Cerebral Hemispheric Infarct Following Ipsilateral IntraCerebral Haemhorrhage: Case Report and Review of Literature : Journal of Cerebrovascular Sciences

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Case Report

Cerebral Hemispheric Infarct Following Ipsilateral IntraCerebral Haemhorrhage

Case Report and Review of Literature

Narang, Sumeet; Dil, Jaspreet Singh; Raja, A; Dil, Sumeet Kaur

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Journal of Cerebrovascular Sciences 10(1):p 53-55, Jan–Jun 2022. | DOI: 10.4103/jcvs.jcvs_26_22
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The authors report the development of a cerebral hemispheric infarct in a patient who was diagnosed to have an intracerebral haematoma and neurologically worsened in the first 6 h. The occurrence of such a phenomenon is rare and scarcely reported. Possible explanations for the development of ischaemia in such a setting have been discussed based on existing literature.


Intra-cerebral Haemorrhage (ICH) is one of the most common of neurosurgical emergencies accounting for one-third of strokes. They are most commonly the result of rupture of intra-cerebral blood vessels due to hypertension and cause acute focal neurological deficit. Despite being a common entity, ICH may take an unexpected course in a patient in the clinical setting.


A 45-year-old female patient presented to the emergency room with a history of sudden-onset weakness in the left half of the body, associated with headache and vomiting. The patient had no previously known comorbidities, with no significant drug history.

On examination, she had a blood pressure recording of 220/120 mmHg, heart rate of 65 beats/min and a score of E2 M5 V3 on the Glasgow Coma Scale, with pupils bilaterally 2 mm in size, well reacting to light.

A computed tomography (CT) scan revealed an intracerebral haematoma (ICH) in the region of the right basal ganglion [Figure 1].

Figure 1:
Computed tomography scan showing right basal ganglionic haematoma at the time of presentation

The patient was admitted to the intensive care unit and was initially managed with anti-oedema measures and antihypertensives. However, within the next 6 h, the patient worsened in sensorium and exhibited decerebrate movements, and the right pupil was seen to have become enlarged and non-reactive to light.

The patient was intubated and mechanically ventilated, and taken up for a right parietotemporal decompression craniotomy and evacuation of the right basal ganglionic haematoma.

Intraoperatively, the brain appeared pale, edematous and non-pulsatile, suggestive of an infarct. A mid-frontal gyrus corticectomy was carried out to reach the haematoma which was suctioned out.

Post-operatively, the patient did not show signs of neurological improvement. A repeat CT scan done 12 h post-operative, revealed a large hemispheric infarct in the right internal carotid artery territory, with evidence of midline shift, corroborative of the intraoperative findings [Figure 2].

Figure 2:
Computed tomography scan showing right hemispheric infarct with midline shift


The occurrence of an infarct following an ICH is an uncommon phenomenon as compared to the reverse, i.e. the haemorrhagic transformation of an infarct. Even more surprising is the short duration within which the chain of events occurred from the time of onset of the haematoma. A review of existing literature shows that such a picture has rarely been reported, and much can be discussed about the pathophysiology of this event and the possible explanations for the same.

According to Besson et al.,[1] there were patients in their study population who developed lacunar infarcts before the onset of ICH, but also some patients who developed lacunar infarcts after, raising the doubt of a common link in the pathogenesis, but while it may be partly true, it was refuted by studies that differentiated the risk factors for both conditions, attributing ICH more to arteriolar pathology.[2]

Kim and Kim[3] have reported their experience with six patients who presented with ICHs but worsened neurologically and developed cerebral infarcts within 10 days; four out of six patients had territorial infarcts. ICHs themselves may predispose the development of infarcts through a combination of mechanisms, including mechanical compression of cerebral vessels, hemodynamic instability and dehydration, inflammation and concomitant small-vessel pathology.[4]

There have also been reported instances of infarcts developing in the background of traumatic subarachnoid haemorrhage, explained by vasospasm.[5]

Several experimental studies have been conducted to evaluate the cerebrovascular mechanisms involved in the development of ischaemia following an ICH. According to Mendelow[6] following ICH, the region of the brain surrounding the haematoma develops extensive ischaemia. The volume of this ischaemic brain may exceed the volume of the haemorrhage several times. There is also a component of the ischaemic process induced by vasoconstrictor substances in the blood and there is a reduction in cerebral perfusion pressure. The focal ischaemic event is initiated at the time of haemorrhage and is largely irreversible. It was also mentioned that early evacuation of the initiating mass lesion may help but is unlikely to reverse the ischaemia.

In another study by Nath et al.,[7] cerebral blood flow was studied in the brain of rats with experimental haemorrhage, and findings suggested that the degree of ischaemia at the time of an intracerebral bleed depended on the size of the lesion squeezing of the microcirculation by the haematoma, rather than a generalised alteration in perfusion pressure, as the cause of ischaemia.

The major question pertains to how this kind of presentation affects clinical management, and the key point is blood pressure regulation as rapid correction may predispose to ischaemia in the perihaematoma area.[8] Owing to the rarity of such a presentation, adequate clinical data are yet to be obtained from larger studies to ascertain the considerations that must be taken in clinical management.


Intracerebral haemorrhage may be complicated by the development of territorial or lacunar infarcts due to changes in cerebrovascular dynamics and can lead to rapid neurological decline.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


1. Besson G, Clavier I, Hommel M, Perret J. Association of lacunar infarction and intracerebral hematoma Rev Neurol (Paris). 1993;149:55–7
2. Beltran I, Lago A, Tembl JI, Landete L, Geffner D. Lacunar infarct and deep cerebral hemorrhage: a comparison of the risk factors Revista de Neurologia.. 1998;27:635–9
3. Kim CH, Kim JS. Development of cerebral infarction shortly after intracerebral hemorrhage Eur Neurol. 2007;57:145–9
4. Qureshi AI, Hanel RA, Kirmani JF, Yahia AM, Hopkins LN. Cerebral blood flow changes associated with intracerebral hemorrhage Neurosurg Clin N Am. 2002;13:355–70
5. Schinke C, Horst V, Schlemm L, Wawra M, Scheel M, Hartings JA, et al A case report of delayed cortical infarction adjacent to sulcal clots after traumatic subarachnoid hemorrhage in the absence of proximal vasospasm BMC Neurol. 2018;18:210
6. Wijman CA, Venkatasubramanian C. The effect of blood pressure on haematoma and perihaematomal area in acute intracerebral haemorrhage Neurosurg Clin N Am. 2006;17(Suppl 1):11–24
7. Mendelow AD. Mechanisms of ischemic brain damage with intracerebral haemorrhage Stroke. 1993;24(Suppl 12):I115–7 discussion I118-9
8. Nath FP, Jenkins A, Mendelow AD, Graham DI, Teasdale GM. Early hemodynamic changes in experimental intracerebral hemorrhage J Neurosurg. 1986;65:697–703

Haematoma; infarct; stroke

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