Correspondence Address:
Dr. Abhishek Juneja
A-15, Old Quarters, Ramesh Nagar, New Delhi - 110 015
India

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Dear Editor,

Occlusion of artery of Percheron (AOP) causes bilateral paramedian thalamic and midbrain infarction.[1] We report a case of a 62-year-old female patient who presented with sudden onset altered sensorium for 2 h. The patient had developed acute onset altered sensorium while she was sitting comfortably at home. There was no history of preceding fever, headache, vomiting, neck pain, or seizure. The patient was a diabetic and hypertensive for the past 10 years on regular treatment. On physical examination, her pulse rate and blood pressure were 92/min and 178/108 mm Hg, respectively. She was not responding to verbal or painful stimuli. Her pupils were normal in size and reactive to light. Bilateral optic fundi were normal. She had no motor response to a deep painful stimulus. Bilateral plantar responses were extensor. Her routine blood investigations were normal. She underwent noncontrast computed tomogram of the head which was normal. She started improving over the next 2 days. She started opening her eyes, moving her limbs and responding to simple verbal commands. She was found to have restricted vertical eye movements while horizontal eye movements were normal. She underwent magnetic resonance imaging (MRI) of head and magnetic resonance (MR) angiogram of head and neck vessels [Figure 1]. MRI brain showed diffusion restriction in bilateral paramedian thalami and rostral midbrain suggestive of AOP infarct. MR angiogram revealed poor flow related signals in the right posterior cerebral artery (PCA) particularly the proximal portion. Her two-dimension echocardiogram showed mild ventricular diastolic dysfunction. Carotid duplex showed bilateral atheromatous plaques without any significant luminal narrowing. The patient was given antiplatelets and hypolipidemic drugs. She gradually improved over the next 2 weeks and was discharged in stable condition.{Figure 1}

Vascular supply of the thalami and midbrain can have multiple anatomical variations. In one such variant, bilateral perforating thalamic arteries arise from one central arterial trunk called the AOP, which arises from P1 segment of one PCA. It supplies the paramedian thalami and the rostral midbrain bilaterally.[2] Other differential diagnoses for bilateral thalamic lesions include infections (viral, tubercular, and fungal) and demyelinating disorders (multiple sclerosis and acute disseminated encephalomyelitis). The clinical triad of altered sensorium, impaired cognition, and vertical gaze palsy is seen typically in AOP infarcts, as seen in our case.[3] Other less common presentations include hemiplegia, ataxia, and oculomotor disturbances. A stroke involving AOP needs to be considered in patients presenting with acute onset of altered sensorium, particularly fluctuating with lesions localizing to bilateral thalamus and/or midbrain. MRI brain with diffusion-weighted images is helpful in detecting the lesions early and establishing the diagnosis. Early diagnosis and prompt institution of appropriate therapy can prevent fatal complications.

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