trochlear nerve palsy may be clinically characterized by vertical diplopia , incomitant hypertropia that increases upon head tilt toward the paralyzed site ( positive bielschowsky 's test ) , excyclotropia , and head tilt . the differentiation between acutely acquired palsy vs. the decompensation of a congenital palsy is important for an accurate diagnosis . the presence of acute unilateral trochlear nerve palsy with claude bernard - horner syndrome represents a rare clinical condition . in a review of 215 cases of trochlear nerve palsy examined over a period of 23 years , the current report describes a patient with trochlear nerve palsy associated with claude bernard - horner syndrome and contralateral hemiparesis , with onset following a hypertensive crisis . a 35-year - old caucasian woman with a history of chronic headache and systemic arterial hypertension was admitted with sudden acute intense bitemporal headache , diplopia , dysarthria , and left hemiparesis . the patient 's blood pressure was lowered with antihypertensive drugs , including sodium nitroprusside , and she regained consciousness the next day . a neurological examination showed right trochlear nerve palsy , slight ipsilateral claude bernard - horner syndrome ( fig . 1 ) , and left hemiparesis . at rest , the patient presented cyclovertical diplopia when her head was tilted down and to the right . magnetic resonance imaging ( mri ) of the brainstem and cerebellum , acquired on the sixth day , showed multiple small areas localized mainly to the pons and mesencephalon that were distinguished by t1 and t2 hyperintense signals and no contrast enhancement ( fig . an mri in the fourth week showed remission of the previous lesions ; the patient was asymptomatic at that time and returned to her daily activities . the most frequent causes of trochlear nerve palsy are traumas , surgical injuries , tumors , demyelinating and inflammatory diseases such as meningitis and cysticercosis . brainstem stroke represents a rare cause of trochlear nerve palsy , in which infarcts may be extensive or restricted to the microvascular territory [ 4 , 5 ] . the patient presented in the current report developed sudden - onset clinical manifestations associated with arterial hypertension . these clinical features were suggestive of a vascular etiology , which was supported by the neuroimaging findings ( fig . 2 ) . most likely , small bleedings at the brainstem and cerebellum occurred as consequence of increased blood pressure . this clinical picture has previously been described in patients with trochlear nerve palsy [ 5 , 6 , 7 ] . the right - side claude bernard - horner syndrome and left - side hemiparesis observed in this patient may be related to the right - side pons lesion that was observed ( fig . in addition , the right - side trochlear palsy was possibly a result of the left dorsal mesencephalic lesion ( fig . after exiting the trochlear nucleus , which is ventrolateral to the cerebral aqueduct , the nerve fascicles course posteroinferiorly around the cerebral aqueduct and decussate in the dorsal midbrain [ 1 , 5 ] . therefore , in the current patient , the involvement of the trochlear nerve must have occurred before the decussation , resulting in contralateral palsy . the literature also contains descriptions of contralateral trochlear nerve palsy with ipsilateral horner 's syndrome . guy et al .   describe nuclear or fascicular involvement of the trochlear nerve prior to decussation in the superior medullary velum and impairment of the adjacent sympathetic fibers . in the current report , the multiplicity of lesions observed in the patient likely was responsible for the unusual clinical presentation . in the case presented here , progressive improvement was observed , and the patient was asymptomatic at the end of the fourth week . similar outcomes have been described in patients with trochlear nerve palsy related to minor vascular lesions . however , there is not sufficient evidence to draw definitive prognostic conclusions in this rare situation [ 3 , 4 , 6 ] .