Multiple sclerosis differential diagnosis: Difference between revisions
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* '''syphilis:''' [[Neurosyphilis]], more commonly seen in [[HIV|HIV+]] patients can be in two forms. One can be seen in late secondary or early tertiary stages as meningovascular involvement and the other one can be seen in later stages as [[parenchymal]] involvement. Meningovascular lesions can present like a [[stroke]] while the other one cause gummas (contrast enhancing lesions). In [[CSF]] there are evidences of [[oligoclonal bands]], [[pleocytosis]] and elevated [[gammaglobulin]].<ref name="pmid16808833">{{cite journal |vauthors=Fadil H, Gonzalez-Toledo E, Kelley BJ, Kelley RE |title=Neuroimaging findings in neurosyphilis |journal=J Neuroimaging |volume=16 |issue=3 |pages=286–9 |year=2006 |pmid=16808833 |doi=10.1111/j.1552-6569.2006.00050.x |url=}}</ref> | * '''syphilis:''' [[Neurosyphilis]], more commonly seen in [[HIV|HIV+]] patients can be in two forms. One can be seen in late secondary or early tertiary stages as meningovascular involvement and the other one can be seen in later stages as [[parenchymal]] involvement. Meningovascular lesions can present like a [[stroke]] while the other one cause gummas (contrast enhancing lesions). In [[CSF]] there are evidences of [[oligoclonal bands]], [[pleocytosis]] and elevated [[gammaglobulin]].<ref name="pmid16808833">{{cite journal |vauthors=Fadil H, Gonzalez-Toledo E, Kelley BJ, Kelley RE |title=Neuroimaging findings in neurosyphilis |journal=J Neuroimaging |volume=16 |issue=3 |pages=286–9 |year=2006 |pmid=16808833 |doi=10.1111/j.1552-6569.2006.00050.x |url=}}</ref> | ||
* '''Progressive multifocal leukoencephalopathy:''' [[Progressive multifocal leukoencephalopathy]] ([[Progressive multifocal leukoencephalopathy|PML]]) is cause by activation of [[JC virus]] and is more commonly seen in [[immunocompromised]] patients. Some evidences shows the relation between [[Progressive multifocal leukoencephalopathy|PML]] and drug [[natalizumab]].<ref name="pmid15947082">{{cite journal |vauthors=Berger JR, Koralnik IJ |title=Progressive multifocal leukoencephalopathy and natalizumab--unforeseen consequences |journal=N. Engl. J. Med. |volume=353 |issue=4 |pages=414–6 |year=2005 |pmid=15947082 |doi=10.1056/NEJMe058122 |url=}}</ref> In [[MRI]] of [[Progressive multifocal leukoencephalopathy|PML]] patients we see multiple [[white matter]] lesions that can become confluent with no enhancement in T1. Diagnosis of [[Progressive multifocal leukoencephalopathy|PML]] is bases on detecting [[JC virus]] in [[CSF]].<ref name="pmid20299430">{{cite journal |vauthors=Bag AK, Curé JK, Chapman PR, Roberson GH, Shah R |title=JC virus infection of the brain |journal=AJNR Am J Neuroradiol |volume=31 |issue=9 |pages=1564–76 |year=2010 |pmid=20299430 |doi=10.3174/ajnr.A2035 |url=}}</ref><ref name="pmid20451009">{{cite journal |vauthors=Shah R, Bag AK, Chapman PR, Curé JK |title=Imaging manifestations of progressive multifocal leukoencephalopathy |journal=Clin Radiol |volume=65 |issue=6 |pages=431–9 |year=2010 |pmid=20451009 |doi=10.1016/j.crad.2010.03.001 |url=}}</ref> | * '''Progressive multifocal leukoencephalopathy:''' [[Progressive multifocal leukoencephalopathy]] ([[Progressive multifocal leukoencephalopathy|PML]]) is cause by activation of [[JC virus]] and is more commonly seen in [[immunocompromised]] patients. Some evidences shows the relation between [[Progressive multifocal leukoencephalopathy|PML]] and drug [[natalizumab]].<ref name="pmid15947082">{{cite journal |vauthors=Berger JR, Koralnik IJ |title=Progressive multifocal leukoencephalopathy and natalizumab--unforeseen consequences |journal=N. Engl. J. Med. |volume=353 |issue=4 |pages=414–6 |year=2005 |pmid=15947082 |doi=10.1056/NEJMe058122 |url=}}</ref> In [[MRI]] of [[Progressive multifocal leukoencephalopathy|PML]] patients we see multiple [[white matter]] lesions that can become confluent with no enhancement in T1. Diagnosis of [[Progressive multifocal leukoencephalopathy|PML]] is bases on detecting [[JC virus]] in [[CSF]].