Akinesia

Akinesia

Akinesia is an inability to initiate voluntary movements. More usually in clinical practice there is a difficulty (reduction, delay), rather than complete inability, in the initiation of voluntary movement, perhaps better termed bradykinesia, reduced amplitude of movement, or hypokinesia. These difficulties cannot be attributed to motor unit or pyramidal system dysfunction. Reflexive motor activity may be preserved (kinesis paradoxica). There may be concurrent slowness of movement, also termed bradykinesia. Akinesia may coexist with any of the other clinical features of extrapyramidal system disease, particularly rigidity, but the presence of akinesia is regarded as an absolute requirement for the diagnosis of parkinsonism. Hemiakinesia may be a feature of motor neglect of one side of the body (possibly a motor equivalent of sensory extinction). Bilateral akinesia with mutism (akinetic mutism) may occur if pathology is bilateral. Pure akinesia, without rigidity or tremor, may occur: if levodopa-responsive, this is usually due to Parkinson’s disease; if levodopa-unresponsive, it may be the harbinger of progressive supranuclear palsy.

Neuroanatomically, akinesia is a feature of disorders affecting:

Frontal-subcortical structures (e.g., the medial convexity subtype of frontal lobe syndrome)
Basal ganglia Ventral thalamus
Limbic system (anterior cingulate gyrus).

Neurophysiologically, akinesia is associated with loss of dopamine projections from the substantia nigra to the putamen.

Pathological processes underpinning akinesia include:

neurodegeneration (e.g., Parkinson’s disease), progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome), multiple system atrophy (striatonigral degeneration); akinesia may occur late in the course of Pick’s disease and Alzheimer’s disease
hydrocephalus
neoplasia (e.g., butterfly glioma of the frontal lobes) cerebrovascular disease.

Akinesia resulting from nigrostriatal dopamine depletion (i.e., idiopathic Parkinson’s disease) may respond to treatment with levodopa or dopamine agonists. However, many parkinsonian/ akinetic-rigid syndromes show no or only partial response to these agents.

 

References

Imai H. Clinicophysiological features of akinesia. European Neurology
1996; 36(suppl1): 9-12

 

Cross References

Akinetic mutism; Bradykinesia; Extinction; Frontal lobe syndromes; Hemiakinesia; Hypokinesia; Hypometria; Kinesis paradoxica; Neglect; Parkinsonism