Multiple sclerosis differential diagnosis: Difference between revisions

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==== Inflammatory/autoimmune conditions: ====
==== Inflammatory/autoimmune conditions: ====
* '''systemic lupus erythematosus:''' [[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 pieces of evidence 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]].
* '''systemic lupus erythematosus:''' [[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 pieces of evidence 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]].<ref name="pmid7854544">{{cite journal |vauthors=Barned S, Goodman AD, Mattson DH |title=Frequency of anti-nuclear antibodies in multiple sclerosis |journal=Neurology |volume=45 |issue=2 |pages=384–5 |year=1995 |pmid=7854544 |doi= |url=}}</ref>
* '''Sjögren’s syndrome:''' [[Sjogren's Syndrome|Sjogren disease]] can cause [[neurological]] manifestations including cerebral [[vasculitis]], [[myopathy]], [[transverse myelitis]] and acute optic [[neuropathy]]. There are evidence of [[Oligoclonal bands|oligoclonal band]] and increased [[IgG]] in [[CSF]] and [[white matter]] lesions in [[MRI]]. [[Sicca syndrome]], rheumatic manifestation and high titers of [[Antinuclear antibodies|ANA]]. SSRo and SS-La will confirm the diagnosis.
* '''Sjögren’s syndrome:''' [[Sjogren's Syndrome|Sjogren disease]] can cause [[neurological]] manifestations including cerebral [[vasculitis]], [[myopathy]], [[transverse myelitis]] and acute optic [[neuropathy]]. There are evidence of [[Oligoclonal bands|oligoclonal band]] and increased [[IgG]] in [[CSF]] and [[white matter]] lesions in [[MRI]]. [[Sicca syndrome]], rheumatic manifestation and high titers of [[Antinuclear antibodies|ANA]]. SSRo and SS-La will confirm the diagnosis.<ref name="pmid3946977">{{cite journal |vauthors=Alexander EL, Malinow K, Lejewski JE, Jerdan MS, Provost TT, Alexander GE |title=Primary Sjögren's syndrome with central nervous system disease mimicking multiple sclerosis |journal=Ann. Intern. Med. |volume=104 |issue=3 |pages=323–30 |year=1986 |pmid=3946977 |doi= |url=}}</ref>
* '''Vasculitis:''' [[Wegener's granulomatosis|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). 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. There are monoclonal bands and increased protein and [[Lymphocyte|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]]. diagnosis is made by evidences of [[vasculitis]] changes in [[angiography]] or [[biopsy]].
* '''Vasculitis:''' [[Wegener's granulomatosis|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).<ref name="pmid1516217">{{cite journal |vauthors=Calabrese LH, Furlan AJ, Gragg LA, Ropos TJ |title=Primary angiitis of the central nervous system: diagnostic criteria and clinical approach |journal=Cleve Clin J Med |volume=59 |issue=3 |pages=293–306 |year=1992 |pmid=1516217 |doi= |url=}}</ref> 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.<ref name="pmid9214418">{{cite journal |vauthors=Calabrese LH, Duna GF, Lie JT |title=Vasculitis in the central nervous system |journal=Arthritis Rheum. |volume=40 |issue=7 |pages=1189–201 |year=1997 |pmid=9214418 |doi=10.1002/1529-0131(199707)40:7&lt;1189::AID-ART2&gt;3.0.CO;2-4 |url=}}</ref> There are monoclonal bands and increased protein and [[Lymphocyte|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]].<ref name="pmid9855557">{{cite journal |vauthors=Berger JR, Wei T, Wilson D |title=Idiopathic granulomatous angiitis of the CNS manifesting as diffuse white matter disease |journal=Neurology |volume=51 |issue=6 |pages=1774–5 |year=1998 |pmid=9855557 |doi= |url=}}</ref> diagnosis is made by evidences of [[vasculitis]] changes in [[angiography]] or [[biopsy]].<ref name="pmid2915784">{{cite journal |vauthors=Moore PM |title=Diagnosis and management of isolated angiitis of the central nervous system |journal=Neurology |volume=39 |issue=2 Pt 1 |pages=167–73 |year=1989 |pmid=2915784 |doi= |url=}}</ref>
* '''Neuro-behçet’s disease:''' [[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. The most common [[neurological]] manifestation of [[Behçet's disease|behcet’s disease]] is [[psychiatric]] symptoms, intranuclear ophthalmoplegia, [[headache]] and sensory/motor deficits. The course of the disease can be relapsing remitting or progresive. In the [[CSF]] specimen we can see high levels of protein, [[pleocytosis]] ([[Granulocyte|granulocyt]]<nowiki/>ic, unlike [[MS]]) and [[oligoclonal bands]] (which can be suppressed by [[corticosteroid]] treatment). In [[MRI]] the most common involvement can be seen in [[brain stem]] and [[basal ganglia]].
* '''Neuro-behçet’s disease:''' [[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.<ref name="pmid10545402">{{cite journal |vauthors=Kidd D, Steuer A, Denman AM, Rudge P |title=Neurological complications in Behçet's syndrome |journal=Brain |volume=122 ( Pt 11) |issue= |pages=2183–94 |year=1999 |pmid=10545402 |doi= |url=}}</ref> The most common [[neurological]] manifestation of [[Behçet's disease|behcet’s disease]] is [[psychiatric]] symptoms, intranuclear ophthalmoplegia, [[headache]] and sensory/motor deficits. The course of the disease can be relapsing remitting or progresive.<ref name="pmid10545401">{{cite journal |vauthors=Akman-Demir G, Serdaroglu P, Tasçi B |title=Clinical patterns of neurological involvement in Behçet's disease: evaluation of 200 patients. The Neuro-Behçet Study Group |journal=Brain |volume=122 ( Pt 11) |issue= |pages=2171–82 |year=1999 |pmid=10545401 |doi= |url=}}</ref> In the [[CSF]] specimen we can see high levels of protein, [[pleocytosis]] ([[Granulocyte|granulocyt]]<nowiki/>ic, unlike [[MS]]) and [[oligoclonal bands]] (which can be suppressed by [[corticosteroid]] treatment).<ref name="pmid1891089">{{cite journal |vauthors=Sharief MK, Hentges R, Thomas E |title=Significance of CSF immunoglobulins in monitoring neurologic disease activity in Behçet's disease |journal=Neurology |volume=41 |issue=9 |pages=1398–401 |year=1991 |pmid=1891089 |doi= |url=}}</ref> In [[MRI]] the most common involvement can be seen in [[brain stem]] and [[basal ganglia]].<ref name="pmid9121642">{{cite journal |vauthors=Tali ET, Atilla S, Keskin T, Simonson T, Işik S, Yuh WT |title=MRI in neuro-Behçet's disease |journal=Neuroradiology |volume=39 |issue=1 |pages=2–6 |year=1997 |pmid=9121642 |doi= |url=}}</ref>
* '''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 a 5-10% change of [[neurological]] involvement and in 50 % of these patients [[neurological]] involvement can be the first [[Sign (medical)|sign]] or [[symptoms]]. 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]]. [[CSF]] analysis can be very same to [[MS]] but in [[sarcoidosis]] we have elevated amount of [[Angiotensin-converting enzyme|angiotensin converting enzyme]].
* '''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 a 5-10% change of [[neurological]] involvement<ref name="pmid3896208">{{cite journal |vauthors=Stern BJ, Krumholz A, Johns C, Scott P, Nissim J |title=Sarcoidosis and its neurological manifestations |journal=Arch. Neurol. |volume=42 |issue=9 |pages=909–17 |year=1985 |pmid=3896208 |doi= |url=}}</ref> and in 50 % of these patients [[neurological]] involvement can be the first [[Sign (medical)|sign]] or [[symptoms]].<ref name="pmid9228380">{{cite journal |vauthors=Sharma OP |title=Neurosarcoidosis: a personal perspective based on the study of 37 patients |journal=Chest |volume=112 |issue=1 |pages=220–8 |year=1997 |pmid=9228380 |doi= |url=}}</ref> 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]].<ref name="pmid2735279">{{cite journal |vauthors=Smith AS, Meisler DM, Weinstein MA, Tomsak RL, Hanson MR, Rudick RA, Farris BK, Ransohoff RM |title=High-signal periventricular lesions in patients with sarcoidosis: neurosarcoidosis or multiple sclerosis? |journal=AJR Am J Roentgenol |volume=153 |issue=1 |pages=147–52 |year=1989 |pmid=2735279 |doi=10.2214/ajr.153.1.147 |url=}}</ref> [[CSF]] analysis can be very same to [[MS]]<ref name="pmid7745401">{{cite journal |vauthors=McLean BN, Miller D, Thompson EJ |title=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 |journal=J. Neurol. Neurosurg. Psychiatry |volume=58 |issue=5 |pages=548–54 |year=1995 |pmid=7745401 |pmc=1073484 |doi= |url=}}</ref> but in [[sarcoidosis]] we have elevated amount of [[Angiotensin-converting enzyme|angiotensin converting enzyme]].


