Cytotoxic lesions of the corpus callosum (CLOCCs)

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~~Transient lesion~~Cytotoxic lesions of the ~~splenium~~corpus callosum (CLOCCs)

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~~Transient~~Cytotoxic lesions of the corpus callosum (CLOCCs) represent a collection of disparate conditions that can cause signal change in the corpus callosum, usually involving the splenium.

Terminology

The term cytotoxic lesions of the corpus callosum (CLOCCs) has been proposed recently¹² as a more precise description of this phenomenon which has previously been known by a variety of terms including transient lesions of the splenium of the corpus callosum, ~~also known as~~ mild encephalitis/encephalopathy with a reversible isolated SCC lesion (MERS), ~~are occasionally encountered on MRI studies~~reversible splenial lesions and ~~may be due~~reversible splenial lesion syndrome (RESLES). CLOCCs not only better reflects current understanding of the underlying pathophysiology of these lesions but also does not explicitly implies that these lesions are confined to the splenium. As such it is probably a ~~number of underlying aetiologies~~better term to use.

Clinical presentation

Unlike many other ~~causes of splenium of corpus callosum (SCC) lesions, the small transient~~ lesions of the ~~splenium seen in epilepsy and antiepileptic drug cessation use~~corpus callosum, CLOCCs do not demonstrate convincing signs or symptoms of hemispheric disconnection, such as pseudo-neglect, alien hand syndrome, ~~apraxia~~apraxia of the left hand, agraphia, alexia, and visual apraxias ⁴.

Pathology

Although numerous underlying aetiologies have been identified these lesions appear to result from a stereotyped cascade of cytokines and stimulated cells. An initial insult results in macrophages releasing inflammatory cytokines (IL-1 and IL-6) which in turn result in a cascade of changes including recruitment T-cells, cause break-down of the blood-brain barrier, production of TNF-α, and activation of astrocytes. The end result is a massive increase in glutamate in the extracellular fluid which, via interactions with a number of cell membrane receptors, results in an influx of water into both astrocytes and neurons which manifests macroscopically as cytotoxic oedema¹².

It appears that the reason the splenium of the corpus callosum is preferentially affected is the presence of a high density of oligodendrocytes expressing large numbers of glutamate affected receptors ¹².

Aetiology

~~Aetiologies include~~ ^1-5:

~~epilepsy~~
- ~~classic presentation is~~Cytotoxic lesions of the corpus callosum are seen in a wide variety of clinical settings, although exactly which conditions are listed in any one publication varies. Classically CLOCCs are seen in patients with seizures or metabolic disturbances, although many other aetiologies are recognised. Reported aetiologies include ^1-5,12:
  - seizures
    - complex relationship – CLOCCs seen in a variety of settings:
      - antiepileptic medications (with or without seizures)
      - sudden cessation of antiepileptic drugs (classic)
      - seizures~~: focal lesions have been described after focal status epilepticus and unusually after single seizures and were explained as focal brain oedema.~~ with or without antiepileptic medications
    - ~~electrolyte imbalance~~
      - ~~including~~ ~~~~extrapontine~~ m ~~yelinolysis~~^10,11~~
    - ~~demyelination~~ metabolic disturbance
      - haemolytic-uraemic syndrome
      - hepatic encephalopathy
      - hypoglycemia
      - Marchiafava-Bignami disease
      - osmotic demyelination (e.g. extrapontine m yelinolysis ^10-12)
      - Wernecke encephalopathy
      - Wilson disease
      - ~~AIDS dementia complex~~
    - infections
      - reported in a wide range of cerebral infections, including cerebral abscess, encephalitis and meningitis
        
        viral: (e.g. influenza, measles,herpes,mumps, adenovirus, varicella zoster, rotavirus ~~and~~ ~~HIV~~)
        
        bacterial~~: salmonella~~ (e.g. salmonella, Legionnaires' disease)
        
        mycobacterial: (e.g. tuberculous meningitis)
    - CNS malignancy
      - many are associated with chemotherapy and/or seizures
    - drugs and toxins
      - antidepressants (e.g amitriptyline)
      - antiepileptics (e.g. carbamazepine, lamotrigine, phenytoin)
      - antipsychotics (e.g. clozapine)
      - chemotherapy (e.g. cyclosporin, fluorouracil)
      - corticosteroids
      - pesticide (e.g. methyl bromide)
    - ~~hypoglycemia~~subarachnoid haemorrhage
      - especially if large volume
      - ~~haemolytic-uremic syndrome with encephalopathy~~not the result of vasospasm
    Radiographic features
    
    Transient lesions of the splenium are only really appreciable on MRI where they have two distinct patterns ⁴:
    1. well circumscribed, small, oval lesions in the midline within the substance of the corpus callosum
    2. more extensive ill-defined irregular lesions extending throughout the splenium and into the adjacent hemispheres (boomerang sign)
    The smaller well-circumscribed lesions are the typical lesion seen in the setting of seizures/cessation of antiepileptic medication, whereas the larger lesion is more typical of other aetiologies.
    
