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. 2020 Oct 23;2020(10):omaa087. doi: 10.1093/omcr/omaa087

Clinical findings of eight-and-a-half syndrome

Hassan A Ahmed 1, Omar Y Al Assaf 1,, Hamdan M Alzarooni 2, Pournamy Sarathchandran 2
PMCID: PMC7583413  PMID: 33133620

CASE

A right-handed male with co morbid diabetes mellitus type 2, presented with sudden onset of dizziness, visual disturbance, slurring of speech and left sided facial droop. He denied any bulbar symptoms, sensory motor symptoms in the limbs, incoordination sphincter disturbances or headache. On physical examination, patient had left horizontal conjugate gaze paresis, and on left gaze, the adduction of the left eye was limited with associated nystagmus of the right eye, while convergence was spared indicating left internuclear ophthalmoplegia). There was no limitation of vertical eye movements. In addition, he had nasolabial fold flattening with inability to fully close the left eye and deviation of right side. (Fig. 1) Rest of the neurological exam was unremarkable.

Figure 1.

Figure 1

(a) Physical examination of our patient, (b) magnetic resonance imaging (MRI) of the Brain showing tegmentum hyperintensity of left lower pons on fluid-attenuated inversion recovery (FLAIR) images, with restriction of diffusion (hyper intense on diffusion-weighted images [DWI] and hypointense on apparent diffusion coefficient [ADC]) suggesting a pontine.

Patient underwent a non-contrast magnetic resonance imaging of the Brain and it was suggestive of left pontine acute ischemic stroke (Fig.1b). CT angiogram of brain and neck vessels, routine laboratory investigations, vasculitis and thrombophilia work-up and ECHO were normal. He was started on dual antiplatelets and atorvastatin and his blood pressure control was optimized. Alternate eye patching was carried out which relieved his blurry vision. Exercises to improve facial weakness were advised.

Eight-and-a-half syndrome is a rare neuro-ophthalmic syndrome where in conjugate horizontal gaze palsy, ipsilateral internuclear ophthalmoplegia and ipsilateral peripheral facial nerve palsy occur together [1]. It is usually due to lesions at the level of the pons, and the most common etiology is ischemic stroke. Demyelinating lesions and space occupying lesions are other uncommon etiologies. [2]

The abrupt onset of symptoms as in our case suggested ischemic stroke. Prognosis depends on the size of the infarct and the ability of the affected area to recover. Usually facial palsy improves first followed by the ocular symptoms. The treatment depends on the underlying etiology, in addition to neurorehabilitation [3, 4].

ACKNOWLEDGMENT

None.

CONFLICT OF INTEREST STATEMENT

None declared.

FUNDING

None.

ETHICS APPROVAL

None required.

CONSENT

Informed consent was obtained from the patient Signed by the patient.

GUARANTOR STATEMENT

Dr. Hassan Ahmed is the guarantor of this article.

REFERENCES

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