Anteromedial thalamic infarct: a rare presentation

Abstract

We report a rare presentation of an anteromedial thalamic infarct in a 50-year-old woman with acute onset left eye ptosis, vertical gaze paresis and confusion. MRI identified an acute left anteromedial thalamic infarct with a severe left P1 stenosis. Thalamic infarcts are associated with marked neurobehavioural disturbances with dominant thalamic lesions causing language deficits, verbal perseveration, memory disturbances, abulia and disorientation. Ocular movement deficits can also be present and typically accompany paramedian lesions. Rarely, patients can develop an ipsilateral ptosis. We discuss these symptoms and review the literature.

Background

The clinical presentation is vital in the evaluation, diagnosis and management of neurological disease. An understanding of brain anatomy, disease and associated features can help guide whether additional workup needs to be done. We report a rare constellation of symptoms resulting from an anteromedial thalamic infarct.

Case presentation

A 50-year-old woman presented with acute onset left eye ptosis, diplopia and confusion. Her medical history was notable only for hypertension for which she was taking low dose amlodipine. On examination, she had a moderate left eye ptosis and impaired vertical movement of the left eye associated with diplopia. There was no diurnal fluctuation or fatigability, anisocoria or anhidrosis. She had minimal word finding difficulty with rare paraphasic errors.

Family reported that she had woken up with these complaints. Initially she was confused, agitated and screaming. She was asking nonsensical questions and speaking of characters in a book as if they were real people who might come visit. The family noticed the ptosis and her speech and brought her into the emergency department for an evaluation. She had no weakness, pain, numbness, paresthesias, ataxia, hyporeflexia or gait instability.

Investigations

The patient had stable vital signs, and routine blood work was unremarkable. MRI revealed an acute left anteromedial thalamic infarct with a severe left P1 stenosis (figures 1 and 2). There were no other areas of acute infarction.

Figure 1.

(A) Diffusion-weighted MRI showing acute left anteromedial thalamic infarct. (B) Apparent diffusion coefficient sequence with corresponding area of low intensity consistent with an acute infarct.

Figure 2.

Loss of flow-related signal involving the P1 segment of the left posterior cerebral artery (PCA) (arrowhead). The right PCA has a fetal origin and demonstrates normal flow-related signal.

Treatment

She underwent a comprehensive stroke workup, had no other vascular risk factors, patent foramen ovale (PFO) or other embolic source. She was treated with aspirin, statin and optimisation of her antihypertensive regimen.

Outcome and follow-up

Her left eye ptosis and vertical gaze paresis persisted at discharge. On follow-up, she reported often having trouble shifting her gaze when looking up and down from notes to a computer screen at work; however, this resolved within a couple months after discharge. Repeat imaging showed recanalisation of the left posterior cerebral artery (PCA).

Discussion

Studies of thalamic vascular supply and associated syndromes identify four major vascular territories. The tuberothalamic artery (also known as the polar artery) originates from the middle third of the posterior communicating artery and primarily supplies the anteromedial thalamus, though there are notable interpersonal variations and as many as one-third of the normal population derives supply from the paramedian artery.¹ The associated clinical syndrome is characterised by marked neurobehavioural disturbances with dominant thalamic lesions causing language deficits, verbal perseveration, memory disturbances, abulia and disorientation.^{2 3}

Rarely, anteromedial thalamic lesions can also cause an ipsilateral ptosis. A search of the English language literature found only a few case reports with unilateral or bilateral ptosis.^4–7 Another recent case report of a 74-year-old woman who presented with a left eye ptosis and found to have a left anteromedial thalamic infarct was attributed by the authors to a Horner’s syndrome from extension of the lesion to the hypothalamus. However, the patient was without any associated signs or symptoms of Horner’s, and the isolated ptosis may have stemmed from the thalamic infarction.⁸ This finding is attributed to a disruption of the supranuclear motor circuit to the levator palpebrae. A ‘cerebral ptosis’ in the setting of a hemispheric insult is well established and ascribed to a cortical region that controls eyelid elevation. It is theorised that any interruption of this supranuclear pathway can cause an ipsilateral ptosis. Ptosis resulting from an anteromedial thalamic lesion possibly involves the topographic correlate to the part of the precentral cortex responsible for eyelid elevation.^{5 9}

Abnormalities of ocular movements resulting from thalamic infarcts typically involve paramedian lesions. In a case series of 18 patients with thalamic infarcts, the highest frequency of horizontal and vertical gaze disturbances, including skew deviation, was associated with paramedian lesions. In this series, 10 patients had either an anterior or medial lesion of which only three had a vertical gaze palsy.¹⁰ Another review of patients with isolated thalamic infarcts identified nine patients with involvement of the anteromedial territory. Among those who had a dominant thalamic lesion, 75% were described to have a vertical eye paresis.² The mechanism underlying this finding is not completely understood though possibly attributable to frontocortical fibres decussating in the medial thalamus.^{11 12}

To our knowledge, this is the first report of a patient presenting with this constellation of symptoms resulting from an anteromedial thalamic infarct.

Learning points.

• The anteromedial thalamic syndrome is characterised by marked neurobehavioural disturbances with dominant thalamic lesions causing language deficits, verbal perseveration, memory disturbances, abulia and disorientation.

• Rarely these lesions can cause ptosis and/or vertical gaze paresis, for which the pathophysiology is not completely understood