* '''Antiphospholipid (Hughes) syndrome:''' In [[antiphospholipid syndrome]], the presence of [[Anti-cardiolipin antibodies|anticardiolipin]] and/or [[lupus anticoagulant]] can cause [[arterial]] and [[venous]] [[thrombosis]]. It can cause [[neurological]] manifestations like [[transient ischemic attack]], ischemic encephalopathy, [[thrombosis]] of cerebral veins, [[seizure]], [[headache]], [[Guillain-Barré syndrome|guillain barre syndrome]], [[dementia]], [[chorea]] and [[optic nerve]] [[neuropathy]]. 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.
* '''Antiphospholipid (Hughes) syndrome:''' In [[antiphospholipid syndrome]], the presence of [[Anti-cardiolipin antibodies|anticardiolipin]] and/or [[lupus anticoagulant]] can cause [[arterial]] and [[venous]] [[thrombosis]].<ref name="pmid6414579">{{cite journal |vauthors=Hughes GR |title=Thrombosis, abortion, cerebral disease, and the lupus anticoagulant |journal=Br Med J (Clin Res Ed) |volume=287 |issue=6399 |pages=1088–9 |year=1983 |pmid=6414579 |pmc=1549319 |doi= |url=}}</ref> It can cause [[neurological]] manifestations like [[transient ischemic attack]], ischemic encephalopathy, [[thrombosis]] of cerebral veins, [[seizure]], [[headache]], [[Guillain-Barré syndrome|guillain barre syndrome]], [[dementia]], [[chorea]] and [[optic nerve]] [[neuropathy]].<ref name="pmid2381525">{{cite journal |vauthors=Levine SR, Deegan MJ, Futrell N, Welch KM |title=Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases |journal=Neurology |volume=40 |issue=8 |pages=1181–9 |year=1990 |pmid=2381525 |doi= |url=}}</ref> 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.<ref name="pmid15644391">{{cite journal |vauthors=Ferreira S, D'Cruz DP, Hughes GR |title=Multiple sclerosis, neuropsychiatric lupus and antiphospholipid syndrome: where do we stand? |journal=Rheumatology (Oxford) |volume=44 |issue=4 |pages=434–42 |year=2005 |pmid=15644391 |doi=10.1093/rheumatology/keh532 |url=}}</ref>
* '''Susac syndrome:''' [[Susac's 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]].
* '''Susac syndrome:''' [[Susac's 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]].<ref name="pmid14694047">{{cite journal |vauthors=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 |title=MRI findings in Susac's syndrome |journal=Neurology |volume=61 |issue=12 |pages=1783–7 |year=2003 |pmid=14694047 |doi= |url=}}</ref>


