Pendular Nystagmus Research Articles

A case of bilateral straatsma syndrome

Straatsma syndrome is characterized by a constellation of conditions including amblyopia, nystagmus, and myopia. We present the case of a 10-year-old boy who complained of involuntary back-and-forth eye movements and reduced vision since birth. His visual acuity was measured at 2/60 in both eyes. Examination revealed horizontal pendular nystagmus without ocular misalignment. Fundus examination showed myopic changes, including an anomalous optic disc with extensive myelinated nerve fibers extending from the optic disc along the superior and inferior arcades to the fovea. Axial length measurements were 28.34 mm and 27.96 mm in the right and left eyes, respectively. SD-OCT imaging confirmed thickening of the retinal nerve fiber layer. Treatment included cycloplegic refraction and occlusion therapy, with regular follow-ups every three months utilizing contact lenses with cycloplegic refraction. The etiology of retinal fiber myelination remains unclear; however, it is hypothesized that blurred retinal imaging during critical ocular development stages may lead to axial elongation and subsequent myopia, potentially delaying the development of the lamina cribrosa and facilitating myelination extension.

Case Report: Pendular Nystagmus Presenting in Usher Syndrome Type I.

We describe a 42-year-old patient with reported "shaking" vision referred due to concerns of possible vestibular system dysfunction. The patient has known history of Usher syndrome type I, bilateral cochlear implants, and severe vision impairment. This case describes an unusual nystagmus previously only reported in individuals with central demyelinating disorders, significant light deprivation, or in congenital / early-onset visual pathway impairment. Case study. Retrospective chart review of vestibular function. Vestibular function was likely absent in this case. There was no evidence of vestibular (jerk) nystagmus for sinusoidal harmonic acceleration stimuli or repeatable responses for cervical vestibular evoked myogenic potentials. Significant pendular low amplitude high frequency oscillations of approximately 6 Hz were present for horizontal and vertical tracings throughout testing. Nystagmus may not always be associated with vestibular system impairment. In this case, the patient's reported "shaking" vision was attributed to pendular low amplitude high frequency nystagmus and hypothesized to relate to long-standing significant vision impairment. This presentation is unusual in adults and has historically been associated with individuals with significant central pathology or in those with long duration light deprivation.

Oculopalatal Tremor: A Narrative Review of Pathophysiology, Clinical Presentation, and Management Strategy

Abstract Oculopalatal tremor (OPT) is a complex neurological disorder characterized by acquired oscillatory nystagmus synchronized with tremors of the soft palate and other muscles. The article discusses the pathology, clinical manifestations, and diagnostic methods of OPT. A comprehensive literature search was conducted in PubMed and Google Scholar using keywords and relevant articles were studied and analysis was done. Vertical pendular nystagmus is the hallmark, while other muscles such as the neck, head, larynx, and diaphragm may be affected. The pathophysiology is due to lesions of the Guillain–Mollaret triangle (GMT), which causes hypertrophy of the inferior olivary. Neuroimaging reveals hypertrophy of the inferior olivary medulla, which aids in diagnosis. Drug treatments such as gabapentin and memantine can reduce nystagmus, although the visual quality may not permanently improve. The study explores the complexity of the pathophysiology and clinical presentation of OPT. New treatments that target abnormal neuronal connections with drugs such as quinine or mefloquine are being investigated. The potential of deep brain stimulation (DBS) remains uncertain, with promising aspects but limited efficacy. A synergy of technology and treatment is proposed to advance OPT treatment. Future studies will aim to clarify the nuances of responses to OPT and may include a comparative study of medication and DBS. OPT is mainly caused by a disruption in GMT/dentato-rubro-olivary pathway, presenting with tremor, and nystagmus is diagnosed with magnetic resonance imaging. Gabapentin and memantine have proved to be effective in improving the condition except for visual changes.

