Asymptomatic Chronic Ischemic Penumbra from Middle Cerebral Artery Occlusion: A Case Report and Literature Review

Acute Middle Cerebral Artery (MCA) occlusion typically causes large hemispherical infarct within hours. However, cellular viability can be maintained in part of the brain tissue for days or months if there is good collateral circulation. We report a case of asymptomatic chronic ischemic penumbra from right MCA occlusion. Introduction Acute occlusion of the Middle Cerebral Artery (MCA) leads to permanent tissue damage and neurological deficit that are proportional to the duration of occlusion [1-3]. A cerebral blood flow of 8-23 ml/100 gram/min may be sufficient for cellular viability but insufficient for normal tissue function. Such potentially salvageable ischemic penumbra was originally described by Astrup et al [1]. Currently, CT perfusion imaging is routinely used to differentiate infarct core from ischemic penumbra [4-6]. The ischemic core is defined by matched decrease in both Cerebral Blood Flow (CBF) and Cerebral Blood Volume (CBV), whereas the ischemic penumbra is defined by a mismatch between CBF and CBV (i.e., delay in Mean Transit Time (MTT) and Time to Peak (TTP), and reduced CBF but normal or even increased CBV). CBV increases in the salvageable tissue due to auto-regulatory vasodilation (Table 1). Here we report a case of asymptomatic chronic ischemic penumbra. Measurement Core Penumbra Time to peak ▲▲ ▲ Mean transit time ▲▲ ▲ Cerebral blood flow ▼▼ ▼ Cerebral blood volume ▼ ▲ or ◄► Flow: volume Ratio Matched Unmatched Case A 50-year-old male presented with left sided numbness and mild hand weakness. Symptom onset was a day prior, approximately 21.5 hours ago. Initial NIHSS score was 2. Non-contrast CT of the head showed a small area of hypodensity in the right posterior insular cortex and a hyperdense right MCA (Figure 1 A and B). CT Angiogram of the brain and neck revealed right proximal MCA occlusion with excellent collaterals (Figure 1 C). CT perfusion delineated a small area of decreased CBV in the posterior insular cortex and a large area of delayed TTP, suggestive of a small ischemic core and a large ischemic penumbra (Figure 1 D and E). MRI Brain confirmed the acute infarct in MCA distribution on diffusion weighted imaging (Figure 1 F). The patient was not indicated for endovascular thrombectomy due to minor deficit and excellent collaterals. Extensive workup was unremarkable except for mild hypercholesterolemia with a total cholesterol level of 209 and LDL 127. The etiology of the stroke was likely intracranial atherosclerotic disease. Patient improved during hospitalization with only residual left sided numbness. Repeat CT perfusion on day 5 showed persistent mismatch between CBV and TTP, indicative of chronic ischemic penumbra. He was treated with maximal medical therapy with aspirin, clopidogrel, and atorvastatin daily. He was discharged with outpatient physical therapy and occupation therapy. The patient Citation: Sweidan AJ and Yu W (2020) Asymptomatic Chronic Ischemic Penumbra from Middle Cerebral Artery Occlusion: A Case Report and Literature Review. Ann Case Report 14: 337. DOI: 10.29011/2574-7754/100337 2 Volume 14; Issue 03 Ann Case Rep, an open access journal ISSN: 2574-7754 did not meet requirements inpatient rehabilitation therapy. He has been doing well without any new symptoms in the last 3 years. Figure 1: Non-contrast CT showed an area of hypodensity in the right insular cortex (A) and a hyperdense right MCA (B). CT angiogram revealed right M1 occlusion with excellent collaterals (C). CT perfusion demonstrated a small infarct core in the right posterior insular cortex (B) and a large area of the Time to Peak (TTP) prolongation, indicative of ischemic penumbra. A MRI brained confirmed acute anfarction in the R MCA distribution (F). Discussion In recent years, 10 randomized controlled trials demonstrated powerful efficacy of Endovascular Thrombectomy (EVT) for acute ischemic stroke from large vessel occlusion with 6-24 hours of symptom onset [7]. However, the treatment is not without risk of complication. The inclusion criteria in most of the recent studies were NIHSS ≥ 6. Our patient had minor deficit from MCA occlusion. CT perfusion showed large ischemic penumbra and excellent collateral circulation. This appears to be the first case report of a patient with documented chronic ischemic penumbra from MCA occlusion and excellent long-term outcome from medical therapy. Hypothetically, the patient may also do well with endovascular therapy due to presence of excellent collaterals [8]. Differentiating between benign oligemia and penumbra will always be a challenge [9]. Cerebral blood flow measurement and other perfusion surrogates are estimates at a given moment and thus our ability to separate benign oligemia, penumbra and core are prone to error [10]. Further studies are warranted to investigate chronic ischemic penumbra and endovascular therapy for patients with minor deficit from MCA occlusion [11].


