1. Multiple Sclerosis :
Diagnosis & Differential Diagnosis
Dr.Ram Raut
JR III (Medicine)
BJMC & SGH Pune

2. Epidemiology
• The most common progressive neurologic
disease of young adults.
• Risk Factors:
–
–
–
–
–
–
–
Female sex, young age
White race
Northern latitude (USA)
High socioeconomic status
Scandinavian ancestry
Month of birth effect
Vitamin D deficiency

3. Diagnosis of Multiple sclerosis
• No single test to diagnose multiple sclerosis.
• Diagnosis relies on recognition of clinical patterns of the disease
as well as exclusion of possible mimics.
• Waxing & waning neurological deficit is the hall mark of disease.
• Supported by MRI studies, CSF & Evoked potential studies.

4. REQUIREMENTS FOR DIAGNOSIS
• Clinically definite MS requires 2 or more episodes of symptoms & 2 or more
signs that reflect pathology in anatomically non-contagious white matter
tracts of the CNS.
• Symptoms must last >24 h &
• Occur as distinct episodes separated by a month or more
• At least 1 of the 2 signs must be present on neurological examination &
• Other may be documented by abnormal paraclinical tests (MRI, VEPs)
• Second clinical event may be supported solely by paraclinical information,
usually the development of new focal white matter lesions on MRI.
• If there is gradual progression of disability > 6 months, & no superimposed
relapses, documentation of Intrathecal IgG synthesis may be used.

5. Clinical Features of Multiple Sclerosis
SYMPTOM
PERCENTAGE
SYMPTOM
PERCENTAGE
Sensory disturbance
34
Facial weakness
1
Weakness
22
Dysarthria
0.6
Visual loss
13
Hearing loss
0.6
Ataxia
11
Cramps
0.6
Diplopia
8
Loss of consciousness
0.6
Vertigo
4.3
Psychiatric symptoms
0.3
Fatigue
2
Poor memory
0.3
Facial pain
2
Dysphagia
0.3
Headache
2
Loss of taste
0.3
Bladder dysfunction
1

6. Ancillary Symptoms of Multiple Sclerosis
1) Heat sensitivity e.g. Uhthoff’s symptom
2) Lhermitte’s symptom
3) Paroxysmal symptoms e.g. paroxysmal tonic seizures,
Dysarthria, sensory symptoms.
4) Trigeminal neuralgia (tic douloereux), hemifacial spasm,
gloosopharyngeal neuralgia.
5) Facial myokymia

7. Clinical course of Multiple Sclerosis

8. Natural History Of Multiple Sclerosis

9. Clinically Isolated Syndrome
• The first demyelinating event that is suggestive of
MS is called CIS.
• Typical course –
60-85% cases of RRMS will eventually progress to
SPMS .The median time is 10 yrs .
• Benign MS –
• Acute Fulminant MS (Marburg variant)

10. Salient Features of PPMS vs RRMS
Differentiating point
Incidence
RRMS
PPMS
Visual loss common
Rare
Equal
30 yrs
Disease burden
Typically asymmetric
weakness /gait disturbance
Female preponderance
Rate of progress
10%
Variable
Symptoms at Onset
85%
40 yrs
slow
50% faster than RRMS
Fewer than RRMS & SPMS

11. KURTZKE’S EDSS

12. DIAGNOSTIC TESTS
MRI
Evoked
potentials
CSF

13. MRI in MS
• Characteristic abnormalities found in >95 % .
• Although sensitive , not specific (many D/Ds for same lesions)
• To study evolution of existing lesions & occurrence of new
lesions.
• Detection of subclinical activity.
• DIS- Simultaneous presence of asymptomatic Gd enhancing &
other non enhancing lesions.
• To evaluate response to treatment.