    MRI
    
    These lesions ~~tend to~~ demonstrate the ~~following signal characteristics~~ expected features of cytotoxic oedema^4,12:
    - T1: hypointense
    - T2: hyperintense
    - DWI/ADC: restricted diffusion
    - T1 C+: no enhancement
    ~~Studies~~Some studies have shown that patients generally recover completely on MRI studies within 1 month, mostly within 1 week following the neurologic recovery ⁷.
    
    Treatment and prognosis
    
    The prognosis generally depends on the underlying cause, but in the setting of epilepsy or antiepileptic drug-related lesions, it is very good.
    Differential diagnosis
    
    Depending on the publication some of the differentials to contemplate are included in the list of aetiologies of CLOCCs. In any case, when confronted with a splenial lesion consider:
    - demyelination
      
      multiple sclerosis (MS)
      
      acute disseminated encephalomyelitis (ADEM)
    - infarction (e.g. pericallosal artery occlusion)
    - posterior reversible encephalopathy syndrome (PRES)
    - trauma (e.g. diffuse axonal injury)
    - tumours (e.g. diffuse glioma, lymphoma)

-<p><strong>Transient lesions of the splenium of the corpus callosum</strong>, also known as<strong> mild encephalitis/encephalopathy with a reversible isolated SCC lesion (MERS)</strong>, are occasionally encountered on MRI studies and may be due to a number of underlying aetiologies.</p><h4>Clinical presentation</h4><p>Unlike other causes of splenium of corpus callosum (SCC) lesions, the small transient lesions of the splenium seen in epilepsy and antiepileptic drug cessation use do not demonstrate convincing signs or symptoms of hemispheric disconnection, such as pseudo-neglect, alien hand syndrome, apraxia of the left hand, agraphia, alexia, and visual apraxias <sup>4</sup>. </p><h4>Pathology</h4><h5>Aetiology</h5><p>Aetiologies include <sup>1-5</sup>: </p><ul>
~~-<li>epilepsy<ul>~~
~~-<li>classic presentation is seen in patients with sudden cessation of antiepileptic drugs</li>~~
~~-<li>seizures: focal lesions have been described after focal status epilepticus and unusually after single seizures and were explained as focal brain oedema.</li>~~
+<p><strong>Cytotoxic lesions of the corpus callosum (CLOCCs) </strong>represent a collection of disparate conditions that can cause signal change in the <a href="/articles/corpus-callosum">corpus callosum</a>, usually involving the splenium. </p><h4>Terminology</h4><p>The term cytotoxic lesions of the corpus callosum (CLOCCs) has been proposed recently<sup>12</sup> as a more precise description of this phenomenon which has previously been known by a variety of terms including<strong> transient lesions of the splenium of the corpus callosum</strong>,<strong> mild encephalitis/encephalopathy with a reversible isolated SCC lesion (MERS)</strong>, <strong>reversible splenial lesions</strong> and <strong>reversible splenial lesion syndrome (</strong><strong>RESLES</strong><strong>)</strong>. CLOCCs not only better reflects current understanding of the underlying pathophysiology of these lesions but also does not explicitly implies that these lesions are confined to the splenium. As such it is probably a better term to use. </p><h4>Clinical presentation</h4><p>Unlike many other <a href="/articles/lesions-of-the-corpus-callosum-differential">lesions of the corpus callosum</a>, CLOCCs do not demonstrate convincing signs or symptoms of hemispheric disconnection, such as <a href="/articles/pseudo-neglect">pseudo-neglect</a>, <a href="/articles/alien-hand-syndrome">alien hand syndrome</a>, <a href="/articles/apraxia">apraxia</a> of the left hand, <a href="/articles/agraphia">agraphia</a>, <a href="/articles/alexia">alexia</a>, and visual apraxias <sup>4</sup>. </p><h4>Pathology</h4><p>Although numerous underlying aetiologies have been identified these lesions appear to result from a stereotyped cascade of cytokines and stimulated cells. An initial insult results in macrophages releasing inflammatory cytokines (IL-1 and IL-6) which in turn result in a cascade of changes including recruitment T-cells, cause break-down of the blood-brain