Clinical studyAkinetic mutism following stroke
Introduction
Akinetic mutism (AM), abulia and apathy are terms that have been used to describe behavioural abnormalities relating to reduced activity and slowness. Several investigators proposed that these clinical states are simply a continuum of severity of reduced behaviour and AM may be an extreme form.1
Following the landmark case report of Cairns et al.,2 the term AM had been used to describe a syndrome characterised by marked reduction of nearly all motor functions including facial expression, gestures and speech output but with some degree of alertness. They described a patient with an epidermoid cyst in the third ventricle whom after several evacuations of the cyst became more alert and responsive. Since then AM had been used in situations with similar clinical picture associated with different aetiologies and pathologies. There is considerable variation in the presentation of such patients and the clinical features of AM correspond more closely to the functional anatomy of the brain regions affected rather to the pathology.
This paper will appraise (i) stroke patients with AM selected to illustrate the variability in the clinical presentation, speech and language characteristics and course of the disease process and (ii) the likely pathophysiological mechanisms that underlie the diverse locations associated with AM.
Section snippets
Right supplementary area and cingulate gyrus
A 77-year-old right handed woman was seen with left-sided hemiplegia on day two. She was drowsy and responded poorly to verbal commands. She had a right gaze palsy with total weakness of the left arm and leg. The tone was decreased and the left plantar was extensor. She was in atrial fibrillation. On day 8 she was alert and non-communicative but seemed to comprehend. Three weeks later although she was alert, she was markedly akinetic with no speech output except for an occasional word. There
Discussion
Eight patients with AM involving different anatomical sites and of maximal importance the frontal lobe (supplementary motor area, cingulate gyrus), basal ganglia (caudate, putamen/globus pallidus) and the mesencephalothalamic regions were selected for consideration. The diagnosis of AM requires certain criteria for this is not only important scientifically but also for use in clinical practice and in research. Furthermore the heterogeneity among the patients with akinetic mutism may raise the
References (28)
- et al.
Prolonged abulia following putaminal haemorrhage
J. Stroke Cerebrovasc. Dis.
(2001) - et al.
Akinetic mutism and mixed transcortical aphasia following left thalamo-mesencephalic infarction
J. Neurol. Sci.
(1999) Cerebral bases of temperament and personality
Lancet
(1954)- et al.
Clinical effects of anterior cerebral artery infarction
J. Stroke Cerebrovasc. Dis.
(1998) - et al.
Caudate infarcts
Arch. Neurol.
(1990) - et al.
Akinetic mutism with an epidermoid cyst of the third ventricle
Brain
(1941) Cerebral vascular disease and behaviour. I. The syndrome of the mesencephalic artery
Arch. Neurol.
(1970)- et al.
Syndrome of the mesencephalic artery: report of a case with CT and neuropsychological findings
J. Neurol. Neurosurg. Psychiatry
(1985) - et al.
Development of akinetic mutism and hyperphagia after left thalamic and right hypothalamic lesions
Childs New System
(1993) - et al.
Anterior cerebral infarctions lausanne stroke registry
Arch. Neurol.
(1990)
Bilateral infarction in the anterior cerebral artery vascular territory due to an unusual anomaly of the circle of Willis
Stroke
Transcortical aphasia: importance of non-speech dominant hemisphere in language repetition
Brain
Hypometria with hemispatial and limb motor neglect
Brain
Structure and function of the supplementary motor area
Neurology
Cited by (96)
Disorders of Consciousness: Classification and Taxonomy
2024, Physical Medicine and Rehabilitation Clinics of North AmericaAkinetic Mutism and Coronavirus Disease 2019: A Narrative Review
2021, Journal of the Academy of Consultation-Liaison PsychiatryApathy: From the underlying pathophysiological mechanisms to future assessments and therapeutic strategies
2021, Encyclopedia of Behavioral Neuroscience: Second EditionOn the pathophysiology and treatment of akinetic mutism
2020, Neuroscience and Biobehavioral ReviewsMoral Motivation and the Basal Forebrain
2020, Neuroscience and Biobehavioral ReviewsCitation Excerpt :For example, the dorsal anterior cingulate region is activated for empathic simulation (Lockwood, 2016), such as sharing others’ pain (Lamm et al., 2011), with evidence for gyral versus sulcal functional subdivisions (Apps et al., 2016). Patients with anterior cerebral artery stroke regularly including the more posterior portions of the dorsal anterior cingulate develop the syndrome of “akinetic mutism” with a general lack of spontaneous activity and speech (Nagaratnam et al., 2004), but little evidence of selective social impairments. It is also important to note that most ventromedial frontal subregions are necessary for prosocial behaviour, such as strategic cooperation, more generally (Melloni et al., 2016) rather than selective for moral motivation.
Cingulate-basal ganglia-thalamo-cortical aspects of catatonia and implications for treatment
2019, Handbook of Clinical NeurologyCitation Excerpt :Over 50% of Fisher's series of 37 cases were secondary to bilateral ACC infarctions and subcortical infarcts affecting the ACC (Fisher, 1983). Nagaratnam et al. (2004) studied eight patients with akinetic mutism and the strokes responsible were in frontal (ACC, SMA, dorsolateral border area) cortices, BG (caudate and putamen), mesencephalon, and thalamus. Mega and Cohenour (1997) theorized that several disconnection points could disrupt the frontal-subcortical/ACC CSTC circuit and lead to akinetic mutism.