Transient global amnesia
Updates to Article Attributes
Transient global amnesia (TGA) is a clinical syndrome with no clear aetiology identified. The syndrome is transient and typically resolves within a few hours.
Epidemiology
Transient global amnesia is most common in the 50-70 year age range ref.
Associations
Clinical presentation
Anterograde and partial retrograde amnesia lasting less than 24 hours without any other neurological or congestive symptoms 6. Episodic memories are more-so affected than semantic memories 6. Most cases show complete resolution of symptoms within a few hours from onset of symptoms 6.
Pathology
Several hypotheses (e.g. epileptic phenomena, stroke, focal focal ischaemia) have have been proposed with no consensus on the exact mechanism 1,6.
Radiographic features
CT brain and conventional sequences of MRI brain may show no abnormalities, especially while the patient is symptomatic.
MRI
Prospective and retrospective studies based on a small number of transient global amnesia patients can detect small punctate regions of abnormally restricted diffusion on DWI/ADC sequences in the CA1 area of the hippocampus(lateral edge of the hippocampal gyrus abutting the temporal horn). These lesions can be bilateral and even multifocal 2-4. These changes generally appear after symptom resolution, and the highest rate of detection is approximately 2 days after symptom onset 6.
Treatment and prognosis
No treatment is required. The condition rarely recurs in ~5% of patients 5,6.
Differential diagnosis
strategic ischaemic stroke (e.g. hippocampal
ischaemicinfarct, bilateral forniceal infarct (amnestic syndrome of the subcallosal artery)), typically exists with other neurological deficits 6,7transient epileptic amnesia, typically presents upon waking while TGA does not 6
psychogenic amnesia, more-so affects semantic memory compared to episodic memory, while TGA is the opposite 6
drug-related amnesia, typically has features of encephalopathy 6
post-traumatic amnesia, has a history of trauma 6
-<p><strong>Transient global amnesia (TGA) </strong>is a clinical syndrome with no clear aetiology identified. The syndrome is transient and typically resolves within a few hours. </p><h4>Epidemiology</h4><p>Transient global amnesia is most common in the 50-70 year age range <sup>ref</sup>.</p><h5>Associations</h5><ul><li><p><a href="/articles/migraine" title="Migraine">migraine</a> <sup>6</sup></p></li></ul><h4>Clinical presentation</h4><p>Anterograde and partial retrograde amnesia lasting less than 24 hours without any other neurological or congestive symptoms <sup>6</sup>. Episodic memories are more-so affected than semantic memories <sup>6</sup>. Most cases show complete resolution of symptoms within a few hours from onset of symptoms <sup>6</sup>.</p><h4>Pathology</h4><p>Several hypotheses (e.g. epileptic phenomena, stroke, focal ischaemia) have been proposed with no consensus on the exact mechanism <sup>1,6</sup>.</p><h4>Radiographic features</h4><p>CT brain and conventional sequences of MRI brain may show no abnormalities, especially while the patient is symptomatic.</p><h5>MRI</h5><p>Prospective and retrospective studies based on a small number of transient global amnesia patients can detect small punctate regions of abnormally restricted diffusion on DWI/ADC sequences in the CA1 area of the <a href="/articles/hippocampus">hippocampus</a> (lateral edge of the hippocampal gyrus abutting the temporal horn). These lesions can be bilateral and even multifocal <sup>2-4</sup>. These changes generally appear after symptom resolution, and the highest rate of detection is approximately 2 days after symptom onset <sup>6</sup>.</p><h4>Treatment and prognosis</h4><p>No treatment is required. The condition rarely recurs in ~5% of patients <sup>5,6</sup>.</p><h4>Differential diagnosis</h4><ul>-<li><p>strategic <a href="/articles/ischaemic-stroke" title="Ischaemic stroke">ischaemic stroke</a> (e.g. hippocampal ischaemic), typically exists with other neurological deficits <sup>6</sup></p></li>- +<p><strong>Transient global amnesia (TGA) </strong>is a clinical syndrome with no clear aetiology identified. The syndrome is transient and typically resolves within a few hours. </p><h4>Epidemiology</h4><p>Transient global amnesia is most common in the 50-70 year age range <sup>ref</sup>.</p><h5>Associations</h5><ul><li><p><a href="/articles/migraine" title="Migraine">migraine</a> <sup>6</sup></p></li></ul><h4>Clinical presentation</h4><p>Anterograde and partial retrograde amnesia lasting less than 24 hours without any other neurological or congestive symptoms <sup>6</sup>. Episodic memories are more-so affected than semantic memories <sup>6</sup>. Most cases show complete resolution of symptoms within a few hours from onset of symptoms <sup>6</sup>.</p><h4>Pathology</h4><p>Several hypotheses (e.g. epileptic phenomena, stroke, focal ischaemia) have been proposed with no consensus on the exact mechanism <sup>1,6</sup>.</p><h4>Radiographic features</h4><p>CT brain and conventional sequences of MRI brain may show no abnormalities, especially while the patient is symptomatic.</p><h5>MRI</h5><p>Prospective and retrospective studies based on a small number of transient global amnesia patients can detect small punctate regions of abnormally restricted diffusion on DWI/ADC sequences in the CA1 area of the <a href="/articles/hippocampus">hippocampus</a> (lateral edge of the hippocampal gyrus abutting the temporal horn). These lesions can be bilateral and even multifocal <sup>2-4</sup>. These changes generally appear after symptom resolution, and the highest rate of detection is approximately 2 days after symptom onset <sup>6</sup>.</p><h4>Treatment and prognosis</h4><p>No treatment is required. The condition rarely recurs in ~5% of patients <sup>5,6</sup>.</p><h4>Differential diagnosis</h4><ul>
- +<li><p>strategic <a href="/articles/ischaemic-stroke" title="Ischaemic stroke">ischaemic stroke</a> (e.g. hippocampal infarct, bilateral forniceal infarct (<a href="/articles/amnestic-syndrome-of-the-subcallosal-artery" title="amnestic syndrome of the subcallosal artery">amnestic syndrome of the subcallosal artery</a>)), typically exists with other neurological deficits <sup>6,7</sup></p></li>
References changed:
- 7. Moussouttas M, Giacino J, Papamitsakis N. Amnestic Syndrome of the Subcallosal Artery: A Novel Infarct Syndrome. Cerebrovasc Dis. 2005;19(6):410-4. <a href="https://doi.org/10.1159/000086104">doi:10.1159/000086104</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/15925871">Pubmed</a>
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