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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neurological spectrum of Borrelia burgdorferi infections is still enlarging. We review epidemiological, pathological and serological data of Lyme disease. The course of the disease is divided in three stages: stage 1 during the first month is characterised by erythema chronicum migrans and associated manifestations; stage 2 includes not only the classical European meningoradiculitis but also less specific neurological symptoms: isolated lymphocytic meningitis with an acute or even relapsing course, apparently idiopathic facial palsy, neuritis of other cranial nerves, polyneuritis cranialis, Argyll-Robertson sign, peripheral nerve involvement, acute transverse myelitis, severe encephalitis, myositis. During stage 3, three to five months or longer after the onset of the disease, chronic arthritis, acrodermatitis chronica atrophicans and various neurological symptoms can be observed: chronic neuropathy with mainly sensory or motor signs, recurrent strokes due to cerebral angiopathy and progressive encephalomyelitis; this third stage the central nervous system involvement is characterised by slowly progressive or fluctuating course during months or years, ataxic or spastic gait disorder, bladder disturbances, cranial nerve dysfunction including optic atrophy and hypoacusia, dysarthria, focal and diffuse encephalopathy. This chronic central nervous system disease can mimic multiple sclerosis, anorexia nervosa, psychic disorders or subacute presenile dementia. It is often associated with pleiocytosis, abnormal EEG and evoked potentials, sometimes multifocal and mainly periventricular white matter lesions visualised by CT or MRI, and as a rule high antibody titers against Borrelia burgdorferi. High doses of penicillin can halt the disease, sometimes induce spectacular regression of symptoms or sometimes be inefficient; ceftriaxone could be a more powerful therapy. Similarities between syphilis and Borreliosis are multiple: both of these spirochetes contain plasmids, can be transmitted through the placenta and progress for many years through successive stages, with multiorgan symptoms, including parenchymatous and vascular lesions of the central nervous system. Borrelia burgdorferi is the new great imitator.
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PMID:[Multiple neurologic manifestations of Borrelia burgdorferi infection]. 307 Jun 90

Acute disseminated encephalomyelitis, an inflammatory and demyelinating disorder of central nervous system white matter, typically occurs following childhood viral infections. Although CT may demonstrate abnormalities, many children have normal CT studies in spite of widespread neurologic abnormalities. We report a series of five patients with the typical clinical presentation of disseminated encephalomyelitis who were studied using magnetic resonance imaging (MRI). In each case the children presented with progressive subacute neurologic abnormalities including headache, diplopia, ataxia, hemiparesis, seizures, dysarthria, and/or coma. CT was nondiagnostic. MRI clearly demonstrated multifocal white matter lesions of the cerebrum, brainstem, and cerebellum which corresponded to clinical signs. The patients improved dramatically with corticosteroid therapy. MRI showed progressive resolution of multifocal lesions in conjunction with clinical improvement.
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PMID:MRI in children with postinfectious disseminated encephalomyelitis. 395 36

A 54-year-old housewife became ill with transient diplopia followed by facial paralysis, tremor of the right hand and a progressively worsening disturbance in gait. Four years after the first appearance of the disease bilateral hypacusia, paralysis of the right hypoglossal nerve, dysarthria, severe spastic tetraparesis with ataxia, urinary retention and an organically induced character change were present. Lumbar puncture fluid contained 51/mm3 lymphocytes and 1164 mg/dl protein. Immunoglobulin A, G and M, synthesised locally, could be detected in cisternal fluid. The serum had a high antibody titre against Ixodes ricinus-Borrelia antigen and the same antibodies, formed locally, were present in the lumbar fluid. The neurological deficiencies improved markedly under parenteral penicillin treatment and the antibody titre decreased. The detection of Borrelian antibodies, especially those synthesised locally in the CSF, enabled an aetiological diagnosis to be made in seven other patients aged 18-47 years in whom the disease had been present for 1 to 8 years. These patients likewise presented symptoms characteristic of a disseminated disease of the CNS, with spastic pareses and evidence in the spinal fluid of chronic inflammation and disruption of CSF barriers in particular. This progressive encephalomyelitis differs from the common and spontaneously healing meningo-polyneuritis (Garin-Bujadoux-Bannworth), the usual manifestation of erythema chronicum migrans of the nervous system, in its progressive nature, its invasion of the CNS and the possible long lasting severe damage when not specifically treated.
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PMID:[Progressive Borrelia encephalomyelitis. Chronic manifestation of erythema chronicum migrans disease of the nervous system]. 400 60