<ref name="pmid20299430">{{cite journal |vauthors=Bag AK, Curé JK, Chapman PR, Roberson GH, Shah R |title=JC virus infection of the brain |journal=AJNR Am J Neuroradiol |volume=31 |issue=9 |pages=1564–76 |year=2010 |pmid=20299430 |doi=10.3174/ajnr.A2035 |url=}}</ref><ref name="pmid20451009">{{cite journal |vauthors=Shah R, Bag AK, Chapman PR, Curé JK |title=Imaging manifestations of progressive multifocal leukoencephalopathy |journal=Clin Radiol |volume=65 |issue=6 |pages=431–9 |year=2010 |pmid=20451009 |doi=10.1016/j.crad.2010.03.001 |url=}}</ref> | ||
* '''HTLV-1 infection:''' Human T lymphotrophic virus, transmitted through sexual activity, can cause tropical spastic paraparesis.<ref name="pmid12619783">{{cite journal |vauthors=Howard AK, Li DK, Oger J |title=MRI contributes to the differentiation between MS and HTLV-I associated myelopathy in British Columbian coastal natives |journal=Can J Neurol Sci |volume=30 |issue=1 |pages=41–8 |year=2003 |pmid=12619783 |doi= |url=}}</ref> The involvement of spinal cord and MRI pattern of Tropical spastic paraparesis can mimic MS disease.<ref name="pmid16338746">{{cite journal |vauthors=Bagnato F, Butman JA, Mora CA, Gupta S, Yamano Y, Tasciyan TA, Solomon JM, Santos WJ, Stone RD, McFarland HF, Jacobson S |title=Conventional magnetic resonance imaging features in patients with tropical spastic paraparesis |journal=J. Neurovirol. |volume=11 |issue=6 |pages=525–34 |year=2005 |pmid=16338746 |doi=10.1080/13550280500385039 |url=}}</ref> In CSF we have positive HTLV-1 titer, lymphocytic pleocytosis, oligoclonal bands and high level of proteins.<ref name="pmid16434682">{{cite journal |vauthors=Umehara F, Tokunaga N, Hokezu Y, Hokonohara E, Yoshishige K, Shiraishi T, Okubo R, Osame M |title=Relapsing cervical cord lesions on MRI in patients with HTLV-I-associated myelopathy |journal=Neurology |volume=66 |issue=2 |pages=289 |year=2006 |pmid=16434682 |doi=10.1212/01.wnl.0000194219.89668.66 |url=}}</ref> | * '''HTLV-1 infection:''' [[Human T-lymphotropic virus|Human T]] lymphotrophic virus, transmitted through sexual activity, can cause [[tropical spastic paraparesis]].<ref name="pmid12619783">{{cite journal |vauthors=Howard AK, Li DK, Oger J |title=MRI contributes to the differentiation between MS and HTLV-I associated myelopathy in British Columbian coastal natives |journal=Can J Neurol Sci |volume=30 |issue=1 |pages=41–8 |year=2003 |pmid=12619783 |doi= |url=}}</ref> The involvement of [[spinal cord]] and [[MRI]] pattern of [[Tropical spastic paraparesis]] can mimic [[MS]] disease.<ref name="pmid16338746">{{cite journal |vauthors=Bagnato F, Butman JA, Mora CA, Gupta S, Yamano Y, Tasciyan TA, Solomon JM, Santos WJ, Stone RD, McFarland HF, Jacobson S |title=Conventional magnetic resonance imaging features in patients with tropical spastic paraparesis |journal=J. Neurovirol. |volume=11 |issue=6 |pages=525–34 |year=2005 |pmid=16338746 |doi=10.1080/13550280500385039 |url=}}</ref> In [[CSF]] we have positive [[Human T-lymphotropic virus|HTLV-1]] titer, [[Lymphocyte|lymphocytic]] [[pleocytosis]], [[oligoclonal bands]] and high level of proteins.<ref name="pmid16434682">{{cite journal |vauthors=Umehara F, Tokunaga N, Hokezu Y, Hokonohara E, Yoshishige K, Shiraishi T, Okubo R, Osame M |title=Relapsing cervical cord lesions on MRI in patients with HTLV-I-associated myelopathy |journal=Neurology |volume=66 |issue=2 |pages=289 |year=2006 |pmid=16434682 |doi=10.1212/01.wnl.0000194219.89668.66 |url=}}</ref> | ||
