Introduction

   Acute esotropia following supranuclear lesions is characterized by tonic ocular inward deviation and limitation of abduction. Although it is a rare clinical manifestation, it may be seen secondary to thalamic and brainstem lesions, which may affect ipsilateral or contralateral eye.⁵⁾⁶⁾⁷⁾ In thalamic hemorrhage, contralateral eye may be more affected and esotropia can be accompanied by upgaze palsy, which is characteristic of a midbrain lesion.^6)7)19) Few reports have described this ocular finding, however, the exact mechanism is not obvious. 
   We describe three patients who presented with ipsilesional or contralesional inward ocular deviation due to thalamic hemorrhage and discuss the possible mechanisms. 

Case Report

1. Patient 1：
   A 76-year-old right-handed man with hypertension developed sudden right hemiparesis and dysarthria. The patient had experienced a stroke 6 years previously and had been treated with aspirin. On admission, the patient's blood pressure was 220/130 mmHg, pulse 75 per minute, and respirations 22 per minute. Neurologic examination disclosed impaired consciousness and right sided weakness(upper limb; grade II, lower limb; grade III). The pupils were equal at 3.0 mm and reactive to light, and no ptosis was evident. In the primary position, the left eye was tonically deviated inward and immobile to left side and did not respond to doll's eye maneuver (Fig. 1). The patient was unable to elevate both eyes upward. The right eye was fully mobile in the horizontal plane. At the time of admission, Computed tomographic scan of the head showed left thalamic and intraventricular hemorrhage descending into the ipsilateral midbrain (Fig. 2). The patient underwent stereotactic catheter insertion. After 4 days, we removed the catheter.
   One month later, bilateral upgaze palsy and the lateral gaze palsy of the left eye slightly improved but double vision persisted.

2. Patient 2：
   A 48-year-old woman presented with sudden left hemiparesis (grade IV). The patient was lethargic, disoriented to time and complained of severe headache and double vision. The patient's blood pressure on admission was 200/120 mmHg, pulse 68 per minute, and respirations 16 per minute. The pupils were equal at 3.0 mm and reactive to light, and no ptosis was evident. In the primary position, the left eye was completely adducted and immobile to voluntary commands or doll's eye maneuvers. The patient was unable to elevate both eyes. The right eye was fully mobile in the horizontal plane. The left lower face was weak and sensation to all modalities was slightly diminished over the left side of the face and the right limbs. 
   At the time of admission, A CT scan revealed right thalamic hemorrhage extending to the posterior wall of third ventricle. Two days later, the voluntary movement of left eye began to improve, but lateral gaze palsy to left persisted. Five days later, she complained of double vision even though the esotropia resolved. Upgaze paresis was still present. Three weeks later, her ocular motility examination had returned to normal. 

3. Patient 3：
   A 73-year-old woman with hypertension presented with right hemiparesis. She was alert. The patient complained of headache and double vision. The patient's blood pressure on admission was 180/100 mm Hg, pulse 73 per minute, and respirations 18 per minute. The pupils were equal at 3.0 mm and reactive to light, and no ptosis was evident. In the primary position, the right eye was completely adducted and immobile to voluntary commands or doll's eye maneuvers. The left eye was fully mobile in both the horizontal and vertical plane. The patient could move both eyes upward and downward, but the right eye remained adducted position. The right lower face was weak, and she had a right hemiparesis (grade IV). The patient showed right-sided lower facial weakness and right-sided sensory loss to all modalities. A CT scan showed left posteromedial thalamic hemorrhage. Two days later, the esotropia resolved and the movement of right eye had returned to normal.