14. Brain MRI in MS
• Leakage of IV Gd in
parenchyma - Marker of
inflammation.
T2-weighted (A) and post-contrast T1-weighted (B) MR images. In A, many whitematter lesions . Two of them enhanced in B with gadolinium-DTPA. This is a sign of
increased blood–bran barrier permeability and continuing inflammation.
• Plaques - as hyper intense
lesion on T2 & proton density
images, & FLAIR images. signifies demyelination
• 1/3rd of the T2 lesions are hypo
intense on T1 (Black Holes)
- signifies irreversible axonal
loss

15. Brain MRI in MS
• On Gadolinium contrast- acute plaques
show contrast enhancement .
- Homogenous or ring pattern &
Persist for 3 weeks
• On sagittal view ,lesions are linear or
flame like streaks perpendicular to the
ventricular surfaces… s/o perivenous
demyelination (Dawson’s fingers).
• Brain atrophy greater than expected for
the age.
• Wallerian Degeneration (rare)

16. MRI lesions of MS in Brain
• SiteMultifocal lesions 1) WML (corpus Callosum, brainstem, cerebellum),
2) GML ( thalami, Basal ganglia),
3) cortical lesions (type 1,2,3).
• SizeLarger than 6 mm, round /ovoid having “fuzzy borders”.
• Burden of the disease
Total volume of T2 weighted signal abnormalities &/or
atrophy.

17. Spinal cord MRI in MS
• Plaques can be seen in the
parenchyma of the cord on T2 /Gd
enhanced T1 imaging.
• Typically oriented longitudinally
along the cord, often posteriorly,
spanning 2-3 segments.
• Focal cord swelling may be present

18. Diagnosis: Imaging
FLAIR
T2
T1
T1 Post C
FLAIR
Characteristic locations of MS lesions on MRI Brain
1) Periventricular-lateral/temporal horns
2) Corpus Callosum/ Callosal-Septal
Interface
3) Sub cortical (best seen on FLAIR)
4) Optic Nerves/Visual Pathways
5) Brain stem/Cerebellar Peduncles
Cortex, and Deep Gray Matter are Rare at 5% at 1.5T; although at 7T in most patients
gray matter/cortical lesions will be visible. Majority of lesions do not enhance.

19. Newer MRI techniques
• MTR (magnetization transfer ratio) imaging- able to
distinguish demyelination from edema.
• Proton magnetic resonance spectroscopic imaging
(MRSI)- quantitate molecules like N-acetyl aspartate
a marker of axonal integrity.

20. Evoked potentials
• Afferent (visual, auditory, somatosensory)
or efferent (motor) CNS pathways.
• Computer averaging to measure CNS electric potentials evoked by
selected peripheral nerves or of the brain.
• Provide most information when pathways studied are clinically
uninvolved.
• Abnormalities occur in 75-90%.
• Not specific but marked asymmetric delay in latency of a specific
EP component is s/o demyelination.

21. EVOKED POTENTIALS
• VER (visual evoked response)
-75% abnormal
regardless of optic neuritis.
• BAER (brainstem auditory
evoked response)
- 30% abnormal
• SSER (somatosensory evoked
response)
- 80% abnormal
Helps distinguish peripheral
from central lesions
Characteristic findings in MS
• Asymmetric delay of
the P-100 potential &
conduction block
(when acute ON)
• Delays or block of
1) N-20 potential of
median nerve
2) p37 potential of
tibial nerve

22. CSF in MS
• Abnormal in 85-90 % cases of MS.
• Mononuclear cell pleocytosis (>5 & <50 cells)
• Increased levels of intrathecally synthesized IgG
• Total CSF protein Normal
Intrathecal synthesis of
IgG can occur in other
conditions like syphilis,
SSPE, Viral encephalitis,
& Lyme disease.
• CSF IgG index = (Ratio of CSF IgG to albumin)/(ratio of serum IgG to
albumin)
• Oligoclonal banding (OCB) by agarose gel electrophoresis.
• Paired serum samples studied to exclude Non CNS origin of any OCBs in
CSF.

