- Inflammatory diseases

Multiple sclerosis

Fig 2: Nodular lesions of the white matter supra , infra tentorial , and cervical...

Generality:

• The most frequent central nervoussystem Inflammatory dysmyelinisantdisease
• Axonal injury.
• Young adults (20–40 ans).
• Feminine predominance.
• Diagnosis: time and spacedissemination criterias (Mac Donald)+ CSF inflammation
• MRI:

White matter signal anomaly

• T1 :iso or hyposignal
• T2, FLAIR : hypersignal > 3mm
• Enhancement: nodular, annular , C shape of lesions in active phase
• Diffusion : hypersignal with lowADC in the periphrey of the lesion in acute phase
• Spectroscopy: variable depending on the phase (acute: diminution of NAA/Cr, rise of Cho/Cr with lipidicspike)
• Corpus callosum atrophy : Evolved form

I- Inflammatory diseases

Neuro-Behçet

Fig 3: 17 years old, ischemic profond CT hypodensitiesWide bilateral asymetric lesions...

Generality:

• Systemic vasculitis of unknown etiology
• Bipolar aphtosis : buccal and genital
• Eye : Uveitis, retinal vasculitis•
• Vascular : arterial and veinous thrombisis
• Joints pain
•  

MRI:

• Vasogenic oedemateous origin
• Multiple nodular and confluent T2 hypersignalsof profond and peri ventricular white matter
• Internal capsule +++
• Patchy moderate enhancement
• Central grey nuclei : thalamus > lenticularnucleus > caudate nucleus
• Vascular disease +++

I- Inflammatory disease

ADEM

Fig 4: Case 3 : 14 years old , history of viral meningitis , :presents acute...

Generality:

• Monophasic CNS inflammatory disease
• Children ++, young adults
• Recent infection / vaccination
• Encephalitis / spinal cord
• CSF: often inflammatory
•  Antibody anti-MOG+
•  

MRI:

• Oedematous lesions of variable size +++
• Supra and infra tentorial white matter
• Asymetric bilateral localization
• Hyposignal T1 and hypersignal T2
• Hypersignal diffusion with rise of ADC
• Ring enhancement , maybe absent

II- Morphological anomalies

Partial agenesis of the corpus callosum

Fig 5: Case 1 : epilepsia assessment Posterior splenium and body agenesis of corpus...

• Generality:
• Difficult diagnosis.
• Short corpus callosum, especially : splenium +++
• Indirect signs : inconstant
•  

MRI:

Direct sign:

• Absence of visualization of a part of the corpus callosum

Indirect sign:

• Colpocephaly

II- Malformative diseases

Total agenesis of corpus callosum

Fig 6: Case 2 : 18 years old, partial epilepsy bec Enlarged appearance of occipital...

Generality:

• Agenesis of the corpus callosum is the most common congenital commissural malformation
• Psychomotor retardation, epileptic seizure.
• Partial/ total.
• Imaging (MRI +++): Diagnostic.
•  

IRM:

Direct sign:

o Absence of visualization of the corpus callosum on the median sagittal section.

Indirect signs:

oDeformations of the frontal horns in "bull horns". oElevation of the roof of the 3rd ventricle. oColpocephaly: isolated dilation with increased gap between the occipital horns. oAbsence of pericallous convolution. oRadial arrangement of the internal cerebral furrows.

II- Morphological anomalies

 Pericallosal lipoma

Fig 8: Case 4 : generalized epilepsy Peri-callosal fat density lesion, not enhanced...

Fig 7: Case 3 : 20 years old, growth retardation and puberty, currently presenting...

Generality:

• Rare congenital lesion
• 90 % median
•  Intracranial lipoma is not a tumor but a malformation due to the abnormal persistence of the "meninx primitiva" / primary meninge and lipomatous differentiation of the latter during the development of the subarachnoid spaces èHETEROTOPIA

MRI:

Two types

1- Anterior or tubulonodular: Rounded or nodular

> 2cm thick

often associated with corpus callosum abnormalities and / or other brain abnormalities

2- Posterior or curvilinear

 Thin and elongated along the margin of the corpus callosum, <1 cm thick

  Back on the splenium

Less often associated with corpus callosum abnormalities and / or other brain abnormalities

III- Tumoral diseases

Glioblastoma

Fig 9: Cas 1 : 51 years old, generalized tonic-clonic seizures. Multiple deep...

Fig 10: Case 2 : 53 years old, right hemiparesis + AEG of progressive onset with...

Generality:

• Frequency rising with age
• (peak 50-60 years)
• survival less than 20% at 1 year
• Old age is the main factor in the poor prognosis.
• Glioblastoma diffuses along:
• Corpus callosum, commissures !!
• Corticospinal bundles.
• The multifocal nature of a necrotico-hemorrhagic lesion is very much in favor of the diagnosis of glioblastoma.
• New WHO classification 2016 !!

CT :

• Heterogeneous, iso or hyperdense islets
• Surrounded by hypodensity
• Heterogeneous or irregular crown enhancement
•   Edema ++

MRI:

• Iso or hypointense T1, hyperintense T2 with heterogeneous signal.
•   The enhancement reflects:

     a break in the BBB

     tumor hypervascularization.

III- Tumoral disease

Lymphoma

Fig 11: Case 3 : 26 years, D9 of treatment, worsening of symptoms with excruciating...

