Correspondence Address: Dr. Neelav Sarma Neurology Outpatient Department, 2nd Floor, Dispur Hospital, Guwahati 781006, Assam India
Source of Support: None, Conflict of Interest: None
Movement disorders following stroke is a well known phenomena both during acute stage as well as in later phases. The type of movement depends on the site of involvement, it is however not uncommon to have more than one type of movement disorder following a stroke. We present a patient with combined dystonia and asterixis following a unilateral thalamic infarct, whose dystonia persisted on follow up while the asterixis faded away with time.
Keywords: Myoclonus dystonia, poststroke movement disorder, thalamic movement disorder
How to cite this article: Sarma N, Mahanta A. Dystonia and asterixis in acute thalamic infarct. Ann Mov Disord 2019;2:78-9
Movement disorders can be a complication in approximately 1%–4% of the patients who develop stroke. They can present as both Parkinsonism More Details and hyperkinetic movement disorder. The common poststroke hyperkinetic movement disorders include chorea, dystonia, tremor, and myoclonus., Although dystonia and asterixis have been described in isolation following stroke, simultaneous presence of both of these phenomena have been rarely described.,, We describe a case of combined dystonia and asterixis presenting as an early manifestation of unilateral thalamic infarct, which has not been described to the best of our knowledge.
A 65-year-old man, who is a known case of diabetes mellitus, presents with sudden-onset weakness in left upper limb and lower limb for 1 day. No history of seizure, loss of consciousness, headache, weakness in any other limbs, and difficulty in speaking or swallowing was reported. Motor examination revealed grade 4- (Medical Research Council Grade) power in wrist extension and hip flexion. On forward posturing of the arms, the patient had dystonic posturing of his left hand in the form of flexion at wrist and metacarpophalangeal joints. No dystonia was observed in lower limb, trunk, or tongue. He also showed intermittent jerks of the left hand suggestive of asterixis [Video 1]. He had normal sensory examination in all four limbs, graphesthesia and stereognosis were normal in left upper limb. Magnetic resonance imaging revealed acute infarct in the right thalamus and in the right temporo-occipital cortex [Figure 1]. The patient was placed on tetrabenazine and sodium valproate. On follow-up visit of 4 months after the day of presentation, the dystonia was persistent with the resolution of asterixis [Video 1].
Figure 1: Magnetic resonance imaging showing diffusion restriction in right thalamus and temporo-occipital cortex (A, B) with hypointensity in corresponding areas in apparent diffusion coefficient (C, D), suggestive of acute infarct
Poststroke movement disorders can present both as an early or delayed manifestation of stroke. Dystonia usually presents as a delayed manifestation of stroke. We present a patient with an early onset of dystonia with accompanying asterixis. The Lausanne Stroke Registry describing 29 cases of poststroke movement disorder out of 2500 stroke patients did not find any patient to have combined asterixis and dystonia. Similarly, a study from Ecuador describing 56 patients of poststroke movement disorder out of 1500 stroke patients did not find a combination of similar movements in their study. This shows the relative rarity of dystonia and asterixis presenting as a poststroke movement disorder in combination. Such movements have however been described in a case series of 11 patients by Perren et al., where one patient had asterixis with dystonia, however, the same patient had bilateral thalamic infarcts. Our patient has a unilateral thalamic infarct, which makes it a unique presentation. Two different case series of poststroke asterixis described by Kim (30 patients) and Tatu et al. (11 patients) did not find accompanying dystonia in those patients. Dystonia, as aforementioned, has a delayed onset following stroke. Factors that have been proposed to play a role include transsynaptic neuronal degeneration, inflammatory changes, oxidative stress, ephaptic transmission, remyelination, central synaptic reorganization, denervation supersensitivity, and neuroplasticity. Although early-onset dystonia has been described following thalamic stroke, it is relatively uncommon. Interruption/injury of the cortico-striato-pallido-thalamo-cortical loop has been implicated to induce dystonia. The two most common stroke locations causing dystonia include the striato-pallidum and thalamus. Asterixis is implicated to occur following the involvement of basal ganglia, thalamus, cerebellum, and frontoparietal cortex and cerebellum.
Asterixis usually has an early onset and has a tendency for early resolution. All the patients described by Kim and Tatu et al. had asterixis in acute phase of stroke and this movement resolved within 12 days in most of them. On the contrary, dystonia has a delayed onset and a lesser likelihood of complete resolution. Our patient showed similar characteristics on follow-up when the dystonic movements persisted with near resolution of asterixis.
To conclude, our case highlights the acute manifestation of dystonia and asterixis. Although such a co-occurrence has been described in a patient with bilateral thalamic infarcts, its presence in the setting of unilateral thalamic infarct makes it a unique presentation.