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Acute demyelination

Cerebral WM changes (WMC) are found in a number of diseases of adulthood, such as the debated Binswanger s disease, multiple sclerosis, acute demyelinating encephalomyelitis, posterior reversible leukoencephalopathy syndrome, cerebral anoxia, leukodystrophies, and mitochondrial encephalopathies, among others. The term leukoaraiosis (LA) is applied for nonspecific WMC, primarily in the elderly, that cannot be attributed to a... [Pg.149]

A 45-year-old woman with a history of epilepsy developed a lumbosacral acute demyelinating polyneuropathy 1 month after her second hepatitis B immunization (22). She had an uncommon syndrome that combined demyelinating and axonal features confined to the lumbosacral roots whose relation to GuiUain-Barre syndrome was unclear. Viral or bacterial causes of the disease could not be found. [Pg.1603]

Creange A, Temam G, Lefaucheur JP. Lumbosacral acute demyelinating polyneuropathy following hepatitis B vaccination. Autoimmunity 1999 30(3) 143-6. [Pg.1607]

Another report included seven cases of acute disseminated encephalomyelitis after administration of Japanese encephalitis vaccine between 1968 and 1990 (10). Three other cases of neurological complications after the use of Japanese encephalitis vaccine have been reported in Denmark. In two cases the clinical picture was consistent with acute demyelinating encephalomyelitis (SEDA-21, 334). [Pg.1957]

Jung et al. (1997) described a patient with a DVA and an acute demyelination around the draining vein. However, there is no evidence that DVA may... [Pg.10]

R.Y. (2010) Compression induces acute demyelination and potassium chatmel exposure in spinal cord. /. Neurotrauma, 27, 1109—1120. doi 10.1089/neu.2010.1271... [Pg.583]

Peripheral neuropathy is degeneration of peripheral nerves. Because motor and sensory axons tun in the same nerves, usually both motor and sensory functions are affected in this disease. Neuropathies may be either acute (e.g., Charcot-Marie-Tooth disease) or chronic (e.g., Guillain-Barre syndrome) and are categorized as demyelinating or axonal. [Pg.938]

Seroconversion neuropathy Inflammatory demyelinating neuropathy Early pre-AIDS Acute Generalized systemic dlness, mononeuropathies Immune dysfunction... [Pg.53]

Acute inflammatory demyelinating polyradiculopathy Early pre-AIDS Acute Motor to sensory signs NCS show demyelinating features Immune dysfunction complement/macrophage-mediated demyelinating neuropathy... [Pg.53]

Opportunistic infection, eg. CMV Progressive polyradiculopathy AIDS Acute, subacute Multiple, asymmetric mononeuropathies, usually painful CMV infection, Schwann cell infection demyelinating neuropathy... [Pg.53]

Uhthoff s phenomenon Acute worsening of multiple sclerosis symptoms on exposure to heat because high body temperatures may exceed the capacitance of the demyelinated nerve and conduction may fail. [Pg.1578]

Acute inflammatoiy demyelinating polyneuropathy is a common cause of reversible paralysis. Acute inflammatory demyelinating polyneuropathy (AIDP), the classic form of the Guillain-Barre syndrome, often begins a week or two after recovery from cytomegalovirus, Epstein-Barr virus or Mycoplasma infection. Patients present with rapidly advancing symmetrical weakness, loss of deep tendon reflexes, often with distal numbness, and limb or back pain. Cerebrospinal fluid (CSF) protein concentration is elevated, but in most cases there is little or no increase in number of inflammatory cells in the CSF. This albumino-cytologic dissociation contrasts with the elevation of both... [Pg.621]

Diabetes mellitus is the most common cause of peripheral neuropathy in the United States. Approximately half of all diabetics demonstrate evidences of neuropathy. The usual clinical pattern is that of a slowly progressive, mixed sensorimotor and autonomic polyneuropathy. More acute, asymmetrical motor neuropathies are also seen, usually affecting the lumbosacral plexus, particularly in older persons with type 2 (non-insulin-dependent) diabetes mellitus. Patients with diabetes mellitus are also prone to develop isolated palsies of cranial nerve III or VII, and there is a high incidence of asymptomatic focal demyelin-ation in the distal median nerve. [Pg.624]

Magira, E. E., Papaioakim, M., Nachamkin, I. et al. Differential distribution of HLA-DQP/DRP epitopes in the two forms of Guillain-Barre syndrome, acute motor axonal neuropathy and acute inflammatory demyelinating... [Pg.626]

A number of animal diseases caused by viruses involve primary demyelination and often are associated with inflammation. These diseases are studied as animal models, which may provide clues about how a viral infection could lead to immune-mediated demyelination in humans [1, 5, 6]. Canine distemper virus causes a demyelinating disease, and the lesions in dog brain show a strong inflammatory response with some similarities to acute disseminated encephalomyelitis in man [ 1 ]. Visna is a slowly progressive demyelinating disease of sheep caused by a retrovirus [ 1 ]. [Pg.641]

A number of OPC are capable of rendering a delayed neurotoxic effect (DNE). This effect becomes apparent gradually, after a certain latent period (usually 14 to 21 days, sometimes 1 to 5 years after the acute poisoning survived) and is characterized clinically by the development of ataxia, muscular weakness, paresis and paralysis of the extremities. Morphologically, it is characterized by fiber demyelinization of spinal pathways and peripheral nerves. Till present time, near 40,000 cases have been described, when paresis and paralysis developed in human beings as a result of their exposure to OPC (TOCP, mipaphox, chloropyrophos, trichlorfon, etc.) [1],... [Pg.103]

Effect of Dose and Duration of Exposure on Toxicity. The severity of neurological effects in humans and animals after acute oral exposure to cyanide is dose-related (Chen and Rose 1952 Lasch and El Shawa 1981). Central nervous system effects have been observed following acute-duration exposures (Levine and Stypulkowski 1959a) and chronic-duration exposures (Hertting et al. 1960), via the inhalation and oral routes. Necrosis is the most prevalent central nervous system effect following acute-duration exposure to high concentrations of cyanide, whereas demyelination is observed in animals that survive repeated exposure protocols (Bass 1968 Ibrahim et al. 1963). [Pg.85]


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Demyelination

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