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

The authors describe the course of herpetic encephalitis in 52 patients aged 16 to 64 years. Five types of the initial manifestations of herpetic infection of the CNS were revealed. In 44.3% of cases the disease started from the general cerebral symptomatology and consciousness disturbance; in 13.6% it started in a brain stroke-like manner followed by the development of the comatose status; in 13.6% of cases from memory disorder and unmotivated actions; in the same percentage of cases, the disease onset was marked by the dominance of dizziness, diplopia, ataxia and central hemiplegia ; in 15.9% the disease started from pains in the stomach, loin and lower limbs. Hemispheric and pseudotumorous stem encephalitides (48.1 and 13.6% respectively) were predominant; in 25% meningoencephalitides and in the remainder, encephalomyelitis running their course in the form of disseminated encephalomyelitis (5.7%), focal myelitis (5.7%) or opticomyelitis (1.9%). The data presented attest to the pleomorphism of the clinical picture of herpetic lesions of the CNS.
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PMID:[Clinical forms of acute herpetic infections of the central nervous system in adults]. 132 73

Magnetic resonance imaging (MRI) with gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA) was used to investigate disruption of the blood-optic nerve barrier associated with acute autoimmune demyelination. Leakage of Gd-DTPA was seen in the optic nerves and optic chiasm of adult guinea pigs sensitized for acute experimental allergic encephalomyelitis, but not in normal unsensitized animals. This finding occurred as early as 5 to 8 days after antigenic sensitization with the myelin emulsion and before the onset of paralysis or ataxia. Pathologic examination at this early stage of experimental allergic encephalomyelitis showed an absence of demyelination in the optic nerves and optic chiasm, although scant perivascular foci of inflammatory cells were seen. Leakage of Gd-DTPA in the optic nerve before demyelination of this white matter tract illustrates that increased permeability of the blood-optic nerve barrier is an early, if not the initial, event in autoimmune demyelination, and the optic nerve is a common site of central nervous system involvement during the initial phase of acute experimental allergic encephalomyelitis. Findings in this animal model appear comparable with the results of MRI with Gd-DTPA in patients with optic neuritis, and they suggest that disruption of the blood-optic nerve barrier is a common denominator for both disorders of primary demyelination.
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PMID:Gadolinium-DTPA-enhanced magnetic resonance imaging in experimental optic neuritis. 234 5

We report two patients with chronic encephalomyelitis due to Borrelia burgdorferi in whom the definite diagnosis was delayed because of atypical clinical features. The first patient presented with chronic spastic paraparesis, slight ataxia and nystagmus of several years' duration. A tentative diagnosis of multiple sclerosis was made in spite of important abnormalities of the CSF biological characteristics. The second patient presented with an acute aphasia and a bilateral Babinski's sign. He was thought to suffer from benign herpetic meningoencephalitis. Several months later, as the patient experienced relapses with cerebellar and spinal cord involvement, falsely positive tests for syphilis were found and an antibiotic treatment was given. High protein content, low glucose levels, pleocytosis and oligoclonal bands were observed in all CSF samples, but the definite diagnosis was based on the detection of serum and CSF antibodies against B. burgdorferi.
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PMID:[Borrelia burgdorferi encephalomyelitis]. 318 97

The dorsal (posterior) root ganglion is a relatively neglected part of the nervous system from the clinical point of view. In recent studies on the pathophysiology of experimental allergic encephalomyelitis (EAE), the main animal model of multiple sclerosis, the DRG of the rabbit was shown to be the site of extensive inflammation and demyelination and of focal conduction block in a high proportion of the large diameter afferents. The resulting severe functional peripheral deafferentation accounts for the postural disturbance, hypotonia, ataxia and areflexia in rabbits with EAE. The vulnerability of the DRG is due to a deficient blood-nerve barrier and possibly also to a susceptibility of the branch point of the ganglion neurone to demyelination-induced conduction block. These and other studies in experimental animals suggest that in man the DRG may be a preferential (but neglected) site of focal structural and functional abnormalities in inflammatory and also other neurological diseases.
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PMID:Vulnerability of the dorsal root ganglion in experimental allergic encephalomyelitis. 384 21

