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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

21 patients studied had persistent or progressive chronic meningitis not associated with a demonstrable infectious or other disease, except Streptococcus milleri antigen in the cerebrospinal fluid of 1 patient. The cerebrospinal-fluid (CSF) abnormalities consisted of a moderate, predominantly mononuclear, pleocytosis, a sharp rise in CSF protein (mean 2.3 g/l), intrathecal synthesis of considerable quantities of oligoclonal immunoglobulin G, and, in half the patients, a fall in the CSF-glucose/blood-glucose ratio. In all patients symptoms began during summer or autumn. In 4 patients the onset was preceded by localised cutaneous lesion, described as erythema chronicum migrans. 4 more patients had been bitten by ticks in the weeks before onset of symptoms. The patients had profound fatigue, malaise, and weight-loss. Half had fever, usually moderate. The neurological abnormalities included aseptic meningitis, cranial neuropathy (mostly facial-nerve paralysis), motor and sensory peripheral radiculoneuropathy, and myelitis. The patients improved or recovered, sometimes dramatically, during a 2-week course of intravenous penicillin G.
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PMID:Chronic meningitis caused by a penicillin-sensitive microorganism? 613 62

We studied 35 patients with chronic meningitis. The neurological abnormalities included aseptic meningitis, cranial neuropathy (mostly facial palsy), motor and sensory peripheral radiculoneuropathy, and myelitis. Neurological symptoms were sometimes preceded by erythema chronicum migrans or an insect bite and were often accompanied by fever, malaise, profound fatigue, and weight loss. The cerebrospinal fluid (CSF) abnormalities consisted of a predominantly mononuclear pleocytosis, an elevated CSF protein (mean 2.3 g/l), intrathecal synthesis of oligoclonal immunoglobulin G, and, in half of the patients, a fall in the CSF/blood glucose ratio. High antibody titers to the Lyme spirochete and the Swedish Ixodes ricinus spirochete were demonstrated by immunofluorescence in 26 of the 35 patients. By imprint immunofixation of electrofocused samples of serum and CSF, intrathecal production of oligoclonal Lyme-spirochete-specific IgG was demonstrated in one patient with chronic meningitis. Four sequential paired samples of serum and CSF from this patient showed local synthesis of spirochete-specific antibodies in CSF. The 35 patients improved or recovered, sometimes dramatically, during a two-week course of intravenous penicillin G.
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PMID:Chronic meningitis and Lyme disease in Sweden. 651 51

Post-polio syndrome (PPS) refers to the new neuromuscular symptoms that occur at least 15 years after stability in patients with prior acute paralytic polio-myelitis. They include: (1) new muscle weakness and atrophy in the limbs, the bulbar or the respiratory muscles [post-poliomyelitis muscular atrophy (PPMA)] and (2) excessive muscle fatigue and diminished physical endurance. PPS is a clinical diagnosis that requires exclusion of all other medical, neurological, orthopedic or psychiatric diseases that could explain the cause of the new symptoms. Routine electromyography is useful to confirm chronic and ongoing denervation and exclude neuropathies. Muscle biopsy, single fiber electromyography (EMG), macro-EMG, serum antibody titers to polio virus, and spinal fluid studies are very useful research tools but they are rarely needed to establish the clinical diagnosis. PPS is a slowly progressive phenomenon with periods of stability that vary from 3 to 10 years. Current evidence indicates that PPS is the evolution of a subclinically ongoing motor neuron dysfunction that begins after the time of the acute polio. It is clinically manifested as PPS when the well-compensated reinnervating process crosses a critical threshold beyond which the remaining motor neurons cannot maintain the innervation to all the muscle fibers within their motor unit territory.
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PMID:The post-polio syndrome as an evolved clinical entity. Definition and clinical description. 761 61

