Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heat stimuli, applied to the skin by non-contact radiation pulses emitted by a CO2-laser, activate simultaneously both A-delta (mean conduction velocity 14 m/s) and C-fibres (0.8 m/s), which terminate in the most superficial skin layers. Correspondingly, brief heat stimuli elicit two pain sensations with mean reaction times of about 500 ms and 1400 ms. Similarly, two evoked potential waveforms were observed in the electroencephalogram: the late components N240/P370 and the ultralate components N1050/P1250. The shape of the two components was reproducible in independent samples of healthy volunteers. In patients with dissociated sensory loss, the laser evoked cerebral potentials are affected, depending on the kind of disturbed nerve and tracts. This is shown in patients with syringomyelia, encephalomyelitis disseminata, myelitis, Brown-Sequard syndrome, Wallenberg syndrome. In cases with hereditary motor and sensory neuropathy type I or with neurosyphilis, ultralate potentials are observed as correlates of delayed pain perception in the affected body areas. The laser evoked cerebral potentials reflected the clinical disorder of pain sensitivity in most cases, whereas somatosensory evoked potentials in response to conventional nerve stimuli failed in objectifying the diagnosis. As such, evoked cerebral potentials in response to laser heat stimuli applied to the hairy skin can be used for an overall examination of the functional integrity of peripheral small fibres, anterolateral tracts and thalamocortical projections.
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PMID:Laser-evoked cerebral potentials in the assessment of cutaneous pain sensitivity in normal subjects and patients. 176 52

An interesting neurological syndrome, characterized by recurrent optic neuritis, cervical myelopathy from syringomyelia, paraparesis, amenorrhea-galactorrhea, and other endocrine problems, has been described among young black women in the French West Indies. The etiology remains unknown, but possible links with Devic's disease, acute disseminated encephalomyelitis, and neurotoxicity from quinolines in Annona muricata teas have been postulated. The largest epidemic of neuropathy in this century occurred in Cuba in 1991-1994. Clinical features and etiologic studies are reviewed. Its primary cause was nutritional. A similar epidemic was recently described in Tanzania. A number of infectious neuropathies and myopathies are reviewed, including leprosy, tuberculosis, hemorrhagic fevers (Ebola and Marburg filoviruses, Lassa, Argentinean and Bolivian arenaviruses), the human retrovirus human T-cell lymphotropic virus type I, Lyme disease and postimmunization neuropathies. The tropics continue to contribute interesting and important clinical conditions that may illuminate the etiopathiogenesis of other common disorders.
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PMID:Tropical myeloneuropathies revisited. 984 4

Diagnosis depends on the clinical manifestations, blood or cerebrospinal fluid study and MRI findings. Acute and subacute intraparenchymal spinal cord disorders are due to vascular disorders or myelitis. Spinal cord infarction is associated with dissecting aortic aneurysm, surgical clipping of aortic aneurysms, aortic atherosclerosis or hypotension from any cause. Hematomyelia results from trauma, vascular malformations, vasculitis, or a coagulation disorder. Acute infectious myelopathies result from direct invasion of the spinal cord by bacteria, parasite, or virus. The cause of acute or subacute inflammatory disease include multiple sclerosis, Devic disease, acute disseminated encephalomyelitis, SLE, or sarciodosis. Sarcoidosis sometimes requires differential diagnosis with cord tumor. Chronic intraparenchymal spinal cord disorders are due to syringomyelia, familial spastic paraplegia, HTLV-1 associated myelopathy, adrenomyeloneuropathy, and vascular malformations. HTLV-1 associated myelopathy present with progressive spastic paraplegia with bladder disturbance and has antibodies to HTLV-1 in the cerebrospinal fluid and serum. Diagnosis of adrenomyeloneuropathy is made by demonstration of elevated levels of very long chain fatty acids in plasma. Vascular malformations are important lesions because they present a treatable cause of progressive myelopathy.
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PMID:[Medical approach to intraparenchymal spinal cord disorders]. 1278 77

A one-year-old female cat was unable to stand. Magnetic resonance imaging was performed, and an enlargement of the lateral, third, and fourth ventricles and syringomyelia were detected. The cat was diagnosed with an isolated fourth ventricle (IFV) with syringomyelia. The serum isoantibody test for the feline infectious peritonitis (FIP) virus was 1:3,200. After the cat died, a pathological examination revealed nonsuppurative encephalomyelitis. We suspected that the IFV, detected in the cat, was associated with FIP encephalomyelitis. To our knowledge, there has been no report on IFV in veterinary medicine.
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PMID:A feline case of isolated fourth ventricle with syringomyelia suspected to be related with feline infectious peritonitis. 1767 10

This report describes the use of magnetic resonance imaging (MRI) to diagnose cervical syringomyelia in 4 cats. MRI revealed enlargement of the lateral ventricle in all the cats. Of the 4 cases, MRI revealed herniation of the cerebellum in 3 cats, an isolated fourth ventricle in 1 cat, severe hydrocephalus in 2 cats and brain masses in 1 cat. In this report, the cervical syringomyelia in these cats may have been due to formation of a secondary syrinx (enlargement of the central canal) as a result of blockage of flow in the outlet of the fourth ventricle caused by FIP encephalomyelitis or secondary cerebellar tonsillar herniation caused by increased intracranial pressure due to intracranial masses or may have been due to caudal compression of the cerebellum caused by increased intracranial pressure due to hydrocephalus.
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PMID:MRI of secondary cervical syringomyelia in four cats. 1972 60

Japanese encephalitis (JE) shows characteristic brain lesions, including bilateral thalamus, midbrain, internal capsule, basal ganglia, and occasionally involves an anterior horn cell. We encountered a case of a 44-year-old man who initially presented with encephalitis, which was finally diagnosed as Japanese encephalomyelitis with syringomyelia. The patient showed severe motor weakness followed by delayed recovery of functional motor activities. Cervical magnetic resonance imaging showed syrinx formation at the C5 level suggesting myelitis, and abnormal electromyographic findings were noted. Clinicians should consider the possibility that the spinal cord may be involved; an example would be syringomyelia due to myelitis in a case of JE presenting with severe and prolonged motor weakness.
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PMID:Prolonged Motor Weakness With Syringomyelia in Japanese Encephalitis: A Case Study. 2660 81