Our patient presented with a transient inability to stand unsupported and marked truncal instability, characterised by contralateral pulsion due to an acute SMA infarction. He noted no other neurological symptoms or signs, such as motor weakness, sensory deficit, incoordination or parkinsonism. Thus, we consider this manifestation as an astasia. Astasia, which is the inability to stand unsupported despite normal strength, resembles the marked balance impairment observed in patients with vestibulocerebellar disease.1
Masdeu and Gorelick2
first described the cases of patients with thalamic astasia, and their patients fell toward the side contralateral to the side of lesions. They also described that thalamic astasia may mimic cerebellar disease. In other reports of astasia associated with other lesions, the direction of astasia was also contralateral to the site of lesions, such as the midbrain or posterior cingulate region.4 6
Our patient has only one lesion located in the unilateral SMA, in the absence of other lesions in the primary motor cortex, thalamus, brainstem or cerebellum. It has been shown that SMA lesions cause various abnormalities of motor function, such as the planning or initiation, including speech function.7 8
Chung et al7
reported the case of a patient who developed severe gait disturbance characterised by markedly impaired postural reflexes after apparent SMA seizure. However, their patient did not show contralateral pulsion. The exact mechanism of contralateral pulsion associated with SMA lesion has not been confirmed in either humans or animals. To the best of our knowledge, no cases of unilateral SMA lesions that cause contralateral pulsion as the sole symptom have been reported.
Astasia as the main clinical manifestation of supratentorial involvement has been associated with the thalamic ventrolateral region,1 3
or midbrain tegmental lesions.6
According to Solomon et al2
fastigial fibers of the vestibulocerebellar pathway project to the medial ventrolateral nucleus of the thalamus, and disruption of this pathway may be responsible for thalamic astasia. SMA also receives a thalamic input from the ventrolateral part of the thalamus, which receives inputs from cerebellar nuclei in animals.9
Disruption of this connection by SMA infarction may have been responsible for astasia in our patient.
Contralateral astasia associated with medial frontal lesions has rarely been described, and recently, only one case has been reported.4
Kataoka et al4
described a patient with posterior cingulate infarction who showed contralateral pulsion similar to that of our patient. They considered their patient's manifestation as astasia. Because the cingulated motor area receives a major thalamic input from the ventrolateral thalamus, disruption of this connection by a posterior cingulate infarction may be responsible for astasia in their patient. Moreover, SMA is also connected to the ventrolateral part of the thalamus, which receives inputs from the basal ganglia9
as well as the cingulated motor area. Disruption of this connection by SMA infarction also have contributed to the patient's astasia.
Astasia in our patient was transient, with resolution within 2 days. This finding was in accordance with those of previous reports.1 3
In Masdeu and Gorelick's report3
the inability to stand unassited lasted for an average of 3 days in six patients with infarction, and two of these patients presented with the inability to stand for only 1 day. They considered that the bilateral representation of fastigial vestibulocerebellar projection to the medial ventrolateral nucleus of the thalamus may be one of the factors for the transient nature of thalamic astasia. This finding may explain in part the transience of astasia in our patient.
In summary, the present finding raises the possibility that unilateral small SMA lesions can cause transient astasia following the disruption of the connection between SMA and the ventrolateral part of the thalamus.
- Astasia is an uncommon clinical feature of stroke, such as thalamic infarction.
- The role of SMA has been demonstrated in animals, but remains unclear in humans. Clinicians should be aware of the possibility of a SMA stroke in patients with contralateral astasia.