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Neurology Today-Neurobowl Case Challenge
Hypertensive Smoker with Left-sided Weakness
Solve this Case!


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In the case first discussed in the February 18 issue (, we told you about a 57-year old man with a history of hypertension and smoking who had a two-hour history of left-sided weakness and numbness. In the emergency department, his blood pressure was 260/130, and he suddenly became less responsive. His eyes were skewed. There was no movement of the right eye; the left eye was able to abduct only. His left arm and leg were weak.

We provided the images (seen here) and asked our readers to localize.

What was the solution? The short answer is that he had a hypertensive hemorrhage in the brainstem producing primarily his visual symptoms of one-and-a-half syndrome (pons). But he also had sensory and motor tract involvement, which contributed to his left side weakness and numbness, and he had sudden change in consciousness.

Among the clues, the one-and-a-half syndrome could be attributed to the observation that he had conjugate gaze palsy to one side (“one”) and impaired adduction on looking to the other side (“and a half”), as well as skewed deviation (localizing to the brainstem, cerebellum, and imbalance of otolith inputs). The horizontal gaze palsy would make one suspect involvement of specific tracts.

Lesions of the medial longitudinal fasiculus (MLF) and the ipsilateral abducens nucleus and/or pontine paramedian reticular formation (PPRF) result in the one-and-a-half syndrome. A lesion in the abducens nucleus (VI) on one side could result in a failure of abduction of the ipsilateral eye and adduction of the contralateral eye and conjugate gaze palsy towards the affected side; interruption of the ipsilateral MLF after it has crossed the midline to the contralateral abducens (VI) nucleus could lead to a failure of adduction of the ipsilateral eye.

Several readers diagnosed the patient with Benedikt's syndrome (ipsilateral oculomotor nerve palsy and cerebellar ataxia including tremor) or Weber's syndrome (ipsilateral oculomotor nerve palsy and contralateral hemiparesis or hemiplegia). Given that the eyes were not down and out, but rather were having difficulty with horizontal conjugate gaze, we must suspect involvement of the MLF or PPRF.

If oculocephalic maneuvers or cold water calorics were performed, we could have differentiated a PPRF lesion from an abducens nucleus lesion. In horizontal gaze palsy from a PPRF lesion, the vestibular projections can help overcome the palsy by activating the vestibular system via oculocephalic maneuvers or an ice water calorics test. However, if the abducens nuclei is lesioned, the horizontal gaze palsy will not resolve.

Another reader mentioned involvement of the omnipause neurons, which are present because they prevent saccades and needs to be inactivated for saccades to occur; but if they are lesioned, this will not occur. The omnipause neurons lie in the nucleus of raphe interpositus, which is located in the midline between the rootlets of abducens nerves. They help maintain the necessary synchronization of the activity of the premotor saccadic burst neurons to drive the eyes rapidly during the saccade and to keep eyes still when saccade is over.

Some readers localized the lesion to the the midbrain. This is a reasonable assumption, but in order to get MLF and PPRF and/or abducens nucleus involvement, we would need to be in the pons. If corticospinal tracts in crus cerebri were involved, CN III exiting could be injured but the eyes would not be down and out. The fact that the midbrain reticular activating system is also in the upper one third of the pons could explain the altered consciousness along with other eye movement issues.

Dr. Patel is a neurology resident at Medical College of Georgia.