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Published on: July 2, 2013
Akinetic mutism following stroke
Nages Nagaratnam1, Kujan Nagaratnam, Kevin Ng
1Blacktown-Mount Druitt Health, NSW 2148, Blacktown, Australia.
Abstract:
This is an appraisal of the varied clinical presentation and the neural substrate for akinetic mutism following stroke. The diagnosis is important as akinetic mutism is often misdiagnosed as depression, delirium and locked-in-syndrome. This is a descriptive study of eight selected patients with akinetic mutism following infarction/haemorrhage in different regions of the brain with characteristic syndromes. They involved the critical areas namely, the frontal (cingulate gyrus, supplementary motor area and dorso-lateral border zone), basal ganglia (caudate, putamen), the mesencephalon and thalamus. The disorders of speech and communication took different forms. The speech disorder included verbal inertia, hypophonia, perseveration, softened and at times slurred. The linguistic disturbances were fluent, non-fluent, anomia and transcortical (motor, mixed) aphasias. The findings were related to what is known about the neuroanatomic location of the lesions and the role of the frontal-subcortical circuitry in relation to behaviour. Akinetic mutism could be explained by damage to the frontal lobe and or interruption of the complex frontal subcortical circuits.
Insights
Akinetic mutism following stroke presents diversely and is often misdiagnosed. Damage to frontal lobe circuits underlies this condition, impacting speech and behavior.
Area of Science:
- Neurology
- Neuroscience
- Clinical Neuroscience
Background:
- Akinetic mutism (AM) is a complex neurological condition characterized by a lack of spontaneous movement and speech.
- Accurate diagnosis of AM is crucial as it is frequently misidentified as depression, delirium, or locked-in syndrome.
- Understanding the neural substrates of AM is essential for improving patient outcomes.
Purpose of the Study:
- To appraise the varied clinical presentations of akinetic mutism post-stroke.
- To investigate the neural substrates associated with akinetic mutism.
- To differentiate akinetic mutism from similar neurological conditions.
Main Methods:
- A descriptive study was conducted on eight patients diagnosed with akinetic mutism following stroke.
- Lesion locations were identified in various brain regions, including the frontal lobe, basal ganglia, mesencephalon, and thalamus.
- Clinical presentations, including speech and communication disorders, were documented and analyzed.
Main Results:
- Akinetic mutism presented with diverse clinical features, affecting speech and communication.
- Observed speech disorders included verbal inertia, hypophonia, perseveration, and slurred speech.
- Linguistic disturbances encompassed fluent, non-fluent, anomic, and transcortical aphasias.
- Lesions were found in critical areas such as the frontal lobe (cingulate gyrus, supplementary motor area, dorso-lateral border zone), basal ganglia (caudate, putamen), mesencephalon, and thalamus.
Conclusions:
- Akinetic mutism following stroke can be attributed to damage in specific brain regions, particularly the frontal lobe.
- Interruption of complex frontal-subcortical circuits is a key factor in the development of akinetic mutism.
- Recognizing the distinct clinical presentation and neural basis of akinetic mutism is vital for accurate diagnosis and management.
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