Introduction
Acute occlusion of the Middle Cerebral Artery (MCA) leads to permanent tissue damage and neurological deficit that are proportional to the duration of occlusion [1][2][3]. A cerebral blood flow of 8-23 ml/100 gram/min may be sufficient for cellular viability but insufficient for normal tissue function. Such potentially salvageable ischemic penumbra was originally described by Astrup et al [1]. Currently, CT perfusion imaging is routinely used to differentiate infarct core from ischemic penumbra [4][5][6]. The ischemic core is defined by matched decrease in both Cerebral Blood Flow (CBF) and Cerebral Blood Volume (CBV), whereas the ischemic penumbra is defined by a mismatch between CBF and CBV (i.e., delay in Mean Transit Time (MTT) and Time to Peak (TTP), and reduced CBF but normal or even increased CBV). CBV increases in the salvageable tissue due to auto-regulatory vasodilation (Table 1). Here we report a case of asymptomatic chronic ischemic penumbra.

Measurement
Core Penumbra

Case
A 50-year-old male presented with left sided numbness and mild hand weakness. Symptom onset was a day prior, approximately 21.5 hours ago. Initial NIHSS score was 2. Non-contrast CT of the head showed a small area of hypodensity in the right posterior insular cortex and a hyperdense right MCA ( Figure 1 A and B). CT Angiogram of the brain and neck revealed right proximal MCA occlusion with excellent collaterals (Figure 1 C). CT perfusion delineated a small area of decreased CBV in the posterior insular cortex and a large area of delayed TTP, suggestive of a small ischemic core and a large ischemic penumbra (Figure 1 D and E). MRI Brain confirmed the acute infarct in MCA distribution on diffusion weighted imaging (Figure 1 F).
The patient was not indicated for endovascular thrombectomy due to minor deficit and excellent collaterals. Extensive workup was unremarkable except for mild hypercholesterolemia with a total cholesterol level of 209 and LDL 127. The etiology of the stroke was likely intracranial atherosclerotic disease. Patient improved during hospitalization with only residual left sided numbness. Repeat CT perfusion on day 5 showed persistent mismatch between CBV and TTP, indicative of chronic ischemic penumbra. He was treated with maximal medical therapy with aspirin, clopidogrel, and atorvastatin daily. He was discharged with outpatient physical therapy and occupation therapy.

Discussion
In recent years, 10 randomized controlled trials demonstrated powerful efficacy of Endovascular Thrombectomy (EVT) for acute ischemic stroke from large vessel occlusion with 6-24 hours of symptom onset [7]. However, the treatment is not without risk of complication. The inclusion criteria in most of the recent studies were NIHSS ≥ 6. Our patient had minor deficit from MCA occlusion. CT perfusion showed large ischemic penumbra and excellent collateral circulation. This appears to be the first case report of a patient with documented chronic ischemic penumbra from MCA occlusion and excellent long-term outcome from medical therapy. Hypothetically, the patient may also do well with endovascular therapy due to presence of excellent collaterals [8]. Differentiating between benign oligemia and penumbra will always be a challenge [9]. Cerebral blood flow measurement and other perfusion surrogates are estimates at a given moment and thus our ability to separate benign oligemia, penumbra and core are prone to error [10]. Further studies are warranted to investigate chronic ischemic penumbra and endovascular therapy for patients with minor deficit from MCA occlusion [11].