diagnostic imaging of central nervous system infections
TRANSCRIPT
C.N.S.CNS Infections
Mohamed Zaitoun
Assistant Lecturer-Diagnostic Radiology Department , Zagazig University Hospitals
EgyptFINR (Fellowship of Interventional
Neuroradiology)[email protected]
Knowing as much as possible about your enemy precedes successful battle
and learning about the disease process precedes successful management
CNS Infections1-Bacterial (Purulent) infections2-Fungal infections3-Parasitic infections4-Viral infections5-Meningitis6-Encephalitis7-Congenital CNS Infections8-AIDS9-Prion Infection
1-Bacterial (Purulent) infections :a) Bacterial Meningitisb) Tuberculous Meningitisc) Empyemad) Brain Abscesse) Lyme Disease
a) Bacterial Meningitis :1-Causes2-Pathological Types3-Predisposing factors4-Radiographic Features5-Complications
1-Causes :-Neonates : Group B Streptococcus , E.coli &
Listeria-Children : Haemophilus , E. coli & Neisseria
meningitidis-Adults : S.pneumoniae & N. meningitidis
2-Pathological Types :a) Leptomeningitis (most common) : arachnoid
and pia involvedb) Pachymeningitis : dura and outer layer of
arachnoid involved
3-Predisposing factors :a) Sinusitisb) Chronic pulmonary infectionc) Tetralogy of Fallotd) Transposition of great vesselse) Other cyanotic heart disease
4-Radiographic Features :a) Meningeal Contrast Enhancementb) Neonatal Cranial US
a) Meningeal Contrast Enhancement :-Normal CT examination is initially most common
finding-Convexity enhancement occurring later is a typical
finding , however , lack of enhancement doesn’t exclude meningitis
-May see generalized brain swelling &/or focal or generalized ischemia
-Hydrocephalus
T1+C shows leptomeningeal enhancement (arrows)
Pachymeningitis in a patient with bacterial meningitis , T1+C shows also subdural empyemas on the left side
Pachymeningitis in a patient with bacterial meningitis , T1+C shows diffuse dural enhancement
T1+C shows left-sided dural enhancement (pachymeningitis) and focal pial enhancement
b) Neonatal Cranial US :-Subtle findings : abnormal parenchymal
echogenicity-Echogenic sulci , 40 %-Extra-axial fluid collections-Ventricular dilatation-Ventriculitis occurs in 70%-90% of cases of
bacterial meningitis , normally thin ventricular wall thickens , wall becomes hyperechoic , debris in CSF
5-Complications :a) Subdural effusion : common in infants and
childrenb)Empyemac) Parenchymal extension : abscess and cerebritisd) Ventriculitise) Hydrocephalus ( communicating >
noncommunicating)f) Venous infarctions secondary to venous
thrombosis
Subdural empyema with strand in a patient with bacterial meningitis , CT+C shows a bilateral subdural effusion with cortical surface enhancement (empyema) , note that the attenuation of the effusion is higher than that of the cerebrospinal fluid
CT without contrast shows mild ventriculomegaly and sulcal effacement
T2 shows only mild ventriculomegaly
Lacunar infarct in a patient with bacterial meningitis , CT shows the distribution of the perforating vessels in the brainstem , basal ganglia & white matter
Bilateral subdural empyema in a patient with bacterial meningitis , CT shows the important diagnostic features of meningitis : prominent enhancement of the margin and increased attenuation of the empyema
Abscess formation in a patient with bacterial meningitis , T1+C shows an abscess formation in the right frontal lobe (arrows) and a right parasagittal subdural empyema (arrowhead)
b) Tuberculous Meningitis :1-Incidence2-Radiographic Features
1-Incidence :-The most common CNS manifestation of TB followed
by intraparenchymal tuberculoma-Seen in all age groups , although has a peak incidence
in childhood (particularly 0-4 years of age) in high prevalence areas , in low prevalence areas it is more frequently encountered in adolescents and adults
-Spread is usually hematogenous from pulmonary TB-Basilar meningeal involvement by chronic
granulomatous process leads to cranial nerve palsies (3rd , 4th & 6th)
2-Radiographic Features :1-Basilar meningitis2-Abscesses (Tuberculoma)
1-Basilar meningitis :-Indistinguishable from fungal , lymphoma and
sarcoid :1-Intense contrast enhancement of basilar meninges
(CT & MRI)2-T2 hypointense meninges3-Later complications may be visible including :a) Hydrocephalusb) Infarcts due to arteritis (especially in children)4-Calcifications occur late in disease