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

Clinical, histological and electrophysiological studies were performed on rabbits with acute experimental allergic encephalomyelitis (EAE). The clinical features were similar to those previously described, with the notable exception of the new findings of areflexia, respiratory slowing and hypothermia. The histological findings were also similar to those previously reported, with inflammatory demyelinating lesions both in the central and peripheral nervous system, especially the dorsal root ganglia. Electrophysiological studies performed one to nine days after the onset of neurological signs demonstrated conduction block in a high proportion of the large diameter afferents in the lumbosacral and thoracic dorsal root ganglia. Single fibre studies with spike-triggered averaging confirmed the conduction block in the dorsal root ganglia. That the conduction block was due to demyelination was indicated by slowing of conduction in large diameter fibres, normal conduction in unmyelinated fibres and the specific effects of temperature and of the potassium channel blocking agent, 4-aminopyridine. These conduction abnormalities in the peripheral nervous system, focused on the dorsal root ganglia, account for the postural disturbance, hypotonia, ataxia and areflexia in rabbits with EAE. Such conduction block is likely to mask the expression of any lesions of the central nervous system that alone could produce similar signs. The implications of these findings for the human demyelinating diseases are discussed.
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PMID:The pathophysiology of acute experimental allergic encephalomyelitis in the rabbit. 608 51

A chronic experimental allergic encephalomyelitis (EAE) has been produced in rabbits sensitized with bovine white matter proteolipid apoprotein. Eleven of 12 animals developed clinical disease one to six months after immunization with a single dose of the apoprotein. The clinical course was characterized by posterior ataxia, flaccid paralysis progressing to spastic paralysis, and incontinence. Spontaneous relapses and remissions were observed in 3 rabbits. Histologically, acute and chronic encephalomyelitis accompanied by primary demyelination were observed. Serum antibody production, assayed by both an enzyme-linked immunosorbent assay and an electroblot procedure, did not correlate with either the clinical course or the histopathological findings. Delayed hypersensitivity to proteolipid apoprotein was observed in all rabbits prior to the onset of clinical signs. The data suggest that lymphocytes specifically sensitized to the proteolipid may be involved in the pathogenesis of the demyelination in chronic EAE.
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PMID:Chronic experimental allergic encephalomyelitis produced by bovine proteolipid apoprotein: immunological studies in rabbits. 618 48

Twelve Lewis rats were inoculated with a guinea pig spinal cord tissue preparation. They developed experimental allergic encephalomyelitis (EAE) after 12-14 days, manifested by weight loss, tail flaccidity, ataxia, hind limb paresis and incontinence. The CNS lesions are produced in this animal model on the basis of inflammatory demyelination, which provides a useful model for multiple sclerosis. Concomitantly with EAE, all animals developed vestibular hyperreactivity (VH) of otolith and canal reflexes. In surviving animals these reflexes renormalized after full clinical recovery. The major effect on the canal response was an increased duration of postrotatory nystagmus caused by an increase in time constant. These findings are similar in part to those previously reported in patients with multiple sclerosis.
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PMID:Physiological abnormalities in experimental allergic encephalomyelitis (EAE). I. Vestibular hyperreactivity (VH) in rats with EAE. 633 52

12 Lewis rats were inoculated with a guinea pig spinal cord tissue preparation. They developed experimental allergic encephalomyelitis (EAE) after 12-14 days manifested by weight loss, tail flaccidity, ataxia, hind limb paresis or paralysis and urinary incontinence. Concomitantly with EAE, all animals developed vestibular hyperreactivity (VH) of canal and otolith reflexes. Other signs of brain-stem dysfunction were also observed: abducens paralysis, facial weakness, tachypnoe and mydriasis with defective pupillary light reflex. The vestibular and other abnormalities subsided with some delay after recovery from clinical EAE, whilst histological abnormalities were still present in the CNS.
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PMID:Physiological abnormalities in experimental allergic encephalomyelitis (EAE): II. Correlation between clinical signs and vestibular hyperreactivity and other signs of brain-stem dysfunction in rats with EAE. 633 24


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