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Table of Contents    
Year : 2016  |  Volume : 64  |  Issue : 7  |  Page : 95-97

Complete middle cerebral artery block without brain infarction

Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication3-Mar-2016

Correspondence Address:
Sunil Pradhan
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Road, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.178048

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 » Abstract 

We report a patient with progressive supranuclear palsy and incidentally detected the absence of right middle cerebral artery (MCA) without any old or acute infarct in its territory. The magnetic resonance angiography and computed tomography angiography failed to detect any significant collateral circulation. We discuss the embryogenesis of brain circulation and offer a possible explanation for the nonvisualization of the right MCA in our patient.

Keywords: Computed tomography angiography; leptomeningeal collaterals; magnetic resonance angiography; middle cerebral artery

How to cite this article:
Pradhan S, Choudhury SS, Paliwal VK. Complete middle cerebral artery block without brain infarction. Neurol India 2016;64, Suppl S1:95-7

How to cite this URL:
Pradhan S, Choudhury SS, Paliwal VK. Complete middle cerebral artery block without brain infarction. Neurol India [serial online] 2016 [cited 2021 Jun 23];64, Suppl S1:95-7. Available from:

 » Introduction Top

Middle cerebral artery (MCA) is the most common site for thrombotic as well as embolic stroke. Embolic stroke results from sudden occlusion of the MCA with consequent hyperacute symptomatology. On the other hand, thrombotic stroke is caused by brain infarct that develops when the gradual narrowing of the blood vessel reaches a critical level. [1],[2],[3] The mild ischemia produced by gradual narrowing of the lumen of MCA provides stimulus for the development of collateral circulation from the adjoining blood vessels. This collateral circulation varies in degree in different individuals and is often not sufficient enough to prevent infarction though it may help in limiting its size. [4],[5],[6] We hereby present a patient who was incidentally found to have the complete occlusion of right MCA but had no brain infarction. Ironically, no significant collateral circulation was observed.

 » Case Report Top

A 73-year-old man, a recently diagnosed case of progressive supranuclear palsy (PSP) on levodopa therapy, presented with abnormal behavior leading to altered consciousness over 3 days. There was no history of headache, seizures, fever, head trauma, preceding diarrhea, or vomiting. The patient had a history of tremors in all four limbs, reduced volume of speech, slowness of daily activities, generalized stiffness leading to difficulty in walking and multiple episodes of backward falls for the last 6 months. There was no history of memory impairment, visual loss, limb weakness, sensory symptoms, or bladder-bowel involvement. The patient also suffered from hypertension and chronic obstructive lung disease and both were controlled on oral medication. The patient was a nonsmoker and occasional alcoholic. On examination, his pulse rate was 88/min, regular with both carotid arteries normally palpable. His blood pressure was 150/90 mm Hg. There was no evidence of renal or carotid bruit. The patient was stuporous (Glasgow Coma Scale - E3V3M5). On oculocephalic testing, his downward vertical gaze was restricted. He had rigidity in all four limbs. Motor examination did not reveal any focal neurological deficit. His routine blood tests revealed hyponatremia (Na = 122mEq/L). His magnetic resonance imaging of the brain showed generalized cortical atrophy without evidence of any old or acute brain infarction [Figure 1]. However, his magnetic resonance angiography showed nonvisualized right MCA without any significant collateral circulation. His single photon emission computed tomography (SPECT) showed normal brain perfusion. CT angiography showed minimal collateral vessels in the right MCA territory. The patient was diagnosed to have hyponatremia, and his consciousness improved over the next 2 days on oral correction by common salt. He continues to be mobile despite the presence of motor signs of PSP for the last 6 months.
Figure 1: (a) Magnetic resonance angiography shows nonvisualized right middle cerebral artery, (b and c) no evidence of acute infarct in the right middle cerebral artery territory on diffusion weighted images, (d and e) no evidence of right hemiatrophy or old infarct on T2-weighted image, and (f) paucity of collaterals in the right middle cerebral artery territory on computed tomography angiography

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 » Discussion Top

Despite complete occlusion of the right MCA, we failed to find any old or acute infarcts in the right MCA territory. The right MCA territory was normally perfused as evidenced by SPECT imaging but without any visible large collateral blood vessels on CT angiography arising either from the anterior or posterior cerebral arteries. Therefore, the possibility of a chronic gradually progressive occlusive disease affecting the right MCA such as atherosclerosis, vasculitis, etc., appears unlikely because such processes would lead to opening of the collaterals usually from the anterior cerebral artery (ACA) and rarely from the posterior circulation. Chronic occlusion of the MCA (or internal carotid artery [ICA]) may sometimes produce collaterals between the MCA and the branches of external carotid arteries. These collaterals are thin-walled blood vessels which do not provide adequate perfusion to prevent brain infarction and sometimes may even produce parenchymal hemorrhage as evidenced in patients with moyamoya disease. [7]