CT+C in a patient with tuberculous meningitis demonstrating marked enhancement in the basal cistern and meninges with dilatation of the ventricles
CT+C of a child with tuberculous meningitis demonstrating acute hydrocephalus and meningeal enhancement
CT+C reveals avid enhancement in the basilar cisterns
T1+C shows basal exudates and hydrocephalous
TB meningitis with tuberculoma
Extensive infarcts of the right basal ganglia and internal capsule after the appearance of vasculitis in the thalamoperforating arteries in a child treated for tuberculous meningitis
2-Abscesses (Tuberculoma) :-Rare unless immunocompromised or from endemic
areas (Indian population)-Usually solitary-Nonspecific enhancing masslike lesions , not always
possible to differentiate a tuberculoma from a pyogenic abscess
-Tends to have central hypointensity on T2 (in contrast to a pyogenic abscess which is hyperintense) , shows restricted diffusion
-Cerebral hemispheres and basal ganglia-Miliary form : multiple tiny intraparenchymal lesions
T2 of a biopsy-proven right parietal tuberculoma , note the low signal intensity rim of the lesion and the surrounding hyperintense vasogenic edema
T1+C in a child with a tuberculous abscess in the left parietal region , note the enhancing thick-walled abscess
Multiple enhancing tuberculomas in both cerebellar hemispheres
Multiple ring enhancing tuberculomas
c) Empyema :1-Incidence2-Radiographic Features
1-Incidence :-An empyema is an infected fluid collection in
subdural (common , subdural effusion) or epidural (uncommon) location
-Empyema is a neurosurgical emergency-Cause : sinusitis (most common ) , otitis ,
trauma & post craniotomy
2-Radiographic Features :1-Subdural or epidural low attenuation fluid
collection with enhancement of adjacent brain2-Thick curvilinear enhancement of empyema3-Venous infarction → edema → mass effect →
midline shift4-Diffusion imaging is highly sensitive : lesions
are DWI bright and ADC dark5-Concomitant signs of sinusitis , otitis
T1+C
T2 T1+C
Diffusion
d) Brain Abscess :1-Common Organism2-Mechanism3-Radiographic Features4-Differential Diagnosis
1-Common Organism :-Children : Staphylococcus (especially after
trauma) , Streptococcus & pneumococcus-Adults : Mixed aerobic and anaerobic flora-Immunosuppression : Toxoplasmosis ,
cryptococcosis , candidiasis , aspergillosis, nocardiosis , mucormycosis (diabetes) , TB & atypical mycobacteria
2-Mechanism :a) Hematogenous dissemination (most common)
:-Intravenous drug abuse-Sepsisb) Direct extension :-Sinusitis-Otitis , mastoiditis-Complication of bacterial meningitis -Open injury (penetrating trauma , surgery)c) Idiopathic
-An abscess evolve over 4 stages :(Early cerebritis >> late cerebritis >> early abscess >>
late abscess) and takes about 2 weeks to fully develop , in the early stage of infection , there is nonspecific T2 prolongation in the affected region with heterogeneous enhancement
-After the abscess become discrete , the classic imaging appearance is a ring enhancing lesion , the rim is hypointe
3-Radiographic Features :a) Locationb) Morphologyc) Diffusion & Perfusiond) MRS
a) Location :1-Hematogenous seeding : multiple lesions at
GM/WM junction2-Penetrating trauma or sinusitis : lesion around
the entry site
b) Morphology :1-Early Stage of Infection2-Thin walled ring enhancement lesion 3-Capsule formation4-Mass Effect5-Ventriculitis6-Daughter Cysts
1-Early Stage of Infection :-In the early stage of infection , there is
nonspecific T2 prolongation in the affected region with heterogeneous enhancement
2-Thin walled ring enhancement lesion :-The classic imaging appearance
3-Capsule formation in 7 to 14 days :-Capsule is thinner on WM side because of lower
perfusion to WM than to GM , because of the thinner capsule , daughter lesions (and intraventricular rupture) occur on the medial side
-Capsule is hypointense on T2 , unlike the rim of a glioma or metastases , an abscess rim is thin & smooth
-Inner margin is often smooth-Capsule formation may be delayed by steroid
administration
4-Mass effect (abscessed cavity , edema)5-Ventriculitis due to ventricular spread :-Increased CSF density (elevated protein
concentration)-Ependymal contrast enhancement-May cause ventricular septations and
hydrocephalus-DWI bright6-Daughter lesions
c) Diffusion & Perfusion :-High DWI signal is usually present centrally-Often this represents true restricted
diffusion (low signal on ADC)-rCBV is reduced in the surrounding edema c.f.
