Rostral brainstem and thalamic infarctions

Julien Bogousslavsky MD (Dr. Bogousslavsky of the Swiss Medical Network has no relevant financial relationships to disclose.)
Jorge Moncayo-Gaete MD (Dr. Moncayo-Gaete of the International University of Ecuador has no relevant financial relationships to disclose.)
Steven R Levine MD, editor. (Dr. Levine of the SUNY Health Science Center at Brooklyn has received honorariums from Genentech for service on a scientific advisory committee and a research grant from Genentech as a principal investigator.)
Originally released November 15, 1996; last updated November 9, 2017; expires November 9, 2020

This article includes discussion of rostral brainstem and thalamic infarctions, Déjerine-Roussy syndrome, thalamic syndrome, Benedikt syndrome, Claude syndrome, Foville syndrome, midbrain infarction, Nothnagel syndrome, paramedian infarction, paramedian thalamic artery syndrome, Parinaud syndrome, thalamic infarction, top of the basilar syndrome, and tuberothalamic artery syndrome. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

The thalamus is a heterogeneous assembly of well-organized nuclei, most of which have extensive reciprocal connections with the cerebral cortex. Hence, the thalamus plays a critical role in sensory, motor, arousal, cognitive, and behavioral functions. The midbrain, which is the smallest and most rostral portion of the brainstem, gives rise mainly to the third and fourth cranial nerves and contains centers and pathways that mediate vertical gaze. The blood supply to both structures is elaborate. Thalamic infarcts are infrequent, and midbrain infarcts are even more so; however, both are associated with a large spectrum of clinical manifestations, which vary according to the vascular territory involved. In this article, the authors present in depth the clinical correlates of midbrain and thalamic ischemic lesions, while also summarizing the advances in treatment and prevention of ischemic lesions involving the different vascular territories of the thalamus and the midbrain.

Key points

 

• The thalamus and midbrain infarcts account for 10% and 1% of all cerebral infarcts, respectively.

 

• Decreased level of consciousness, vertical gaze paresis, and contralateral hypoesthesia are the main clinical manifestations of paramedian thalamic infarcts.

 

• Posterolateral infarction syndrome is characterized by contralateral pure sensory deficit, sensory motor stroke, or sensory motor deficit with abnormal involuntary movements.

 

• Oculomotor and supranuclear (conjugate or disconjugate) vertical gaze palsies are the most localizing manifestations of midbrain infarction.

 

• Small vessel disease is the prime etiology in thalamic infarcts.

 

• The etiology of midbrain infarcts remains undetermined in up to 50% of cases.

Historical note and terminology

Thalamic syndrome due to vascular lesions involving the ventrolateral nucleus of the thalamus was first delineated early in the nineteenth century by Jules Déjerine and colleagues (Dejerine and Roussy 1906). The main clinical findings were considered to be hemihypesthesia, nonsensory components (mild hemiparesis and hemiataxia), followed by choreoathetosis and delayed onset of pain in the same affected limbs (Dejerine and Roussy 1906).

Approximately 25 years later, Charles Foix described the anatomy of the arterial supply of the thalamus and was the first to associate thalamic infarction to occlusive disease of the posterior cerebral artery (Foix and Hillemand 1925). During the second half of the twentieth century, more important details of the vascular anatomy of the thalamus were provided mainly by Percheron (Percheron 1976).

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