barrier, production of TNF-α, and activation of astrocytes. The end result is a massive increase in glutamate in the extracellular fluid which, via interactions with a number of cell membrane receptors, results in an influx of water into both astrocytes and neurons which manifests macroscopically as <a href="/articles/cytotoxic-cerebral-oedema">cytotoxic oedema</a> <sup>12</sup>. </p><p>It appears that the reason the splenium of the corpus callosum is preferentially affected is the presence of a high density of oligodendrocytes expressing large numbers of glutamate affected receptors <sup>12</sup>. </p><h5>Aetiology</h5><p>Cytotoxic lesions of the corpus callosum are seen in a wide variety of clinical settings, although exactly which conditions are listed in any one publication varies. Classically CLOCCs are seen in patients with seizures or metabolic disturbances, although many other aetiologies are recognised. Reported aetiologies include <sup>1-5,12</sup>: </p><ul>
+<li>seizures<ul><li>complex relationship – CLOCCs seen in a variety of settings:<ul>
+<li>antiepileptic medications (with or without seizures)</li>
+<li>sudden cessation of antiepileptic drugs (classic)</li>
+<li>seizures with or without antiepileptic medications</li>
~~-</li>~~
-<li>electrolyte imbalance<ul><li>including <a title="Extrapontine myelinolysis" href="/articles/extrapontine-myelinolysis-1">extrapontine </a><a title="Extrapontine myelinolysis" href="/articles/extrapontine-myelinolysis-1">m</a><a title="Extrapontine myelinolysis" href="/articles/extrapontine-myelinolysis-1">yelinolysis</a> <sup>10,11</sup>
~~-<li><a href="/articles/demyelination">demyelination </a></li>~~
~~-<li><a href="/articles/multiple-sclerosis">multiple sclerosis (MS)</a></li>~~
~~-<li><a href="/articles/acute-disseminated-encephalomyelitis-adem-1">acute disseminated encephalomyelitis (ADEM)</a></li>~~
~~-<li><a href="/articles/posterior-reversible-encephalopathy-syndrome-1">posterior reversible encephalopathy syndrome (PRES)</a></li>~~
+<li>metabolic disturbance<ul>
+<li>electrolyte imbalance (e.g. hyperammonemia, hyper- and hyponatremia)</li>
+<li><a href="/articles/haemolytic-uraemic-syndrome">haemolytic-uraemic syndrome</a></li>
+<li><a href="/articles/hepatic-encephalopathy">hepatic encephalopathy</a></li>
+<li><a href="/articles/hypoglycaemic-encephalopathy">hypoglycemia</a></li>
~~-<li><a href="/articles/diffuse-axonal-injury">diffuse axonal injury (DAI)</a></li>~~
~~-<li><a href="/articles/hiv-associated-dementia">AIDS dementia complex</a></li>~~
~~-<li>infections<ul>~~
~~-<li>viral: influenza, measles, herpes, <a href="/articles/mumps">mumps</a>, adenovirus, varicella zoster, rotavirus and <a href="/articles/hivaids">HIV</a>~~
+<li>
+<a href="/articles/osmotic-demyelination-syndrome">osmotic demyelination</a> (e.g. <a href="/articles/extrapontine-myelinolysis-1">extrapontine </a><a href="/articles/extrapontine-myelinolysis-1">m</a><a href="/articles/extrapontine-myelinolysis-1">yelinolysis</a> <sup>10-12</sup>)</li>
+<li>
+<a href="/articles/wernicke-encephalopathy">Wernecke </a><a href="/articles/wernicke-encephalopathy">encephalopathy</a>
+</li>
+<li><a href="/articles/wilson-disease-cns-manifestations-1">Wilson disease</a></li>
+</ul>
+</li>
+<li>infections<ul><li>reported in a wide range of cerebral infections, including <a href="/articles/brain-abscess-1">cerebral abscess</a>, <a href="/articles/viral-encephalitides">encephalitis</a> and <a href="/articles/leptomeningitis">meningitis</a><ul>
+<li>viral (e.g. influenza, measles, <a href="/articles/herpes-simplex-encephalitis">herpes</a>, <a href="/articles/mumps">mumps</a>, adenovirus, varicella zoster, rotavirus)</li>
+<li>bacterial (e.g. salmonella, <a href="/articles/legionella-pneumonia">Legionnaires' disease</a>)</li>
+<li>mycobacterial (e.g. <a href="/articles/tuberculous-meningitis">tuberculous meningitis</a>)</li>
+</ul>
+</li></ul>
~~-<li>bacterial: salmonella, <a href="/articles/legionella-pneumonia">Legionnaires' disease</a>~~
+<li>CNS malignancy<ul><li>many are associated with chemotherapy and/or seizures</li></ul>
+</li>
+<li>drugs and toxins<ul>
+<li>antidepressants (e.g amitriptyline)</li>