==== Infections: ====
==== Infections: ====
* '''Lyme disease:''' [[Borrelia burgdorferi]] is transmitted through a [[tick]] bite and can cause rash ([[erythema chronica migrans]]) typical for [[lyme disease]]. This disease can affect [[cranial nerves]] especially [[Seventh cranial nerve|seventh nerve]]. It is usually easily differentiated from [[MS]] because of [[Meninges|meningitis]] involvement in [[MRI]] and [[pleocytosis]] as well as high lyme titer in [[CSF]].
* '''Lyme disease:''' [[Borrelia burgdorferi]] is transmitted through a [[tick]] bite and can cause rash ([[erythema chronica migrans]]) typical for [[lyme disease]]. This disease can affect [[cranial nerves]] especially [[Seventh cranial nerve|seventh nerve]]. It is usually easily differentiated from [[MS]] because of [[Meninges|meningitis]] involvement in [[MRI]] and [[pleocytosis]] as well as high lyme titer in [[CSF]].<ref name="pmid16909774">{{cite journal |vauthors=Drozdowski W |title=[Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?] |language=Polish |journal=Przegl Epidemiol |volume=60 Suppl 1 |issue= |pages=39–45 |year=2006 |pmid=16909774 |doi= |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 pieces of evidence of [[oligoclonal bands]], [[pleocytosis]], and elevated [[gammaglobulin]].
* '''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 pieces of evidence 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]]. 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 based on detecting [[JC virus]] in [[CSF]].
* '''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 based 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-lymphotropic virus|Human T]] lymphotrophic virus, transmitted through sexual activity, can cause [[tropical spastic paraparesis]]. The involvement of [[spinal cord]] and [[MRI]] pattern of [[Tropical spastic paraparesis]] can mimic [[MS]] disease. In [[CSF]] we have positive [[Human T-lymphotropic virus|HTLV-1]] titer, [[Lymphocyte|lymphocytic]] [[pleocytosis]], [[oligoclonal bands]] and high level of proteins.
* '''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]] infection frequently involves [[CNS]] and can be the initial manifestation of the disease. In an [[MRI]], there are [[white matter]] lesions. In a [[CSF]] analysis, there are high levels of proteins and cell counts but [[oligoclonal bands]] are rarely seen.  
* '''HIV-Related Disorders of the CNS:''' [[HIV]] infection frequently involves [[CNS]] and can be the initial manifestation of the disease. In an [[MRI]], there are [[white matter]] lesions. In a [[CSF]] analysis, there are high levels of proteins and cell counts but [[oligoclonal bands]] are rarely seen.<ref name="pmid3316921">{{cite journal |vauthors=McArthur JC |title=Neurologic manifestations of AIDS |journal=Medicine (Baltimore) |volume=66 |issue=6 |pages=407–37 |year=1987 |pmid=3316921 |doi= |url=}}</ref>