Sixty-three patients with tick-borne encephalitis were studied for sequelae up to 5 years after the acute illness (median: 12 months, range: 1-44 months). Patients were examined clinically, by neuropsychological testing and by electroencephalography. The clinical presentation during the acute stage was as follows: Meningitis (M,n = 12), Meningoencephalitis (Me,n = 27), Meningoencephalomyelitis (My,n = 15), and Meningoencephaloradiculitis (R,n = 9). A total of 59 patients reported a neurasthenic syndrome after discharge, which correlated with the severity of the acute illness. Twenty patients were not able to work because of reduced stress tolerance, fatigue or an elevated emotional sensitivity, which lasted for 3 months at most. In some patients hypacusis (n = 7), severe dysarthria and dysphagia (n = 4) remained essentially unimproved for years following the acute illness. While in 8/9 patients with radiculitis paresis of the extremities improved well over months to years, improvement was quite limited in all patients with myelitis. In 41/55 patients, investigations by electroencephalography revealed normal findings even within months after acute illness. Persistent cognitive deficits were present only in 7/11 patients with a severe course of disease.
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PMID:[Follow-up and prognosis of early summer meningoencephalitis]. 927 61

The patient was a 33 year female. In 2001, she was diagnosed with systemic lupus erythematosus (SLE) and treated with prednisolone and ciclosporin. In May 2006, she noticed slight muscle weakness in the bilateral lower limbs. In July of the same year, she experienced gait difficulty and was admitted to our hospital because of fatigue, appetite loss, fever and disorientation. Soon afterwards, she had a fit of general convulsion and suffered from urinary retention and fecal incontinence. A brain magnetic resonance image revealed atrophy of the thoracic cord in T2 weighted images, and cerebrospinal fluid examination showed high total protein and interleukin-6 concentration, indicating complication of lupus myelitis as well as cerebral involvement. Steroid pulse and oral prednisolone treatment resulted in ameriolation of cerebral complications such as disorientation and convulsion, but muscle weakness and paresthesia in the lower limbs and urinary retention persisted. Cyclophosphamide pulse therapy was started and resulted in a marked recovery from muscle weakness, paresthesia and urinary retention, and she could discharge. We conclude that steroid and cyclophosphamide pulse therapy for a SLE patient with CNS lupus and lupus myelitisis is effective for ameriolation of symptoms such as disorientation, convulsion, urinary retension, fecal incontinence, muscle weakness and paresthesia in the lower limbs as well as elevated level of serum anti-ribosomal P antibody.
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PMID:[Successful therapy with steroid and cyclophosphamide pulse for CNS lupus and lupus myelitis]. 1798 83

This case report describes the use of acupuncture for back pain, knee pain and insomnia in a 49 year old woman with a recent diagnosis of transverse myelitis with paraplegia, sensory disturbance, and bladder and bowel dysfunction. She was receiving intensive in-patient multi-disciplinary rehabilitation but was struggling to participate fully due to pain and poor sleep quality. She received a course of acupuncture in addition to standard care and reported substantial benefits including reduction in pain, improved sleep and mood, and reduction in daytime fatigue. Effective symptom control allowed this patient to participate more fully in her rehabilitation programme. Reduction of knee pain and sleep disturbance was maintained until discharge, 15 weeks after the last acupuncture treatment. This case report suggests that acupuncture may be an option to consider for other patients with pain or sleep disturbance that is interfering with their rehabilitation programme.
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PMID:Acupuncture for back pain, knee pain and insomnia in transverse myelitis - a case report. 1881 65

Lyme borreliosis is a multisystem disorder caused by Borrelia burgdorferi (Bb). Neurological symptoms such as lymphocytic meningoradiculoneuritis (Bannwart's syndrome), cranial neuritis (II,III,IV,V,VI), encephalitis, transverse myelitis are found in about 10% of cases during the second phase of the disease. In the chronic stage, many months or years after the initial infection, other neurologic complications may occur, such as encephalomyelitis, epileptic crises, cognitive impairment, peripheral neuropathy and psychiatric disturbances such as depression, anxiety, panicc attacks, catatonia, psychosis etc. Some patient continue to experience symptoms of fatigue, insomnia or psychiatric disorder in the post borrelia syndrome. We describe here a patient with a triad of unusual symptoms in chronic LNB including tremor, seizures and psychosis. Standardized medical interview, neurologic examination, neuroimaging, serum and CSF serology as well as EEG and EMNG evaluation were performed. The patient was treated with intravenous ceftriaxone and doxycycline and responded with rapid clinical and functional improvement.Newertheless, he suffered from multiple systemic and neurologic sequelas that influenced his daily activities in post treatment period. Emphasis is placed on the atypical onset and evolution, the difficulties encountered in formulating diagnosis, early treatment and the uncertainties concerning the sequelae after treatment. In patients with non-specific long lasting symptoms in the absence of overt clinical signs suggesting CNS involvement, routine treatment with i.v. ceftriaxone is not to be encouraged.
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PMID:Tremor, seizures and psychosis as presenting symptoms in a patient with chronic lyme neuroborreliosis (LNB). 2164 54

