear cell infiltrates in 3/4 cases; characterization of these cells showed that they were predominantly non monoclonal T8 lymphocytes. Other symptoms of "AIDS-related complex" were present in all five patients. None had other causes of peripheral neuropathy. Thus, peripheral neuropathy can be the initial manifestation of LAV/HTLV III infection. Isolation of the virus from the nerve in one published case, and arguments for intrathecal synthesis of LAV-specific IgG suggest the direct role of this agent; however, the lymphocytic infiltration seen in three of our cases favours an indirect immune mechanism, as in other organs, such as lungs and lymph nodes.
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PMID:[Peripheral neuropathy in relation to LAV/HTLV III retrovirus infection. A clinical, anatomical and immunological study. 5 cases]. 302 90

The common and not so common neurologic lesions due to sarcoidosis include cranial nerve palsies, meningitis, hypothalamic and pituitary lesions, basilar meningitis, polyneuropathy, space occupying lesions and spinal cord involvement. The diagnosis of neurosarcoidosis requires a compatible clinical or radiologic picture of sarcoidosis and histological confirmation of noncaseating granulomas. Serum ACE, Gallium-67 lung scan and bronchoalveolar lavage are of help in supporting the diagnosis and establishing activity of the disease. A CT scan with enhancement is the diagnostic procedure of choice. Corticosteroids are the cornerstone of therapy.
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PMID:Neurosarcoidosis. A report of ten patients illustrating some usual and unusual manifestations. 303 91


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