Crossed cerebellar diaschisis
Updates to Article Attributes
Crossed cerebellar diaschisis (CCD)refers to a depression of blood flowin function, metabolism, and metabolismperfusion affecting a cerebellar hemisphere occurring as a result of a contralateral focal supratentorial lesion, classically an infarct.
Clinical presentation
Other than neurological deficits and other clinical features associated with the contralateral supratentorial lesion, this condition is generally asymptomatic 1.
Pathology
Diaschisis in the brain, by definition, refers to an acute inhibition of function and metabolism produced by a focal disturbance in a portion of the brain at a distance from the original site of injury but connected via white matter tracts 1. Although initially defined as caused by an acute lesion, many sources in the literature employ a more liberal definition and refer to it being related to a lesion of any temporal duration 1.
When affecting the cerebellum, it is a well-recognised phenomenon following cerebral infarction 2-4, although it can be a sequela of any significant supratentorial lesion (e.g. tumours 1, intracerebral haemorrhage 5, encephalitis 5, Dyke-Davidoff-Masson syndrome 6, radiation necrosis, etc.). The most likely mechanism is thought to be interruption of cortico-ponto-cerebellar white matter tracts, which then results in deafferentation and hypometabolism of the contralateral cerebellar hemisphere 2.
The same phenomenon can also occur in other regions of the brain after various insults 8,9:
- ipsilateral thalamic diaschisis, occurring after an ipsilateral middle cerebral artery territory infarction
- crossed transhemispheric diaschisis, occurring after a contralateral infarct
- ipsilateral thalamocortical diaschisis, occurring after an ipsilateral thalamic infarct
Radiographic features
By definition, nuclear medicine should be performed to formally detect hypometabolism in the contralateral cerebellar hemisphere 1, however other imaging modalities may be useful if interpreted in the correct clinical context.
CT perfusion / MRI perfusion
CT perfusion performed during an acute stroke may show a contralateral perfusion abnormality in about 20% of cases 4. In particular, CBF and CBV maps show only mild-to-moderate reduction in these parameters, which are not low enough to classify as infarctions 7. MR perfusion can also play a similar role 3,4. In chronic stages, there can be associated volume loss to the contralateral cerebellar hemisphere, known as crossed cerebellar atrophy 1,2.
Nuclear medicine
FDG PET-PET shows hypometabolism in the affected cerebellar hemisphere, which is diagnostic of this conditionphenomenon 1.
Treatment and prognosis
No treatment, other than management of the supratentorial insult and prevention of further insults, is available or necessary.
History and etymology
The term 'diaschisis' was first coined by Constantin von Monakow (1853-1930), a Russian neuropathologist, in 1914 8,10, although the concept was first proposed by Charles-Édouard Brown-Séquard (1817-1894) who debated the topic with Jean-Martin Charcot (1825-1893) in the late 1800s 8,11.
-<p><strong>Crossed cerebellar diaschisis (CCD)</strong> refers to a depression of blood flow and metabolism affecting a <a href="/articles/cerebellum">cerebellar hemisphere</a> occurring as a result of a contralateral focal supratentorial lesion, classically an infarct. </p><h4>Clinical presentation</h4><p>Other than neurological deficits and other clinical features associated with the contralateral supratentorial lesion, this condition is generally asymptomatic <sup>1</sup>.</p><h4>Pathology</h4><p>Diaschisis in the brain, by definition, refers to an acute inhibition of function and metabolism produced by a focal disturbance in a portion of the brain at a distance from the original site of injury but connected via white matter tracts <sup>1</sup>. Although initially defined as caused by an acute lesion, many sources in the literature employ a more liberal definition and refer to it being related to a lesion of any temporal duration <sup>1</sup>.</p><p>When affecting the cerebellum, it is a well-recognised phenomenon following cerebral infarction <sup>2-4</sup>, although it can be a sequela of any significant supratentorial lesion (e.g. <a href="/articles/brain-tumours">tumours</a> <sup>1</sup>, <a href="/articles/intracerebral-haemorrhage">intracerebral haemorrhage</a> <sup>5</sup>, encephalitis <sup>5</sup>, <a href="/articles/dyke-davidoff-masson-syndrome">Dyke-Davidoff-Masson syndrome</a> <sup>6</sup>, <a href="/articles/cerebral-radiation-necrosis-1">radiation necrosis</a>, etc). The most likely mechanism is thought to be interruption of cortico-ponto-cerebellar white matter tracts, which then results in deafferentation and hypometabolism of the contralateral cerebellar hemisphere <sup>2</sup>.</p><h4>Radiographic features</h4><p>By definition, nuclear medicine should be performed to formally detect hypometabolism in the contralateral cerebellar hemisphere <sup>1</sup>, however other imaging modalities may be useful if interpreted in the correct clinical context. </p><h5>CT perfusion / MRI perfusion</h5><p>CT perfusion performed during an acute stroke may show a contralateral perfusion abnormality in about 20% of cases <sup>4</sup>. In particular, <a href="/articles/cerebral-blood-flow-cbf">CBF</a> and <a href="/articles/cerebral-blood-volume-cbv">CBV</a> maps show only mild-to-moderate reduction in these parameters, which are not low enough to classify as infarctions <sup>7</sup>. MR perfusion can also play a similar role <sup>3,4</sup>. In chronic stages, there can be associated volume loss to the contralateral cerebellar hemisphere, known as crossed cerebellar atrophy <sup>1,2</sup>.