Herpes simplex encephalitis
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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. Extralimbic involvement is more common in children than in adult, seen most commonly in the parietal lobe, with sparing of basal ganglia.
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 tohaemorrhage
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 vasogenicodema
- 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 imaging diffeential considerations include
- limbic encephalitis
- gliomatosis cerebri
- statusepilepticus
- 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
-<p><strong>Herpes simplex (HSV) encephalitis</strong> is the most common cause of fatal sporadic viral encephalitis and has characteristic imaging findings. </p><p>Two sub types are <span>recognised</span> which differ in demographics, virus and pattern of involvement. They are <sup>1</sup>:</p><ol style="PADDING-RIGHT: 5px; BACKGROUND-POSITION: 2px 2px; PADDING-LEFT: 5px; PADDING-BOTTOM: 0px; MARGIN: 10px; BORDER-LEFT: rgb(185,196,208) 20px solid; PADDING-TOP: 0px; BACKGROUND-COLOR: rgb(255,255,255); background-origin: initial; background-clip: initial">-<li>-<span>neonatal</span> herpes encephalitis</li>-<li>-<span>childhood</span> and adult herpes encephalitis</li>-</ol><p>This article concerns itself with the latter. For a discussion of the former, please refer to the article <a href="/articles/neonatal-herpes-simplex-encephalitis" title="neonatal herpes simplex encephalitis">neonatal herpes simplex encephalitis</a>. </p><h4>Epidemiology</h4><p>Childhood and adult herpes encephalitis <span>is</span> usually due to HSV-1 (90%) with the rest due to HSV-2 <sup>5</sup>. There is no particular age, sex or seasonal predilection. </p><h4>Clinical presentation</h4><p>Presentation is unfortunately relatively non-specific consisting of fever, headaches, focal neurological deficits, seizures, and altered or decreased level of <span>conciousness</span>. </p><p>Diagnosis is established <span>with</span> 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. </p><h4>-<span>Radiographic</span> features</h4><p>In the adult immunocompetent patient, the pattern is quite characteristic, involving the medial temporal lobes, insular cortex and <span>inferolateral</span> frontal lobes. The basal ganglia are typically spared, helping to distinguish it from a <a href="/articles/middle-cerebral-artery-infarction" title="MCA infarct">middle cerebral artery infarct</a>. </p><p>In immunocompromised patients, involvement can be more diffuse, and more likely to involve the <a href="/articles/brainstem" title="Brainstem"><span>brainstem</span></a> <sup>5</sup>. </p><p>It is important to appreciate that the pattern of involvement in children and adults is different to that of <a href="/articles/neonatal-herpes-simplex-encephalitis" title="Neonatal HSV encephalitis" style="COLOR: rgb(63,117,216); TEXT-DECORATION: none">neonatal HSV encephalitis</a>. <span>Extralimbic</span> involvement is more common in children than in <span>adult</span>, seen most commonly in the parietal lobe, with sparing of basal ganglia.</p><h5>CT</h5><p>Early diagnosis is difficult and a 'normal' <span>scan</span> 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 <span>lobed</span> and the <a href="/articles/island-of-reil">island of Reil</a> (insular cortex) <sup>2</sup>. If scanned later <span>then</span> the changes may become more obvious and even progress to <span>haemorrhage</span>. </p><p>Contrast enhancement is uncommon during the first week of the disease. Thereafter patchy low level enhancement may be seen <sup>5</sup>. </p><h5>MRI</h5><p>Affected areas however have a similar appearance, in terms of signal characteristics :</p><ul>-<li>- +<p><strong>Herpes simplex (HSV) encephalitis</strong> is the most common cause of fatal sporadic viral encephalitis and has characteristic imaging findings. </p><p>Two sub types are recognised which differ in demographics, virus and pattern of involvement. They are <sup>1</sup>:</p><ol>
- +<li>neonatal herpes encephalitis</li>
- +<li>childhood and adult herpes encephalitis</li>
- +</ol><p>This article concerns itself with the latter. For a discussion of the former, please refer to the article <a href="/articles/neonatal-herpes-simplex-encephalitis">neonatal herpes simplex encephalitis</a>. </p><h4>Epidemiology</h4><p>Childhood and adult herpes encephalitis is usually due to HSV-1 (90%) with the rest due to HSV-2 <sup>5</sup>. There is no particular age, sex or seasonal predilection. </p><h4>Clinical presentation</h4><p>Presentation is unfortunately relatively non-specific consisting of fever, headaches, focal neurological deficits, seizures, and altered or decreased level of conciousness.</p><p>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. </p><h4>Radiographic features</h4><p>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 <a href="/articles/middle-cerebral-artery-infarction">middle cerebral artery infarct</a>. </p><p>In immunocompromised patients, involvement can be more diffuse, and more likely to involve the <a href="/articles/brainstem">brainstem</a> <sup>5</sup>. </p><p>It is important to appreciate that the pattern of involvement in children and adults is different to that of <a href="/articles/neonatal-herpes-simplex-encephalitis">neonatal HSV encephalitis</a>. Extralimbic involvement is more common in children than in adult, seen most commonly in the parietal lobe, with sparing of basal ganglia.</p><h5>CT</h5><p>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 <a href="/articles/island-of-reil">island of Reil</a> (insular cortex) <sup>2</sup>. If scanned later then the changes may become more obvious and even progress to haemorrhage. </p><p>Contrast enhancement is uncommon during the first week of the disease. Thereafter patchy low level enhancement may be seen <sup>5</sup>. </p><h5>MRI</h5><p>Affected areas however have a similar appearance, in terms of signal characteristics:</p><ul>