We report a 63-year-old man with progressive gait disturbance and dysarthria. The patient was apparently well until the age of 62 (February, 1990) when he noted unsteadiness of gait. Two months later, dysarthria appeared. He was admitted to Juntendo Izunagaoka Hospital on April 23, 1990. Neurologic examination revealed a mentally sound man with normal higher cerebral functions. Cranial nerves were unremarkable except for scanning speech. His gait was ataxic with positive Romberg sign. No motor weakness was noted, however, he had hypotonia and cerebellar ataxia. Deep tendon reflexes were retained and the plantar response was flexor. Pain, touch and vibration senses were diminished in the distal parts of the lower extremities. Laboratory examination revealed a 2.5 cm mass in the left lung field. Cranial MRI revealed a small T1-low and T2-high signal intensity lesion in the left temporal lobe. Abdominal CT scan revealed multiple low density lesions in the liver. His subsequent course was complicated by progressive deterioration in his gait and loss of deep tendon reflexes. He expired on November 24, 1990. The patient was discussed in the neurological CPC and the chief discussant arrived at the conclusion that the patient had anti-Hu associated paraneoplastic encephalomyelitis and sensory neuropathy. Some other participants thought that the patient had carcinomatous cerebellar degeneration. Postmortem examination revealed a 4x4 cm mass lesion involving the left S4-S5 segments. Histologic examination of the tumor was small cell carcinoma. Many metastatic foci were found in the liver. The cerebral hemispheres were unremarkable except for a small wedge-shaped tissue defect in the left temporal lobe which appeared to have been caused by old head trauma which the patient had received. The cerebellar vermis showed slight enlargement of cortical sulci, however, the cerebellar hemispheres appeared unremarkable. Upon histologic examination, marked loss of Purkinje cells was noted, particularly in the cerebellar anterior lobe. The dentate nucleus showed slight cell loss with increase in fat granule cells. The inferior olive was normal. The histologic characteristics were consistent with the pathologic diagnosis of carcinomatous cerebellar degeneration. No evidence of limbic encephalitis was seen. The peripheral nerve was not examined.
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PMID:[A 63 year-old man with progressive gait disturbance and dysarthria]. 888 38

Viliuisk encephalomyelitis (VE) is an unique neurological disease occurring in the Iakut (Sakha) people of Siberia. Evolution of the disease follows one of three broad clinical forms: subacute, slowly progressive or chronic. Death occurs within 3 to 6 months in subacute cases and within 6 years in the slowly progressive cases. Chronic cases lack a subacute phase but show a slowly progressive dementia associated with bradykinesia, dysarthria and spastic paraparesis that stabilizes late in the disease process. In subacute and slowly progressive cases, focal necrotizing encephalomyelitis is seen at necropsy. Chronic cases show multifocal areas of lysis with a gliotic margin, predominantly within grey matter, lacking associated chronic inflammatory changes seen in the other forms of the disease. Epidemiological studies are consistent with a disease of low-grade communicability, but laboratory studies have so far failed to reveal an infectious organism. The spectrum of neuropathological changes are reviewed in this examination of 11 cases. Although the aetiology of VE remains obscure, further studies are warranted since it may represent a novel disease process.
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PMID:Viliuisk encephalomyelitis--review of the spectrum of pathological changes. 922 30

We report a 49-year-old previously healthy woman with acute onset of decrease in attention, dysarthria and ataxia, accompanied by drowsiness. On admission, there were cloudness of consciousness, hallucination and left hemiparesis. Cerebrospinal fluid study revealed a cell count of 1/mm3, and the cytology was class I with a slight increase in protein. MRI of the brain performed on admission showed multiple gadolinium-enhanced lesions with a T2 weighted high intensity area in the cerebral white matter. At first the patient was diagnosed as acute disseminated encephalomyelitis (ADEM), and treated with methylprednisolon pulse therapy. Soon after, she showed transient clinical improvement, but her condition soon worsened. MR spectroscopy revealed elevated choline peak, decreased NAA peak and lactate peak, which indicated a neoplastic lesion. The brain biopsy disclosed diffuse intravascular lymphoma (IVL). MRS was useful in the differential diagnosis of IVL from ADEM.
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PMID:[MR spectroscopy findings of a case of intravascular malignant lymphoma: usefulness for differential diagnosis]. 1288 28

