Journal of Postgraduate Medicine
 Open access journal indexed with Index Medicus & EMBASE  
     Home | Subscribe | Feedback  

CASE REPORT
[Download PDF
 
Year : 1990  |  Volume : 36  |  Issue : 4  |  Page : 230-2  

Anterior cerebral artery territory infarction (a case report).

MA Kothari, AV Pathare, NJ Burkule, VV Joshi, AA Chikhalikar, SG Dalvi 
 Department of Medicine, Seth G.S. Medical College, Parel, Bombay.

Correspondence Address:
M A Kothari
Department of Medicine, Seth G.S. Medical College, Parel, Bombay.




How to cite this article:
Kothari M A, Pathare A V, Burkule N J, Joshi V V, Chikhalikar A A, Dalvi S G. Anterior cerebral artery territory infarction (a case report). J Postgrad Med 1990;36:230-2


How to cite this URL:
Kothari M A, Pathare A V, Burkule N J, Joshi V V, Chikhalikar A A, Dalvi S G. Anterior cerebral artery territory infarction (a case report). J Postgrad Med [serial online] 1990 [cited 2017 Oct 22 ];36:230-2
Available from: http://www.jpgmonline.com/text.asp?1990/36/4/230/821


Full Text




  ::   IntroductionTop


It is important to recognize the anomalies of the cerebral circulation. This is especially true of the anterior cerebral arteriesacas, as they supply blood to both the hemispheres[1],[2]. Anomalies of the anterior cerebral arteries are not quite rare as believed[3],[4]. Baptista[3] demonstrated anomalies of the ACA in 25% of the brain specimens he studied. A review of literature reveals that accessory ACA is the most common anomaly with an incidence varying from 0.5 to 20%, followed by bihemispheric ACA (12 to 13.3%), unpaired or azygous ACA (0.3 to 3.2%) (Table 1) and aplastic ACA (0.3 to 1.1%)

We describe here an unusual presentation of cerebrovascular accident in the ACA territory with an aplastic ACA.


  ::   Case reportTop


MYK a 64-year-old mate was admitted to the King Edward Memorial Hospital in March 1989, complaining of sudden onset of throbbing, bifrontal headaches associated with non-projectile vomiting, followed 72 hours later by incontinence of urine and inability to get up from the bed and walk on his own. However, he could move all his limbs in bed. There was no history of unconsciousness, convulsions or any cranial nerve involvement. He also did not complain of fever or neck pains. He was a non-hypertensive, non-diabetic individual and had suffered an anteroseptal myocardial infarction two years ago.

On general examination, his vital parameters were normal. His pulse was 80 beats/minute and blood-pressure in right brachial artery in supine position was 170190 mm of Hg. All the peripheral pulses including the carotids were well felt. On central nervous system examination, he was conscious, cooperative, well oriented in time, space and person. Examination of the motor system, sensations and deep tendon reflexes were normal. The planter reflex was extensor in both the lower limbs. There were no cerebella signs. He also did not have any signs of frontal lobe involvement such as the palmomental reflex, contra lateral grasp reflex, the sucking reflex etc. Examination of the other systems was unremarkable.

On investigations his hemogram, routine urine, stool examination and blood chemistry were all normal. His ECG revealed evidence of an old anteroseptal infarction. Two dimensional echocardiography was normal with no dyskinetic segment. Radiograph of his chest and skull were normal. His cerebrospinal fluid examination was normal with no evidence of haemorrhage or xanthochromia. His computer axial topography revealed hypo dense lesions in both the frontal lobes (See [Figure:1] and [Figure:2]). The ventricles were mildly dilated and there was minimal post-contrast enhancement of the hypo dense lesions in both the frontal lobes, suggestive of bilateral infarctions. Bilateral carotid angiograms were then performed. Right common carotid injection did not pacify the right ACA; however, left common carotid injection of contrast revealed simultaneous pacification of both the ACA branches (See [Figure:3], [Figure:4], [Figure:5], [Figure:6]), thus establishing the diagnosis of an aplastic right ACA.


  ::   DiscussionTop


Considerable variations occur in the origin and course of the ACAs[3],[4]. However, three distinct patterns are well recognised[3]. The most common anomaly is the accessory ACA. In this case, besides the right and the left ACAs, a third, middle or median artery is present and distributes blood to either or both the hemispheres. The next most common anomaly is the bihemispheric ACA. In this case, both the right and the left ACAs are present. However, one of them sends, one or more branches which cross the midline to distribute blood to the medial surfaces of both the cerebral hemispheres. The least common anomaly is the unpaired or azygous ACA, in which case, instead of a right or left ACA, only a single unpaired artery is present and it supplies blood to the medial surfaces of both the cerebral hemispheres.

