T1-weighted MRI of brain demonstrates diffuse enhancement of the meninges in viral

meningoencephalitis.

Figure 1: (a) Axial T2-weighted image showing small hyperintense lesions (black
arrows) in bilateral centrum semiovale. (b and c) Axial diffusion-weighted images
showing restricted diffusion of these lesions (open arrows). (d and e) Postcontrast
axial T1-weighted images show patchy and peripherally enhancing lesions in
bilateral corona radiata and centrum semiovale (arrowhead). (f) Postcontrast
coronal T1-weighted image shows diffuse meningeal enhancement (white arrow)
Axial T1 C+
C+ T1 Axial Marked leptomeningeal enhancement is seen with multiple tuberculomas and enhancing exudates
in basal cisterns.

Tubercular meningitis with

Sumber:

tuberculomas
Case contributed by Dr Praveen Jha
https://radiopaedia.org/cases/tubercular-meningitis-with-tuberculomas

Multiple ring enhancing lesions as described, along with basal enhancing exudates.

Case Discussion

Tuberculous meningitis is the most common presentation of intracranial tuberculosis, and

usually refers to infection of the leptomeninges. Uncommonly tuberculosis can be limited to the
pachymeninges (dura mater), it is called as tuberculous pachymeningitis and is discussed
separately.
The remainder of this article pertains to leptomeningeal tuberculosis, which involves
the arachnoid mater and pia mater.

Epidemiology
Tuberculous meningitis, although seen in all age groups, 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.

Important risk factors include:

HIV/AIDS
immunosuppression
diabetes mellitus
alcoholism

Clinical presentation
Low grade fever with headache is prodromal manifestation. Most common clinical manifestation
is fever, headache, vomiting and neck stiffness. Cranial nerve palsies of 3rd, 4th and 6th nerves
may be seen. Seizures, focal neurological deficits, stupor and coma may be seen in late stages.

CSF analysis reveals lymphocytosis, increased protein level and decreased glucose levels.

Pathology
Tuberculous meningitis is caused by Mycobacterium tuberculosis. The infection spreads
haematogeneously from a distant focal point, usually pulmonary tuberculosis and lodges
immediately deep to the pia forming Rich foci. These can rupture into the subarachnoid space,
forming an exudate. This purulent material is primarily located in vicinity of basal cisterns:
inferomedial surface of frontal lobe, anteromedial surface of temporal lobes,
superior cerebellum and floor of the fourth ventricle.

From here, infection spreads to interpeduncular cisterns, around optic chiasm and to
pontomesencephalic, ambient and suprasellar cisterns. Although the exudate can reach
the Sylvian fissures it uncommonly extends over the cerebral convexities 3.

Choroid plexitis may also be a late manifestation as is mass-like regions of caesous necrosis
within this exudate.
Radiographic features
CT
non-contrast scans may be normal
later complications may be visible including:
o hydrocephalus
o infarcts due to arteritis (especially in children)

Following contrast administration a number of additional features may be visible:

basal enhancing exudates

leptomeningeal enhancement, along sylvian fissures, tentorium uncommonly convexities
ependymitis may be present

MRI
T1
o normal initially
o T1 shortening may be seen after progression of disease 3
T2
o normal initially
o T2 shortening is seen after disease progression 3
T1 C+ (Gd): diffuse basal enhancement with enhancing exudates
magnetization transfer (MT) spin echo: significantly lower MT ratio is seen in
tuberculous meningitis as compared to fungal and pyogenic meningitis

Treatment and prognosis

Anti-tuberculosis regimen is started after confirmation of diagnosis. Treatment of complications
(e.g. drainage of hydrocephalus) is also performed.

Complications
hydrocephalus
arteritis that may result in ischaemic infarcts 5
o affects one-third of cases
o more common in children
cranial neuropathies: most affected nerves are 3rd, 4th and 6th nerves
Differential diagnosis
General imaging differential considerations include:

pyogenic meningitis
leptomeningeal carcinomatosis
disseminated oligodendroglial-like leptomeningeal tumour of childhood
fungal meningitis
neurosarcoidosis

MRI of the brain demonstrates prominent sulcal high T2 signal on post Gad FLAIR and much
less florid leptomeningeal enhancement. Prominent papilloedema is visible, best seen on thin
T2. Otherwise the study is unremarkable.

