The MCA is the largest branch of the internal carotid artery and is the continuation of this artery into the Sylvian fissure; the MCA starts just below the medial part of the anterior perforated substance. This artery is the source of blood supply of most of the lateral surface of the cerebral hemisphere in addition to deep structures (white and grey matters) of the frontal and parietal lobes.1
In terms of vascular anatomy, the MCA is divided into three ‘segments’: the proximal, Sylvian and the distal segments. The penetrating lenticulostriate arteries arise from the posterior and superior aspect of the ‘proximal’ segment; the adjacent corona radiate, external capsule, claustrum, putamen, parts of the globus pallidus, body of the caudate nucleus and the upper parts of the anterior and posterior limbs of the internal capsule are nourished by these penetrating arteries. The Sylvian segment gives rise to branches in the Sylvian fissure that supplies the insula of Reil. Then, the distal segment of the stem may face one of three paths: it may bifurcate into two branches in 78% of individuals, it may trifurcate into three arteries in 12% of individuals or it may divide into multiple trunks with variable sizes and length.2
Therefore, the commonest event is that the MCA divides into anterior and posterior branches that supply most of the lateral surface of the cerebral hemisphere. Because of this variable vascular anatomy, the clinical picture of MCA occlusion is highly variable and may be isolated to a specific area—for example, complete proximal main stem occlusion, deep arterial territory infarction or superficial cortical (anterior or posterior) syndromes.3 4
Acute unilateral ischaemic stroke confined to the lenticular nucleus (putamen and globus pallidus) is a rare event comprising 1.6% of the deep MCA territory ischaemia. The overall clinical pictures of isolated deep MCA ischaemic strokes are usually dominated by damage to the internal capsular structures rather than the damaged lenticular nucleus; therefore, faciobrachiocrural paresis is the most prominent feature in most patients.5
Ghika et al6
and Moulin et al7
reported pure infarctions limited to the internal capsule with a multitude of presentations; however, pure ischaemic stroke confined to the lenticular nucleus remains poorly defined. According to Giroud et al
the presentation of lenticular nuclear damage may include a cognitive-behavioural syndrome (mainly from pallidal lesions) or a motor syndrome (resulting from putamenal damage). However, this distinction is blurred in most cases by the variable vascular supply and efficiency of the collaterals.
Our patient developed an acute ischaemic infarction involving the left putamen, globus pallidus, part of the caudate nucleus and the anterior limb of internal capsule—a coma-shaped area on brain CT scan or MRI. Most likely, this has resulted from occlusion of the lateral striate branches of the proximal segment of the MCA ending with the so-called striato-capsular syndrome.9
This syndrome comprises hemiparesis (usually affects the arm more than the leg) and cortical signs (from damage to the subcortical fibres connecting the cortex and deep structures) such as non-fluent aphasia, neglect, apraxia and so forth.9
The patient's speech disturbance is clinically consistent with an expressive type of dysphasia. Very rarely, the speech disturbance of striato-capsular infarctions may manifest itself as a mild limb weakness but with severe dysarthria.9
However, Bhata and Marsden10
suggested that abulia is the commonest behavioural abnormality in patients with focal basal ganglia lesions; this might easily be considered a dysphasic component of the symptomatology. Nadeau and Crosson11
critically reviewed the available literature of ‘subcortical aphasia’. They concluded that the language defects of striatocapsular infarctions are due to sustained hypoperfusion of the overlying cortex that is not visible on the conventional imaging studies. Conventional four-vessel cerebral angiography is a very valuable tool in defining the vascular occlusion and its anatomy; unfortunately, the lack of expertise in our hospital radiology department with regard to this invasive investigation cancelled the use of this option.
We believe that the resultant cytotoxic oedema of the infracted tissue has resulted in a mass effect and impingement of the underlying thalamus and upper midbrain with secondary dysfunction of the ascending reticular activating system; the possible cause behind this patient's coma. However, this is unlikely to develop within a ‘few hours’ of the vascular occlusion. The patient's daughter insisted that her mother did not complain of any weakness and the family did not notice any abnormalities in their mother's speech; the only notion was that the patient's consciousness progressively deteriorated to the point of reaching coma within a few hours. We question the duration of the patient's initial presentation; we believe that the duration of the deterioration of her consciousness is much longer.
The patient came back after 2 weeks for a scheduled follow-up visit. She demonstrated a right-sided pyramidal weakness of grade 3 and an extensor planter. During the visit, she did utter a few sounds but no single word. During this visit, we noticed right-sided spasticity. We specifically asked the family if there was any ‘dystonic’ posturing or any abnormal movement of the right arm/leg during the past 2 weeks and the reply was no. Giroud, Bhatia and Marsden8 10 12
noticed that dystonia was the commonest acute, subacute or delayed manifestation of lenticular damage. Our patient did not develop such a manifestation and this observation is consistent with that of Russmann and colleagues5
; none of their 13 patients with pure lenticular infarctions developed any form of movement disorders.
- The MCA is a medium-sized artery that supplies most of the hemispheric structures, both superficial and deep.
- The variable vascular anatomy of the MCA may result (when occluded) in a multitude of hemispheric ischaemic strokes syndromes with atypical presentations and brain imaging findings. The inexperienced physician might easily misdiagnose these syndromes as neoplastic or infectious process.
- The occurrence of ‘sudden’ or rapidly progressive neurological dysfunction(s) should always prompt the physician to search for a vascular cause, even if the brain imaging findings are atypical.
- Isolated ischaemic infarction of the lenticular nucleus and part of the caudate is a very rare event resulting from occlusion of the lateral striate arteries; because of the location and shape of the damaged area, an alternative diagnosis, other than stroke, usually comes into mind.
- Pure lenticular infarction may not commonly result in dystonia in contrast to what is mentioned in previous literature.