24. 2010 Revised McDonald MS Diagnostic Criteria
Diagnosis of MS requires elimination of more likely diagnoses
& demonstration of Dissemination of lesions in space ( in space ( DIS) and time (DIT)
Clinical
Attacks
Lesions
Additional criteria for Diagnosis
2 or more
Objective clinical evidence of ≥ 2 lesions
or
objective clinical evidence of 1 lesion with
reasonable historical evidence of a prior
attack
None.
Clinical evidence alone will suffice, additional
evidence desirable but must be consistent
with MS
2 or more
Objective clinical evidence of 1 lesion
DIS ; OR await further clinical attack
implicating a different CNS site
1
1
0
(progressio
n from
onset)
Objective clinical evidence of ≥2 lesions
Objective clinical evidence of 1 lesion
DIT ; OR await a second clinical attack.
DIS ; OR await further clinical attack
implicating a different CNS site AND
DIT ; OR await a second clinical attack
One year of disease progression (retrospective or prospective) AND at least 2 of the
following 3 :
DIS in brain based on ≥ 1 T2 lesion in periventricular, juxtacortical or infratentorial region ;
DIS in the spinal cord based on ≥ 2 T2 lesions; or
positive CSF (e/o OCB and/or elevated IgG index)

25. PARA CLINICAL EVIDENCE IN MS DIAGNOSIS
EVIDENCE FOR DISSEMINATION OF
LESIONS IN SPACE (DIS)
EVIDENCE FOR DISSEMINATION OF
LESIONS IN TIME (DIT)
≥ 1 T2 lesion in at least 2 of 4 areas of
CNS (periventricular, juxtacortical,
infratentorial, spinal cord.
•A new T2 &/or Gd enhancing
lesion(s) on f/u MRI with ref to a
baseline scan irrespective of the
timing of baseline MRI or
• Gd enhancement not required for DIS
•Simultaneous presence of
• If brainstem or spinal cord syndrome, asymptomatic Gd enhancing & non
the symptomatic lesions are excluded & enhancing lesions at any time
do not contribute to the lesion count.
Evidence for Positive CSF
Oligoclonal IgG bands in CSF
( & not serum) or Elevated IgG index
These criteria are developed thru the
consensus of the inter national panel
on the diagnosis of MS

26. Differential Diagnosis Of Multiple sclerosis
•
•
•
•
•
•
•
•
•
Acute disseminated encephalomyelitis
(ADEM)
Antiphospholipid antibody syndrome
Behcet’s disease
Cerebral autosomal dominant
arteriopathy, sub cortical infarcts, &
leucoencephalopathy (CADASIL)
Congenital leucodystrophies
(adrenoleucodystrophy, metachromatic
leucodystrophy)
HIV infection
Ischemic optic neuropathy (arteritic &
non arteritic)
Lyme disease
Mitochondrial encephalopathy with lactic
acidosis & stroke (MELAS)
•
•
•
•
•
•
•
•
•
•
Neoplasms (lymphoma, glioma,
meningioma)
Sarcoid
Sjogren’s syndrome
Stroke & ischemic cerebrovascular
diseases
Syphillis
SLE & related collagen vascular
diseases
Tropical spastic paraparesis (HTLV
I/II infection)
Vascular malformations (especially
spinal dural AV fistulas)
Vasculitis (Primary CNS or other)
Vitamin B12 deficiency

27. When to consider alternative diagnosis
•
•
•
•
•
•
•
•
•
•
•
•
Fever
Concomitant systemic disease.
Dermatologic involvement other than psoriasis
Endocrine disease other than autoimmune thyroid disease
Mucosal ulcerations
Sicca
Bone lesions
Tendon Xanthomas
Hematologic manifestations
Systemic thrombosis
Recurrent spontaneous abortions
Onset after 50 yrs of age

28. Neurologic features that warrant further diagnostic considerations
•
•
•
•
•
•
•
•
•
Peripheral neuropathy
Myopathy
Hearing loss
Multiple cranial neuropathy
Neuropsychiatric illness other
than unipolar depression
Prominent cognitive symptoms
from onset
CVST/Cortical & lacunar infarcts
Extrapyramidal features
Amyotrophy
•Meningismus/ meningeal
enhancement on imaging
•Unilateral lesions
•Myelopathy alone
•Normal brain MRI
•Retinopathy
•CNS hemorrhage
•Simultaneous enhancement
of all lesions