* '''HIV-Related Disorders of the CNS:''' | * '''HIV-Related Disorders of the CNS:''' HIV infection frequently involves CNS and can be the initial manifestation of the disease. In MRI there are white matter lesions and in CSF analysis there are high levels of proteins and cell counts but oligoclonal bands are rarely seen. | ||
==== Metabolic and genetic disorders: ==== | ==== Metabolic and genetic disorders: ==== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
- Overview
Differentiating multiple sclerosis from other diseases
Multiple sclerosis must be differentiated from other diseases that can mimic this disease clinically or radiologically such as:
Inflammatory/autoimmune conditions:
- systemic lupus erythematosus: Systemic lupus erythromatosus can cause neurological manifestations such as seizures, movement disorders, transverse myelitis, cranial and peripheral neuropathies and optic nerve involvement. In the brain MRI of SLE patients there are evidences of atrophy and subcortical white matter lesions. SLE is diagnosed based on systemic manifestations, present of oligoclonal bands and IgG in CSF and high titer of antinuclear antibodies.[1]
- Sjögren’s syndrome: Sjogren disease can cause neurological manifestations including cerebral vasculitis, myopathy, transverse myelitis and acute optic neuropathy. There are evidence of oligoclonal band and increased IgG in CSF and white matter lesions in MRI. Sicca syndrome, rheumatic manifestation and high titers of ANA, SSRo and SS-La will confirm the diagnosis.[2]
- Vasculitis: Wegener’s granulomatosis and polyarteritis nodosa are sometimes categorized as a differential diagnosis of MS, but the most common vasculitis which can mimic MS is isolated angitis of the central nervous system (IACNS).[3] IACNS is an inflammatory disease with an unknown cause. It affects small and medium sized arteries in the brain parenchyma and meninges. Neurological manifestation of this disease is headache, personality change, paresis, seizures, cranial neuropathy and intracerebral /subarachnoid hemorrhages.[4] There are monoclonal bands and increased protein and lymphocytic pleocytosis and IgG levels in the CSF of this patients. MRI may show patchy or diffuse increased signal in periventricular and subcortical white matter.[5] diagnosis is made by evidences of vasculitis changes in angiography or biopsy.[6]
- Neuro-behçet’s disease: Behcet’s disease is an idiopathic inflammatory disorder and can manifest as a triad of oral and genital ulcers and anterior uveitis. Lungs, gastrointestinal tract, joint and skin can be involved too. Rarely, neurological signs can be the first manifestation of the disease.[7] The most common neurological manifestation of behcet’s disease is psychiatric symptoms, intranuclear ophthalmoplegia, headache and sensory/motor deficits. The course of the disease can be relapsing remitting or progresive.[8] In the CSF specimen we can see high levels of protein, pleocytosis (granulocytic, unlike MS) and oligoclonal bands (which can be suppressed by corticosteroid treatment).[9] In MRI the most common involvement can be seen in brain stem and basal ganglia.[10]
- sarcoidosis: Sarcoidosis is an inflammatory disease with formation of non caseating epitheloid granulomata. It’s a multisystem disease but affects lungs more than other organs. There is 5-10% change of neurological involvement[11] and in 50 % of these patients neurological involvement can be the first sign or symptoms.[12] It usually affects cranial nerves, hypothalamus and pituitary gland. involvement of optic nerve, brain stem and spinal cord can mimic MS symptoms. In MRI we can see an isolated or diffuse lesion in brain parenchyma or even periventricular white matter lesion like MS.[13] CSF analysis can be very same to MS[14] but in sarcoidosis we have elevated amount of angiotensin converting enzyme.