A CASE OF SENSORY ATAXIA AND ITS MANAGEMENT THROUGH PANCHAKARMA

Sensory ataxia is both a symptom and a sign in neurology. It is a form of ataxia (loss of coordination) caused not by cerebellar dysfunction but by loss of sensory input into the control of movement. Sensory ataxia is dis-tinguished from cerebellar ataxia by the presence of near-normal coordination when the patient visually observes the movement but marked worsening of coordination when the eyes are shut, indicating a positive Romberg's sign. Sensory ataxia also lacks the associated features of cerebellar ataxia, such as pendular tendon reflexes, scanning dysarthria, nystagmus and broken pursuit eye movements. Sensory ataxia can manifest in sensory large fibre peripheral neuropathies and conditions causing dysfunction of the spinal cord's dorsal columns due to vari-ous disorders: infectious, auto-immune, metabolic, toxic, vascular and hereditary diseases. There is no direct correlation to sensory ataxia in Ayurvedic classics; based on pathology, it is nearer to Kaphavrita vyana vata. Objectives--By considering sensory ataxia as Kaphavrita vyana vata, the present study has attempted to evalu-ate the efficiency of Ayurvedic formulation in the conservative management of sensory ataxia. Met hod-A case of sensory ataxia, initially patient was treated with Dashamoola kaya seka followed by Shastika shalipindasweda, followed by Balavarnakara niruha basti1 and Anuvasana basti with ksheera bala taila as per Kala Basti schedule (modified), followed by Shaman aushadhi. Result-Patient was observed for symptomatic improvement based on the questionnaire over graded signs & symptoms, also observed for clinical examination before & after treatment. Conclusion: The study has shown that conservative management of sensory ataxia can be managed effectively through the Ayurvedic principle and improve quality of life.

Update on central oculomotor disorders and nystagmus

The diagnosis of ocular motor disorders and the different forms of a nystagmus is based on a systematic clinical examination of all types of eye movements: eye position, spontaneous nystagmus, range of eye movements, smooth pursuit, saccades, gaze-holding function, vergence, optokinetic nystagmus, as well as testing of the function of the vestibulo-ocular reflex (VOR) and visual fixation suppression of the VOR. Relevant anatomical structures are the midbrain, pons, medulla, cerebellum, and cortex. There is a simple clinical rule: vertical and torsional eye movements are generated in the midbrain, horizontal in the pons. The cerebellum is relevant for almost all types of eye movements; typical pathological findings are saccadic smooth pursuit, gaze-evoked nystagmus or dysmetric saccades.Nystagmus is defined as a rhythmic, most often involuntary eye movement. It normally consists of a slow (pathological) drift of the eyes and a fast central compensatory movement of the eyes back to the primary position (re-fixation saccade). There are three major categories: first, spontaneous nystagmus, i. e. nystagmus which occurs in the gaze straight ahead position as upbeat or downbeat nystagmus; second, nystagmus that becomes visible at eccentric gaze only and third, nystagmus which can be elicited by certain maneuvers, e. g. head-shaking, head positioning, air pressure or hyperventilation, most of which are of peripheral vestibular origin. The most frequent central types of spontaneous nystagmus are downbeat and upbeat, infantile, pure torsional, pendular fixation, periodic alternating, and seesaw nystagmus. Many types of central nystagmus allow a precise neuroanatomical localization: for instance, downbeat nystagmus, which is most often caused by a bilateral floccular lesion or dysfunction, or upbeat nystagmus, which is caused by a lesion in the mesencephalon or medulla oblongata. Examples of pharmacotherapy are the use of 4-aminopyridine for downbeat and upbeat nystagmus, memantine or gabapentin for fixation pendular nystagmus or baclofen for periodic alternating nystagmus.

Nystagmus Characteristics in Albinism: Unveiling the Link to Foveal Hypoplasia and Visual Acuity.

The purpose of this study was to describe the association among nystagmus characteristics, foveal hypoplasia, and visual acuity in patients with albinism. We studied nystagmus recordings of 50 patients with albinism. The nystagmus waveform was decomposed into two types: dominantly pendular and dominantly jerk. We correlated the nystagmus type, amplitude, frequency, and percentage of low velocity (PLOV) to Snellen visual acuity and foveal hypoplasia grades. The grade of foveal hypoplasia and visual acuity showed a strong correlation (r = 0.87, P < 0.0001). Nystagmus type and PLOV had the strongest significant (P < 0.0001) correlation with visual acuity (r = 0.70 and r = -0.56, respectively) and with foveal hypoplasia (r = 0.76 and r = -0.60, respectively). Patients with pendular nystagmus type had the lowest PLOV, and the highest grade of foveal hypoplasia (P < 0.0001). Severe foveal hypoplasia (grade 4), was almost invariably associated with pendular nystagmus (86%). Foveal hypoplasia grade 4 is associated with pendular nystagmus, lower PLOV, and worse visual acuity. Based on these results, nystagmus recordings at a young age may contribute to predicting visual outcomes.

Unilateral Pendular Nystagmus in Multiple Sclerosis: A Case Series.