==== Metabolic and Genetic/Heriditary Disorders: ====
==== Metabolic and Genetic/Heriditary Disorders: ====
* '''Migraine:''' [[Migraine Headache|Migraine]] is a throbbing [[headache]], which worsens by sound and light. It can cause a variety of transient [[neurological]] manifestation including [[sensory loss]], [[visual loss]], ophtalmoparesis, and [[vertigo]]. These manifestations can occur before or with the [[migraine headache]] but in some cases, which we call “amigrainous migraine”, we have [[neurological]] problems without [[headache]]. In an [[MRI]] of these patients, we can see small areas of deep [[frontal]] [[white matter]] lesions.
* '''Migraine:''' [[Migraine Headache|Migraine]] is a throbbing [[headache]], which worsens by sound and light. It can cause a variety of transient [[neurological]] manifestation including [[sensory loss]], [[visual loss]], ophtalmoparesis, and [[vertigo]]. These manifestations can occur before or with the [[migraine headache]] but in some cases, which we call “amigrainous migraine”, we have [[neurological]] problems without [[headache]]. In an [[MRI]] of these patients, we can see small areas of deep [[frontal]] [[white matter]] lesions.<ref name="pmid1860133">{{cite journal |vauthors=Igarashi H, Sakai F, Kan S, Okada J, Tazaki Y |title=Magnetic resonance imaging of the brain in patients with migraine |journal=Cephalalgia |volume=11 |issue=2 |pages=69–74 |year=1991 |pmid=1860133 |doi=10.1046/j.1468-2982.1991.1102069.x |url=}}</ref><ref name="pmid16728687">{{cite journal |vauthors=Rocca MA, Ceccarelli A, Falini A, Colombo B, Tortorella P, Bernasconi L, Comi G, Scotti G, Filippi M |title=Brain gray matter changes in migraine patients with T2-visible lesions: a 3-T MRI study |journal=Stroke |volume=37 |issue=7 |pages=1765–70 |year=2006 |pmid=16728687 |doi=10.1161/01.STR.0000226589.00599.4d |url=}}</ref>
* '''Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy:'''
* '''Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy:'''
*  '''Leber’s hereditary optic neuropathy:''' [[Leber's hereditary optic neuropathy|Leber’s hereditary optic neuropathy]] is caused by [[Mitochondria|mitochondirial]] DNA [[mutation]]. It presents as acute bilateral [[blindness]]. The [[MRI]] finding of [[MS]] and [[Leber's hereditary optic neuropathy|LHON]] are alike and make it difficult to differentiate them.  
*  '''Leber’s hereditary optic neuropathy:''' [[Leber's hereditary optic neuropathy|Leber’s hereditary optic neuropathy]] is caused by [[Mitochondria|mitochondirial]] DNA [[mutation]]. It presents as acute bilateral [[blindness]].<ref name="pmid3201231">{{cite journal |vauthors=Wallace DC, Singh G, Lott MT, Hodge JA, Schurr TG, Lezza AM, Elsas LJ, Nikoskelainen EK |title=Mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy |journal=Science |volume=242 |issue=4884 |pages=1427–30 |year=1988 |pmid=3201231 |doi= |url=}}</ref> The [[MRI]] finding of [[MS]] and [[Leber's hereditary optic neuropathy|LHON]] are alike and make it difficult to differentiate them.<ref name="pmid8867076">{{cite journal |vauthors=Jansen PH, van der Knaap MS, de Coo IF |title=Leber's hereditary optic neuropathy with the 11 778 mtDNA mutation and white matter disease resembling multiple sclerosis: clinical, MRI and MRS findings |journal=J. Neurol. Sci. |volume=135 |issue=2 |pages=176–80 |year=1996 |pmid=8867076 |doi= |url=}}</ref>


