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| Year : 2007 | Volume
: 2
| Issue : 2 | Page : 92-93 |
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Post traumatic ischemic stroke in posterior and middle cerebral arteries following evacuation of extradural hematoma
Abrar A Wani, ML Babu, RU Altaf, K Altaf, AR Bhatt, T Raina, W Asrar, D Tanveer
Department of Neurosurgery, Sher-i-Kashmir Institute of Medical Sciences, Srinagar, India
Correspondence Address:
Abrar A Wani
Department of Neurosurgery, Sher-i-Kashmir Institute of Medical Sciences, Soura, Srinagar, J and K
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1817-1745.36775
How to cite this article:
Wani AA, Babu M L, Altaf R U, Altaf K, Bhatt A R, Raina T, Asrar W, Tanveer D. Post traumatic ischemic stroke in posterior and middle cerebral arteries following evacuation of extradural hematoma. J Pediatr Neurosci 2007;2:92-3 |
How to cite this URL:
Wani AA, Babu M L, Altaf R U, Altaf K, Bhatt A R, Raina T, Asrar W, Tanveer D. Post traumatic ischemic stroke in posterior and middle cerebral arteries following evacuation of extradural hematoma. J Pediatr Neurosci [serial online] 2007 [cited 2023 Dec 2];2:92-3. Available from: https://www.pediatricneurosciences.com/text.asp?2007/2/2/92/36775 |
 Introduction | |  |
Cerebral trauma leading to vascular occlusion is not a common entity, with incidence being reported in the range of 1.9-3.5%. [1],[2] It may occur in isolation or in association with other intracranial pathology, like epidural hematoma (EDH). [3],[4] The common territory found to be involved is that of the posterior cerebral artery because of compression of the vessel against free edge of tentorium due to rise in supratentorial pressure due to EDH. [2],[5] In the region of middle cerebral artery (MCA), infarct can occur due to displacement of MCA branches due to midline shift or shearing effect and dissection of MCA because of close proximity to lower wing of sphenoid. [4] Other causes of vascular occlusion are cerebral vasospasm and thrombosis.
| Case Report | | |
A 13-year-old girl had road traffic accident, and she reported to the Emergency Department with a Glasgow coma score (GCS) of 4. There had been a delay of 5 h in transporting the patient since the time of injury. She was intubated and resuscitated, and a CT scan was done, which revealed left parietal epidural hematoma [Figure - 1]. An urgent craniotomy and evacuation of the hematoma was done. She failed to improve in her sensorium and hence a check CT scan was done, which showed evolving left PCA infarct [Figure - 2]. Two days later another CT scan was done, which revealed fully evolved PCA infarct and small infarct in MCA territory which seemed to involve one of the terminal divisions, as involved region was small [Figure - 3]. Carotid Doppler study did not reveal any evidence of carotid dissection. After a few days, the patient's respiration improved but a low GCS of 5 persisted. A tracheostomy was done, and after 3 weeks the patient was discharged with a GCS of 7. Three months after injury, she was able to perform many of her household activities but still was not able to go to school.
| Discussion | | |
Cerebral infarction due to vascular occlusion is not a common entity. [1],[2] Since most of the trauma patients are evaluated using CT scan, it is to be differentiated from the other common lesion, viz., edema. Infarct corresponds to a particular vascular territory, is often wedge shaped with broad base externally and shows evolution. This evolution was seen in our case as well, since in the first postoperative scan there was minimal hypo density in PCA territory; and in the second postoperative scan there was complete infarct in PCA territory with occurrence of infarct in MCA territory as well.
The major cause of infarction following EDH is compression of the artery, which in case of PCA occurs due to rapid rise in supratentorial pressure leading to herniation and compromise of PCA due to compression against free margin of tentorium. [3] In case of MCA, it is usually due to the impact of relatively fixed M1 segment on the posterior margin of lower wing of sphenoid. [4] This can lead to subintimal injury leading to thrombosis or arterial dissection leading to occlusion of the vessel. [7],[8],[9] In case of MCA, infarction can also occur due to occlusion of small perforating branches, secondary to displacement of midline cerebral structures due to a mass lesion like extradural hematoma. [3]
The most common cause of subarachnoid hemorrhage is trauma. Blood in subarachnoid space can cause vasospasm and this can be a cause of infarction following trauma. [9],[10] In addition hyperpyrexia and epileptic seizure activity may elevate metabolic demand, inducing a relative state of ischemia. [11] Combination of EDH and infarction, though being a known entity, has been described only in a few papers. [2],[3],[12],[13],[14]
Mortality after posttraumatic infarction is variable. In some studies, mortality in craniocerebral trauma with complicating posttraumatic cerebral infarction does not differ significantly from that in craniocerebral trauma patients without posttraumatic cerebral infarction when matched for admission Glasgow coma score results. Thus, aggressive management should be considered even in the presence of posttraumatic cerebral infarction. [1] Meanwhile, some studies suggest infarction is an indicator of a poor clinical outcome, especially among patients with associated subdural hematoma, brain swelling/ edema and subarachnoid hemorrhage. In a series of studies by Server et al ., it was 43.8%. [4]
| Conclusion | | |
Occurrence of infarction after EDH implies a grave prognosis with high morbidity. Combination of PCA and MCA territory infarction following EDH is a rare entity. This can be avoided by rapid transportation of such patients to a neurocenter and rapid evacuation before occurrence of ischemic changes.
| References | | |
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| 4. | Mobbs RJ, Chandran KN. Traumatic middle cerebral artery occlusion: Case report and review of pathogenesis. Neurol India 2001;49:158-61. |
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| 10. | Wilkins RH, Odom GL. Intracranial arterial spasm associated with craniocerebral trauma. J Neurosurg 1970;32:626-33. [PUBMED] |
| 11. | Gade GF, Becker DP, Miller JD, Dwan PS. In: Pathology and pathophysiology of head injury. Neurological surgery. Youmans JR, editor. WB Saunders Company: Philadelphia; 1990. p. 1965-2016. |
| 12. | Fujimara M, Kaneyarna M, Motohashi O, Ishi K, Onuma T. Cerebral infarcts in caudate nucleus associated with EDH and diffuse brain injury in a child after severe head injury. Childs Nerv Syst 2004;20:430-3. |
| 13. | Patermiti S, Fiore P, Macri E, Marra G, Cambria M, Fakone F, et al . Extradural hematomas: Report of 37 consecutive cases with survival. Acta Neurochir (Wein) 1994;131:207-10. |
| 14. | De Caro M, Munari PF, Parenti A. Middle cerebral artery thrombosis after blunt head trauma. Clin Neuropathol 1998;17:1-5. |
[Figure - 1], [Figure - 2], [Figure - 3]
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