Fisher described the lacunar infarct syndrome of ‘ataxic hemiparesis’ first in 1965, and later included other strokes that present with dysmetria that is out of proportion and ipsilateral to the side of weakness.2
A number of these patients presented with stuttering symptoms similar to the case reported here. Lesions that simultaneously interrupt pyramidal systems and adjoining frontopontocerebellar systems produce ataxic hemiparesis. Common locations are both anterior and posterior limb of the internal capsule, upper pons, and more rarely corona radiata, lentiform nucleus and thalamus.2,3
Gorman et al
have argued that lacunar infarctions originating in the capsule cannot be distinguished clinically from pontine stroke.4
It was for this reason that the follow-up MRI was performed with thin section coronal imaging through the brainstem. However, by the time the follow-up study was performed the patient’s symptoms had improved dramatically and the diffusion weighted image (DWI) lesion resolved concurrently. The brainstem was still unremarkable. Upon discharge 24 h later, the examination revealed no weakness and only subtle residual deficits with rapid alternating movements and orbiting (making circular motions with the arms as if boxing). The patient’s gait was stable and he was deemed safe to ambulate unassisted.
Prior case reports have demonstrated reversal of abnormality on DWI in patients with transient ischaemic attack (TIA) when imaged soon after symptom onset.5–7
A larger series published subsequently found that four of nine patients with TIAs had no residual evidence of infarct on follow-up imaging.8
However, a still more recent study demonstrated focal atrophy and T2 prolongation in nearly 80% of TIA related DWI abnormalities suggesting that the vast majority of such small areas of low diffusivity result in permanent tissue injury.9
A substantial small animal MRI literature indicates that reversible ischaemic abnormality on DWI is due transient decrease in mitochondrial ATP production and resulting cell membrane sodium–potassium pump dysfunction. In rat models, variation in the duration and intensity of ischaemia leads to wide variation in the percentage of affected neurons that die, but some cell death is seen even in brief ischaemia accompanied by complete normalisation of diffusivity.1,10
This supports the hypothesis that TIAs in human patients result from a degree or duration of ischaemia that causes relatively little permanent cell death.11
Likewise studies of average apparent diffusion coefficient (ADC) in regions of abnormality on DWI have shown higher ADC in patients with TIA when compared with stroke patients.12
On the other hand, recent human imaging studies have shown that improving the spatial resolution of clinical DWI sequences substantially increases the detection of ischaemic low diffusivity lesions on MRI of patients with stroke, raising the possibility that clinical TIA without detectable abnormality on DWI may actually represent infarcts too small to be detected by current clinical DWI techniques.13
While ongoing advances in imaging fuel controversy about both the pathophysiology and appropriate nosology of transient ischaemic clinical syndromes with detectable abnormality on DWI, there is emerging agreement that this entity requires prompt aggressive investigation and treatment because it signals an increased early risk for additional TIA and stroke.14,15
Our report contributes to this growing literature by providing a clear, well documented and temporally correlated case of normalisation of clinical and DWI abnormality within a very short time in an untreated patient with a stuttering presentation of ataxic hemiparesis.
- ‘Ataxic hemiparesis’ implies dysmetria that is out of proportion to weakness and can result from a lacunar stroke or transient ischaemic attack (TIA).
- Focal transient ischaemia may produce reversible abnormalities on diffusion weighted imaging (DWI) of the brain, emphasising the continuum between TIA and stroke.
- Transient ischaemic clinical syndromes with abnormalities on DWI warrant aggressive investigation and treatment to avoid additional ischaemic injury.