Baptista[2] defines a bihemispheric ACA as one, which in its initial portion furnishes branches only to the homolateral cerebral hemisphere and then, at some point in its further course sends, one or more branches across to supply the opposite cerebral hemisphere. He has further sub-classified them into eight sub-groups[3], based on the different variations. However, our patient does not fit into any of these sub-groups as no portion of the right ACA was visualised on anglography, (See [Figure:3]-[Figure:4]), signifying that our patient had a rudimentary or an aplastic ACA.

Aplasia of the ACA is quite rare. As quoted by Krayenbuhl and Yasargil[5], it was observed, (1) once by Curry and Culbreth and once in 360 cases by Von Mitterwallner, and in none of the 83 brain specimens examined by Adachi and Hasebe. Angiographically, as quoted by kreyan bulak and Yasargils Tonnis and Schiefer reported aplasia of ACA in two (0.7%) of their 265 cases, whereas Krayenbuhl and Yasargil have observed it in only two (1.1%) of their 185 cases.5 The bilateral carotid angiograms in our patient clearly demonstrates aplasia of the right ACA and a bihemispheric distribution of the blood supply through the left ACA.

Incontinence and gait aplaxia are two of the commonest manifestations of ACA territory infarction. However, the clinical picture depends on the location and size of the infarct, which in turn relates to the site of occlusion, the pattern of blood flow through the circle of Willis and other ischaemia-inodifying factors[4].

Unilateral occlusion of the stem of the ACA proximal to its connection with the anterior communicating artery is usually well tolerated since adequate collateral flow comes from the ACA of the opposite side. Maximal disturbance occurs when both arteries arises from one ACA stem, in which case there will be infarction of the medial parts of both the cerebral hemispheres. This produces Para paresis; with weakness more marked peripherally, urinary incontinence and aboulic and aphasic symptoms. These patients lie in bed unwilling to initiate any voluntary movement including speaking, appear to watch other people by following them with their eyes, take food and drink only if it is placed in their mouth and make sucking noises and chewing movements but otherwise seem uninterested in their surroundings[5].

Complete infarction due to occlusion of one ACA distal to the anterior communicating artery results in a sensory-motor deficit of the opposite foot and leg and a lesser degree of paresis of the arm with sparing of the face[1]. Urinary incontinence, contra lateral grasp and sucking reflexes and Para tonic rigidity (Gegenhalten) may be evident. Foot drop is a constant finding and difficulty in walking is even greater than expected from the weakness present because aplaxia of gait is an additional problem and may be combined with loss of position sense in the affected limb[5]. Also, transcortical motor aphasia could occur with the occlusion of Hetibner's branch of the left ACA[4]. Branch occlusion of the ACA produce only fragments of the total syndrome, as would be expected, usually produces a spastic weakness or cortical sensory loss in the opposite foot and leg[1].


  ::   AcknowledgmentTop


We thank the Dean, Seth GS Medical College and King Edward Memorial Hospital, Bombay, for permission to present this case report.

References

1 Adams RD, Victor M. Cerebrovascular diseases. In: “Principles of Neurology”, IIIrd Edition, New York: McGraw-Hill Book Company; 1985, pp 569-640.
2Baptista AG. Studies on the arteries of the brain. II. The anterior cerebral artery: some anatomic features and their clinical implications. Neurology 1963; 13:825-835.
3Critchley M. The anterior cerebral artery and its syndromes. Brain 1930; 53:120-165.
4Kistler JP, Ropper AH, Martin JB. Cerebrovascular Disease. In: "Harrison's Principles of Internal Medicine," JD Wilson, E Braunwald, KJ Isselbacher, KG Petersdorf, JB Martin, AS Fauci, RY Root, editors. 12th Edition, New York: McGraw-Hill Inc; 1991, pp 1977-2001
5Krayenbuhl H, Yasargil MG. Radiological anatomy and topography of the cerebral arteries. In: "Handbook of Clinical Neurology." PJ Vinken, GW Brulyn, editors. Vol. No. 11. Vascular diseases of the nervous system. Part 1. Amsterdam: North-Holland Publishing Company; 1972, pp 65-101.

 
Sunday, October 22, 2017
 Site Map | Home | Contact Us | Feedback | Copyright  and disclaimer