to both normal white matter and tumor edema seen in high grade gliomas
d) MRS :-Recognition of amino acids , acetate and
succinate in pyogenic abscesses and lipid peak in tubercular abscesses
(a) T1+C , (b) T2 , (c) Diffusion , (d) ADC
T1+C
Diffusion
Diffusion
CT without contrast CT+C
CT+C
With Ventriculitis
4-Differential Diagnosis :1-Metastasis or high grade glioma (e.g. GBM) :-Abscesses tend to have smoother inner wall -Satellite lesions favour infection-Abscesses may have low intensity capsule-rCBV elevated in high grade gliomas , reduced in
abscesses 2-subacute infarction , hemorrhage or contusion3-Demyelination4-Radiation necrosis
GBM
Mets
Demyelination
Radionecrosis
Enhancing subacute hemorrhagic stroke
e) Lyme Disease :-Caused by the spirochete Borrelia burgdorfrei -Can cause white matter disease with a
nonspecific imaging appearance of T2 prolongation predominantly in the subcortical white matter
-Associated enhancement of multiple cranial nerves or meningeal enhancement may suggest the diagnosis
FLAIR shows several foci of high T2 signal in periventricular white matter on left side above the trigone of left lateral ventricle
FLAIR shows multiple nonspecific foci of T2 prolongation in white matter
Sagittal (A and B) and axial (C) FLAIR show arcuate and confluent subcortical white matter involvement and callososeptal interface involvement remarkably similar to that in MS but without involvement of the periventricular white matter
Facial neuritis , a 48 year old woman with headache and peripheral right facial palsy , prominent enhancement of the fundal tuft and labyrinthine segment of the seventh cranial nerve on postinfusion axial T1 (A) and coronal spoiled gradient-recalled sequences (B)
T1+C (A and B) with enhancing bilateral third and fifth cranial nerves , C, Nine days later , the patient developed left facial palsy with enhancing fundal tuft and labyrinthine and tympanic segments of the seventh cranial nerve
(a) Axial T1+C shows enhancement of left seventh cranial nerve (arrow) , (b) Coronal T1+C shows left trigeminal nerve enhancement (arrow)
T1+C depict enhancement of (a) right trigeminal nerve (arrow) and (b) descending portion of the right facial nerve (arrow)
2-Fungal Infections :a) Causesb) Radiographic Features
a) Causes :1-Immunocompetent patients :-Coccidioidomycosis , histoplasmosis &
blastomycosis2-Immunocompromised patients (AIDS ,
chemotherapy , steroids & transplant recipients ) :
-Nocardiosis , aspergillosis, candidiasis , cryptococcosis & mucormycosis
b) Radiographic Features :1-Basilar Meningitis2-Abscesses3-Helpful Criteria
1-Basilar Meningitis :-Intense contrast enhancement of basilar meninges
(similar to TB)
2-Abscesses :-Early : granuloma-Late: abscess with ring enhancement and central
necrosis (A ring-enhancing T2 heterointense lesion with irregular walls and irregular projections into the cavity with low ADC and no contrast enhancement)
3-Helpful Criteria :a) Aspergillosisb) Mucormycosis c) Coccidiodomycosis d) Cryptococcosis
a) Aspergillosis :1-Hemorrhagic infarcts from vascular invasion2-Often coexistent sinus disease that has extended to CNS3-Dissimenated Aspergillosis (T2W isointense /
hypointense masslike lesions)
b) Mucormycosis :-Indistinguishable from aspergillosis
c) Coccidiodomycosis :-Indistinguishable from TB
Aspergillosis in a 36-year-old woman with HIV infection who experienced a rapid decline in consciousness , axial unenhanced CT reveals a large parenchymal hemorrhage involving the left hemisphere that caused mass effect and midline shift
Disseminated aspergillosis in a 38-year-old man with HIV infection , CT+C shows multiple circumscribed regions of hypoattenuation with faint peripheral enhancement
Disseminated aspergillosis in a 39-year-old AIDS patient , (a) T2 FLAIR shows two well-circumscribed foci of hyperintensity within the centrum semiovale , there is no significant surrounding edema , (b) T1+C shows low signal intensity lesions that do not demonstrate enhancement