Acquired pendular nystagmus is most often seen in patients with demyelinating disease. Although it is often bilateral, rare cases may be monocular. There is paucity of data on the spectrum of clinical presentation, underlying mechanism, and response to treatment in patients with monocular pendular nystagmus. Retrospective case series of patients with monocular pendular nystagmus seen in 2 tertiary neuro-ophthalmology clinics between January 2019 and June 2022. All patients underwent a complete neuro-ophthalmological assessment and MRI. We describe 5 patients (3 women) aged 31-49 with monocular pendular nystagmus. All had a diagnosis of multiple sclerosis. Three patients had horizontal and 2 had vertical pendular nystagmus. The Snellen visual acuity in the eye with pendular nystagmus varied from 20/20 to 20/200. Two patients were asymptomatic and 3 suffered visually debilitating oscillopsia. Treatment response was available for 2 patients, both of which responded well to treatment with memantine. The pendular nystagmus was observed in the eye with worse visual acuity in 4 of 5 cases (80%). Three patients had bilateral pontine lesions, and 2 had unilateral pontine lesion ipsilateral to the side of nystagmus. Monocular pendular nystagmus in adults is seen most often in patients with multiple sclerosis. Asymmetry in brainstem lesions and afferent visual input may be the culprit. Treatment with memantine may result in significant improvement in symptomatic patients.

Impaired Direction Selectivity in the Nucleus of the Optic Tract of Albino Mice.

Human albinos have a low visual acuity. This is partially due to the presence of spontaneous erroneous eye movements called pendular nystagmus. This nystagmus is present in other albino vertebrates and has been hypothesized to be caused by aberrant wiring of retinal ganglion axons to the nucleus of the optic tract (NOT), a part of the accessory optic system involved in the optokinetic response to visual motion. The NOT in pigmented rodents is preferentially responsive to ipsiversive motion (i.e., motion in the contralateral visual field in the temporonasal direction). We compared the response to visual motion in the NOT of albino and pigmented mice to understand if motion coding and preference are impaired in the NOT of albino mice. We recorded neuronal spiking activity with Neuropixels probes in the visual cortex and NOT in C57BL/6JRj mice (pigmented) and DBA/1JRj mice with oculocutaneous albinism (albino). We found that in pigmented mice, NOT is retinotopically organized, and neurons are direction tuned, whereas in albino mice, neuronal tuning is severely impaired. Neurons in the NOT of albino mice do not have a preference for ipsiversive movement. In contrast, neuronal tuning in visual cortex was preserved in albino mice and did not differ significantly from the tuning in pigmented mice. We propose that excessive interhemispheric crossing of retinal projections in albinos may cause the disrupted left/right direction encoding we found in NOT. This, in turn, impairs the normal horizontal optokinetic reflex and leads to pendular albino nystagmus.

Palato-ocular synchrony: Seeing what is behind closed eyelids in palatal tremor (P5-11.010)

<h3>Objective:</h3> To call attention to palato-ocular synchrony, a little-known manifestation of palatal tremor. <h3>Background:</h3> Palatal tremor due to a lesion of the dentato-rubro-olivary pathway (Guillain-Mollaret triangle) may spread to contiguous or remote muscles. When it involves the eyes it is known as oculopalatal tremor (OPT) manifesting as pendular nystagmus, typically vertical and/or torsional, causing oscillopsia. Nystagmus may be minimal or absent with eyes open and appear only under closed eyelids, a phenomenon described in 1976 by Jacobs and Bender, and called palato-ocular synchrony (Arch Neurol;33:289). These authors observed that palato-ocular synchrony was caused by eyelid closure rather than simply the removal of vision. <h3>Design/Methods:</h3> Two illustrative video case reports. <h3>Results:</h3> Following brainstem hemorrhage (patient 1 – midbrain; patient 2 – pons) involving the Guillain-Mollaret triangle, two patients developed hypertrophic olivary degeneration and asymptomatic palatal tremor. In patient 1, there was no nystagmus with eyes open, but under closed eyelids, vertical oscillations were readily apparent. In patient 2, there was very subtle torsional pendular nystagmus without oscillopsia, but large vertical oscillations were apparent with eyelid closure that were synchronous with PT. The mechanism of palato-ocular synchrony is unknown but may be related to the observation that palatal tremor, due to a lesion of the Guillain-Mollaret triangle, is one of the few movement disorders that persist during sleep, and this may simply reflect eyelid closure. <h3>Conclusions:</h3> A lesion, typically stroke, involving the Guillain-Mollaret triangle often leads to delayed development of palatal tremor. Such patients should undergo a careful ocular motor examination looking for oculopalatal tremor; if absent, then the globes should be observed during active eye closure. A visible or palpable ocular oscillation under closed eyelids is known as palato-ocular synchrony, an underappreciated phenomenon that extends the spectrum of manifestations of palatal tremor. <b>Disclosure:</b> Dr. Reich has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Best Doctors. Dr. Reich has received personal compensation in the range of $500-$4,999 for serving as a Consultant for UpToDate. Dr. Reich has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Enterin. Dr. Reich has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for NIH. Dr. Reich has received personal compensation in the range of $10,000-$49,999 for serving as an Expert Witness for Various law firms. The institution of Dr. Reich has received research support from ninds. Dr. Reich has received publishing royalties from a publication relating to health care. Dr. Reich has received publishing royalties from a publication relating to health care. Dr. Gold has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Springer .