* '''Vitamin B12 deficiency:''' [[Vitamin B12|B12]] deficiency can cause [[neurological]] manifestation including [[peripheral neuropathy]], [[optic neuropathy]], cervical myelopathy, and fatigue. [[MRI]] findings include contrast enhancement of posterior and lateral [[spinal cord]] columns preferably in cervical and thoracic levels.
* '''Vitamin B12 deficiency:''' [[Vitamin B12|B12]] deficiency can cause [[neurological]] manifestation including [[peripheral neuropathy]], [[optic neuropathy]], cervical myelopathy, and fatigue.<ref name="pmid8618695">{{cite journal |vauthors=Chatterjee A, Yapundich R, Palmer CA, Marson DC, Mitchell GW |title=Leukoencephalopathy associated with cobalamin deficiency |journal=Neurology |volume=46 |issue=3 |pages=832–4 |year=1996 |pmid=8618695 |doi= |url=}}</ref> [[MRI]] findings include contrast enhancement of posterior and lateral [[spinal cord]] columns preferably in cervical and thoracic levels.<ref name="pmid10068811">{{cite journal |vauthors=Locatelli ER, Laureno R, Ballard P, Mark AS |title=MRI in vitamin B12 deficiency myelopathy |journal=Can J Neurol Sci |volume=26 |issue=1 |pages=60–3 |year=1999 |pmid=10068811 |doi= |url=}}</ref>
* '''Lysosomal disorders:'''
* '''Lysosomal disorders:'''
# [[Metachromatic leukodystrophy]]: MLD is an [[autosomal recessive]] [[Lysosomal storage diseases|lysosomal storage disease]] that leads to accumulation of galactosyl sulfatide.
# [[Metachromatic leukodystrophy]]: MLD is an [[autosomal recessive]] [[Lysosomal storage diseases|lysosomal storage disease]] that leads to accumulation of galactosyl sulfatide.<ref name="pmid14086829">{{cite journal |vauthors=AUSTIN JH, BALASUBRAMANIAN AS, PATTABIRAMAN TN, SARASWATHI S, BASU DK, BACHHAWAT BK |title=A CONTROLLED STUDY OF ENZYMIC ACTIVITIES IN THREE HUMAN DISORDERS OF GLYCOLIPID METABOLISM |journal=J. Neurochem. |volume=10 |issue= |pages=805–16 |year=1963 |pmid=14086829 |doi= |url=}}</ref><ref name="pmid14338983">{{cite journal |vauthors=MEHL E, JATZKEWITZ H |title=EVIDENCE FOR THE GENETIC BLOCK IN METACHROMATIC LEUCODYSTROPHY (ML) |journal=Biochem. Biophys. Res. Commun. |volume=19 |issue= |pages=407–11 |year=1965 |pmid=14338983 |doi= |url=}}</ref>
# [[Fabry’s disease]]: [[X-linked]] disease with impaired activity of a-galactosidase leading to accommodation of globotriaosylceramide in many organs including [[ganglion cells]] of the [[autonomic nervous system]].
# [[Fabry’s disease]]: [[X-linked]] disease with impaired activity of a-galactosidase leading to accommodation of globotriaosylceramide in many organs including [[ganglion cells]] of the [[autonomic nervous system]].<ref name="pmid6023233">{{cite journal |vauthors=Brady RO, Gal AE, Bradley RM, Martensson E, Warshaw AL, Laster L |title=Enzymatic defect in Fabry's disease. Ceramidetrihexosidase deficiency |journal=N. Engl. J. Med. |volume=276 |issue=21 |pages=1163–7 |date=May 1967 |pmid=6023233 |doi=10.1056/NEJM196705252762101 |url=}}</ref><ref name="pmid5411915">{{cite journal |vauthors=Kint JA |title=Fabry's disease: alpha-galactosidase deficiency |journal=Science |volume=167 |issue=3922 |pages=1268–9 |date=February 1970 |pmid=5411915 |doi= |url=}}</ref>
# [[Krabbe’s disease]]: [[Autosomal recessive]] disease with impaired activity of galactocerebrosidase leading to destruction of [[CNS]] and [[PNS]] [[myelin]] and axonal degeneration.
# [[Krabbe’s disease]]: [[Autosomal recessive]] disease with impaired activity of galactocerebrosidase leading to destruction of [[CNS]] and [[PNS]] [[myelin]] and axonal degeneration.<ref name="pmid5271165">{{cite journal |vauthors=Suzuki K, Suzuki Y |title=Globoid cell leucodystrophy (Krabbe's disease): deficiency of galactocerebroside beta-galactosidase |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=66 |issue=2 |pages=302–9 |date=June 1970 |pmid=5271165 |pmc=283044 |doi= |url=}}</ref>
* '''Adrenoleukodystrophy:''' [[Adrenoleukodystrophy|ALD]] disease causes accumulation of [[long chain fatty acids]]. [[X-linked]] type of this disease ([[adrenomyeloneuropathy]]) will cause [[spinal cord]] disease and peripheral [[neuropathy]] and can be considered as a [[differential diagnosis]] of [[MS]] disease.
* '''Adrenoleukodystrophy:''' [[Adrenoleukodystrophy|ALD]] disease causes accumulation of [[long chain fatty acids]]. [[X-linked]] type of this disease ([[adrenomyeloneuropathy]]) will cause [[spinal cord]] disease and peripheral [[neuropathy]] and can be considered as a [[differential diagnosis]] of [[MS]] disease.<ref name="pmid3978476">{{cite journal |vauthors=Dooley JM, Wright BA |title=Adrenoleukodystrophy mimicking multiple sclerosis |journal=Can J Neurol Sci |volume=12 |issue=1 |pages=73–4 |year=1985 |pmid=3978476 |doi= |url=}}</ref>
* '''mitochondrial encephalopathy epilepsy lactic acidosis and stroke:''' One of the [[mitochondrial diseases]] that can categorized as a [[MS]] [[differential diagnosis]] in [[Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes|mitochondrial encephalopathy epilepsy lactic acidosis and stroke]] ([[MELAS]]). The manifestations include: [[Seizures]], exercise intolerance, [[limb]] [[weakness]], [[stroke]] like episodes, [[hemiparesis]] and [[hemianopia]]. There are evidences of calcium deposition in [[caudate nucleus]] and [[globus pallidus]] in [[CT scan]] and cortical involvement in [[MRI]] imaging.
* '''mitochondrial encephalopathy epilepsy lactic acidosis and stroke:''' One of the [[mitochondrial diseases]] that can categorized as a [[MS]] [[differential diagnosis]] in [[Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes|mitochondrial encephalopathy epilepsy lactic acidosis and stroke]] ([[MELAS]]). The manifestations include: [[Seizures]], exercise intolerance, [[limb]] [[weakness]], [[stroke]] like episodes, [[hemiparesis]] and [[hemianopia]]. There are evidences of calcium deposition in [[caudate nucleus]] and [[globus pallidus]] in [[CT scan]] and cortical involvement in [[MRI]] imaging.<ref name="pmid2398945">{{cite journal |vauthors=Rosen L, Phillips S, Enzmann D |title=Magnetic resonance imaging in MELAS syndrome |journal=Neuroradiology |volume=32 |issue=2 |pages=168–71 |year=1990 |pmid=2398945 |doi= |url=}}</ref>