29. MS Variants
1)
Marburg variant (Acute MS)
2)
Balo’s Concentric Sclerosis
3)
Disseminated subpial demyelination
4)
Schilder’s Disease –
A rare progressive demyelinating disorder (Myelinoclastic
diffuse sclerosis) which usually begins in childhood. It is not same as
Addison-Schilder disease (adrenoleucodystrophy).
5)
Mass Lesion
6)
Neuromyelitis Optica (Devic Syndrome)
7)
Opticospinal MS
8)
Tumefactive MS

30. NEUROMYELITIS OPTICA (NMO)
NMO (Devic’s syndrome) -An aggressive inflammatory disorder
of acute ON & myelitis.
• Attacks of ON can be bilateral (unilateral in MS)
• Myelitis can be severe & transverse (rare in MS) & typically longitudinally
extensive involving 3 or more contagious vertebral segments
• Lesions - Hypothalamus, periaqueductal brainstem, or ‘cloud like WML’ in
cerebral hemispheres are suggestive of NMO.
• Spinal cord MRI – focal enhancing region of swelling & cavitation extending
over 3 or more spinal cord segments & often in central gray matter.
• Up to 40 % have systemic autoimmune disorder. Other causes are infection,
para neoplastic or idiopathic.
• Aquaporin-4 auto-antibody against water channel protein is present in 60 70%

31. Progressive Myelopathy
• Typically presents as asymmetric progressive Myelopathy with insidious
onset.
• Onset usually older than RRMS
• M:f= 1:1
• CSF analysis is essential for diagnosis. But 10-15 % will not have
increased IT IgG.
• D/Ds – neoplasm, AV malformations, B12 def, Sarcoid, Sjogren's, HSP,
Syphillis, HIV, HTLV.
• Esp. Dural AVM in old people having progressive Myelopathy.
• Accordingly Invx include- MRI Spine, B12 levels, MMA, Homocystine,
Sr.ACE levels, RF, VLFA, Anti-SSA & B, ANA, VDRL, FTPA, HIV & HTLV .

32. Progressive cognitive impairment
with symmetric white matter disease.
• In adults, leucodystrophies often present with progressive cognitive
impairment.
• WML similar to MS are seen on imaging .
• But these are more confluent & symmetric. (focal plaques in MS)
• D/Ds- adrenoleucodystrophy, Metachromatic leucodystrophy, Krabbe’s
disease, MTHFR def, Biotinidase def, CADASIL.
• Some leucodystrophies are associated with peripheral neuropathy.
• NCV with nerve biopsy can narrow the diagnostic considerations.

33. Cranial neuropathies
• Ms can affect cranial nerves like optic nerve & can cause facial paresis.
• Similar features are seen in Behcet’s, Sjogren’s, skull base infiltrating
tumors, TB, Sarcoidosis.
• Behcet’s syndrome – Cranial neuropathies, oro-genital ulcerations,
dermatographia, elevated ESR.
• Sjogren’s syndrome- sicca syndrome, confirmed by biopsy of minor
salivary or lacrimal gland.
• MRI/ CT are useful in skull base infiltrating tumors.
• CSF analysis, cytology, PCR, & culture can identify neoplastic cells or
mycobacterium.

34. Acute transverse myelitis (ATM)
• Spinal cord inflammation resulting in
motor & sphincter impairment with
neurological level.
Spinal Imaging - To exclude
compressive etiology, tumors &
AVM.
• Usually bilateral & tends to be more
severe.
Brain imaging - Look for
disseminated demyelination.
• Causes – HZV, HSV, collagen vascular
diseases, sarcoidosis & idiopathic.
CSF analysis & blood studies- For
e/o systemic inflammation &
infection.
• ATM can be a presenting feature of
NMO.
• Anti NMO IgG antibody should be
checked if there is longitudinally
extensive myelitis
Infarcts of anterior spinal artery,
may be distinguished by preserved
dorsal column signs & CSF analysis
(no leucocytosis & no IT IgG
synthesis.