Aspergillosis in an HIV-infected patient who presented with rapidly progressive proptosis , T1+C shows a peripherally enhancing low signal intensity mass within the left orbit that is causing proptosis , intracranial extension is present, as evidenced by dural enhancement in the middle cranial fossa (arrow) , opacification and enhancement of the left ethmoid air cells is seen , in addition , enhancement is seen within the periorbital soft tissue and in the left temporalis muscle
d) Cryptococcosis : Most common1-Incidence2-Radiographic Features
1-Incidence :-The most common CNS fungal infection in patients
with AIDS & is caused by Cryptococcus neoformans
-It is the 3rd most common CNS infection in AIDS overall , after HIV encephalopathy & Toxoplasmosis
-Similar to toxoplasmosis , AIDS patients become susceptible to Cryptococcus with a CD4 count less than 100 cells/µl
2-Radiographic Features :- The imaging findings may consist of
meningoencephalitis , intraventricular or intraparenchymal cryptococcomas , gelatinous pseudocysts or hydrocephalus
-Cryptococcus spreads along the basal ganglia perivascular spaces leaving behind gelatinous pseudocysts which appears as round water signal lesions on T1 & T2
-Intraventricular or intraparenchymal cryptococcomas (ring enhancing granulomas)
-Consider this diagnosis in an HIV-positive patient with communicating hydrocephalus
T2 shows multiple foci of high signal intensity within the bilateral basal ganglia , findings consistent with gelatinous pseudocysts in dilated perivascular spaces (arrows) , enlargement of the ventricles , consistent with hydrocephalus , is also present
Cryptococcal meningoencephalitis (a) T2 shows high signal intensity in the right occipital lobe with foci of hyperintensity are present in the bilateral basal ganglia (arrows) findings consistent with gelatinous pseudocysts , (b) T1 shows low signal intensity in the right occipital lobe that corresponds to the area of hyperintensity seen in a (c) T1+C shows leptomeningeal enhancement in the region of the T2 hyperintensity
Cryptococcoma (a) T1 shows a low signal intensity mass lesion in the right cerebellum , (b) T2 shows the mass is heterogeneous in signal intensity but predominantly hyperintense with a surrounding rim of T2 hyperintensity , a finding consistent with edema , (c) T1+C reveals peripheral nodular enhancement of the lesion
3-Parasitic Infections :a) Neurocysticercosisb) Toxoplasmosisc) Hydatid Disease
a) Neurocysticercosis : (NCC)1-Etiology2-Evolution of Lesions3-Locations4-Radiographic Features
1-Etiology :-Most common parasitic CNS infection of
immunocompetent patients-Caused by Taenia solium (pork tapeworm)-Ingestion of contaminated water or pork , ingested
eggs penetrate intestine , disseminate hematogenously and encyst in muscle , brain and ocular tissue
-Cysts first contain a living larva which ultimately dies causing inflammation (contrast enhancement) and calcifications
-75% of infected patients have CNS involvement , seizures are the most common presentation
2-Evolution of Lesions :a) Nonenhancing cyst : live larvaeb) Ring enhancing lesion : dying larvae cause
inflammatory reactionc) Calcification: old lesion
3-Locations :a) Parenchymal (most common)b) Intraventricular (may cause obstruction)c) Subarachnoid
4-Radiographic Features :a) Four Stages in Brain Parenchymab) Typical Appearance of Cystsc) Other Findings
a) Four Stages in Brain Parenchyma :1-Vesicular stage2-Colloid stage 3-Nodular granular stage4-Calcified stage
1-Vesicular stage :-Cyst + scolex , non-enhancement 2-Colloid stage :-Ring enhancement , edema3-Nodular granular stage : -Decreased enhancement & edema , begins
calcification 4-Calcified stage :-Obvious calcifications on CT & MRI (T2*W)
b) Typical Appearance of Cysts :1-Multiple cystic lesions of water density2-Larvae (scolices) appear of variable signal intensity on T23-Ring enhancement (inflammatory response caused by dying
larvae)4-The cyst with dot sign :-Represents the parasytic cyst with (usually excentric) scolex-It can be seen on both MRI and CT at :a) The vesicular stage (CSF like density cyst & hyperintense scolex)b) Colloidal vesicular stage (enhancement of wall and scolex)