==== CNS lymphoma ====
==== '''CNS lymphoma''' ====
[[Primary CNS lymphoma]] is mostly [[diffuse large B-cell lymphoma]] ([[Diffuse large B cell lymphoma|DLBCL]]). These patients more commonly present with [[neurological]] manifestation rather than [[B symptoms]]. In [[MRI]] evaluation, because of high cell count and scant [[cytoplasm]] lesions become isotense to hypointense on T2. In [[CSF]] analysis, there are increased number of [[WBC]] and proteins, low levels of glucose and positive [[cytology]] for cells with enlarged [[nucleus]] and course [[chromatin]].
[[Primary CNS lymphoma]] is mostly [[diffuse large B-cell lymphoma]] ([[Diffuse large B cell lymphoma|DLBCL]]).<ref name="pmid9166827">{{cite journal |vauthors= |title=A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project |journal=Blood |volume=89 |issue=11 |pages=3909–18 |year=1997 |pmid=9166827 |doi= |url=}}</ref> These patients more commonly present with [[neurological]] manifestation rather than [[B symptoms]].<ref name="pmid10659013">{{cite journal |vauthors=Bataille B, Delwail V, Menet E, Vandermarcq P, Ingrand P, Wager M, Guy G, Lapierre F |title=Primary intracerebral malignant lymphoma: report of 248 cases |journal=J. Neurosurg. |volume=92 |issue=2 |pages=261–6 |year=2000 |pmid=10659013 |doi=10.3171/jns.2000.92.2.0261 |url=}}</ref> In [[MRI]] evaluation, because of high cell count and scant [[cytoplasm]] lesions become isotense to hypointense on T2.<ref name="pmid15925998">{{cite journal |vauthors=Küker W, Nägele T, Korfel A, Heckl S, Thiel E, Bamberg M, Weller M, Herrlinger U |title=Primary central nervous system lymphomas (PCNSL): MRI features at presentation in 100 patients |journal=J. Neurooncol. |volume=72 |issue=2 |pages=169–77 |year=2005 |pmid=15925998 |doi=10.1007/s11060-004-3390-7 |url=}}</ref> In [[CSF]] analysis, there are increased number of [[WBC]] and proteins, low levels of glucose and positive [[cytology]] for cells with enlarged [[nucleus]] and course [[chromatin]].<ref name="pmid16083830">{{cite journal |vauthors=Fitzsimmons A, Upchurch K, Batchelor T |title=Clinical features and diagnosis of primary central nervous system lymphoma |journal=Hematol. Oncol. Clin. North Am. |volume=19 |issue=4 |pages=689–703, vii |year=2005 |pmid=16083830 |doi=10.1016/j.hoc.2005.05.009 |url=}}</ref>


