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Year : 1999  |  Volume : 47  |  Issue : 2  |  Page : 157-8

A case of unpaired anterior cerebral artery occlusion producing akinetic mutism.






How to cite this article:
Oomman A, Madhusudhanan M. A case of unpaired anterior cerebral artery occlusion producing akinetic mutism. Neurol India 1999;47:157


How to cite this URL:
Oomman A, Madhusudhanan M. A case of unpaired anterior cerebral artery occlusion producing akinetic mutism. Neurol India [serial online] 1999 [cited 2020 Aug 7];47:157. Available from: http://www.neurologyindia.com/text.asp?1999/47/2/157/1624



Aplasia or congenital absence of one anterior cerebral artery (ACA) is seen in only 1% of angiograms. ACA territory infarcts constitute only 0.6% to 3% of all acute ischaemic strokes.[1],[2] Bilateral infarcts due to unpaired ACA occlusion is still more rare. A case of unpaired ACA occlusion by an embolus from the heart after a silent myocardial infarction producing akinetic mutism is presented.

A 49 year old former airman was admitted with history of sudden onset of loss of consciousness and right focal seizures becoming generalized. He had exertional breathlessness for two days prior to admission. He was a heavy smoker and alcoholic. On admission, he was unconscious but his vital signs were stable. Ocular fundi were normal. He was moving all the four limbs equally. Plantars were equivocal. There was a loud fourth heart sound but no cardiac enlargement or murmurs. Seizures were controlled with intravenous phenytoin and diazepam. The next day, the patient was noticed to be more alert. He was opening his eyes, had spontaneous blinking and was following the examiner with his eyes. He was however mute and incontinent. All deep tendon jerks were brisk. Gegenhalten and grasp reflex were present bilaterally. Sensations could not be tested.

His electro cardiogram was consistent with anterior wall myocardial infarction. 2D doppler study showed a large anteroapical dyskinetic area which was almost aneurysmal with a sessile mass (1.2 x 1.3cm.) suggestive of a clot at the apex. CT scan showed bilateral medial frontal, well delineated low attenuation areas more marked on the right side without contrast enhancement. DSA study revealed evidence of solitary (unpaired) ACA [Figure 1].

ACA territory is an uncommon site for occlusive vascular strokes. Bilateral infarcts form a very small subset among ACA territory infarcts. Many anatomic variations of ACA are found angiographically. ACA may be hypoplastic on one side in 4% and aplastic in 1.3% of cases. Variations in the post-communical segment include unpaired (0.5-5% ), bihemispherical (1%) and triplex (1-2%). The relative rarity of ACA territory infarcts can be highlighted by the fact that Nakajima[3] experienced only 27 cases of ACA occlusion from 1977 to 1989 of which only 4 were bilateral. Bogousslavaski[4] found ACA occlusion in only 1.8% of 1490 patients admitted with acute stroke. None of them came across bilateral ACA territory occlusion due to unpaired ACA block.

Akinetic mutism is a disorder of consciousness characterized by unresponsiveness but with superficial appearance of alertness. Akinetic mutism can occur with lesions of anteromedial frontal lobes, tumour of third ven tricle, surgical occlusion of both anterior cerebral arteries, bilateral cingulate gyrus lesions, spontaneous or embolic bilateral anterior cerebral artery occlusions, multiple sclerosis etc.[5],[6] Wide cavum septum pellucidum may play an important role in the occurrence of akinetic mutism in hydrocephalic patients.[7]

The present case had a silent anterior wall myocardial infarction with a clot as demonstrated by 2D doppler study. This case shows a constellation of relatively rare neurological findings. The embolic occlusion from a truly silent myocardial infarction, in anterior cerebral artery territory occurs in only 1-3% of all occlusive stokes. Secondly, bilateral ACA territory occlusion from obstruction of unpaired ACA is quite rare. Thirdly, akinetic mutism occurs only in less than one third of ACA strokes.

 

 

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Online since 20th March '04
Published by Wolters Kluwer - Medknow