Brain Lectures

“Quiz & Conclusion”

Prof. Dr. Mamdouh Mahfouz

COLLECTED BY

AHMAD MOKHTAR ABODAHAB

ASS. LECTURER OF RADIOLOGY
SOHAG UNIVERSITY
BRAIN TUMORS
CONCLUSION
I.C. CYSTS
Intracranial cysts
Extra-axial cysts Intra-axial cysts

 Arachnoid cyst Astrocytoma [ cystic types ]

 Epidermiod cyst Hydatid cyst
 Dermoid cyst Pore cephalic cyst
 Abscesses
Colloid cyst  Cysticercosis
 Leptomeningeal cysts
 Cystic deposits
 Meningioma with cystic part
Epidermoid cyst
0.2 % - 1.8% of brain masses
CP angle, supra and parasellar
region middle cranial fossa
and cisterna magna
• CT: hypodense lesions may
simulate arachnoid cyst
– Surface is lobulated
– May show calcifications
 MRI : hypo intense T1 between
CSF and brain parenchyma
 Marked hyperintense T2 > CSF
 Almost never isointense to the
brain parenchyma in PD
 Epidermiod cyst

 CSF like contents on CT, MRI

 DD arachnoid cyst
 FLAIR → intermediate signal of epidermoid cyst
 Diffusion WIs → Free diffusion of water molecules in
CSF → Low signal in arachnoid cyst
 While restricted diffusion by protein macromolecules
in epidermoid cyst → high signal
 Calcification is uncommon .
 No enhancement
 Dermoid cyst
 Rare than epidermoid cyst
 Midline plane [ posterior fossa,
suprarenal area] Intraventricular
 CT: fat density ± calcification, no
enhancement
 MRI: high signal in T1 [ fat ]
 Rupture intraventricular or
subarachnoid → fat /fluid level
 Hydatid cyst
2% of intracranial SOLs

CT Unilocular cyst CSF density

No edema no enhancement
± calcification
MRI low signal T1 , high signal T2
Porencephaly
Focal cavity filled with CSF communicating with the ventricle

Primary Type
Secondary Type
Colloid cyst
2% of all glial neoplasms
Characteristic site anterior 3rd ventricle
Characteristic contents dense viscid mucoid material
(old blood, cholesterol crystals, CSF, various ions)
• CT: hyper dense midline lesion no enhancement

F 31Y
Colloid cyst
2% of all glial neoplasms
• MRI: variable signals depending on the contents
T1 hyperintense or hypo intense
T2 hyperintense or hypo intense
POSTERIOR FOSSA LESIONS
Notice Intra-canalicular Extension
Multiple in Von Hipple Lendu
Syndrome
INTRA CRANIAL VASCULAR LESIONS
Intracrainal
infections
Intracranial infections
Congenital
Encephalitis
Meningitis ,empyema
Cerebritis , abscess , ependymitis
Granulomatous infection
Fungal and parasitic infections
HIV intracranial manifestations
Characteristic Imaging Findings
 Diffuse meningeal enhancement Meningitis
 Marginal enhancement Abscess (intracerebral
or extra axial)
 Peri-ventricular calcifications  Toxoplasmosis, CMV,
Cysticercosis
 Intraaxial cyst with no enhancement  Hydatid
 Bilateral temporal non enhancing lesion  Herpes encephalitis
 Enhancement of the ventricular walls  Ependymitis
Congenital and neonatal Infections

The classic TORCH infections include:

• Toxoplasmosis
• Rubella
• Cytomegalovirus (CMV)
• Herpes simplex virus (HSV) type2
Encephalitis
Acute non focal [ diffuse] inflammatory disease of brain
 Usually caused by viruses
 CT and MRI NON SPECIFIC FINDINGS

 Multiple hypodense areas [CT]

 Low signal in T1 and high signal in T2 [ MRI]
 Contrast injection gyral pattern of enhancement
▄ █

Toxoplasmosis
Encephalitis
Some viruses may have a more specific imaging appearance
Herpes Simplex 1:750,000

Type I Childhood or Adult encephalitis

Type II Neonatal encephalitis

 Herpes simplex virus – type1 is the cause of 95% all HE

[The most common fatal encephalitis in the childhood and adults ]

 Brain biopsy is not usually needed since imaging is diagnostic

 Mortality rate 50% - 70%
 ACUTE DEMELINATING ENCEPHALOMYELITIS

 Demyelinating lesions throughout the white matter

 Posterior fossa involvement is common in children
 Multiple lesions with no mass effect
 25% will have permanent defect with 10% mortality
 DD Multiple sclerosis [MS ]
Antecedent viral illness or vaccination
Monophasic disease
 Clinically early [ headache , drowsiness , fever]
later [ neurological deficits , seizures , death ]
 Meningitis
Meningitis is the most common from CNS infection

 Pyogenic meningitis
 Viral meningitis
 Granulomatous meningitis (TB )
 Meningitis
Complications of meningitis include:
Hydrocephalus
Sinus thrombosis
Subdural / epidural empyema
Parenchymal infection, infarction
Ventriculitis / ependymitis
Sterile subdural effusions are common in infantile meningitis
Cerebritis
Is the earliest stage of purulent infection
Extends intra-cranially by blood , directly from sinuses ,
trauma
•Early cerebritis (3 to 5 days) : typically ill- defined
nonenhancing focus.

