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Year : 2010  |  Volume : 13  |  Issue : 2  |  Page : 148-149

Internal carotid artery dissection: An unusual cause of occipital infarction

National Hospital, Sri Lanka

Date of Submission28-Sep-2009
Date of Decision17-Oct-2009
Date of Acceptance20-Jan-2010
Date of Web Publication25-Jun-2010

Correspondence Address:
Inuka K Gooneratne
10/1 Borella Cross Road, Colombo 8
Sri Lanka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-2327.64634

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How to cite this article:
Gooneratne IK, Gamage R, Gunarathne KS. Internal carotid artery dissection: An unusual cause of occipital infarction. Ann Indian Acad Neurol 2010;13:148-9

How to cite this URL:
Gooneratne IK, Gamage R, Gunarathne KS. Internal carotid artery dissection: An unusual cause of occipital infarction. Ann Indian Acad Neurol [serial online] 2010 [cited 2022 Jul 4];13:148-9. Available from:

Carotid artery dissections (CAD) are uncommon but not rare. Incidence studies indicate between 2.5 and 3 cases per 100 000 population for all age groups, mean age of onset in the early 40s. [1] Traumatic carotid artery dissection is a recognized complication following severe head injury and trauma to the neck. CAD is an identified cause of stroke and accounts for 20% of strokes in the young. [2] Incidence of stroke before the age of 40 years accounts to nearly 10% of all strokes in the South Asian region. [3] Internal carotid artery dissections usually produce stroke in the middle cerebral artery territory or the border zone between the middle and anterior cerebral arteries. It is unusual for occipital infarction in the posterior cerebral artery (PCA) territory to be caused by internal carotid artery disease. The following describes a patient with this unusual presentation and highlights the mechanism of such a stroke and its implications.

A 22 year old male came to hospital complaining of headache, neck pain, and sudden onset left-sided hemianopia, upper limb paresis, and loss of sensation for a day. He had sustained blunt trauma to the head which involved neck hyper-extension, a week ago. He was discharged and was symptom free for approximately a week. Examination revealed a Glasgore Coma Score (GCS) of 15, left homonymous hemi-anopia, and left upper limb spastic mono-paresis with sensory loss. The rest of the examination was unremarkable.

CT brain showed a right occipital infarct [Figure 1]. Magnetic resonance angiography (MRA) showed an absent right posterior cerebral artery (PCA) [Figure 2]. All other intracranial vessels were normal. Digital subtraction angiography demonstrated occlusion of the right cervical internal carotid artery due to dissection [Figure 3] and normal flow in all other extra cranial vessels. Cardiac source of embolism and thrombophilc states were excluded. The patient was anticoagulated.

Traumatic carotid artery dissection is a recognized complication following head injury and trauma to the neck. The mechanism of injury involves hyper-extension of the neck resulting in tethering of the internal carotid at the base of the skull or stretching over the lateral processes of the upper cervical vertebrae. [4] This results in the tearing of the vessel between adventia and intima or intima and media. Rupture through the intima causes the formation of thrombus within the lumen and may lead to a critical occlusion of the internal carotid artery or a thrombo-embolic episode. CAD on angiography shows irregular, and often tapered, stenosis with the characteristic "string sign," "flame-shaped" occlusion [Figure 3].

Symptoms in blunt carotid injury classically do not appear until 12 to 24 h after injury. Neurologic symptoms sometimes may be delayed for several weeks [5] The clinical picture of CAD is variable, with either pure local symptoms, such as Horner syndrome associated with headache or cervical pain, or cerebral ischemia in up to 80% of patients. [6]

Incidence studies suggest PCA territory infarcts to be more common among strokes in the young. [7] This patient presented with hemiplegia and hemsensory loss which are features of middle cerebral artery territory infarction, along with visual field defects. Previous studies have shown that 17% of patients with pure cortical PCA strokes have face-arm-leg motor deficits and 23% have sensory deficits in the same distribution. [8]

This patient's imaging demonstrates a right CAD absent right PCA [Figure 2] and an infarct in the right PCA territory [Figure 1]. Such an occurrence is possible when a persistent fetal PCA, which takes direct origin from the internal carotid artery, acts as a conduit for embolism from the anterior circulation. The adult configuration PCAs branch off the top of the basilar artery and supply parts of the midbrain, subthalamic and basal nuclei, thalamus, inferior temporal lobe, and occipitoparietal cortices. The PCA is divided in to two parts by the posterior communicating artery (PcomA), the proximal part is named as the pre-communicating part (P1) and the distal part as the post-communicating part (P2). In the fetal PCA, the diameter of the ipsilateral pre-communicating (P1) segment of PCA is less than PcomA, so that the blood supply to the occipital lobe is mainly via the internal carotid arteries. Fetal PCA arising predominantly from the ICA is seen in 4.4% of the Sri Lankan population, while in India the incidence remains as high as 25%. [9] This mechanism of stroke has been described. [10]

Traumatic CADs are often missed, as there is a delay in the onset of signs and symptoms and when these signs do develop, they are often attributed to an associated head injury rather than a vascular injury. Failure to make a diagnosis of CAD may result in long-term neurologic sequelae or death, although spontaneous resolution of the condition does sometimes occur.

   References Top

1.Stapf C, Elkind MS, Mohr JP. Carotid artery dissection. Annu Rev Med 2000;51:329-47.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Smith S. Cervical arterial dissection: causes and treatment. Stroke Rounds 2003;1:2.   Back to cited text no. 2      
3.Das SK, Banerjee TK, Biswas A, Roy T, Raut DK, Mukherjee CS, et al. A prospective community-based study of stroke in Kolkata, India. Stroke 2007;38:906-10.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Li MS, Smith BM, Espinosa J, Brown RA, Richardson P, Ford R. Nonpenetrating trauma to the carotid artery: seven cases and a literature review. J Trauma 1994;36:265-72.  Back to cited text no. 4  [PUBMED]    
5.Crissey MM, Bernstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1974;75:543-9.  Back to cited text no. 5  [PUBMED]    
6.Biousse V, D'Anglejan-Chatillon J, Touboul PJ, Amarenco P, Bousser MG. Time course of symptoms in extracranial carotid artery dissections: a series of 80 patients [review]. Stroke 1995;26:235-9.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Naess H, Waje-Andreassen U, Thomassen L. Occipital lobe infarctions are different. Vasc Health Risk Manag 2007;3:413.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Kumral E, Bayulkem G, Atac C, Alper Y. Spectrum of superficial posterior cerebral artery territory infarcts. Eur J Neurol 2004;11:237-46.  Back to cited text no. 8      
9.De Silva KR, Silva TR, Gunasekera WS, Jayesekera RW. Variation in the origin of the posterior cerebral artery in adult Sri Lankan brains. Neurol India 2009;57:46-9.   Back to cited text no. 9      
10.Kόker W, Mull M, Block F, Thron A. Carotid artery dissections presenting as isolated posterior cerebral artery infarctions. J Neurol 1997;244:324-7.  Back to cited text no. 10      


  [Figure 1], [Figure 2], [Figure 3]


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