- Antiphospholipid (Hughes) syndrome: In antiphospholipid syndrome, the presents of anticardiolipin and/or lupus anticoagulant can cause arterial and venous thrombosis.[15] It can cause neurological manifestations like transient ischemic attack, ischemic encephalopathy, thrombosis of cerebral veins, seizure, headache, guillain barre syndrome, dementia, chorea and optic nerve neuropathy.[16] In MRI there is evidence of white matter T2 hyperintense and/or cortical lesions. The latter is in favor of APS. In CSF analysis lack of oligoclonal bands is against the MS diagnosis. Differentiating MS from APS is so difficult that it’s recommended to treat MS patients for APS too.[17]
- Susac syndrome: Susac syndrome is an idiopathic disease that causes microangiopathy of brain, retina and cochlea arterioles. Involvement of this arterioles leads to visual disturbance, hearing loss and encephalopathy. In MRI there is white and gray matter lesions and leptomeningeal involvement. CSF analysis shows elevated protein level and pleocytosis.[18]
Infections:
- Lyme disease: Borrelia burgdorferi is transmitted trough tick bite and cause rash (erythema chronica migrans) typical for lyme disease. This disease can affect cranial nerves especially seventh nerve. It is usually easily differentiated from MS because of meningitis involvement in MRI and pleocytosis and high lyme titer in CSF.[19]
- syphilis: Neurosyphilis, more commonly seen in HIV+ patients can be in two forms. One can be seen in late secondary or early tertiary stages as meningovascular involvement and the other one can be seen in later stages as parenchymal involvement. Meningovascular lesions can present like a stroke while the other one cause gummas (contrast enhancing lesions). In CSF there are evidences of oligoclonal bands, pleocytosis and elevated gammaglobulin.[20]
- Progressive multifocal leukoencephalopathy: Progressive multifocal leukoencephalopathy (PML) is cause by activation of JC virus and is more commonly seen in immunocompromised patients. Some evidences shows the relation between PML and drug natalizumab.[21] In MRI of PML patients we see multiple white matter lesions that can become confluent with no enhancement in T1. Diagnosis of PML is bases on detecting JC virus in CSF.[22][23]
- HTLV-1 infection: Human T lymphotrophic virus, transmitted through sexual activity, can cause tropical spastic paraparesis.[24] The involvement of spinal cord and MRI pattern of Tropical spastic paraparesis can mimic MS disease.[25] In CSF we have positive HTLV-1 titer, lymphocytic pleocytosis, oligoclonal bands and high level of proteins.[26]
- HIV-Related Disorders of the CNS: HIV infection frequently involves CNS and can be the initial manifestation of the disease. In MRI there are white matter lesions and in CSF analysis there are high levels of proteins and cell counts but oligoclonal bands are rarely seen.
Metabolic and genetic disorders:
- Vitamin B12 deficiency:
- Lysosomal disorders:
- Adrenoleukodystrophy:
- Mitochondrial disorders:
- Clinically defined genetic disorders:
CNS lymphoma
spinal diseases
References
- ↑ Barned S, Goodman AD, Mattson DH (1995). "Frequency of anti-nuclear antibodies in multiple sclerosis". Neurology. 45 (2): 384–5. PMID 7854544.
- ↑ Alexander EL, Malinow K, Lejewski JE, Jerdan MS, Provost TT, Alexander GE (1986). "Primary Sjögren's syndrome with central nervous system disease mimicking multiple sclerosis". Ann. Intern. Med. 104 (3): 323–30. PMID 3946977.
- ↑ Calabrese LH, Furlan AJ, Gragg LA, Ropos TJ (1992). "Primary angiitis of the central nervous system: diagnostic criteria and clinical approach". Cleve Clin J Med. 59 (3): 293–306. PMID 1516217.
- ↑ Calabrese LH, Duna GF, Lie JT (1997). "Vasculitis in the central nervous system". Arthritis Rheum. 40 (7): 1189–201. doi:10.1002/1529-0131(199707)40:7<1189::AID-ART2>3.0.CO;2-4. PMID 9214418.
- ↑ Berger JR, Wei T, Wilson D (1998). "Idiopathic granulomatous angiitis of the CNS manifesting as diffuse white matter disease". Neurology. 51 (6): 1774–5. PMID 9855557.
- ↑ Moore PM (1989). "Diagnosis and management of isolated angiitis of the central nervous system". Neurology. 39 (2 Pt 1): 167–73. PMID 2915784.
- ↑ Kidd D, Steuer A, Denman AM, Rudge P (1999). "Neurological complications in Behçet's syndrome". Brain. 122 ( Pt 11): 2183–94. PMID 10545402.
- ↑ Akman-Demir G, Serdaroglu P, Tasçi B (1999). "Clinical patterns of neurological involvement in Behçet's disease: evaluation of 200 patients. The Neuro-Behçet Study Group". Brain. 122 ( Pt 11): 2171–82. PMID 10545401.
- ↑ Sharief MK, Hentges R, Thomas E (1991). "Significance of CSF immunoglobulins in monitoring neurologic disease activity in Behçet's disease". Neurology. 41 (9): 1398–401. PMID 1891089.
- ↑ Tali ET, Atilla S, Keskin T, Simonson T, Işik S, Yuh WT (1997). "MRI in neuro-Behçet's disease". Neuroradiology. 39 (1): 2–6. PMID 9121642.
