HappyPoet wrote:Differential diagnosis of MS - most extensive list I've ever found:
http://www.medmerits.com/index.php/arti ... lerosis/P8
Postinfectious and postvaccinal encephalomyelitis follow inflammation-induced sensitization to myelin antigens. These reactions cause inflammatory demyelination that is localized (eg, transverse myelitis, optic neuritis) or diffuse (eg, encephalomyelitis). Symptoms often develop after upper respiratory tract infections (usually viral or mycoplasma) or vaccinations, leading to acute disseminated encephalomyelitis. Oligoclonal bands in CSF are less common than in multiple sclerosis and, if present, often disappear. MRI lesions should all be of the same age, but several weeks after onset, partially-resolved lesions can appear to be different ages. The perivascular inflammation and demyelination is similar to the pathology of multiple sclerosis, but these fever-associated disorders are monophasic (Tselis and Lisak 1995).
CADASIL, Binswanger disease, hemiplegic migraine, Sjögren syndrome, and Behçet disease can cause episodic, multifocal central nervous system lesions that can be confused with multiple sclerosis clinically and on MRI.
“Phenocopies” of multiple sclerosis appear on MRI scans. CADASIL, hypertensive vascular disease, Susac syndrome, leukodystrophies, vanishing white matter disease, Alexander disease, sarcoid, and migraine all overlap with the MRI appearance of multiple sclerosis.
Multiple sclerosis eventually develops in 20% to 33% of ADEM patients. Thus, most patients with ADEM (66% to 80%) do not develop multiple sclerosis and should not be treated for multiple sclerosis when oligoclonal bands are negative.
Amyloid angiopathy causes cerebral microhemorrhages but also a leukoencephalopathy that involves the U-fibers. Iron in lesions can be seen on T2*-weighted MRI.
Copper deficiency causes a progressive myelopathy and neuropathy, often related to gastrointestinal disorders, post-gastric bypass, and zinc excess (similar to the cuprizone model in rodents).
...Folate deficiency can cause encephalopathy and spastic paraparesis.
...Vitamin B12 deficiency causes subacute combined degeneration with centrocecal scotomata, optic atrophy, MRI lesions around the corpus callosum (not Dawson fingers), partially reversible leukoencephalopathy, and long tract signs from cord degeneration.
Vitamin E deficiency causes ataxia, myelopathy, and neuropathy
Devic disease, or neuromyelitis optica, is a demyelinating, sometimes necrotic, inflammatory disease of the spinal cord and the optic nerves. Attacks are more severe and more frequent than in multiple sclerosis. In Asia and South America and in Native American Indians, Devic disease is more common than multiple sclerosis. In Europe and the United States, multiple sclerosis is far more common.
.....Rituximab was therapeutic in a series of 8 patients (Cree et al 2005). Plasmapheresis may also reduce symptoms. Interferon therapy, however, may cause worsening (Javed and Reder 2006; Wang et al 2006; Warabi et al 2007), but because this disease is so active, apparently adverse interferon effects could be spurious (Javed 2011).
Inflammatory bowel disease with brain lesions.
Parasites can migrate into the CNS and cause focal symptoms and must be excluded in patients from endemic areas, eg, cysticercosis.
Cancer--primary and secondary brain tumors. Hemophagocytic lymphohistiocytosis, Langerhans cell histiocytosis, and neoplastic angioendotheliosis can be confused with multiple sclerosis.
....Storage disorders and other genetic diseases versus childhood multiple sclerosis. Leukodystrophies are usually confluent and bilateral on MRI. Juvenile metachromatic leukodystrophy and late onset Tay-Sachs disease have MRI signatures that could be confused with multiple sclerosis. Also to be considered are adult polyglucosan body disease (glycogen-branching enzyme mutation causes accumulation of polyglucosan bodies throughout the nervous system and cerebral myelin loss),....
Susac syndrome. Retrobulbar vasculopathy of Susac causes encephalopathy, branch (distal) retinal artery occlusions, and hearing loss (Weinshenker and Lucchinetti 1998). It affects 20- to 40-year-old women and is associated with headaches, hearing loss, tinnitus, pseudobulbar speech, and encephalopathy. There are microangiopathic infarcts in gray and white matter, and bilateral branch artery occlusions in the retina. MRI shows many multifocal white matter lesions of the central corpus callosum, plus lesions in deep gray, posterior fossa, brain parenchyma, and occasionally the leptomeninges. Acute large “snowballs” and multiple older small “punched-out” areas riddle the central corpus callosum (Susac et al 2003). Intravenous immunoglobulin and corticosteroids improve hearing and MRI.
Vaccination (polio and possibly influenza). Associations reported in a few papers are likely spurious, as the vast majority of studies find no link. Some find a 3-fold increase in the incidence of multiple sclerosis after vaccination with recombinant hepatitis B vaccine, but not with vaccines against other viruses (Hernan et al 2004), yet others report no increase.
Viruses or viral encephalitis (measles, mumps, rubella, chickenpox, cytomegalovirus, hepatitis A and B, herpes zoster vasculopathy, HHV-6 encephalomyelitis, acute HIV infection, HTLV-I (also associated with Sjögren syndrome), infectious mononucleosis, Japanese encephalitis (a flavivirus with bilateral thalamic lesions and polio-like flaccid paralysis), post-measles autoimmunity and subacute sclerosing panencephalitis, poliomyelitis (central cord lesions on MRI), West Nile virus (flavivirus) with a polio-like presentation. Japanese macaque encephalitis causes multifocal inflammatory demyelinating plaques of varying ages. It is caused by a gamma-2 herpesvirus with 50% homology to human Kaposi sarcoma-associated virus.
Also to be considered are adult polyglucosan body disease (glycogen-branching enzyme mutation causes accumulation of polyglucosan bodies throughout the nervous system and cerebral myelin loss),....
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