(a) Pathognomonic subcortical cyst left showing the scolex with a close by calcification , calcified subcortical cyst right with perifocal/perilesional edema , calcification in the left temporal muscle , (b) ring enhancing lesion due to a degenerating subcortical cyst in the right occipital lobe , (c) several scattered intraparenchymal calcifications most likely in the context of NCC
CT without contrast CT+C
T1 T1+C
T1+C
CT without contrast shows calcifications
CT without contrast shows calcifications
Intraventricular NCC resulting in acute hydronephrosis
T1 shows extraparenchymal subarachnoid cysticercosis with multiple lobulated cystic lesions predominantly in the subarachnoid space (prepontine , suprasellar cistern and cisterna ambiens) as well as probable intraventricular lesions with potential dilation of the 4th ventricle
c) Other Findings :1-Hydrocephalus2-Chronic meningitis3-Calcification of skeletal muscle
b) Toxoplasmosis :1-Incidence2-Clinical Picture3-Radiographic Features4-Differential Diagnosis
1-Incidence :-2nd most common opportunistic CNS infection
in AIDS (with CD4 count less than 100 cells/µl) with HIV encephalitis is the most common
-Is the most common cause of cerebral abscess in these patients
-Caused by Toxoplasma gondii (reservoir : infected cats)
2-Clinical Picture :a) Congenital :-Meningitis , encephalitis : calcification-Encephalomalacia , atrophy-Chorioretinitis
b) Immunocompetent adults :-Systemic disease with lymphadenopathy and
fever-CNS is not involved (in contradistinction to AIDS)c) Immunocompromised patients :-Fulminant CNS disease-Predilection for basal ganglia and grey-white
matter junction
3-Radiographic Features :-Solitary or multiple ring-enhancing lesions with
marked surrounding edema in basal ganglia , thalami and grey-white matter junction
-Target appearance of lesions is common-Treated lesions may calcify or hemorrhage
NECT shows a large area of edema in the LT basal ganglia (yellow arrows) , centered on a subtle hyperattenuating mass (red arrow)
Multiple ring-enhancing lesions with surrounding vasogenic edema
Ring enhancing lesion with surrounding vasogenic edema
T1+C shows smooth ring-enhancement of the lesion (red arrow)
T1+C shows multiple enhancing lesions
Ring enhancing lesions
T1+C shows ring-enhancing lesions with eccentric nodules : the “target sign” (arrows)
FLAIR shows the extensive edema surrounding a heterogeneous rounded mass (red arrow) in the LT basal ganglia
F-18 FDG PET scan shows asymmetrical , relatively decreased metabolism of the LT basal ganglia (blue arrows)
4-Differential Diagnosis : From Lymphoma1-Periventricular location and subependymal spread
favors lymphoma2-Empirical treatment with antiprotozoal drugs
followed by reassessment of lesions is often used to distinguish between the two
3-Multiple lesions more suggestive of toxoplasma4-SPECT thallium : lymphoma appears as hot lesions ,
toxoplasmosis appears as cold lesions5-Perfusion : Increased relative cerebral blood
volume in lymphoma6-PET : Toxoplasmosis is hypometabolic7-MRS : Lymphoma shows high choline peak ,
Toxoplasmosis shows high lipid peak
c) Hydatid Disease :1-Incidence2-Radiographic Features
1-Incidence :-Intracranial hydatid disease is very rare , most
of cerebral hydatid cysts are located in supratentorial structures in the vascular territory of middle cerebral artery
-Caused by Echinococcus granulosus
2-Radiographic Features :-Well-defined circumscribed spherical non-enhancing
intra-axial cystic lesion-Lies in the territory of the middle cerebral artery-Cyst fluid is isointense with CSF in all pulse sequences-No calcification and typically no surrounding edema ,
presence of perilesional edema usually indicates complication as rupture or secondary infection
CT without contrast CT+C
T1 T2
T1+C
DWI ADC
4-Viral infections : 1-Herpes Simplex Virus Encephalitis2-HIV Encephalopathy3-CMV Encephalitis
