Horizontal gaze pathology: pathogenesis, clinical signs of ophthalmoplegia and one-and-a-half syndrome (clinical case)

The purpose of this article is to familiarize practitioners with current ideas about the clinical picture, pathogenesis, and causes of various eye movement disorders that occur during eye movements in the horizontal plane and are manifestations of neurological diseases of various etiologies. Generalized information is provided on the mechanisms of occurrence, clinical signs, and differences between infranuclear, nuclear, intranuclear, and supranuclear ophthalmoplegia, which appear in cases of damage to various anatomical structures of the nervous system. Current data on the mechanisms of functioning and interaction of a number of neurological structures that ensure coordinated eye movements in the horizontal plane are presented, emphasizing the special role of the medial longitudinal fasciculus, cortical and pontine gaze centers. Based on an analysis of the literature, the mechanisms of occurrence and clinical manifestations of inter-nuclear ophthalmoplegia are described, which appears in the presence of damage to the medial longitudinal fasciculus and manifests as impaired adduction of the eye on the affected side, accompanied by monocular nystagmus in the contralateral abducted eye. Particular attention is paid to the description of the combination of clinical signs of unilateral complete damage to the medial longitudinal fasciculus at the level of the middle third of the pons with damage to the pontine gaze center, leading to the onset of one-and-a-half syndrome (1.5 syndrome) with a characteristic clinical picture — on the side of the lesion, the eye looks straight ahead and does not move in the horizontal plane in either direction («one»), while the other eye can only move outward («half») with the appearance of monocular abduction nystagmus. It is emphasized that, according to modern concepts, one-and-a-half syndrome can be combined with damage to other adjacent structures, leading to the appearance of a number of its variants — oculomotor syndromes, whose names are formed by adding 1.5 to the number of the affected pair of cranial nerves — 8.5; 9; 13.5; 15.5; 16.5. There is an opinion that the most common combination in clinical practice is ipsilateral damage to the VII pair of cranial nerves with one-and-a-half syndrome, which creates syndrome 8.5 («eight and a half»). The article presents and analyzes a clinical case of ischemic stroke in the right pons in a 57-year-old patient with the onset of one-and-a-half syndrome 9 in neurological status.