A previously neurodevelopmentally intact 5-year-old male was admitted to hospital with a right lower lobe pneumonia with pleural effusion, subsequently confirmed to be a Mycoplasma pneumoniae infection. On the seventh day of the illness he had a prolonged generalized tonic or tonic-clonic convulsion, requiring intubation and ventilation. He was slow to regain consciousness (Child's Glasgow Coma Score 7-10 over 6 days) and brain imaging with CT and then MRI demonstrated bilateral thalamic lesions with oedema and central haemorrhage suggestive of acute bilateral thalamic necrosis, without striatal or white-matter involvement. He was treated with a 2-week course of erythromycin, and as an autoimmune process was considered possible, 5 days of intravenous methylprednisolone (20 mg/kg/day) followed by a 4-week oral prednisolone taper. He made a slow recovery over the next few weeks with almost complete neurological recovery by 2 months but with significant dysarthria, drooling, and a mild left hemiparesis. At 9 months, significant dystonia continued to affect his speech and, together with tremor, his upper-limb fine motor function bilaterally. His gait, personality, and higher cognitive functions appeared to have recovered fully. Although acute striatal necrosis, acute disseminated encephalomyelitis, and encephalitis have been reported with Mycoplasma pneumoniae and a similar picture of acute bilateral thalamic necrosis with influenza-A ('acute necrotizing encephalopathy'), this is the first reported case of Mycoplasma pneumoniae-associated isolated acute bilateral thalamic necrosis.
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PMID:Acute bilateral thalamic necrosis in a child with Mycoplasma pneumoniae. 1499 91

A previously healthy female, aged 4 years 3 months, developed brainstem encephalitis with clinical manifestations of fever, decreased level of consciousness, and left facial and abducens paralysis 1 week after bilateral parotitis. Twenty days after remission of encephalitis, she manifested new symptoms of ataxia, dysarthria, and fever. Magnetic resonance imaging revealed multiple hyperintense lesions which were increased in size when compared with the first magnetic resonance imaging. She was treated with glucocorticoids and intravenous immunoglobulin. Forty-eight days after therapy, she was able to walk with support and recovered completely on follow-up. Brainstem encephalitis and acute disseminating encephalomyelitis are discussed as rare complications of mumps.
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PMID:Brainstem encephalitis and acute disseminated encephalomyelitis following mumps. 1498 8

A 65-year-old man was admitted to our hospital complaining of diplopia, dysarthria, difficulty in walking and progressive dysesthesia that developed in his left hand and leg. Brain MRI revealed high signal intensity regions on T2-weighted and FLAIR images of the hippocampus and the corpus amygdaloideum. After admission, the patient's neurological symptoms progressed to delirium and dementia with hallucinations. When he eventually developed severe respiratory failure requiring ventilatory support, brain MRI revealed new high signal intensity regions on T2-weighted images of the medulla oblongata and pons. Chest CT scans showed a mass under the aortic arch, and based on subsequent histopathological examination of a transesophageal endoscopic ultrasonography-guided fine needle aspiration biopsy of the tumor, a diagnosis of small cell lung cancer was made. In addition, anti-Hu antibody was found in the patient's serum, leading to a diagnosis of paraneoplastic encephalomyelitis/sensory neuropathy. One course of chemotherapy (carboplatin + etoposide) was administered; however, the protocol was not completed because the patient developed severe pneumonia. Given that neurological symptoms usually precede a diagnosis of malignancy in paraneoplastic neurological syndromes, it is important that these are considered carefully, as they may contribute to early diagnosis and treatment. Here we report a rare case of severe central hypoventilation in paraneoplastic encephalomyelitis/sensory neuropathy.
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PMID:[Paraneoplastic neurological syndrome accompanied by severe central hypoventilation and expression of anti-Hu antibody in a patient with small cell lung cancer]. 1851 96

Anabolic androgenic steroid (AAS) abuse has increased among athletes in recent years. However, AAS abuse can increase hypercoagulopathy and cause cerebrovascular disease. We report a case of a 27-year-old man who had right hemiparalysis, hemianopia, dysarthria, and double vision in the middle of muscle training. He suspected acute disseminated encephalomyelitis at first, because of a preceding respiratory infection. However, extensive work-up was performed, including brain magnetic resonance imaging, transcranial Doppler and transesophageal echocardiography, confirming the final diagnosis of cardioembolic stroke. Physicians should be aware that cerebrovascular disease may be a side effect of AAS, even in younger populations.
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PMID:Cerebral infarction in a young man using high-dose anabolic steroids. 2190 17


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