1-Herpes Simplex Virus Encephalitis :a) Typesb) Clinical Picturec) Locationd) Radiographic Featurese) Differential Diagnosis
a) Types :1-HSV 2 , genital herpes :-Neonatal TORCH infection (see Congenital
Infections)-Acquired during delivery-Diffuse encephalitis (non-focal)
2-HSV 1 , oral herpes :-Children and adults-Usually activation of latent virus in trigeminal
ganglion-Altered mental status , fulminant course-Limbic system , frequently bilateral but
asymmetrical
b) Clinical Picture :-Non specific consisting of fever , headaches ,
focal neurological deficits , seizures and altered or decreased level of consciousness
-Diagnosis is established with PCR of CSF with the clinical Picture , CSF demonstrating pleocytosis and elevated protein
-Herpes should be the first consideration in any patient with fever , mesial temporal lobe signal abnormality and acute altered mental status
c) Location :-In the adult immunocompetent patient , the
pattern is quite characteristic involving the medial temporal lobes & Cingulate gyrus, the basal ganglia are typically spared , helping to distinguish it from a MCA infarct
-In immunocompromised patients , involvement can be more diffuse and more likely to involve the brainstem
d) Radiographic Features : (of HSV-1)1-CT2-MRI
1-CT :-Often normal in early HSV encephalitis-Low attenuation in within the anterior and
medial parts of the temporal lobes and the insular cortex
-Later then the changes may become more obvious and even progress to hemorrhage
2-MRI :*T1 :-May show general edema (hypointense) in
affected region -If complicated by subacute hemorrhage there may
be areas of hyperintense signal*T2 :-Hyperintensity of affected white matter and cortex
*T1+C :-Early : enhancement is usually absent-Later enhancement is variable in pattern :1-Gyral enhancement2-Leptomeningeal enhancement 3-Ring enhancement4-Diffuse enhancement*DWI / ADC :-Restricted diffusion is common due to cytotoxic
edema (T1 hypointense/T2 hyperintense)
T2 Diffusion
T2 Diffusion
T2
T1 shows multifocal hemorrhages
e) Differential Diagnosis :-The D.D. of medial temporal lobe lesions
include : MCA infarction , infiltrating glioma , limbic encephalitis and seizure related changes
-Fever is typically absent in infarction & glioma-Herpes encephalitis should be the first
consideration in any patient with fever & signal abnormality in the medial temporal lobe
2-HIV Encephalopathy :-AIDS dementia complex-The most common CNS infection in AIDS patients-MRI : diffuse cerebral atrophy & symmetric T2
prolongation on the periventricular & deep white matter , no mass effect , no enhancement
-In contrast to PML , HIV encephalitis spares the subcortical U-fibers & tends to be symmetric
(a) NECT shows prominence of the sulci and ventricles , findings consistent global volume loss , symmetric low attenuation is present in the periventricular white matter , (b) T2 shows prominence of the sulci and ventricles , findings consistent with diffuse atrophy , symmetric periventricular hyperintensity corresponds to the regions of low attenuation seen on the CT , no mass effect , (c) T1+C shows that no enhancement is associated with the regions of T2 hyperintensity
T2 FLAIR
FLAIR
3-CMV Encephalitis :-Only affects the immunosuppressed , typically
when the CD4 cell count is less than 50 cells/µl -The most common CNS manifestation of CMV
infection is ventriculitis or meningoencephalitis
-The characteristic imaging feature of CMV ventriculitis include subependymal FLAIR hyperintensity & enhancement throughout the ventricular system
(a) FLAIR shows circumferential hyperintensity surrounding the lateral and fourth ventricles , nonspecific T2 signal is present in the white matter , (b) T1+C reveals thin , linear periventricular enhancement , the nonspecific T2 hyperintensity in the white matter did not enhance
T2 FLAIR
5-Meningitis :-Diagnosis is made by lumbar puncture not
imaging -Indications for neuroimaging in possible
meningitis are to assess complications (see before)
