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Year : 2019  |  Volume : 67  |  Issue : 4  |  Page : 1126--1128

A Case of Artery of Percheron Infarct: Need for High Clinical and Radiological Suspicion

Arun K Agrawal, Kuljeet S Anand, Pawan Kumar, Jyoti Garg 
 Department of Neurology, PGIMER and DR RML Hospital, New Delhi, India

Correspondence Address:
Dr. Arun K Agrawal
Department of Neurology, PGIMER and DR RML Hospital, New Delhi - 110 001

How to cite this article:
Agrawal AK, Anand KS, Kumar P, Garg J. A Case of Artery of Percheron Infarct: Need for High Clinical and Radiological Suspicion.Neurol India 2019;67:1126-1128

How to cite this URL:
Agrawal AK, Anand KS, Kumar P, Garg J. A Case of Artery of Percheron Infarct: Need for High Clinical and Radiological Suspicion. Neurol India [serial online] 2019 [cited 2021 Jan 21 ];67:1126-1128
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Occlusion of artery of Percheron (AOP) causes infarction of bilateral paramedian thalami and midbrain.[1] It often poses a diagnostic difficulty to clinicians and diagnosis may often be missed due to varying clinical presentation and occasional inability to detect the infarct on early brain imaging. We had an interesting case presenting with acute onset altered sensorium and having bilateral thalamic and midbrain infarcts due to occlusion of AOP. A 68-year-old diabetic, hypertensive, and hypothyroid female, well controlled on regular medication, presented to emergency room with history of found lying unconscious in her bed in early morning hours. There was no history of fever, vomiting or headache, head trauma, substance abuse, hypoglycemia, seizures, or transient ischemic attack (TIA). On examination, blood pressure (BP) was 160/90 mm Hg with rest vitals normal. Glasgow Coma Scale (GCS) was 6 with flaccid quadriparesis, bilateral extensor plantars, and absent neck rigidity. Pupils were unequal, dilated on right side, and constricted on left side with no reaction to light. Fundus showed grade I retinopathy changes. Blood sugar, serum sodium, and rest emergency metabolic profile were normal. Urgent non-contrast computed tomography (NCCT) head showed no acute lesions and ruled out hemorrhage. Furthermore, a CT angiogram of brain excluded any major intracranial artery occlusion. Possibility of acute ischemic stroke was kept. The patient remained unconscious for the next 2 days and thereafter started opening eyes gradually and also moving her limbs. She started following verbal commands, but her sensorium was fluctuating and she remained drowsy most of the time. At this time, complete dropping of right upper eyelid was noted. Further examination revealed complete right-sided third cranial nerve palsy. Three days later, MRI brain showed bilateral paramedian ventromedial thalamic and bilateral paramedian ventral midbrain (right > left) suggestive of AOP infarct [Figure 1]. Two-dimensional (2D) echo showed grade I left ventricular diastolic dysfunction and concentric left ventricular hypertrophy (LVH) with LV ejection fraction (LVEF) 55%. There were no clots or vegetations. An extended continuous electrocardiogram (ECG) monitoring for 72 h also did not show any evidence of paroxysmal arrhythmias. Bilateral carotid Doppler showed thickening of intima media, but no significant luminal narrowing was observed. Her HbA1c was 6.3. Lipid profile and thyroid function tests were within normal limits. She was started on antiplatelets and statins. Gradually her sensorium improved well over a period of 2 weeks, but ptosis and extraocular movements did not improve.{Figure 1}

There are four normal anatomic variations in vascular supply of the thalami and midbrain. In variant IIb, which is quite uncommon, bilateral perforating thalamic arteries arise from one central arterial trunk called the AOP, which arises from P1 segment of one posterior cerebral artery (PCA). It supplies the paramedian thalami and the rostral midbrain bilaterally.[2] AOP infarction comprises around 0.1%–0.3% of all ischemic strokes. Lazzaro et al. described the four distinct ischemic patterns of AOP infarction involving bilateral paramedian thalami with varying involvement of midbrain and anterior thalamus. The V sign [axial T2/FLAIR magnetic resonance imaging (MRI) through the midbrain showing a V-shaped hyperintensity along the pial surface of the midbrain at the interpeduncular fossa), as seen in the index case, was identified in 67% of cases of AOP infarction with midbrain involvement and supports the diagnosis when present.[3] Common differentials for a patient presenting with acute alteration of sensorium and having bilateral lesions of thalamus include thrombotic and embolic vascular occlusions (arterial like top of basilar syndrome and venous like sinus thrombosis), infections (viral, tubercular, fungal, malarial, toxoplasma), and demyelinating disorders [acute disseminated encephalomyelitis (ADEM), multiple sclerosis (MS)]. Strokes with occlusion of AOP showing mid brain involvement demonstrate poor long-term prognosis as in our case third cranial nerve palsy did not improve. Clinical triad of fluctuating sensorium, impaired cognition, and vertical gaze palsy is seen typically in AOP infarcts, as seen in index case.[4] Less common presentations include hemiplegia, ataxia, and oculomotor disturbances (thalamopeduncular syndrome). Patients with basilar artery syndrome with occluded AOP can be considered for intra-arterial thrombolysis, but in our case time of onset of stroke was not clear, thus thrombolysis was avoided. Stroke involving AOP should be kept as a differential diagnosis in patients presenting with acute onset of altered sensorium particularly fluctuating with lesions localizing to bilateral thalamus and/or midbrain. MRI brain with diffusion/susceptibility weighted images are very helpful in detecting the lesions early and establishing the diagnosis, although this is not always true and initial imaging may also be normal. Less common presentations of AOP infarction should also be kept in mind. Other differential diagnosis should be carefully ruled out. Early establishment of diagnosis and institution of appropriate treatment is important for better recovery.

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