- ↑ Stern BJ, Krumholz A, Johns C, Scott P, Nissim J (1985). "Sarcoidosis and its neurological manifestations". Arch. Neurol. 42 (9): 909–17. PMID 3896208.
- ↑ Sharma OP (1997). "Neurosarcoidosis: a personal perspective based on the study of 37 patients". Chest. 112 (1): 220–8. PMID 9228380.
- ↑ Smith AS, Meisler DM, Weinstein MA, Tomsak RL, Hanson MR, Rudick RA, Farris BK, Ransohoff RM (1989). "High-signal periventricular lesions in patients with sarcoidosis: neurosarcoidosis or multiple sclerosis?". AJR Am J Roentgenol. 153 (1): 147–52. doi:10.2214/ajr.153.1.147. PMID 2735279.
- ↑ McLean BN, Miller D, Thompson EJ (1995). "Oligoclonal banding of IgG in CSF, blood-brain barrier function, and MRI findings in patients with sarcoidosis, systemic lupus erythematosus, and Behçet's disease involving the nervous system". J. Neurol. Neurosurg. Psychiatry. 58 (5): 548–54. PMC 1073484. PMID 7745401.
- ↑ Hughes GR (1983). "Thrombosis, abortion, cerebral disease, and the lupus anticoagulant". Br Med J (Clin Res Ed). 287 (6399): 1088–9. PMC 1549319. PMID 6414579.
- ↑ Levine SR, Deegan MJ, Futrell N, Welch KM (1990). "Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases". Neurology. 40 (8): 1181–9. PMID 2381525.
- ↑ Ferreira S, D'Cruz DP, Hughes GR (2005). "Multiple sclerosis, neuropsychiatric lupus and antiphospholipid syndrome: where do we stand?". Rheumatology (Oxford). 44 (4): 434–42. doi:10.1093/rheumatology/keh532. PMID 15644391.
- ↑ Susac JO, Murtagh FR, Egan RA, Berger JR, Bakshi R, Lincoff N, Gean AD, Galetta SL, Fox RJ, Costello FE, Lee AG, Clark J, Layzer RB, Daroff RB (2003). "MRI findings in Susac's syndrome". Neurology. 61 (12): 1783–7. PMID 14694047.
- ↑ Drozdowski W (2006). "[Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?]". Przegl Epidemiol (in Polish). 60 Suppl 1: 39–45. PMID 16909774.
- ↑ Fadil H, Gonzalez-Toledo E, Kelley BJ, Kelley RE (2006). "Neuroimaging findings in neurosyphilis". J Neuroimaging. 16 (3): 286–9. doi:10.1111/j.1552-6569.2006.00050.x. PMID 16808833.
- ↑ Berger JR, Koralnik IJ (2005). "Progressive multifocal leukoencephalopathy and natalizumab--unforeseen consequences". N. Engl. J. Med. 353 (4): 414–6. doi:10.1056/NEJMe058122. PMID 15947082.
- ↑ Bag AK, Curé JK, Chapman PR, Roberson GH, Shah R (2010). "JC virus infection of the brain". AJNR Am J Neuroradiol. 31 (9): 1564–76. doi:10.3174/ajnr.A2035. PMID 20299430.
- ↑ Shah R, Bag AK, Chapman PR, Curé JK (2010). "Imaging manifestations of progressive multifocal leukoencephalopathy". Clin Radiol. 65 (6): 431–9. doi:10.1016/j.crad.2010.03.001. PMID 20451009.
- ↑ Howard AK, Li DK, Oger J (2003). "MRI contributes to the differentiation between MS and HTLV-I associated myelopathy in British Columbian coastal natives". Can J Neurol Sci. 30 (1): 41–8. PMID 12619783.
- ↑ Bagnato F, Butman JA, Mora CA, Gupta S, Yamano Y, Tasciyan TA, Solomon JM, Santos WJ, Stone RD, McFarland HF, Jacobson S (2005). "Conventional magnetic resonance imaging features in patients with tropical spastic paraparesis". J. Neurovirol. 11 (6): 525–34. doi:10.1080/13550280500385039. PMID 16338746.
- ↑ Umehara F, Tokunaga N, Hokezu Y, Hokonohara E, Yoshishige K, Shiraishi T, Okubo R, Osame M (2006). "Relapsing cervical cord lesions on MRI in patients with HTLV-I-associated myelopathy". Neurology. 66 (2): 289. doi:10.1212/01.wnl.0000194219.89668.66. PMID 16434682.