Pyogenic meningitis
Dr Bruno Di Muzio et al.
Pyogenic meningitis, also referred as bacterial meningitis, is a life-
threatening CNS infectious disease affecting the meninges, with an elevated
mortality and disability rates. Three bacteria (Haemophilus
influenzae, Streptococcus pneumoniae, Neisseria meningitidis) account for the
majority of cases .4,5

Epidemiology
The epidemiological spectrum of pyogenic meningitis has changed in the last two
decades in some countries due routine vaccination. Largely the use of the H.
influenzae type b (Hib) conjugate vaccine for infants and the heptavalent protein-
polysaccharide pneumococcal conjugate vaccine (PCV7) are good examples that
explain the significant reduction on H. influenza and pneumococcal disease
incidences. Near elimination of serogroup C meningococcal meningitis and H.
influenzae meningitis has been documented in wealthy nations . 3,4

The median age at diagnosis of bacterial meningitis has increased in the last
decades as a result of children vaccination, although infants under 2 months of
age have not experienced this incidence reduction .3

It is important to note that chronic and immunocompromising conditions were

common predisposing factor for bacterial meningitis among adults, such as : 5

elderly patients (>65 years)

splenectomy and hyposplenic state
alcoholism
HIV/AIDS
diabetes mellitus
cancer
anatomical defect (related with recurrent meningitis)
organ transplant recipients
Clinical presentation
In older children and adults there are typical symptoms and signs, such as: fever,
headache, stiff neck, committing and mental dysfunction hanging from lethargy to
coma. The signs are less clear in infants, being related to non-specific signs of
sepsis and seizures . 2

The diagnosis is usually confirmed by lumbar puncture.

Pathology
Bacteria may arise at the CNS as a result of direct implantation, contagious
infection from a local septic process (e.g. sinusitis) or an infected foreign body
(e.g. a shunting catheter), or by haematogenous spread . 2

Aetiology
group B streptococcus (GBS): is the major cause of bacterial meningitis in
infants under 2 months of age
Neisseria meningitidis: is the major cause of bacterial meningitis in older
children and young adults
Streptococcus pneumoniae: is the the most common pathogen in adults

Radiographic features
As the response to these insults are limited and follows a stereotypical fashion,
the imaging findings are mostly nonspecific with respect to the causative
pathogen. Nevertheless, imaging findings are helpful in detecting an abnormality
and making differential diagnosis with other noninfectious causes . 1

CT and MRI
typically shows thin and linear leptomeningeal enhancement
Complications
The complications of meningitis can be remembered using the
mnemonic HACTIVE . 6

H: hydrocephalus
A: abscess
C: cerebritis / cranial nerve lesion
T: thrombosis
I: infarct
V: ventriculitis / vasculopathy
E: extra-axial collection: empyema and hygroma

Treatment and prognosis

Empirical antimicrobial therapy for purulent meningitis is guided by the age of the
patient .
3

The adult case fatality has a straight correlation with increasing age, the overall
rate is estimated around 16% in the USA, ranging from ~9% among patients 18
to 34 years of age vs. ~23% among those older than 65 years . 3

Differential diagnosis
fungal meningitis: usually exhibit a thicker, lumpy or nodular enhancement 1

viral meningitis
sumber : https://radiopaedia.org/articles/pyogenic-meningitis
There is marked diffuse leptomeningeal enhancement most pronounced over the cerebellum
and in the basal cisterns. There is also nodular enhancement in the right basal ganglia likely via
the perivascular spaces.

There is a focus of restricted diffusion in the left inferomedial cerebellum compatible with a
small PICA branch infarction. There is no hemorrhage.

Small polyps or retention cysts in the maxillary sinuses.

Herpes simplex encephalitis

A.Prof Frank Gaillard et al.

Herpes simplex (HSV) encephalitis is the most common cause of fatal sporadic
fulminant necrotising viral encephalitis and has characteristic imaging findings.
Two subtypes are recognised which differ in demographics, virus and pattern of
involvement. They are : 1

1. neonatal herpes encephalitis

2. childhood and adult herpes encephalitis

This article concerns itself with the latter. For a discussion of the former, please
refer to the article neonatal herpes simplex encephalitis.