a) Bacterial Meningitis :-See beforeb) T.B. Meningitis :-See beforec) Subdural Effusion / Empyema :-See befored) Cerebritis :-Diffuse area of parenchymal low attenuation which may
develop into abscesse) Abscess :-See beforef) Viral Meningitis :-Neuroimaging usually entirely normal
6-Encephalitis :a) HSV Encephalitis :-See beforeb) Slow Viruses :1-Subacute Sclerosing Panencephalitis (SSPE) :-Known as Dawson Disease-Progressive increase T2 signal and atrophy
several years after primary measles infection
T2 shows asymmetric high signal intensity lesions in both hemispheres , lesions in the right thalamus and globus pallidus are noted
2-Rasmussen’s Encephalitis :-Progressive neurological deficits and intractable
seizures in children with progressive atrophy of the involved hemisphere with large ventricle
-Increased T2 signal and atrophy in one cerebral hemisphere
-N.B. :*Notice that , opposed to hemimegalencephaly , the
smaller hemisphere is the site of abnormality and the lateral ventricle is larger in the smaller hemisphere
Axial FLAIR and coronal T2WI show atrophy of the left cerebral hemisphere with enlargement of the lateral ventricle
T1 & T2 shows prominent sulci , dilated lateral ventricle and hemiatrophy on the left
Axial brain CT scan showing dilated left lateral ventricle and prominent left sulci , in keeping with left hemiatrophy
T2 shows dilated left cerebral sulci and dilated left lateral ventricle
Rasmussen’s Encephalitis (LT side) Hemimegalencephaly (RT side)
7-Congenital CNS Infections :a) Etiologyb) Radiographic Features
a) Etiology :1-TORCH :TOxoplasmosis (second most common)RubellaCMV infection (most common)Herpes simplex2-Other :HIV infectionSyphilisVaricella
b) Radiographic Features :1-CMV Infection : (PV) -Periventricular calcification : thick and chunky -CT is adequate for diagnosis in 40%-70% of cases with
typical calcifications , however , calcifications may be in atypical locations such as basal ganglia (calcification generally appears faint and punctate , a characteristic that helps distinguish basal ganglia calcification due to congenital CMV infection from that due to other causes which tends to be more florid) or subcortical regions
-At MR , calcification appears as areas of low signal intensity on T2-weighted images , this appearance is especially evident on T2* weighted gradient-echo images which are highly sensitive for depiction of intracranial calcification
-Neuronal migration anomalies , especially polymicrogyria
-Infection acquired during first two trimesters causes congenital malformations , whereas infection in the third trimester manifests as destructive lesions
(a) Axial unenhanced CT shows periventricular calcification (arrow) and cerebellar atrophy (arrowhead) , (b) Axial unenhanced CT shows basal ganglia and thalamic calcification (arrow) as well as ventriculomegaly with severe generalized loss of volume
T2 , calcifications (arrow)
Atypical location , BG
With lissenencephaly
Diffuse pachygyria (arrows) , ventriculomegaly and white matter lesions (arrowhead)
Right frontal focal polymicrogyria (arrows) , ventriculomegaly and white matter lesions (arrowheads)
Diffuse increased signal intensity of white matter , a finding indicative of delayed myelination
2-Congenital Toxoplasmosis : (B&P)-Basal ganglia and Parenchymal calcification
(diffuse) , intracranial calcifications may regress or resolve over time in cases of treated toxoplasmosis
-Hydrocephalus-Chorioretinitis-Migrational anomalies & encephalomalacia
Disappearing calcification in congenital toxoplasmosis , (a) unenhanced axial images of the brain in a 12 month old infant shows ventricular enlargement , (b) CT at 4 years of age show that brain calcification is lessening over time
3-Rubella :-Microcephaly-Basal ganglia and parenchymal calcifications-Atrophy
Punctate calcifications of the basal ganglia (arrow) and low attenuation of the white matter
4- HSV-2 :-Multifocal GM and WM involvement-Hemorrhagic infarction , consider this diagnosis in a neonate who
presents in the second or third week of life with diffuse brain edema and leptomeningeal enhancement