- +<li>
-<li>-<span>may</span> show general <span>oedema</span> in <span>affected region</span>-</li>-<li>-<span>if</span> complicated by sub acute <span>haemorrhage</span> there may be areas of hyper intense signal</li>- +<li>may show general oedema in affected region</li>
- +<li>if complicated by sub acute haemorrhage there may be areas of hyper intense signal</li>
-</li>-<li>- +</li>
- +<li>
-<li>-<span>enhancement</span> is usually absent early on</li>-<li>-<span>later</span> enhancement is variable in pattern <sup>5</sup><ul>-<li>-<span>gyral</span> enhancement</li>-<li>-<span>leptomeningeal</span> enhancement </li>-<li>-<span>ring</span> enhancement</li>-<li>-<span>diffuse</span> enhancement</li>- +<li>enhancement is usually absent early on</li>
- +<li>later enhancement is variable in pattern <sup>5</sup><ul>
- +<li>gyral enhancement</li>
- +<li>leptomeningeal enhancement </li>
- +<li>ring enhancement</li>
- +<li>diffuse enhancement</li>
-</li>- +</li>
-</li>-<li>- +</li>
- +<li>
-<li>-<span>hyperintensity</span> of affected white matter and cortex</li>-<li>-<span>more</span> established <span>haemorrhagic</span> components may the hypo <span>intense</span>-</li>- +<li>hyperintensity of affected white matter and cortex</li>
- +<li>more established haemorrhagic components may the hypo intense</li>
-</li>-<li>- +</li>
- +<li>
-<li>-<span>more</span> sensitive than T2 weighted images</li>-<li>-<span>restricted</span> diffusion is common due to cytotoxic <span>oedema</span>-</li>-<li>-<span>beware</span> of <a href="/articles/t2-shine-through" title="T2 shine-through">T2 shine through</a> due to <span>vasogenic</span> <span>odema</span>-</li>-</ul>-</li>-<li>-<strong>GE / SWI</strong> - may demonstrate blooming if <span>haemorrhagic</span> (rare in neonates, common in older patients)</li>-</ul><h4>Treatment and prognosis</h4><p>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 <span>have</span> a much poorer outcome <sup>3</sup>. Overall mortality is over 70% with only 2.5% of affected patients every fully recovering <sup>5</sup>. </p><p>Treatment is with intravenous antivirals (e.g. <span>acyclovir</span>) </p><h4>Differential diagnosis</h4><p>General imaging diffeential considerations include</p><ul>-<li><a href="/articles/limbic-encephalitis"><span>limbic</span> encephalitis </a></li>-<li><a href="/articles/gliomatosis_cerebri"><span>gliomatosis</span> cerebri</a></li>-<li><a href="/articles/status-epilepticus"><span>status</span> <span>epilepticus</span></a></li>-<li>-<a href="/articles/middle-cerebral-artery-infarction" title="middle cerebral artery (MCA) infarction"><span>middle</span> cerebral artery (MCA) infarction</a> - typically involves the basal ganglia</li>-<li><span>trauma</span></li>-<li>-<span>many</span> other <a href="/articles/viral-encephalitides" title="viral encephalitides">viral encephalitides</a>, can have very similar appearances and are difficult to separate clinically. Diagnosis usually requires PCR. These include <sup>4</sup>:-<ul>-<li>Epstein-Barr virus (EBV)</li>-<li>-<span>human</span> herpes virus 6 (HHV-6)</li>-<li>Varicella-Zoster virus (VZV)</li>-<li>-<span>influenza</span> A</li>- +<li>more sensitive than T2 weighted images</li>
- +<li>restricted diffusion is common due to cytotoxic oedema</li>
- +<li>beware of <a href="/articles/t2-shine-through">T2 shine through</a> due to vasogenic odema</li>
- +</ul>
- +</li>
- +<li>
- +<strong>GE / SWI</strong> - may demonstrate blooming if haemorrhagic (rare in neonates, common in older patients)</li>
- +</ul><h4>Treatment and prognosis</h4><p>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 <sup>3</sup>. Overall mortality is over 70% with only 2.5% of affected patients every fully recovering <sup>5</sup>. </p><p>Treatment is with intravenous antivirals (e.g. acyclovir)</p><h4>Differential diagnosis</h4><p>General imaging diffeential considerations include</p><ul>
- +<li><a href="/articles/limbic-encephalitis">limbic encephalitis </a></li>
- +<li><a href="/articles/gliomatosis-cerebri">gliomatosis cerebri</a></li>
- +<li><a href="/articles/status-epilepticus">status epilepticus</a></li>
- +<li>
- +<a href="/articles/middle-cerebral-artery-infarction">middle cerebral artery (MCA) infarction</a> - typically involves the basal ganglia</li>
- +<li>trauma</li>
- +<li>many other <a href="/articles/viral-encephalitides">viral encephalitides</a>, can have very similar appearances and are difficult to separate clinically. Diagnosis usually requires PCR. These include <sup>4</sup>:<ul>
- +<li>Epstein-Barr virus (EBV)</li>
- +<li>human herpes virus 6 (HHV-6)</li>
- +<li>Varicella-Zoster virus (VZV)</li>
- +<li>influenza A</li>
-</li>- +</li>
Images Changes:
Image 8 MRI (T2) ( create )
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