Another possibility was a normal variation of the circle of Willis with the absence of MCA. [8] Normal variations or anomalies that are known to affect MCA includes (1) duplication: Two vessels originating from the origin from ICA, (2) accessory MCA: Anomalous vessel originating from ACA that runs parallel to M1 segment of MCA, (3) early branching: Division of MCA close to its origin from ICA, (4) fenestration: Dual channels at origin from ICA, and (5) single trunk (nonbranching) MCA and trifurcated, quadrifurcated MCA. Congenital agenesis, aplasia, or hypoplasia of MCA is not known. However, congenital agenesis of ICA and ACA are reported. [9] We presume that our patient may represent one rare occurrence where the development of right MCA was arrested during embryogenesis. Embryologically, by 7-8 weeks of gestation and with ongoing development of the cerebral hemispheres, the circle of Willis is formed. [10] The major vessels, mainly the MCA gives rise to an annular network of leptomeningeal arteries that are classified as paramedian, short and long circumferential arteries depending upon their length or course over the cerebral hemispheres before they penetrate the neuropil. The penetrating branches of leptomeningeal arteries mainly supply the cerebrum. These penetrating arteries are classified as cortical, medullary, and straital. The cortical branches supply the cortex. The medullary branches further supply the deep brain regions such as the internal capsule and the basal nuclei. Both cortical and medullary arteries supply in a ventriculopetal (centripetal) manner as they course inward from the cortical surface towards the ventricles. In contrast, the straital arteries arborize close to the ventricles and mainly supply more central portions of the cerebrum and run towards the cortical surface (ventriculofugal arteries). During the first trimester, the ventriculopetal system remains the dominant arterial blood supply for the brain. However, by the third trimester, the central MCAs becomes dominant and anastomose with anterior and posterior cerebral arteries as the circle of Willis matures, and the leptomeningeal supply of the brain gradually becomes less dominant. [10] At some point of development of the central MCA, its occlusion or failure to grow (hypoplasia) might result in persistent leptomeningeal supply of MCA territory, as may be presumed in our patient. These persistent leptomeningeal perforators may not be large enough to appear on CT angiography. However, these may be seen on digital subtraction angiography (DSA). Unfortunately, we failed to perform DSA in our patient due to our inability to obtain consent for the same.

We conclude that nonvisualized MCA without any brain infarction in the MCA territory may represent a rare occurrence of a hypoplastic MCA with normal perfusion of its territory possibly by the remnant leptomeningeal collaterals.

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Conflicts of interest

There are no conflicts of interest.

 » References Top

Writing Group Members, Lloyd-Jones D, Adams RJ, Brown TM, Carnethon M, Dai S, et al. Heart disease and stroke statistics - 2010 update: A report from the American Heart Association. Circulation 2010;121:e46-215.  Back to cited text no. 1
Truelsen T, Piechowski-Józwiak B, Bonita R, Mathers C, Bogousslavsky J, Boysen G. Stroke incidence and prevalence in Europe: A review of available data. Eur J Neurol 2006;13:581-98.  Back to cited text no. 2
WHO. Global Burden of Stroke; 2010. Available from:   Back to cited text no. 3
Liebeskind DS. Understanding blood flow: The other side of an acute arterial occlusion. Int J Stroke 2007;2:118-20.  Back to cited text no. 4
Liebeskind DS. Collateral circulation. Stroke 2003;34:2279-84.  Back to cited text no. 5
Liebeskind DS. Neuroprotection from the collateral perspective. IDrugs 2005;8:222-8.  Back to cited text no. 6
Baltsavias G, Khan N, Valavanis A. The collateral circulation in pediatric moyamoya disease. Childs Nerv Syst 2015;31:389-98.  Back to cited text no. 7
Umansky F, Dujovny M, Ausman JI, Diaz FG, Mirchandani HG. Anomalies and variations of the middle cerebral artery: A microanatomical study. Neurosurgery 1988;22 (6 Pt 1):1023-7.  Back to cited text no. 8
Lie TA. Congenital anomalies of the carotid arteries. Amsterdam: Excerpta Medica; 1968. p. 35-51.  Back to cited text no. 9
Standring S. Gray′s Anatomy: The Anatomical Basis of Clinical Practice. 41 st ed. Amsterdam: Elsevier Health Sciences; 2015.  Back to cited text no. 10


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