35. The Mimics
Patients may have radiologic findings consistent with MS
But have symptoms that are not.
Another distinguishing feature of MS mimickers is that standard MS
treatments often fail.

36. Acute disseminated Encephalomyelitis (ADEM)
•
•
•
•
•
•
Monophasic illness. Rapid onset.
Multifocal inflammation & demyelination.
Children>adults
Altered sensorium & seizures are common.(rare in MS)
MRI - Multiple lesions often contrast enhancing (acute)
CSF- Lymphocytic pleocytosis, protein elevation, IT IgG
Causes
Post infectious –
Measles, chickenpox, mumps,
mononucleosis, influenza,
parainfluenza, rubella, mycoplasma.
Autoimmune
response to MBP
(Molecular mimicry)
Post vaccination.
-Rabies, smallpox.
Hurst disease- Type of ADEM with acute Fulminant hemorrhagic leucoencephalitis.

37. Inflammatory
Acute Disseminated Encephalomyelitis
FLAIR
FLAIR
T2
ADEM is characterized by supratentorial and infratentorial deep white matter lesions with poorly
defined margins and periventricular sparing. Bilateral gray nuclei lesions in the basal ganglia and
thalamus.
Diffuse thoracic spinal cord lesions will be over 2 segments long.
More likely to enhance and be peripheral not periventricular.
Differentiation of MS from ADEM is more likely if 2 of 3 criteria are met; absent diffuse bilateral
lesion pattern, presence of black holes, and 2 or more periventricular lesions.
T2

38. Inflammatory
Neuromyelitis Optica
FLAIR
FLAIR
FLAIR
T2
T1 Post C
Linear lesions can be found in the medulla and the spinal cord (spanning at least three vertebral
segments and frequently causing cord expansion).
Where MS lesions contain a central vein and a hypo-intense rim, NMO lesions are frequently
observed in the deep white matter, brainstem, and adjacent to the third and fourth ventricles .
Optical coherence tomography reveals more nerve fiber damage than in MS, and cortical lesions are
uncommon in NMO.

39. Inflammatory
Behcet’s
FLAIR
FLAIR
T2
T1 Post C
Lesions are commonly found in the brainstem, white matter (periventricular and
superficial), internal capsule, basal ganglia, and thalamus.
Brain atrophy as well as changes in lesion shape and size, and 7% have enhancing lesions
makes differentiation from MS difficult, to add the course can be monophasic,
polyphasic or progressive.
Brainstem atrophy may predict a progressive course in neuro-Behcet’s. Lesions in the
spinal cord (spanning multiple segments in the cervical or thoracic spine) are rare.

40. Inflammatory
Sarcoid
T1 Post C
T1 Post C
T1 Post C
T1 Post C
Multiple hyper intense intraparachymal lesions.
Many cases will display chronic basilar leptomeningitis a finding not seen in MS,
Enhancement along the Virchow-Robin spaces appears linear. Hydrocephalus is a
common finding.
Leptomeningeal enhancement along the third cranial nerve, and spinal nerve roots.
Enhancement of the lacrimal gland (indicated by the arrow).
T1 Post C

41. Susac's syndrome
• Susac syndrome is a microangiopathy (Retinocochleocerebral Vasculopathy).
• Characterized by encephalopathy, branch retinal artery occlusions & hearing loss.
T1 Post C
FLAIR
FLAIR
Small white matter lesions are observed on MRI.
Lesions like “black holes” of MS, but have a more prominent hypo intensity on T1.
T2 hyper intense lesions are seen in central corpus Callosum and the deep gray matter.
Parenchymal and leptomeningeal enhancement (not seen in MS).
Diffusion tensor imaging shows fiber tract loss. Cortical atrophy also has been observed.

42. Inflammatory
Systemic Lupus Erythematosus
T2
FLAIR
MRA/MRV
MTT
Focal & punctate hyper-intensities in white and/or gray matter are indicative of vasculitis.
Unlike MS, white matter lesions in vasculitis are less periventricular & more peripheral .
MRA can show occlusions leading to abnormal blood flow.
Perfusion images, particularly MTT studies, can be more sensitive.
White matter hyper-intensities are more common if neuropsychiatric symptoms present.