•Late cerebritis (4 to 14 days): patchy enhancement and edema

Cerebritis
• Early capsule [about 2 weeks] thin enhancing rim
• Late capsule [weeks or months] thick enhancing rim
Cerebritis ,
Resolution of imaging findings lags behind clinical improvement

abscess
Complications of pyogenic abscess include:
 Formation of satellite or “daughter” abscesses
 Ventriculitis, ependymitis
 Purulent leptomeningitis
 Ventriculitis

 Ventriculitis/
ependymitis is more likely
to occur from surgical procedures than
from ruptured brain abscess or meningitis
Uncommon , but serious
Choroid plexitis [enlargement and
enhancement ]
Granulomatous Diseases

There is an increasing prevalence of TB in developed

countries due to HIV , IV drug abuse , immune compromised
states, homelessness, crowded conditions in confined
populations (e.g., prisons and nursing homes), and
immigration from endemic areas.
CNS tuberculosis can cause
a. Meningitis
b. Encephalitis

c. Tuberculoma or abscess
Cysticercosis

 The most common CNS parasitic infection

 Taenia solium
 Ingestion of contaminated water or food parasite in
the body. Embryo lodges in the brain tissue or meninges
cyst around the scolex [ vesicular stage ]
intense inflammatory reaction formation of capsule
[ colloidal stage ]
 Larva dies calcification
Cysticercosis
 Two types
Cysticercus cellulosae [ cyst with scolex inside ]
Cysticercus racemose [ grape like cysts ,no scolex ]
 Intraventricular Cysticercosis 7- 20 %
4th ventricle is the most common
Single or multiple
Free or Subependymal
Neuro cysticercosis [ 3 imaging features ]
 Peri ventricular calcification
 Cysts with scolex inside
 Subarachniod cysts
 Hydatid cyst
2% of intracranial SOLs

CT unilocular cyst CSF density

No edema, no enhancement
± calcification
MRI low signal T1 and high signal T2
CNS Manifestations of HIV Infection
INFECTIONS AND NEOPLASMS
Common infectious CNS organisms
HIV, Toxoplasmosis, Cryptococcus
Cytomegalovirus
Papovavirus [Progressive multifocal
leukoencephalopathy PML]

Common neoplastic diseases

Primary and secondary CNS lymphoma
MENINGITIS IN
AIDS PATIENT
CNS Manifestations of HIV Infection

 Non pyogenic abscesses are

more likely to occur in immune
compromised patients and include
toxoplasma, myocobacterium,
fungi, nocardia, actinomycosis
 PML

 Reactivated Papovirus acquired during childhood

 Destroys oligodendrocytes failure to maintain
myelination
 4% of AIDS patients develop PML
 Weakness , aphasia , ataxia , hemi paresis
 No dementia [ present in HIV encephalitis ]
 Poor prognosis death within 3-18 month
 White matter lesions located superficially then deep
 No edema , no mass effect , no enhancement
So >>> Characteristic Imaging Findings

 Diffuse meningeal enhancement Meningitis

 Marginal enhancement Abscess (intracerebral
or extra axial)
 Periventricular calcifications  Toxoplasmosis, CMV,
Cysticercosis
 Intraaxial cyst with no enhancement  Hydatid
 Bilateral temporal non enhancing lesion  Herpes
encephalitis
 Enhancement of the ventricular walls  Ependymitis
Migrational Disorders of the Brain

Gyral abnormalities
• Agyria [Lissencephaly]
• Pacchygyria
• Polymicrogyria

 Schizencephaly
 Gray matter heterotopia
 Unilateral megalencephaly
 Migration disorders

Diffuse Focal
Band heterotopia Subependymal and
Lissencephaly subcortical heterotopia

Rests , nodules , mass

CT and MR features similar to the normal cortex
Lissencephaly F 5M

A rare congenital brain

malformation that means
smooth brain (agyria),
represents a spectrum of
disorders ranging from total
agyria to mixed agyria and
pachygyria
Exact cause is not known
Gray matter Heterotopia
Neurons in abnormal location due
to arrest of radial migration to the
surface of the brain
Types:
• Subependymal heterotopia
• Focal heterotopia
• Diffuse band heterotopia
[ Double cortex syndrome]
Focal Heterotopia
MRI findings
Focal masses within the deep white matter
Isointense to the cortex in all sequences
No perilesional edema
No mass effect
Ipsilateral dysmorphology of the lateral ventricle
Disorders of cortical organization
Abnormal organization

14-20 weeks Sylvian and parieto-

occipiral sulci

32-33 week Large number of sulci

are formed

38-40 week normal adult sulcal

pattern is reached

Disruption of the process of gyral formation

Polymicrogyria
Schizencephaly
Polymicrogyria PMG
 Thickened cortex with many
small gyria
 Gyri may be so small to be
identified on imaging Flat
thick cortex similar to
pachygyria or agyria
 3D reformatted images
 Bilateral opercular
(perisylvian ) syndrome
* Bilateral symmetric PMG of the operculum
* Primitive sylvian fissures
 Schizencephaly
[ gray matter-lined clefts]

 Small clefts with coapted

walls [Closed lip type]
 Large clefts with free
communication between
the ventricle and
subarachnoid spaces
[ Open lip type]

Atlas SW , MRI of the Brain and Spine ,2nd Edition ,1996

 Type I: (closed lip)

Schizencephaly • Fused cleft lined with

gray matter

Originally described as bilateral

symmetrical full thickness cleft within the
cerebral hemispheres.
The cleft is lined by gray matter and
commonly involves the parasylvian
regions.
The cause is unknown
The severity of disease correlates with the Type II: (open lip)
extent of schizencephaly.
• Large true
hemispheric cleft lined
by a membrane of two
layers of gray matter
Type II Schizencephaly

[ Robertson SJ, Wolpert SM:Brain: congenital.In Runge

VM, editor: clinical MRI, Philadelphia, 1990]

Porencephaly
Open lip schizencephaly

surface reconstruction from a 3-D data set

Blaser & Jay,Neuroimaging Clinics , 1999
Schizencephaly Closed Lip
M 7.5Y