+<li>antiepileptics (e.g. carbamazepine, lamotrigine, phenytoin)</li>
+<li>antipsychotics (e.g. clozapine)</li>
+<li>chemotherapy (e.g. cyclosporin, fluorouracil)</li>
+<li>corticosteroids</li>
+<li>pesticide (e.g. methyl bromide)</li>
+</ul>
+</li>
+<li>
+<a href="/articles/subarachnoid-haemorrhage">subarachnoid haemorrhage</a><ul>
+<li>especially if large volume</li>
+<li>not the result of <a href="/articles/cerebral-vasospasm-following-subarachnoid-haemorrhage">vasospasm</a>
~~-<li>mycobacterial: <a href="/articles/tuberculous-meningitis">tuberculous meningitis</a> </li>~~
~~-<li>hypoglycemia</li>~~
~~-<li>haemolytic-uremic syndrome with encephalopathy</li>~~
-</ol><p>The smaller well-circumscribed lesions are the typical lesion seen in the setting of seizures/cessation of antiepileptic medication, whereas the larger lesion is more typical of other aetiologies. </p><h5>MRI</h5><p>These lesions tend to demonstrate the following signal characteristics <sup>4</sup>: </p><ul>
+</ol><p>The smaller well-circumscribed lesions are the typical lesion seen in the setting of seizures/cessation of antiepileptic medication, whereas the larger lesion is more typical of other aetiologies. </p><h5>MRI</h5><p>These lesions demonstrate the expected features of <a href="/articles/cytotoxic-cerebral-oedema">cytotoxic oedema</a> <sup>4,12</sup>: </p><ul>
-</ul><p>Studies have shown that patients recover completely on MRI studies within 1 month, mostly within 1 week following the neurologic recovery <sup>7</sup>.</p><h4>Treatment and prognosis</h4><p>The prognosis generally depends on the underlying cause, but in the setting of epilepsy or antiepileptic drug-related lesions, it is very good. </p>
+</ul><p>Some studies have shown that patients generally recover completely on MRI studies within 1 month, mostly within 1 week following the neurologic recovery <sup>7</sup>.</p><h4>Treatment and prognosis</h4><p>The prognosis generally depends on the underlying cause, but in the setting of epilepsy or antiepileptic drug-related lesions, it is very good. </p><h4>Differential diagnosis</h4><p>Depending on the publication some of the differentials to contemplate are included in the list of aetiologies of CLOCCs. In any case, when confronted with a splenial lesion consider:</p><ul>
+<li>
+<a href="/articles/demyelination">demyelination</a><ul>
+<li><a href="/articles/multiple-sclerosis">multiple sclerosis (MS)</a></li>
+<li><a href="/articles/acute-disseminated-encephalomyelitis-adem-1">acute disseminated encephalomyelitis (ADEM)</a></li>
+</ul>
+</li>
+<li>infarction (e.g. <a href="/articles/pericallosal-artery">pericallosal artery</a> occlusion)</li>
+<li><a href="/articles/posterior-reversible-encephalopathy-syndrome-1">posterior reversible encephalopathy syndrome (PRES)</a></li>
+<li>trauma (e.g. <a href="/articles/diffuse-axonal-injury">diffuse axonal injury</a>)</li>
+<li>tumours (e.g. <a href="/articles/diffuse-glioma">diffuse glioma</a>, <a href="/articles/cns-lymphoma-1">lymphoma</a>)</li>
+</ul>

References changed:

12. Starkey J, Kobayashi N, Numaguchi Y, Moritani T. Cytotoxic Lesions of the Corpus Callosum That Show Restricted Diffusion: Mechanisms, Causes, and Manifestations. Radiographics. 2017;37(2):562-76. <a href="https://doi.org/10.1148/rg.2017160085">doi:10.1148/rg.2017160085</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/28165876">Pubmed</a>

Updates to Synonym Attributes

Title was changed:

Mild encephalitis ~~/ encephalopathy~~/encephalopathy with a reversible isolated SCC lesion (MERS)

Updates to Synonym Attributes

Title was changed:

Mild encephalitis ~~/ encephalopathy~~/encephalopathy with a reversible isolated SCC lesion

Updates to Synonym Attributes

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Cytotoxic lesions of the corpus callosum (CLOCCs)

Updates to Article Attributes

Terminology

Clinical presentation

Pathology

Aetiology

Radiographic features

MRI

Treatment and prognosis

Differential diagnosis

Updates to Synonym Attributes

Updates to Synonym Attributes

Updates to Synonym Attributes

Updates to Synonym Attributes

Updates to Synonym Attributes