43. Inflammatory
Chronic Inflammatory Demyelinating Polyneuropathy
FLAIR
FLAIR
T1 Post C
Schwann cell proliferation causes peripheral nerve enlargement (onion bulb).
Hypertrophic spinal nerves can be detected on MRI.

44. Balos Concentric Sclerosis: A MS Variant
Demyelinating disease similar to standard MS, in which demyelinated tissues
form concentric layers.
T2
T2
T2*
Concentric rings are seen on T2 imaging.
T1 Gadolinium enhancing rings are visible in areas of increased BBB permeability.
Micro hemorrhages and ectatic veins can be observed on 7T SWI.

45. Infectious
Human Immunodeficiency Virus
T2
T2
T2
T2
•Periventricular white matter lesions can be observed on T2 images. Atrophy is a
HIV's entrance into the brain causes CNS inflammation via cytokine release. The virus attacks oligodendrocytes,
predominant finding. inflammation HAART, atrophyas gliosis and myelin pallor.changes can
causing demyelination. Chronic Despite results in changes such & inflammatory CD4+ count can be
correlated to the lesion patterns on MRI, such as gray and white matter loss and increases in venticular and sulcal CSF.
progress. Hepatitis C is also believed to play a role in white matter lesions. Gliosis and inflammation lead to
Coinfection with
cognitive impairment and eventually dementia. The blood brain barrier prevents the passage of medications, making
•HIVtreatment difficult. exhibit DTI abnormalities like in MS .
patients also
•Basal ganglia involvement is more in HIV than MS.
•The axial spine image shows enhancement in the corticospinal tracts bilaterally.
• Diffuse white matter T2 signal abnormality (myelin pallor), often seen in PLHIV.

46. Infectious
Progressive Multifocal Leucoencephalopathy
FLAIR
T2
White matter hyper intensities observed particularly in FLAIR and T2 sequences.
T2 imaging shows increased signal radiating away from the ventricles along with
corpus Callosum like MS, or can be more of a T2 pallor like in HIV .
Hypo intense lesions on T1 images are similar to “black holes” seen in MS.
Sub cortical U fibers are also affected in PML but cortical ribbon and gray matter
are spared.

47. Infectious
Neuroborreliosis (Lyme)
FLAIR
T1 Post C
T1 Post C
The tickborne spirochete, Borrelia burgdorfera, causes Lyme disease. Patients present with a range of non-specific
symptoms (headache, fatigue, myalgia). Patients may also present with multiple episodes of neurological deficits. The
classic hallmark of Lyme disease is erythema migrans. Although 10-15% of patients have some sort of CNS
involvement, the disease rarely affects the spinal cord. Antibiotic treatment is highly effective. Increased total protein,
pleocytosis, and Bb (Borrelia burgdorfera) antibodies are present in CSF. The hallmarks of neuroborreliosis are
meningitis, cranial neuritis and radiculoneuritis. Facial palsy is also common. Patients may also present with optic
neuritis.
DWI and FLAIR imaging will show ischemic lesions.
MRA or Trans-cranial Doppler will show vasculitis changes and TIA-like
lesions.
Meningeal and cranial nerve III enhancement are seen .

48. Infectious
Toxoplasmosis
FLAIR
FLAIR
T2
FLAIR
Multifocal hyper common CNS infection inin the white matter HIV patients infected with the parasite will
Toxoplasmosis is the intense lesions AIDS patients. Almost half of on T2 imaging.
eventually develop toxoplasmosis. Approximately 20% - 70% of the American population is seropositive for Toxoplasma
gondii. Patients present with headache and focal neurological deficits.
Ring enhancing target-like lesions with surrounding edema are observed.
Lesions also seen in the corticomedullary junction and periventricular areas.
MRI can be diagnostic of toxoplasmosis if mass effect seen in basal ganglia or
thalamic lesions.