==== spinal diseases ====
==== spinal diseases ====
[[Dural arteriovenous fistula]] and true malformations can be mistaken with [[MS]] since they can all cause thoracic [[myelopathy]].
[[Dural arteriovenous fistula]] and true malformations can be mistaken with [[MS]] since they can all cause thoracic [[myelopathy]].<ref name="pmid8271855">{{cite journal |vauthors=Deen HG, Nelson KD, Gonzales GR |title=Spinal dural arteriovenous fistula causing progressive myelopathy: clinical and imaging considerations |journal=Mayo Clin. Proc. |volume=69 |issue=1 |pages=83–4 |date=January 1994 |pmid=8271855 |doi= |url=}}</ref>


==References==
==References==

Revision as of 21:07, 4 December 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Irfan Dotani

Overview

Multiple sclerosis must be differentiated from other diseases that can mimic this disease clinically or radiologically such as Inflammatory/autoimmune conditions, Infections,Metabolic, and Genetic/Heriditary Disorders such as CNS lymphoma and spinal diseases.

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:

Infections:

Metabolic and Genetic/Heriditary Disorders:

  1. Metachromatic leukodystrophy: MLD is an autosomal recessive lysosomal storage disease that leads to accumulation of galactosyl sulfatide.[34][35]
  2. Fabry’s disease: X-linked disease with impaired activity of a-galactosidase leading to accommodation of globotriaosylceramide in many organs including ganglion cells of the autonomic nervous system.[36][37]
  3. Krabbe’s disease: Autosomal recessive disease with impaired activity of galactocerebrosidase leading to destruction of CNS and PNS myelin and axonal degeneration.[38]

CNS lymphoma

Primary CNS lymphoma is mostly diffuse large B-cell lymphoma (DLBCL).[41] These patients more commonly present with neurological manifestation rather than B symptoms.[42] In MRI evaluation, because of high cell count and scant cytoplasm lesions become isotense to hypointense on T2.[43] In CSF analysis, there are increased number of WBC and proteins, low levels of glucose and positive cytology for cells with enlarged nucleus and course chromatin.[44]

spinal diseases

Dural arteriovenous fistula and true malformations can be mistaken with MS since they can all cause thoracic myelopathy.[45]