-Neonatal herpes encephalitis causes widespread MR imaging signal abnormalities that are hypointense on T1 and hyperintense on T2
-Neonatal herpes encephalitis usually involves the periventricular white matter and spares the temporal and inferior frontal lobe associated with adult herpes infection
(a) T1 shows area of hypointensity in white matter of left temporal-occipital region , two small areas of hemorrhage involve gray-white junction , (b) T2 shows hyperintensity in involved white matter
5-Congenital HIV (Primary HIV Encephalitis) :-Diffuse atrophy-Basal ganglia calcification after 1 year
Progressive mineralizing vasculopathy of the basal ganglia
8-AIDS :-Central nervous system involvement in HIV is
the result of one of four mechanisms : 1-Direct Consequence of the HIV virus2-Opportunistic Infections3-Neoplasms in the Immunocompromised Host4-Treatment / Drug Related Complications
1-Direct Consequence of the HIV virus : AIDS Dementia Complex
-HIV encephalopathy : See before
2-Opportunistic Infections :a) Viralb) Fungalc) Protozoaid) Bacterial
a) Viral :1-CMV Encephalitis : See before2-PML : See before
b) Fungal :1-Cryptococcus :-See Fungal Infections
2-Aspergillus & Candida :-See Fungal Infections-Rare in HIV , commoner in other immunocompromised
groups , e.g. bone marrow transplant recipients
c) Protozoai : (Toxoplasmosis)-See before
d) Bacterial :-Typical pyogenic infections-T.B. :Tuberculous meningitis with leptomeningeal
thickening , hydrocephalus , perforating vessel infarcts , cerebritis & abscess
3-Neoplasms in the Immunocompromised Host:
-Lymphoma-See Brain Tumors
4-Treatment / Drug Related Complications :-Immune reconstitution inflammatory syndrome
(IRIS) is the phenomenon of paradoxical deterioration of an AIDS related illness following initiation of highly active anti-retroviral therapy (HAART)
-IRIS has been described with several opportunistic pathogens , including TB , CMV , PML and cryptococcosis as well as Kaposi sarcoma
-The imaging features may mimic worsening on the underlying condition or be atypical
IRIS in a patient with biopsy-proved PML (a) T2 shows hyperintensity in the bilateral (right greater than left) periatrial white matter , (b) T1+C reveals diffuse patchy enhancement in the region of the T2 hyperintensity , (c) FLAIR obtained 2 weeks later demonstrates progression of the T2 hyperintensity with an increase in mass effect , (d) T1+C reveals progression of the patchy enhancement in the 2-week interval
9-Prion Infection : Creutzfeldt-Jakob Disease (CJD)
a) Definitionb) Typesc) Locationd) MRI Findings
a) Definition :-CJD is a transmissible fatal neurodegenerative disorder
caused by prions-Diagnosis is by EEG & detection of 14-3-3 protein in CSFb) Types :-There are four main subtypes: sporadic , familial ,
iatrogenic and variant CJD with the latter being associated with mad cow disease
c) Location :-The cerebral cortex and basal ganglia typically being
involved
d) MRI Findings :-Typical MRI appearance is cortical ribboning which
describes ribbon-like FLAIR hyperintensity & restricted diffusion of the cerebral cortex , the basal ganglia & thalami are also involved , there is often sparing of the motor cortex
-Pulvinar sign or hockey stick sign = typical bilateral lesions in the pulvinar nuclei of the thalamus (dorsomedial thalamus)
*Restricted diffusion seen at diffusion weighted MR imaging is attributed to spongiform neuronal degeneration and is more sensitive than T2 imaging findings in detecting CJD , especially for cortical lesions
FLAIR (top row) , DWI (bottom row) show diffusely increased FLAIR signal with restricted diffusion in the cerebral cortex , basal ganglia & dorsomedial thalamus , there is relative sparing of the motor cortex (red arrows) , a hockey stick sign is visible on the 1st FLAIR image (yellow arrows)
Hockey stick sign
(a) T2 & (b) DWI show bilaterally symmetric areas of T2 prolongation and restricted diffusion in the medial pulvinar nuclei of the medial thalamus (pulvinar sign or hockey stick sign) (arrows)
