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Special Considerations in Gaze
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
When the head is steady, integration in the horizontal direction is mediated by nucleus prepositus hypoglossi (NPH) and medial vestibular nucleus (MVN), whereas the interstitial nucleus of Cajal (INC) performs the same function for vertical and torsional eye position.1–3 Both of these are referred to as ocular motor integrators.
Three-, Rather Than Two-Dimensional Burst Generation for Spontaneous Saccadic Eye Movements
Published in Michael Fetter, Thomas Haslwanter, Hubert Misslisch, Douglas Tweed, Three-Dimensional Kinematics of Eye, Head and Limb Movements, 2020
A.J. van Opstal, K. Hepp, Y. Suzuki, V. Henn
The direct pathway is assumed to be prone to noise, thus giving rise to small random errors. These errors would rapidly accumulate by a random walk, if no appropriate action would be taken by the saccadic system. A second neural pathway involves the SC-cNRTP-CV-brainstem path (the ‘indirect’ path) and is proposed to play a decisive role in torsional error correction. To that means, the error correction system, presumably embodied by the cerebellar vermis, needs to have access to both the desired eye displacement of the next saccade, as well as of current eye position in 3D. Neuroanatomical evidence indicates that the vermis may receive these signals through the cNRTP (Gerrits and Voogd, 1986), and the nucleus prepositus hypoglossi (Yamada and Noda, 1987), respectively.
Viscerosensory Processing in Nucleus Tractus Solitarii: Structural and Neurochemical Substrates
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
D.A. Ruggiero, V.M. Pickel, T.A. Milner, M. Anwar, K. Otake, E.P. Mtui, D. Park
Other cells were labeled in the ventral subolivary nucleus, nucleus pars α and ventral raphe. In the rostral dorsomedial medulla a small cell column was labeled in the periventricular gray and spatially segregated from unlabeled soma in the nucleus prepositus. Others extended into the dorsomedial reticular formation. NTS projection cells in the aforementioned columns were directly contiguous with those in lamina V-VII and X, respectively. Labeled cells in the spinal trigeminal nucleus caudalis pars zonale and paratrigeminal nucleus extended caudally into superficial laminae of the cervical dorsal horn.
Emerging evidence for noninvasive vagus nerve stimulation for the treatment of vestibular migraine
Published in Expert Review of Neurotherapeutics, 2020
Vagal afferents and efferents terminate in four medullary vagal nuclei: the nucleus tractus solitarius (NTS), nucleus ambiguus, trigeminal spinal nucleus, and dorsal motor vagus nucleus (DMX) [8]. The NTS is the first major relay station for vagal afferents, contains trigemino-vestibulo-vagal neurocircuitry, and plays an important role in motion sickness and migraine-related nausea [11–13]. It receives afferents from the ipsilateral medial vestibular nucleus (via the lateral pathway), the ipsilateral nucleus prepositus hypoglossi (via the medial pathway), and bilateral inferior vestibular nuclei [8]. The NTS receives vestibulo-cerebellar and vestibulo-hypothalamic afferents via the parabrachial and Kolliker-Fuse nuclei [14,15]. Indicating a role in migraine, neurons connecting the parabrachial nucleus and NTS express calcitonin gene-related peptide [16,17], and play a major role in conditioned taste aversion (the animal model for motion sickness) [18]. The DMX receives vestibular afferents [19,20], and projects to the cerebellar vermis, fastigial nucleus, and nucleus interpositus [21], structures that are important in ocular motor control [22]; these connections suggest a pathway by which nVNS modulates VM-associated vertigo and nystagmus. Other brainstem nuclei that host vestibulo-vagal connections, and thus provide a possible substrate for nVNS to act on VM episodes include the rostro-ventro-lateral medulla, reticular formation, locus coeruleus, and nucleus intercalatus [8,19,20].
Fixation stability as a biomarker for differentiating mild traumatic brain injury from age matched controls in pediatrics
Published in Brain Injury, 2021
Melissa Hunfalvay, Nicholas P. Murray, Frederick Robert Carrick
In clinical examination and clinical studies using questionnaires fixation stability is a standard part of the oculomotor exam (29). The gap between clinical practice and research reveals the need for examination of fixation stability in a quantifiable manner to determine if this construct helps further differentiate patients with TBI, especially mTBI which are the most difficult to diagnose, from those with no history of TBI and pediatrics. This study was conducted to add another element, specifically fixations, to the already important analysis of oculomotor behavior for examining mTBI. Introducing novel discriminatory measures relative to fixation assessments provides a less complicated measure of performance and thus represents a reliable and simple scheme of detection and analysis of oculomotor deficits associated with brain injury. Metrics for quantifying fixations include measurements of Bivariate Contour Ellipse Area (BCEA), Convergence Point, Depth, Disassociated Phoria, and Targeting Displacement (30). Due to the elliptical nature of fixation points, x and y coordinates are used to find an ellipse that fits the central set of x and y data points for left right and both eyes (31). Microsaccades and drifts of the human eye cause corrections of the eye back to a central point. These slight eye movements form an area of dispersion in the shape of an ellipse that is measured by the BCEA (32,33). A larger BCEA indicates a less stable fixation. Impaired fixation stability may indicate dysfunction in brainstem lesions affecting the Nucleus Prepositus Hypoglossi-Medial Vestibular Nucleus Region (NPH-MVN) which is essential for neural integration and vestibular imbalance (34,35).
Episodic ataxia type 2 characterised by recurrent dizziness/vertigo: a report of four cases
Published in International Journal of Neuroscience, 2019
Xia Ling, Dan-hua Zhao, Jing Zhao, Bo Shen, Xu Yang
Gaze nystagmus is often present, especially during side-glancing and looking down, and may be accompanied by rebound nystagmus, which is one of the clinical features of EA2 [3]. Furthermore, spontaneous vertical nystagmus, especially downbeat nystagmus, can occur in a third of patients during the attack period [3]. Gaze-evoked nystagmus and downbeat nystagmus often suggest lesions in the interstitial nucleus of Cajal [10]/flocculus cerebellum and paraflocculus [11,12]. Horizontal gaze nystagmus often indicates impaired horizontal gaze integration of the eyeball, such as in the brainstem nucleus prepositus hypoglossi and medial vestibular nucleus [10]. In summary, the production of gaze nystagmus is mainly due to the dysfunction of the cerebellum and brainstem [10]. In this study, patient 1 showed horizontal nystagmus when gazing left. Besides gaze nystagmus, left optokinetic nystagmus disappeared and right optokinetic nystagmus weakened in patient 1. The asymmetry of optokinetic nystagmus often suggests impaired eye movement, for example, caused by unilateral cortical or pontine damage [13]. Eye movement disorder has been reported in EA2 patients, mainly paroxysmal tonic upward gaze and saccadic abnormalities [14]. Optokinetic nystagmus disappearance has not been reported. Moreover, patient 1 presented abnormal smooth pursuit, suggesting lesions may involve visual tracking, eye movement and control pathways. In this study, the head shaking test produced left horizontal nystagmus in patient 1. An abnormal head shaking test is observed in central vestibular disease and peripheral vestibular disease. The patient’s caloric test was normal. These results suggest normal peripheral vestibular function. Therefore, we presume that head shaking-evoked nystagmus may be caused by central damage.