Post by janed on Mar 28, 2012 2:52:55 GMT -5
Herpes simplex (HSV) encephalitis is the most common cause of fatal sporadic viral encephalitis and has characteristic imaging findings.
Two sub types are recognised which differ in demographics, virus and pattern of involvement. They are 1:
neonatal herpes encephalitis
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 5. There is no particular age, sex or seasonal predilection.
Clinical presentation
Presentation is unfortunately relatively non-specific consisting of fever, headaches, focal neurological deficits, seizures, and altered or decreased level of conciousness.
Diagnosis is established with PCR of CSF, although the combination of clinical scenario, CSF demonstrating pleocytosis and elevated protein, and appropriate imaging is usually highly suggestive and permits commencement of treatment.
Radiographic features
In the adult immunocompetent patient, the pattern is quite characteristic, involving the medial temporal lobes, insular cortex and inferolateral frontal lobes. The basal ganglia are typically spared, helping to distinguish it from a middle cerebral artery infarct.
In immunocompromised patients, involvement can be more diffuse, and more likely to involve the brainstem 5.
It is important to appreciate that the pattern of involvement in children and adults is different to that of neonatal HSV encephalitis.
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 lobed and the island of Reil (insular cortex) 2. If scanned later then the changes may become more obvious and even progress to haemorrhage.
Contrast enhancement is uncommon during the first week of the disease. Thereafter patchy low level enhancement may be seen 5.
MRI
Affected areas however have a similar appearance, in terms of signal characteristics :
T1
may show general oedema in affected region
if complicated by sub acute haemorrhage there may be areas of hyper intense signal
T1 C+ (Gd)
enhancement is usually absent early on
later enhancement is variable in pattern 5
gyral enhancement
leptomeningeal enhancement
ring enhancement
diffuse enhancement
T2
hyperintensity of affected white matter and cortex
more established haemorrhagic components may the hypo intense
DWI / ADC
more sensitive than T2 weighted images
restricted diffusion is common due to cytotoxic oedema
beware of T2 shine through due to vasogenic odema
GE / SWI : 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 3. Overall mortality is over 70% with only 2.5% of affected patients every fully recovering 5.
Treatment is with intravenous antivirals (e.g. acyclovir)
Differential diagnosis
General considerations include
limbic encephalitis
gliomatosis cerebri
status epilepticus
middle cerebral artery (MCA) infarction : typically involves the basal ganglia
trauma
many other viral encephalitides, can have very similar appearances and are difficult to separate clinically. Diagnosis usually requires PCR. These include 4:
Epstein-Barr virus (EBV)
human herpes virus 6 (HHV-6)
Varicella-Zoster virus (VZV)
influenza A
T2
DWI
Two sub types are recognised which differ in demographics, virus and pattern of involvement. They are 1:
neonatal herpes encephalitis
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 5. There is no particular age, sex or seasonal predilection.
Clinical presentation
Presentation is unfortunately relatively non-specific consisting of fever, headaches, focal neurological deficits, seizures, and altered or decreased level of conciousness.
Diagnosis is established with PCR of CSF, although the combination of clinical scenario, CSF demonstrating pleocytosis and elevated protein, and appropriate imaging is usually highly suggestive and permits commencement of treatment.
Radiographic features
In the adult immunocompetent patient, the pattern is quite characteristic, involving the medial temporal lobes, insular cortex and inferolateral frontal lobes. The basal ganglia are typically spared, helping to distinguish it from a middle cerebral artery infarct.
In immunocompromised patients, involvement can be more diffuse, and more likely to involve the brainstem 5.
It is important to appreciate that the pattern of involvement in children and adults is different to that of neonatal HSV encephalitis.
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 lobed and the island of Reil (insular cortex) 2. If scanned later then the changes may become more obvious and even progress to haemorrhage.
Contrast enhancement is uncommon during the first week of the disease. Thereafter patchy low level enhancement may be seen 5.
MRI
Affected areas however have a similar appearance, in terms of signal characteristics :
T1
may show general oedema in affected region
if complicated by sub acute haemorrhage there may be areas of hyper intense signal
T1 C+ (Gd)
enhancement is usually absent early on
later enhancement is variable in pattern 5
gyral enhancement
leptomeningeal enhancement
ring enhancement
diffuse enhancement
T2
hyperintensity of affected white matter and cortex
more established haemorrhagic components may the hypo intense
DWI / ADC
more sensitive than T2 weighted images
restricted diffusion is common due to cytotoxic oedema
beware of T2 shine through due to vasogenic odema
GE / SWI : 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 3. Overall mortality is over 70% with only 2.5% of affected patients every fully recovering 5.
Treatment is with intravenous antivirals (e.g. acyclovir)
Differential diagnosis
General considerations include
limbic encephalitis
gliomatosis cerebri
status epilepticus
middle cerebral artery (MCA) infarction : typically involves the basal ganglia
trauma
many other viral encephalitides, can have very similar appearances and are difficult to separate clinically. Diagnosis usually requires PCR. These include 4:
Epstein-Barr virus (EBV)
human herpes virus 6 (HHV-6)
Varicella-Zoster virus (VZV)
influenza A
T2
DWI