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RESEARCH PRODUCT
Seventh nerve palsies may be the only clinical sign of small pontine infarctions in diabetic and hypertensive patients
Hanns Christian HopfFrank ThömkeJürgen MarxPeter P. UrbanAnnette Mika-grüttnersubject
AdultMalemedicine.medical_specialtyBrain Stem InfarctionsNeurologyFunctional LateralityDiabetes ComplicationsOcular Motility DisordersPonsInternal medicineNeural PathwaysDiabetes MellitusVestibulocochlear Nerve DiseasesmedicineHumansCranial nerve diseaseStrokeAgedRetrospective StudiesParesisbusiness.industryMiddle AgedVestibular nervemedicine.diseaseMagnetic Resonance ImagingFacial nerveFacial paralysisSurgeryFacial NerveNeurologyBasilar ArteryHypertensionCardiologyFemaleDisease SusceptibilityNeurology (clinical)Facial Nerve Diseasesmedicine.symptombusinessJaw jerk reflexdescription
Backgroud: 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 7th 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 7th 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 7th 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 7th 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.
year | journal | country | edition | language |
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2002-11-01 | Journal of Neurology |