References

Template:WH Template:WS

  1. ↑ Barned S, Goodman AD, Mattson DH (1995). "Frequency of anti-nuclear antibodies in multiple sclerosis". Neurology. 45 (2): 384–5. PMID 7854544.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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&lt;1189::AID-ART2&gt;3.0.CO;2-4. PMID 9214418.
  5. ↑ 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.
  6. ↑ Moore PM (1989). "Diagnosis and management of isolated angiitis of the central nervous system". Neurology. 39 (2 Pt 1): 167–73. PMID 2915784.
  7. ↑ Kidd D, Steuer A, Denman AM, Rudge P (1999). "Neurological complications in Behçet's syndrome". Brain. 122 ( Pt 11): 2183–94. PMID 10545402.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ Stern BJ, Krumholz A, Johns C, Scott P, Nissim J (1985). "Sarcoidosis and its neurological manifestations". Arch. Neurol. 42 (9): 909–17. PMID 3896208.
  12. ↑ Sharma OP (1997). "Neurosarcoidosis: a personal perspective based on the study of 37 patients". Chest. 112 (1): 220–8. PMID 9228380.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ Drozdowski W (2006). "[Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?]". Przegl Epidemiol (in Polish). 60 Suppl 1: 39–45. PMID 16909774.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ 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.
  27. ↑ McArthur JC (1987). "Neurologic manifestations of AIDS". Medicine (Baltimore). 66 (6): 407–37. PMID 3316921.
  28. ↑ Igarashi H, Sakai F, Kan S, Okada J, Tazaki Y (1991). "Magnetic resonance imaging of the brain in patients with migraine". Cephalalgia. 11 (2): 69–74. doi:10.1046/j.1468-2982.1991.1102069.x. PMID 1860133.
  29. ↑ Rocca MA, Ceccarelli A, Falini A, Colombo B, Tortorella P, Bernasconi L, Comi G, Scotti G, Filippi M (2006). "Brain gray matter changes in migraine patients with T2-visible lesions: a 3-T MRI study". Stroke. 37 (7): 1765–70. doi:10.1161/01.STR.0000226589.00599.4d. PMID 16728687.
  30. ↑ Wallace DC, Singh G, Lott MT, Hodge JA, Schurr TG, Lezza AM, Elsas LJ, Nikoskelainen EK (1988). "Mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy". Science. 242 (4884): 1427–30. PMID 3201231.
  31. ↑ Jansen PH, van der Knaap MS, de Coo IF (1996). "Leber's hereditary optic neuropathy with the 11 778 mtDNA mutation and white matter disease resembling multiple sclerosis: clinical, MRI and MRS findings". J. Neurol. Sci. 135 (2): 176–80. PMID 8867076.
  32. ↑ Chatterjee A, Yapundich R, Palmer CA, Marson DC, Mitchell GW (1996). "Leukoencephalopathy associated with cobalamin deficiency". Neurology. 46 (3): 832–4. PMID 8618695.
  33. ↑ Locatelli ER, Laureno R, Ballard P, Mark AS (1999). "MRI in vitamin B12 deficiency myelopathy". Can J Neurol Sci. 26 (1): 60–3. PMID 10068811.
  34. ↑ AUSTIN JH, BALASUBRAMANIAN AS, PATTABIRAMAN TN, SARASWATHI S, BASU DK, BACHHAWAT BK (1963). "A CONTROLLED STUDY OF ENZYMIC ACTIVITIES IN THREE HUMAN DISORDERS OF GLYCOLIPID METABOLISM". J. Neurochem. 10: 805–16. PMID 14086829.
  35. ↑ MEHL E, JATZKEWITZ H (1965). "EVIDENCE FOR THE GENETIC BLOCK IN METACHROMATIC LEUCODYSTROPHY (ML)". Biochem. Biophys. Res. Commun. 19: 407–11. PMID 14338983.
  36. ↑ Brady RO, Gal AE, Bradley RM, Martensson E, Warshaw AL, Laster L (May 1967). "Enzymatic defect in Fabry's disease. Ceramidetrihexosidase deficiency". N. Engl. J. Med. 276 (21): 1163–7. doi:10.1056/NEJM196705252762101. PMID 6023233.
  37. ↑ Kint JA (February 1970). "Fabry's disease: alpha-galactosidase deficiency". Science. 167 (3922): 1268–9. PMID 5411915.
  38. ↑ Suzuki K, Suzuki Y (June 1970). "Globoid cell leucodystrophy (Krabbe's disease): deficiency of galactocerebroside beta-galactosidase". Proc. Natl. Acad. Sci. U.S.A. 66 (2): 302–9. PMC 283044. PMID 5271165.
  39. ↑ Dooley JM, Wright BA (1985). "Adrenoleukodystrophy mimicking multiple sclerosis". Can J Neurol Sci. 12 (1): 73–4. PMID 3978476.
  40. ↑ Rosen L, Phillips S, Enzmann D (1990). "Magnetic resonance imaging in MELAS syndrome". Neuroradiology. 32 (2): 168–71. PMID 2398945.
  41. ↑ "A clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma. The Non-Hodgkin's Lymphoma Classification Project". Blood. 89 (11): 3909–18. 1997. PMID 9166827.
  42. ↑ Bataille B, Delwail V, Menet E, Vandermarcq P, Ingrand P, Wager M, Guy G, Lapierre F (2000). "Primary intracerebral malignant lymphoma: report of 248 cases". J. Neurosurg. 92 (2): 261–6. doi:10.3171/jns.2000.92.2.0261. PMID 10659013.
  43. ↑ Küker W, Nägele T, Korfel A, Heckl S, Thiel E, Bamberg M, Weller M, Herrlinger U (2005). "Primary central nervous system lymphomas (PCNSL): MRI features at presentation in 100 patients". J. Neurooncol. 72 (2): 169–77. doi:10.1007/s11060-004-3390-7. PMID 15925998.
  44. ↑ Fitzsimmons A, Upchurch K, Batchelor T (2005). "Clinical features and diagnosis of primary central nervous system lymphoma". Hematol. Oncol. Clin. North Am. 19 (4): 689–703, vii. doi:10.1016/j.hoc.2005.05.009. PMID 16083830.
  45. ↑ Deen HG, Nelson KD, Gonzales GR (January 1994). "Spinal dural arteriovenous fistula causing progressive myelopathy: clinical and imaging considerations". Mayo Clin. Proc. 69 (1): 83–4. PMID 8271855.
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