Post-stroke dyskinesias

Abstract

Strokes, whether ischemic or hemorrhagic, are among the most common causes of secondary movement disorders in elderly patients. Stroke-related (vascular) movement disorders, however, are uncommon complications of this relatively common disease. The spectrum of post-stroke movement disorders is broad and includes both hypo- and hyperkinetic syndromes. Post-stroke dyskinesias are involuntary hyperkinetic movements arising from cerebrovascular insults and often present with mixed phenotypes of hyperkinesia which can sometimes be difficult to classify. Nevertheless, identification of the most relevant motor phenotype, whenever possible, allows for a more specific phenomenological categorization of the dyskinesia and thus helps guide its treatment. Fortunately, post-stroke dyskinesias are usually self-limiting and resolve within 6 to 12 months of onset, but a short-term pharmacotherapy might sometimes be required for symptom control. Functional neurosurgical interventions targeting the motor thalamus or globus pallidus interna might be considered for patients with severe, disabling, and persistent dyskinesias (arbitrarily defined as duration longer than 12 months).

Keywords: movement disorders; stroke; vascular dyskinesia.

Figure 1

Major types of post-stroke movement disorders. Hyperkinetic disorders are the most frequent, at least in the first year following the stroke. Choreiform dyskinesias are the most common phenotype, followed by dystonia, but non-choreo-dystonic dyskinesias (eg, tremor and asterixis) are generally far less common.

Figure 2

A simplified diagram of the motor control circuitry. The motor cortex projects to the cerebellum and basal ganglia and receives feedback signals from them. Although cerebellar output is tonically excitatory and basal ganglia output is tonically inhibitory, the balance between these two systems is of pivotal importance for motor control and coordination. GLU and GABA are the major excitatory and inhibitory neurotransmitters in this network, respectively. Abbreviations: GLU, glutamate; GABA, gamma-aminobutyric acid.

Figure 3

A simplified diagram of the basal ganglia motor circuitry, including its direct and indirect pathways. DA plays a central role in this circuit and acts as a neuromodulator that regulates the striatal function. Abbreviations: DA, dopamine; GLU, glutamate; GABA, gamma-aminobutyric acid; GPe, external globus pallidus; GPi, internal globus pallidus.

Figure 4

A simplified diagram of the cerebellar motor circuitry. The dentato-rubro-olivary circuit (Guillain-Mollaret triangle) is part of the cortico-cerebellar loop. The dentate nucleus projects to red nucleus via the SCP, which in turn connects to inferior olivary nucleus via the CTT. The latter nucleus projects back to the dentate nucleus via ICP. Abbreviations: SCP, superior cerebellar peduncle; CTT, central tegmental tract; ICP, inferior cerebellar peduncle.