Neuromyelitis optica (NMO) is usually a relapsing demyelinating disease of the central nervous system associated with optic neuritis, transverse myelitis involving three or more contiguous spinal cord segments, and seropositivity for NMO-IgG antibody. NMO is often mistaken for multiple sclerosis and there are relatively sporadic publications about NMO and overlapping systemic or organ-specific autoimmune diseases, such as systemic lupus erythematosus (SLE). We described a unique case of a 25-year-old Arab young woman who was diagnosed with SLE, depending on clinical, laboratory investigations and after she had fulfilled the diagnostic criteria for SLE and had presented the following findings: constitutional findings (fatigue, fever, and arthralgia); dermatologic finding (photosensitivity and butterfly rash); chronic renal failure (proteinuria up to 400 mg in 24 hours); hematologic and antinuclear antibodies (positivity for antinuclear factor (ANF), anti-double-stranded DNA antibodies, direct Coombs, ANA and anti-DNA, low C4 and C3, aCL by IgG and IgM). Recently, she presented with several episodes of transverse myelitis and optic neuritis. Clinical, radiological, and laboratory findings especially seropositivity for NMO-IgG were compatible with NMO. Accurate diagnosis is critical to facilitate initiation of immunosuppressive therapy for attack prevention. This case illustrates that NMO may be associated with SLE.
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PMID:Systemic Lupus Erythematosus (SLE) Complicated by Neuromyelitis Optica (NMO - Devic's Disease): Clinic-Pathological Report and Review of the Literature. 2494 69

Hepatitis C virus (HCV) infection is considered a systemic disease because of involvement of other organs and tissues concomitantly with liver disease. Among the extrahepatic manifestations, neuropsychiatric disorders have been reported in up to 50% of chronic HCV infected patients. Both the central and peripheral nervous system may be involved with a wide variety of clinical manifestations. Main HCV-associated neurological conditions include cerebrovascular events, encephalopathy, myelitis, encephalomyelitis, and cognitive impairment, whereas "brain fog", depression, anxiety, and fatigue are at the top of the list of psychiatric disorders. Moreover, HCV infection is known to cause both motor and sensory peripheral neuropathy in the context of mixed cryoglobulinemia, and has also been recently recognized as an independent risk factor for stroke. These extrahepatic manifestations are independent of severity of the underlying chronic liver disease and hepatic encephalopathy. The brain is a suitable site for HCV replication, where the virus may directly exert neurotoxicity; other mechanisms proposed to explain the pathogenesis of neuropsychiatric disorders in chronic HCV infection include derangement of metabolic pathways of infected cells, alterations in neurotransmitter circuits, autoimmune disorders, and cerebral or systemic inflammation. A pathogenic role for HCV is also suggested by improvement of neurological and psychiatric symptoms in patients achieving a sustained virologic response following interferon treatment; however, further ad hoc trials are needed to fully assess the impact of HCV infection and specific antiviral treatments on associated neuropsychiatric disorders.
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PMID:Chronic hepatitis C virus infection and neurological and psychiatric disorders: an overview. 2574 Nov 33

The hallmark signs and symptoms of anemia are directly related to a decrease in oxygen delivery to vital tissues and organs and include pallor, fatigue, lightheadedness, and shortness of breath. Neurologic complications are often nonspecific and can include poor concentration, irritability, faintness, tinnitus, and headache. If undiagnosed or untreated, anemia can progress to cognitive dysfunction, psychosis, encephalopathy, myelopathy, peripheral neuropathy, and more focal syndromes, such as stroke, seizures, chorea, and transverse myelitis. Imaging can play an important role in the early diagnosis and treatment of these neurologic and systemic complications associated with anemia, and hence, better outcome.
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PMID:Imaging Manifestations of Neurologic Complications in Anemia. 2744 95


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