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Locked-In Syndrome
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Almost all movement becomes impossible in locked-in syndrome. That's because most of your motor nerves that travel through your brain stem are cut off from sending signals to your muscles. Quadriplegia—the complete inability to move the trunk and all four limbs—is just the beginning. The person also experiences swallowing palsy, meaning that they cannot use the muscles involved in eating, and aphonia, meaning that they cannot use the muscles involved in speaking. Their facial muscles are also typically paralyzed, including some of their eye movements. Specifically, a person with locked-in syndrome typically cannot look from side to side due to horizontal gaze palsy.
Stroke
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
The PPRF (answer A) is involved in the sleep-wake cycle. A lesion here would present with the patient looking away from the side of the lesion (contralateral gaze deviation). A bilateral PPRF lesion would cause a horizontal gaze palsy.
Disruptions in physical substrates of vision following traumatic brain injury
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
The supranuclear portion of the oculomotor system is less commonly involved in TBI and, when present, usually is secondary to a contusion to the general area of the frontal eye fields or its connections. This results in horizontal gaze palsy. Horizontal and vertical gaze palsy can result in brain stem lesions, but in those conditions, there is usually a plethora of other brain stem neurological abnormalities on exam. Disorders of the primary visual system, the retinogeniculocortical tract, results in scotoma or visual field defect. A scotoma is defined as an area of partial attenuation or loss of visual acuity surrounded by an area of normal preserved vision. Lesions in the optic nerve cause monocular scotoma, the shape of which is dependent upon which nerve fibers are involved. Lesions of the optic chiasm usually result in a bitemporal hemianopsia or blindness in the temporal half of both visual fields. Retrochiasmal lesions cause contralateral hemianopsia, which is blindness in one half of the visual field. Lesions in the optic tract produce incongruous visual field defects because the fibers from each eye are still not adjacent to each other. Posterior optic radiation lesions result in homonymous quadranopsias, primary visual cortex lesions sparing the posterior portion result in macular sparing homonymous hemianopsias, and total bilateral primary visual cortex lesions cause bilateral homonymous hemianopsias.
Horizontal Gaze Palsy with Progressive Scoliosis: A Case Report and Literature Review
Published in Neuro-Ophthalmology, 2019
The ROBO3 gene plays a role in the regulation of hindbrain axonal midline crossing and helps cell migration. Mutations of ROBO3 result in abnormal horizontal eye movement, progressive scoliosis, brainstem malformation, and defective crossing of brainstem neuronal pathways.6,9 Horizontal gaze palsy is a major ophthalmologic finding. Nystagmus and ametropia are other important ophthalmologic findings for these patients, which can lead to amblyopia and permanent poor vision.10–13 Horizontal gaze palsy in these patients is probably related to aberrant supranuclear input onto the abducens motoneurons from the pontine reticular formation that cannot cross the midline, and inability of the developing axons in the medial longitudinal fasciculus to cross the midline. The mechanism of the scoliosis aspect is less clear, but it may result from a lack of normal contralateral pathways to spinal muscles.14–16
Vertical One-and-a-Half Syndrome with Pseudoabducens Palsy and Midbrain Horizontal Gaze Paresis
Published in Journal of Binocular Vision and Ocular Motility, 2022
Yasser Aladdin, Bader Shirah, Khurshid Khan
Paramedian mesencephalic lesions can cause contralateral horizontal gaze palsy due to a combined paresis of contralateral saccade and monocular adduction paresis in the ipsilesional eye.1,2 The contralateral saccadic failure results from the interruption of the corticofugal pathways from the frontal eye field and the colliculofugal tracts from the superior colliculus.1 The dissociated horizontal gaze palsy in this patient with preserved horizontal VOR indicates interruption of these supranuclear tracts within the midbrain before their decussation at the level of the inferior colliculus.
Horizontal Gaze Palsy and Progressive Scoliosis in Dizygotic Twins
Published in Journal of Binocular Vision and Ocular Motility, 2022
Catarina Xavier, Miguel Vieira, Ana Filipa Duarte, Ana Xavier, Eduardo D. Silva
Dizygotic twins of 14 years old were studied, a girl (patient 1) and a boy (patient 2), born and living in Fogo Island, Cape Verde, were evacuated to Dona Estefânia Hospital (under cooperation agreement) for diagnosis and treatment at our institution, due to severe scoliosis. Both patients presented with clinical features of horizontal gaze palsy and progressive scoliosis. Their parents are non-consanguineous, both born on Fogo Island. No similar cases were known in the family.