BACKGROUND: Small brainstem infarctions are increasingly recognized as a cause of isolated ocular motor and vestibular nerve palsies in diabetic and/or hypertensive patients. This raises the question whether there are also isolated 7(th) nerve palsies due to pontine infarctions in patients with such risk factors for the development of cerebrovascular diseases. METHODS: Over an 11-year-period, we retrospectively identified 10 diabetic and/or hypertensive patients with isolated 7(th) nerve palsies and electrophysiological abnormalities indicating pontine dysfunction. All patients had examinations of masseter and blink reflexes, brainstem auditory evoked potentials, direct current electro-oculography including bithermal caloric testing, and T1- and T2-weighted MRI (slice thickness: 4-7 mm). RESULTS: Electrophysiological abnormalities on the side of the 7(th) nerve palsy included delayed masseter reflex latencies (4 patients), slowed abduction saccades (4 patients), vestibular paresis (2 patients), and abnormal following eye movements (2 patients). Electrophysiological abnormalities were always improved or normalized at re-examination, which was always associated with clinical improvement. MRI revealed an ipsilateral pontine infarction in 2 patients. Another 2 had bilateral hyperintense intrapontine lesions, and one an ipsilateral cerebellar infarction. CONCLUSIONS: Simultaneous improvement or recovery of abnormal clinical and electrophysiological findings strongly indicated that both were caused by the same actual pontine lesions. A 7(th) nerve palsy may be the only clinical sign of a pontine infarction in diabetic and/or hypertensive patients. Such mechanism may be underestimated if based on MRI only.
BACKGROUND: Small brainstem infarctions are increasingly recognized as a cause of isolated ocular motor and vestibular nerve palsies in diabetic and/or hypertensivepatients. This raises the question whether there are also isolated 7(th) nerve palsies due to pontine infarctions in patients with such risk factors for the development of cerebrovascular diseases. METHODS: Over an 11-year-period, we retrospectively identified 10 diabetic and/or hypertensivepatients with isolated 7(th) nerve palsies and electrophysiological abnormalities indicating pontine dysfunction. All patients had examinations of masseter and blink reflexes, brainstem auditory evoked potentials, direct current electro-oculography including bithermal caloric testing, and T1- and T2-weighted MRI (slice thickness: 4-7 mm). RESULTS: Electrophysiological abnormalities on the side of the 7(th) nerve palsy included delayed masseter reflex latencies (4 patients), slowed abduction saccades (4 patients), vestibular paresis (2 patients), and abnormal following eye movements (2 patients). Electrophysiological abnormalities were always improved or normalized at re-examination, which was always associated with clinical improvement. MRI revealed an ipsilateral pontine infarction in 2 patients. Another 2 had bilateral hyperintense intrapontine lesions, and one an ipsilateral cerebellar infarction. CONCLUSIONS: Simultaneous improvement or recovery of abnormal clinical and electrophysiological findings strongly indicated that both were caused by the same actual pontine lesions. A 7(th) nerve palsy may be the only clinical sign of a pontine infarction in diabetic and/or hypertensivepatients. Such mechanism may be underestimated if based on MRI only.