Generality:

• Primary lymphoma (non-Hodgkin's type B +++)
• Frequent involvement of the corpus callosum, peri-ventricular regions, subcortical and central gray nuclei.
• All ages (6th and 7th decades •
•   Male predominance: SR = 2/3 •
•   Evolution :
• Good response under chemoT +++ / ± radioT(no surgery !!!)
• Complete remission (80% of cases)
• Frequent recurrences (50-60% of cases),

MRI:

• T1: hypointense
• T2: iso- or hypointense +++ the lesion is molded by the edema which surrounds it
• T1 Gado: intense and homogeneous enhancement
• Diffusion: Hyperintense lesion with restriction of ADC
• Spectroscopy:

1. Marked elevation of the Cho
2. Decreased NAA and Cr peaks
3. Corresponding increase in Cho / NAA and Cho / Cr ratios
4.   Presence of an often very clear resonance of lactates and especially free lipids

III- Tumoral diseases

Corpus callosum metastasis

Fig 11: Case 3 : 26 years, D9 of treatment, worsening of symptoms with excruciating...

Generality:

• Rare (Corpus callosum poorly vascularized)
• 20% of CNS tumors

MRI:

• Variable signal in T1 and T2
• Enhancement after injection

Spectroscopy:

• Decreased NAA
• Lipid peak
• Increased choline

III- Tumoral diseases

Dysembryoplastic neuroepithelialtumors(DNET)

Fig 12: Case 4: 37 years old, operated grade II astrocytoma, treated by radiotherapy...

Generality:

• Lesions considered benign and stable of questionable origin (malformative vs tumor)
• Rare
• most often before 20 years
• Male predominance: SR = 3/2
•   Clinical: refractory partial epilepsy starting before 20 years ++
• Very rare recurrence, even in the event of incomplete excision

MRI:

• Supratentorial lesion of cortical topography
• Well limited lesion,
• very variable in size
• T2 hypersignal è pseudopolycysticappearance in soap bubbles ’
• T1 hyposignal
• Variable FLAIR signal è Evocativeborder of perilesional hypersignal
• Lack of mass effect or perilesionaledema
• Contrast uptake in 20% to 50% of cases, nodular, annular or heterogeneous
•  
•  

IV- Infectious diseases

Tuberculoma

Fig 13: Case 5 : 10 years old, fronto-callosum tumor with partial resection....

Generality:

• Tuberculosis of the central nervous system (CNS) is quite common and severe.
• The involvement is always secondary, even if the primary focus remains latent.
• Immunosuppression +++
• Tuberculoma the most common lesion
• Solitary or multiple.

CT:

• -C: Hypodense lesions, rounded, surrounded by perilesional edema.
• Nodular or crown enhancement with hypodense center.

MRI:

• Variable signal in T2 depending on the evolutionary stage
• Early: hypo T2, discrete hyperT1, nodular enhancement
• Mature tuberculoma: gray matter isosignal capsule
• The center in hypo / hyper T2 (caseous necrosis / liquefaction).
• Annular enhancement
• Spectro: The choline / creatinine ratio> 1 in tuberculomas.

V- Traumatic diseases

 Traumatic lesions

Generality:

• Rare
• Two mechanisms:
• 1.By contact effect à areas of contusion 2.By stretching and twisting axons à diffuse axonal lesions

MRI:

Contusion focus

• T2 hypersignal, FLAIR and diffusion
• T2 hypointense haemorrhage *

Diffuse axonal lesions

Two types

• Haemorrhagic: hypo signal T2 *
• Edematous: FLAIR hyper signal with restriction of diffusion without T2 abnormality *

VI- Vascular diseases

 Ischemic stroke

Generality:

• Ischemic stroke: absolute neurological emergency!
• Imaging should:
• Rule out a differential diagnosis and in particular hemorrhage
• Establish a positive diagnosis of an ischemic lesion and specify its topography and extent.
• Specify the level of arterial occlusion.
• Determine the degree of cerebral perfusion.
• Appreciate the pathophysiological stage

MRI:

• Hypersignal in T2 or FLAIR-weightedsequence (before the 8th hour)
• Hyposignal in T1-weighted sequence.
• Diffusion (excellent sensitivity): Hypersignal withreduced ADC in the hyperacute phase
• Arterial occlusion: intra-arterialhypersignal in T2 or FLAIR (disappearance of intravascularhyposignal due to flow (flow void),
• T2 *: signal gap èhemorrhage stigmata
• 3D TOF: search for occlusion or arterialstenosis
•  
•  

VII- Metabolic diseases

Centro and extraponticmyelinolysis

Generality:

• Or osmotic demyelination syndrome
• demyelination of the central part of the protuberance or other parts of the brain.
• The main predisposing factors are chronic alcoholism, states of undernutrition and too rapid correction of hyponatremia.

MRI:

• T1-weighted hypointense
• hypersignal on T2 and FLAIR weighted sequences
• Enhancement possible by contrast
• Normal initial MRI does not rule out the diagnosis à repeat the exam.
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•  
•  
• VII- Metabolic disease

 Marchiafava-Bignami Disease

Generality:

• Rare complication occurring after acute intoxication in a chronic alcoholic
• Acute demyelination of the corpus callosum and necrosis
• A deficiency of the group B vitamin complex is the main etiopathogenichypothesis.
• Good improvement after administration of these compounds.

CT:

• Hypodensity of the corpus callosum
• Bleeding changes and possible contrast enhancements

MRI:

• In the acute phase.
• T1: hypointense
• T2 / FLAIR: hyperintense
• Diffusion: hypersignal with ADC restriction,
• T1 Gado: no contrast enhancement
• In the chronic phase:
• HypoT1 / hyperT2 cystic necrosislesions diffuse or localized CC involvement

VIII- Degenerative disease

• Corpus callosum atrophy