49. Infectious
Creutzfeldt-Jakob Disease
T2
FLAIR
ADC
FLAIR
Bilateral and symmetric increased signal intensity in Basal ganglia.
White arrows on the ADC image indicate the cortical ribbon sign.
Symmetrical hyper intensities in the pulvinar nuclei (“hockey stick” sign) indicated by black
arrows in the first two images.
FLAIR imaging shows the Pulvinar sign. The criteria for which include:
1. Appropriate clinical history
2. Bilateral hyper intensity in the pulvinar, greater than that in the putamen;
3. Appropriate imaging sequences have been performed, preferably including a FLAIR
sequence in the axial plane.

50. Infectious
Human T- Lymphotropic Virus Type 1
FLAIR
T2
T2
Thoracic spinal cord atrophy on T2 sagittal images, are observed in the later
stages of the disease.
T2 hyper intense lesions were correlated with motor impairment, increased
IgG in CSF, and a rapid clinical course.

51. Infectious
Tuberculosis
T1 Post C
T1 Post C
T1 Post C
T1 Post C
Infarction and hydrocephalus, leptomeningeal enhancement and arachnoiditis.
Both tuberculomas and pyogenic abscess are ring-enhancing with central hypo intense
area, but the tuberculomas will show no restriction on ADC.
MRA shows segmental areas of narrowing.
In TBM, proteinaceous exudates is hyper intense on FLAIR.
Spectroscopy shows a lipid peak, which can be seen in MS also due to myelin breakdown.
MR Spectroscopy is also useful with tubercular abscesses showing elevated lipid/lactate
without elevated amino acids.

52. Neoplasm
Metastatic Cancer
FLAIR
FLAIR
T1 Post C
T2GRE
The most common metastases are breast cancer, lung cancer, and melanoma. The blood brain barrier restricts drug
delivery from the bloodstream, making the treatment of metastatic disease difficult. Metastatic brain disease has a high
mortality and morbidity rate. Patients can present with seizures, cognitive impairment, and mood disorders.
Gadolinium-enhanced MRI is the gold standard for detecting metastatic
disease.
This patient had a history of breast cancer and presented 10 years later with cognitive dysfunction, depression, and
neuropathy.
DWI correlates with histology, grade, architecture, Ki67 proliferation index,
fibrosis, and prognosis. Note the lack of periventricular lesions.
ADC

53. Metabolic / Genetic
Adrenoleukodystrophy
FLAIR
FLAIR
T1 Post C
T1 Post C
Demyelination in the visual and audio pathways, pyramidal tracts, external
capsule, and cerebellar white matter is observed .
Affected white matter will have prolonged T1 and T2 relaxation times.
Blood brain barrier abnormalities on T1-Gd as an enhancing demyelinating edge.
Typically, sub cortical U fibers are spared as in the sagittal FLAIR image, unlike
the above axial FLAIR image . There is a posterior predominance of the disease.

54. Metabolic / Genetic
Metachromatic Leucodystrophy
T2
T2
FLAIR
FLAIR
Symmetric volume loss and demyelination can be seen initially in the periventricular
white matter, & then extend to the sub cortical white matter .
Atrophy, dilated ventricles, and multifocal white mater lesions in the frontal lobes
have been observed.

55. Tumefactive MS (Tumor like MS)
GBM
Tumefactive MS
CNS Lymphoma
T1 Post C
TB
T2
T2
T2
Tumefactive MS is characterized by a single intracranial well-circumscribed lesion > 2
centimeters in diameter with incomplete rim enhancement and often with mass effect.
T2
The lesion can have the classic "butterfly shape" of GBM and lymphoma.
Multiple smaller lesions in the basal ganglia, corpus Callosum, spinal cord, parietal and
frontal lobes suggest the true diagnosis.
MR Spectroscopy may show increased glutamate/glutamine peaks. Increased choline to Nacetyl-aspartate ratios are seen in Tumefactive MS and malignancy.
FDG-PET can be differentiating (hyper-metabolism in malignancy is > than Tumefactive MS).