Post ischemic stroke - spasticity vs dystonia

Case contributed by Ettie Ben-Shabat
Diagnosis almost certain


Vertigo, left sided weakness and sensory loss.

Patient Data

Age: 65 years
Gender: Male

The images demonstrate an acute infarct involving the right PICA territory.

In addition, there is cortical signal abnormality and likely restricted diffusion involving the superomedial right frontal lobe, extending posterosuperiorly. There is also small area of restricted diffusion laterally in the right frontal lobe. Imaging findings are consistent with infarction within the right anterior cerebral artery territory and small foci of infarction in the right MCA territory.

There is mild hemorrhagic transformation within the right cerebellar infarct, with abnormal signal on the susceptibility weighted imaging but no increased T1 signal.

Case Discussion

Rehabilitation notes

Two years after the stroke, the patient presented with significant foot hypertonicity that interfered with their walking. The rehabilitation clinicians used neuroimaging to assist in differentiating between spasticity and dystonia. Neuroimaging also served to guide treatment decisions.


The term hypertonicity is often used interchangeably with the term spasticity, even though originally the term spasticity referred to a hypersensitive stretch reflex 1. Furthermore, spasticity has been shown to be associated with loss of motor function (muscle strength) 2.

Lesions that affect the primary motor cortex and/or corticospinal tracts and/or basal ganglia are commonly seen in people affected by lower limb spasticity 3. In this case, most of the primary motor cortex was intact. In addition, both the corticospinal tracts and basal ganglia were fully intact.


Patients affected by hypertonicity due to dystonia may present with a similar walking pattern to patients affected by spasticity. However, when dystonia is present, the stretch reflex and motor functions may be intact, as they were in this case. A distinct clinical feature that characterized this case was the significant sensory loss.

Abnormal brain function associated with upper limb dystonia has been observed in the premotor cortex 4. In this case, the frontal lesion affected the premotor cortex and supplementary motor area. A second lesion was found in the cerebellum, which impacted sensation (whilst the parietal lobe was intact). The literature also suggests that there is an association between sensory deficits and the presence of dystonia 5.

In this case, both lesion location (as shown on the MRI) and clinical presentation, supported the presentation of hypertonicity consistent with dystonia rather than spasticity.


Distinction between spasticity and dystonia is important because it may affect treatment choices. The patient in this case, was treated initially with Botulinum toxin A injections for reduction of hypertonicity, with limited effect (as the patient was not affected by spasticity).

On the other hand, treatment of dystonia, which included sensory training and sensory motor integration, was effective.


Observation of hypertonicity may be similar whether it was caused by spasticity or dystonia. Yet neuroimaging for lesion localization and careful clinical examination, can aid the clinician in differentiating between the two. Such distinction is important because it carries therapeutic consequences.

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