</p><h5>Nuclear medicine</h5><p>FDG PET shows hypometabolism in affected cerebellar hemisphere, which is diagnostic of this condition <sup>1</sup>.</p>- +<p><strong>Crossed cerebellar diaschisis </strong>refers to a depression in function, metabolism, and perfusion affecting a <a href="/articles/cerebellum">cerebellar hemisphere</a> occurring as a result of a contralateral focal supratentorial lesion, classically an infarct. </p><h4>Clinical presentation</h4><p>Other than neurological deficits and other clinical features associated with the contralateral supratentorial lesion, this condition is generally asymptomatic <sup>1</sup>.</p><h4>Pathology</h4><p>Diaschisis in the brain, by definition, refers to an acute inhibition of function and metabolism produced by a focal disturbance in a portion of the brain at a distance from the original site of injury but connected via white matter tracts <sup>1</sup>. Although initially defined as caused by an acute lesion, many sources in the literature employ a more liberal definition and refer to it being related to a lesion of any temporal duration <sup>1</sup>.</p><p>When affecting the cerebellum, it is a well-recognised phenomenon following cerebral infarction <sup>2-4</sup>, although it can be a sequela of any significant supratentorial lesion (e.g. <a href="/articles/brain-tumours">tumours</a> <sup>1</sup>, <a href="/articles/intracerebral-haemorrhage">intracerebral haemorrhage</a> <sup>5</sup>, encephalitis <sup>5</sup>, <a href="/articles/dyke-davidoff-masson-syndrome">Dyke-Davidoff-Masson syndrome</a> <sup>6</sup>, <a href="/articles/cerebral-radiation-necrosis-1">radiation necrosis</a>, etc.). The most likely mechanism is thought to be interruption of cortico-ponto-cerebellar white matter tracts, which then results in deafferentation and hypometabolism of the contralateral cerebellar hemisphere <sup>2</sup>.</p><p>The same phenomenon can also occur in other regions of the brain after various insults <sup>8,9</sup>:</p><ul>
- +<li>ipsilateral thalamic diaschisis, occurring after an ipsilateral <a href="/articles/middle-cerebral-artery">middle cerebral artery</a> territory infarction</li>
- +<li>crossed transhemispheric diaschisis, occurring after a contralateral infarct</li>
- +<li>ipsilateral thalamocortical diaschisis, occurring after an ipsilateral thalamic infarct</li>
- +</ul><h4>Radiographic features</h4><p>By definition, nuclear medicine should be performed to formally detect hypometabolism in the contralateral cerebellar hemisphere <sup>1</sup>, however other imaging modalities may be useful if interpreted in the correct clinical context. </p><h5>CT perfusion / MRI perfusion</h5><p>CT perfusion performed during an acute stroke may show a contralateral perfusion abnormality in about 20% of cases <sup>4</sup>. In particular, <a href="/articles/cerebral-blood-flow-cbf">CBF</a> and <a href="/articles/cerebral-blood-volume-cbv">CBV</a> maps show only mild-to-moderate reduction in these parameters, which are not low enough to classify as infarctions <sup>7</sup>. MR perfusion can also play a similar role <sup>3,4</sup>. In chronic stages, there can be associated volume loss to the contralateral cerebellar hemisphere, known as crossed cerebellar atrophy <sup>1,2</sup>.</p><h5>Nuclear medicine</h5><p>FDG-PET shows hypometabolism in the affected cerebellar hemisphere, which is diagnostic of this phenomenon <sup>1</sup>.</p><h4>Treatment and prognosis</h4><p>No treatment, other than management of the supratentorial insult and prevention of further insults, is available or necessary.</p><h4>History and etymology</h4><p>The term 'diaschisis' was first coined by <strong>Constantin von Monakow</strong> (1853-1930), a Russian neuropathologist, in 1914 <sup>8,10</sup>, although the concept was first proposed by <strong>Charles-Édouard Brown-Séquard</strong> (1817-1894) who debated the topic with <strong>Jean-Martin Charcot</strong> (1825-1893) in the late 1800s <sup>8,11</sup>.</p>
References changed:
- 8. Carrera E, Tononi G. Diaschisis: past, present, future. (2014) Brain : a journal of neurology. 137 (Pt 9): 2408-22. <a href="https://doi.org/10.1093/brain/awu101">doi:10.1093/brain/awu101</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/24871646">Pubmed</a> <span class="ref_v4"></span>
- 9. Reidler P, Thierfelder KM, Fabritius MP, Sommer WH, Meinel FG, Dorn F, Wollenweber FA, Duering M, Kunz WG. Thalamic Diaschisis in Acute Ischemic Stroke. (2018) Stroke. <a href="https://doi.org/10.1161/STROKEAHA.118.020698">doi:10.1161/STROKEAHA.118.020698</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/29523650">Pubmed</a> <span class="ref_v4"></span>
- 10. von Monakow C. Die Lokalisation im Grosshirn und der Abbau der Funktion durch Kortikale Herde. (1914) Wiesbaden, Germany JF Bergmann.
- 11. Brown-Séquard CE. Seance du 18 decembre, C R Soc Biol. (1875). Vol. 424.
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