Purpose or Case Report: Case:

We present the case of a 3 year old male patient who presented to ED with right sided weakness and facial drooling post fall with head injury. On examination, there was residual right sided weakness with poor eye contact and communicative difficulties.

Urgent CT Head revealed a focal, well defined hypo-attenuation in the left basal ganglia (Figure 1).

Subsequent MRI Head and Angiogram demonstrated an anomalous origin of the left middle cerebral artery (MCA) and lenticulostriate arteries on Time of Flight (TOF) angiographic images. The left internal cerebral artery (ICA) gives off the left posterior communicating artery which loops back on it giving off a very small MCA and forming a large, odd looking A1 anterior cerebral artery (ACA) (Figure 2). The left lenticulostriate arteries arise on the horizontal segment of the loop which forms the A1 ACA (Figure 2).

The left perforator territory demonstrates high T2/FLAIR signal with diffusion restriction involving the left putamen and upper aspect of the left caudate nucleus as seen on CT (Figure 3).

The patient was initiated on antiplatelet therapy with aspirin. He subsequently represented two months later with transient left sided weakness. Neurological examination was grossly normal apart from a slow gate.

Repeat MRI demonstrated reduction in the extent of the previous T2 signal abnormality within the left putamen consistent with expected evolution of previous infarct (Figure 4).

Dual antiplatelet therapy with the addition of clopidogrel was initiated. Subsequent clinical follow up found improvement in his verbal ability and eye contact.

Discussion:

There are numerous reported anatomical variants involving the MCA, such as a duplicated, accessory and fenestration, which are related to the embryological development of the MCA (1-3). Recently, twig-like MCA’s have been reported which are likely thought to be a secondary consequence to developmental stenosis of the proximal MCA (4). There are currently no case reports describing the anomalous distal ICA, ACA and MCA findings such as those in our case report. We hypothesise that the patient clinical symptoms are likely due to the anomalous origin and tortuosity of the lenticulostriate arteries resulting in hypoperfusion and ischaemia (5). Clinical improvement was demonstrated after initiating antiplatelet therapy. Moreover, interestingly despite the small calibre MCA there was no evidence of ischaemia within this territory.
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