Acute exotropia and blepharospasm due to bilateral paramedian thalamic infarct

Hypersomnolent state, severe amnesia, transient coma and vertical gaze abnormalities are characteristic features of bilateral paramedian thalamic infarcts. Vergence disorders or blepharospasm has recently been reported but there is no study reporting blepharospasm together with exotropia. In this paper, we present a case with bilateral paramedian thalamic infarct who had blepharospasm and acute exotropia. A 60-year-old, right-handed, male patient who was unconscious was admitted to the hospital. His history revealed a speech disorder and a headache preceding his unconsciousness. On physical examination the pulse rate was 86/min/regular, the blood pressure 200/120 mm Hg, and respirations 14 per minute. On neurologic examination, he was stuporous and his pupils were equal and myotic. Bilateral light reaction was diminished. There was bilateral persistent tonic spasm of the eyelids and the eyes were in divergence position. Plantar reflexes were bilateral extensor. Cranial CT disclosed bilateral hypodense infarct areas in the paramedian thalamic localisation. The patient was treated with an antiaggregant, dexamethasone and antihypertensive. No change was found in blepharospasm and divergence position during therapy. The patient died on the seventh day after stroke onset. The supranuclear organisation of the vergence system is not well-known, though conjugate eye movements are mostly understood. Dysfunction of the vergence in structures contributing to neural integration may be due to disordered convergence secondary to organic conditions. Although the anatomic pathway of these signals has not yet been identified, divergence eye movements have been assumed to result from a complementary input from divergence neurons to the lateral rectus motoneurons. Divergence position in our case might be related to convergence paralysis or excessive stimulation of divergence neurons due to involvement of vergence pathways. Data from previous studies indicate that convergence paralysis might be more responsible for acute exotropia in bilateral paramedian thalamic lesions. The pathophysiological mechanism for disorders of eyelid movements is not well known. Bilateral eyelid opening in awake patients by unilateral stimulation in the prefrontal, occipital and rarely precentral cortices has been demonstrated. Reflex blepharospasm or excessive eyelid closure that is provoked by attempts to hold the eyelids open is seen with nondominant hemispheric infarction, brainstem lesions or rarely in thalamic vascular events. In conclusion, we propose that vergence and eyelid functions are already closely linked with the paramedian thalamic area and the descending cortical pathways which pass through the paramedian thalamus and exert an inhibitory input to premotor vergence neurons in the midbrain. We would like to point out the fact that although paramedian thalamic infarcts are considered not to be fatal, our patient died on the seventh day after stroke onset. This case raises the question of whether acute vergence together with eyelid function abnormalities could be a negative prognostic sign.