Epidemiology
Childhood and adult herpes encephalitis is usually due to HSV-1 (90%) with the
rest due to HSV-2 . There is no particular age, sex or seasonal predilection.
5

Clinical presentation
The presentation is unfortunately relatively non-specific consisting of fever,
headaches, focal neurological deficits, seizures, and altered or decreased level
of consciousness.

Diagnosis is established with PCR of CSF, although the combination of the

clinical scenario, CSF demonstrating pleocytosis and elevated protein, and
appropriate imaging is usually highly suggestive and permits commencement of
treatment.

Pathology
HSV is an obligatory intracellular virus that enters via infecting nasopharyngeal
cells into the sensory branch of lingual nerve then ascends to trigeminal ganglion
and remains latent for a lifetime. Reactivation in the case of immunosuppression,
trauma, or other stresses can result in fulminant haemorrhagic necrotising
encephalitis. HSV has a high affinity for limbic systems with bilateral but
asymmetrical involvement.
Histology
Perivascular cuffs of lymphocytes, large inclusions in neurons and glial cells
called "owl's eye", neurophagia, necrosis and haemorrhage are characteristics of
HSE.

Radiographic features
In the immunocompetent adult patient, the pattern is quite typical and manifests
as a bilateral asymmetrical involvement of the limbic system, medial temporal
lobes, insular cortices and inferolateral frontal lobes. The basal ganglia are
typically spared, helping to distinguish it from a middle cerebral artery infarct.

Extralimbic involvement is more prevalent in children than in adults, seen most

commonly in the parietal lobe, with sparing of basal ganglia. Eventually, it results
in marked cystic encephalomalacia and volume loss in affected areas.

In immunocompromised patients, involvement can be more diffuse, and more

likely to involve the brainstem .
5

CT
Early diagnosis is difficult and a 'normal' scan should not dissuade from the
diagnosis. If findings are present, they typically consist of subtle low density
within the anterior and medial parts of the temporal lobe and the island of
Reil (insular cortex) . If scanned later then the changes may become more
2

apparent and even progress to haemorrhage.

Contrast enhancement is uncommon during the first week of the disease. After
that patchy low-level enhancement may be seen . 5

MRI
Affected areas, however, have a similar appearance, in terms of signal
characteristics:

T1
 o may show general oedema in the affected region
o if complicated by subacute haemorrhage there may be areas of
hyperintense signal
T1 C+ (Gd)
o enhancement is usually absent early in the disease
o enhancement occurs later and is variable in pattern 5

gyral enhancement
leptomeningeal enhancement
ring enhancement
diffuse enhancement
T2
o hyperintensity of affected white matter and cortex
o more established haemorrhagic components may the hypointense
DWI/ADC
o more sensitive than T2 weighted images
o restricted diffusion is common due to cytotoxic oedema
o restricted diffusion is less intense compared to infarction
o beware of T2 shine through due to vasogenic oedema
GE/SWI
o may demonstrate blooming if haemorrhagic (rare in neonates,
common in older patients)

Treatment and prognosis

Mortality ranges dramatically depending on how early treatment is instituted.
Even in patients who are young and otherwise well, and only lethargic still have a
mortality of 25%. Older patients or those comatose at the time treatment is
started invariably have a much poorer outcome . Overall mortality is over 70%
3

with only 2.5% of affected patients every fully recovering . 5

Treatment is with intravenous antivirals (e.g. acyclovir).

Differential diagnosis
General imaging differential considerations include:

limbic encephalitis
gliomatosis cerebri
status epilepticus
middle cerebral artery (MCA) infarction: typically involves the basal ganglia
trauma
viral encephalitides: many can have very similar appearances and are
difficult to separate clinically, and the diagnosis usually requires PCR4

o Epstein-Barr virus (EBV) encephalitis

o human herpes virus 6 (HHV-6) encephalitis
o Varicella-Zoster virus (VZV) encephalitis
o influenza A virus encephalitis
o rabies encephalitis
sumber : https://radiopaedia.org/articles/herpes-simplex-encephalitis