Temporary Demyelinating Diseases?

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Temporary Demyelinating Diseases?

Postby Lyon » Sat Jun 03, 2006 9:35 am

oo
Last edited by Lyon on Fri May 06, 2011 9:24 pm, edited 1 time in total.
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demyeli-nation

Postby jimmylegs » Sat Jun 03, 2006 10:06 am

there are a few monophasic illnesses or nutritional deficiencies that can involve demyelination.

here's one:

Neurol India. 2002 Sep;50(3):238-43.
Acute disseminated encephalomyelitis.
Murthy JM.

Department of Neurology, The Institute of Neurological Sciences, CARE Hospitals, Nampally, Hyderabad - 500 001, India. drjmk@sol.net.in

Acute disseminated encephalomyelitis (ADEM) is an uncommon inflammatory demyelinating disease of the central nervous system. The true incidence of the disease in India is undetermined and is likely to be more frequent than reported, as the common antecedent events, exanthematous fevers and Semple antirabies vaccination, which predispose to ADEM, are still prevalent. The existing evidence suggests that ADEM results from a transient autoimmune response towards myelin or other self-antigens, possibly via molecular mimicry, or by non-specific activation of auto-reactive T cell clones. ADEM is a monophasic illness with favourable long-term outcome. Involvement of neuroaxis is variable and can be diffuse or multifocal and site restricted. Magnetic resonance imaging (MRI) is highly sensitive in detecting white matter lesions and the lesions described are rather extensive and subcortical in location. Involvement of the deep gray matter, particularly basal ganglia, is more frequent. Oligoclonal bands in CSF are usually absent. No therapy has been established by controlled trials in ADEM. Use of high-dose methylprednisolone, plasma exchange, and IVIG are based on the analogy of the pathogenesis of ADEM with that of multiple sclerosis (MS). Differentiation of ADEM from the first attack of MS is important from prognostic as well as therapeutic point of view. However, in the absence of biological marker, at times differentiation of ADEM from the initial presentation of MS may not be possible even by combination of clinical, CSF analysis, and MRI. This differentiation is more relevant to India where the incidence of MS is low.

****
http://www.neuroweb.us/Chapters/acute%2 ... y/text.htm

Acute disseminated encephalomyelitis (ADEM): The age of onset is highly variable 2nd to 6th decades. ADEM follows viral exanthema, respiratory and other infections (measles, rubella, corona virus, mycoplasma, chlamydia, campylobacter, streptococcus, influenza, parainfluenza, CMV, EBV, HSV-6, chicken pox, HIV and hepatitis A and B) or vaccinations for smallpox, rabies (Semple vaccin), mumps, hepatitis B, diphtheria-tetanus-pertusis, polio, rubella, influenza and live measles in almost 50% of patients. However in over 45% of cases ADEM is reported to be idiopathic. The clinical course is highly variable, ranging from a slow progression over weeks to a fulminant course over hours to days. Characteristic clinical features include a monophasic focal or multifocal neurologic disturbances particularly sensory deficits and pyramidal motor signs, brainstem dysfunction, and less frequently visual field defects, aphasia, ataxia, myelitis and signs of acute meningoencephalitis with meningismus, alteration in consciousness, focal and generalized seizures, and psychosis. Optic neuritis is rare. Maximal deficits are reached within several days, weeks or even months. CSF shows pleocytosis (up to 150-200 WBCs) in 80%, protein level is usually elevated, but generally not higher than 180 mg/dl, and OCB may be found. In the acute phase, CSF studies may show increased cell counts (initially neutrophils predominance) with elevated protein and decreased glucose levels as sign of active inflammatory process. Despite this, CSF may be normal in up to 20% of cases. Finding the causative agent is most often elusive. Screening for antibodies against HSV, EBV, CMV, VZV, Coxsackie, adenovirus, enterovirus and B. Burgerdorfi in CSF is advised. MRI reveals large, confluent asymmetric multifocal areas of increased signal intensity on T2-weighted sequences, affecting predominantly white matter in addition to brainstem and thalami (unlike MS). Unlike in MS, corpus callosum is rarely affected . Mass effect can be present and florid gadolinium enhancement can be found. With respect to enhancement and unlike in MS, all lesions should have the same enhancement properties. CSF and MRI can however not fully discriminate between ADEM and MS. 50% of patients with ADEM have MRI features of MS. In addition 35% of patients with ADEM develop clinical definite MS over a mean period of 3 year. In 26% of patients MRI lesions resolve. Dramatic improvement of neurological deficit is observed with high-dose corticosteroids (methylprednisolone 1g over 30 minutes for 5 days). In addition, iv immunoglobulin have been proven to be effective. The definitive diagnosis of ADEM requires biopsy. ADEM usually resolves in a few weeks or months and complete recovery occurs in about 50%. Mortality is 10-30%. Differential diagnosis should include leucodystrophies, multiple cerebral emboli, abscesses, HIV encephalopathy, fungal and bacterial infections (including Lyme disease, brucellosis), postmalarial neurological syndrome (endemic area), toxic encephalopathies, metabolic (including mitochondrial) encephalopathies (e.g. Marchiafava-Bignami disease), RPLE, inflammatory (neurosarcoidosis) and autoimmune diseases (SLE, APLS, neuroBehçet), vasculitis (PACNS), PMFLE, multifocal glioma, CNS lymphoma, Devic syndrome and "Acute MS", which is never monophasic, except Schilder disease and Balo excentric sclerosis. Related disorders are AHLE, Bickerstaff brainstem encephalitis, optic neuritis, ATM, cerebellitis and multiphasic form of ADEM and MS.

i like this, because to me it means i might have it not MS. i mean, it even says you can have OCBs in the CSF! i also think i have subacute combined degeneration of the spinal cord already (another source of demyelination, this time from my cobalamin deficiency), and the acute progression in january could have been related to my hep b vaccine for my trip. (BUT, i don't know exactly how my serum looked compared to CSF with respect to OCBs, and i don't know exactly how serum would look if you were getting csf ocbs after a hep b vaccine) anyway, i also don't have any of the typical ms optic problems. mind you, i think i have lesions in or near the corpus callosum but i'd have to double check my mris.

anyway so ya! there are definitely other demyelinating things out there that can be fixed!
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Postby Lyon » Sat Jun 03, 2006 10:30 am

oo
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Postby Lyon » Sat Jun 03, 2006 10:41 am

oo
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date of dx

Postby jimmylegs » Sat Jun 03, 2006 12:08 pm

january. still in complete denial!
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Postby Lyon » Sat Jun 03, 2006 12:48 pm

oo
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denial

Postby jimmylegs » Sat Jun 03, 2006 1:22 pm

ugh the first little while is surely a bugger on the emotional state. poor wifey :(

every day i desperately searched for shreds of hope and over time, i found them. time will tell if i need to deal with the real MonSter, or if i can squeak past it with this warning episode.
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Re: denial

Postby Lyon » Sat Jun 03, 2006 2:08 pm

oo
Last edited by Lyon on Fri May 06, 2011 9:23 pm, edited 1 time in total.
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end of ms

Postby jimmylegs » Sat Jun 03, 2006 2:21 pm

i hope you're right lyon. i'll try the grape koolaid cure too, just ruling out coffee therapy at the moment ;)
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Postby Lyon » Sat Jun 03, 2006 2:33 pm

oo
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