Discussion

   Acute esotropia from supanuclear cerebral lesion is chacterized by tonic inward ocular deviation.⁵⁾ Few reports have described this ocular finding in patients with thalamic and brainstem lesions.^{3)4)6)7)8)11)15)16)} However, the exact mechanism of this ocular deviation is not obvious.
   Anatomic experiments in monkey show that the neurons of medial rectus subnucleus are grouped in subgroups A, B, and C.²⁾ Group C neurons may be more involved in tonic contraction of medial rectus, which is perhaps important mechanism of convergence.^2)11)15) Descending cortico-oculomotor pathways for convergence pass through the thalamus and the mesodiencephalic junction and terminate directly in oculomotor complexes. These projection systems exist bilaterally and contralateral pathway exerts an inhibitory influence upon the neurons of the oculomotor nucleus via convergence neurons, particularly those in subgroup C. Inhibitory descending pathway may decussate in the subthalamic region (Fig. 3). Acute disinhibition of these neurons would result in a sustained but transient discharge of the medial rectus and tonic activation.^{4)9)10)11)15)} Thus, patients may develop acute esotropia with abduction deficit and the transient unresponsiveness to oculocephalic and vestibulo-ocular stimulation could be observed.⁶⁾ In the monkey, vergence neurons have been found dorsal and lateral to the oculomotor nucleus.^12)13)15)
   Patient 2 and patient 3 developed unilateral esotropia contralateral to thalamic hemorrhage and patient 1 had ipsilesional esotropia (Fig. 1). The contralesional esotropia may be explained by damage to the ipsilesional descending convergence pathway in the thalamus and rostral subthalamus before decussation. Ipsilesional esotropia may be caused by damage to the ipsilesional descending convergence pathway after decussation in the caudal subthalamus, near the mesodiencephlaic junction or by irritation of the ipsilesional convergence neuron.^{4)10)11)15)16)} Thus, a lesion involving both the midbrain and subthalamic region could cause bilateral esotropia (Fig. 3). In thalamic hemorrhage, contralateral eye may be more affected and esotropia can be accompanied by upgaze palsy, which is characteristic of a midbrain lesion.^6)7)19) 
   The mesodiencephalic junction contains the rostral interstitial of the medial longitudinal fasciculus (riMLF), the interstitial nucleus of Cajal (INC), the mesencephalic reticular formation (MRF), and the posterior comissure (PC), which are involved in the premotoneuron control of vertical eye movements.^1)4)18) Vertical saccades are generated by burst neurons, which are found in the riMLF, in the rostral midbrain.¹⁾¹⁷⁾ Burst neurons for upward and downward saccades were believed to intermingle without topographic pattern within the riMLF.⁴⁾¹⁴⁾ Burst neurons responsible for downgaze project directly to the ipsilateral inferior rectus subnucleus and trochlear nucleus without decussation, while neurons for upgaze project bilaterally to the oculomotor nucleus through the posterior commissure (Fig. 3). Thus, this makes isolated riMLF lesions more likely to impair downward saccades.^{1)4)14)18)20)} Selective upward gaze palsy after unilateral lesions may be explained by damage to the projection fibers from the riMLF mediating upward saccades.
   Patient 1 and patient 2 showed upgaze paralysis. This suggests that the esotropia in these two patients was associated with a midbrain lesion. We thought that patient 1 developed upgaze palsy (Fig. 1) due to extension of the hemorrhage into the midbrain (Fig. 2) and patient 2 due to compression of the midbrain from edema. Thalamic hemorrhage may be not directly responsible for the eotropia. It is thought to be due to associated midbrain lesion.⁶⁾ 
   The prognosis for recovery of the esotropia is known to be good. Few reports exists on esotopia from thalamic and brainstem lesion, partly because the condition is uncommon. However it is possible that acute esotropia is under-recognized.

Conclusions

   Acute esotropia may develop in thalamic and brainstem lesions. The esotropia may caused by damage to descending convergence pathway or by damage to neural structures involved in the vergence and vertical gaze in the mesodiencephalic junction. The upgaze palsy seen in our patients could be due to extension of hemorrhage into or compression of the midbrain. Attention to these deficits may be clues to the diagnosis of thalalmic and brainstem lesions.

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