Hypertrophic olivary degeneration associated with bilateral vocal cord adductor dystonia

BackgroundHypertrophic olivary degeneration (HOD) is a rare condition caused by lesions within the dentato-rubro-olivary pathway, resulting in ocular nystagmus and palatal myoclonus (oculopalatal tremor) but not usually dystonia. Dystonia is an uncommon association, and we present the first reported association of hypertrophic olivary degeneration with bilateral vocal cord dystonia.Case presentationA 33 year old male presented initially with acute hydrocephalus on the background of previous ventriculoperitoneal (VP) shunting for previously treated medulloblastoma. After revision of the VP shunt, the patient developed progressive hiccups and stridor leading to respiratory failure requiring intubation. Ocular pendular nystagmus and palatal myoclonus at 3 Hz was observed. Flexible nasendoscopy (FNE) demonstrated bilateral tonic adduction of the vocal folds with 3 Hz coarse supraglottic, pharyngeal and palatal rhythmic myoclonus. MRI imaging demonstrated T2 hyperintensity within the bilateral inferior olivary nuclei consistent with stage 3 radiological HOD.ConclusionsDystonia is a rarely reported phenomenon in HOD but is not unexpected with the inferior olivary nucleus implicated in dystonic disorders. We report the association of HOD with bilateral vocal cord adductor dystonia, a potentially life threatening condition.

Oculocutaneous Albinism.

A 5-year-old Chinese girl presented intense photophobia and blurring vision from birth. Her uncorrected visual acuity was 20/200 for the right eye and 10/200 for the left eye. The best-corrected visual acuity was 30/200 and 20/200, respectively. Both eyes had horizontal pendular nystagmus. The iris of both eyes was diaphanous translucent. Retinal examination showed a lack of pigment, notably large choroidal vessels, and macular hypoplasia (Fig. 1). Optical coherence tomography results demonstrated an absence of the foveal pit and loss of usual thinning of macula. She also had white eyelashes and hypopigmentation of skin and hair (Supplementary Digital Content, Fig. 1, https://links.lww.com/APJO/A131). Her parents are cousins, and both had neither albinism nor other systematic or ocular diseases. Sunglasses were recommended to relieve the symptom of photophobia. Appropriate sunscreens and periodic inspection for early detection of skin cancer were advised.Figure 1: Color images of anterior segment indicated diaphanous translucent iris. The fundus images showed lack of pigment, notably large choroidal vessels, as well as macular hypoplasia for the retina of the patients.

Horizontal Gaze Palsy with Progressive Scoliosis Syndrome: A Concise Synopsis from the Ophthalmologist’s Perspective

The aim of this article is to provide a concise synopsis of Horizontal Gaze Palsy and Progressive Scoliosis syndrome and give the ophthalmologist’s perspective. Horizontal Gaze Palsy and Progressive Scoliosis is a rare autosomal recessive genetic condition. It has been described in both consanguineous and non-consanguineous families. It is caused by mutations in the round-about guidance receptor 3 (ROBO3) gene. Based on our literature review, to date, roughly 100 patients with this rare syndrome and 55 round-about guidance receptor 3 gene mutations have been reported. The age of onset of symptoms varies from 2 months up to 60 years, but usually start in early childhood. Musculoskeletal symptoms include scoliosis and difficulties with posturing. Mental retardation and global developmental delay may also ensue. Ophthalmological manifestations include convergent squint, pendular nystagmus and horizontal gaze palsy. Vertical and convergence eye movements are preserved. Lid position, pupillary reflexes and fundus examination are usually normal as well. Brain neuroimaging reveals striking radiological findings, including brainstem hypoplasia with an anterior and dorsal pontine cleft and a butterfly shaped medulla and absence of the normal promontories of the facial colliculi. To date, there is no definitive treatment of this condition. Convergent squint can be corrected with prisms or surgery. Spectacles are used to correct any significant refractive error. Patching or atropine drops can be used for the treatment of amblyopia. This rare syndrome is a systemic condition that requires a multidisciplinary team to treat the patients with a holistic approach, address their needs and alleviate the emotional burden. It should always be included in the differential diagnosis in patients who present with skeletal anomalies and ocular motility disorders.

Binocular, accommodative and oculomotor alterations in multiple sclerosis

AbstractMultiple sclerosis (MS) is an acquired demyelinating and inflammatory neurodegenerative disease affecting the central nervous system (CNS). Clinical and subclinical ocular disturbances occur in almost all patients with MS. Among them, oculomotor, accommodative and binocular alterations have been reported in MS. Our research group has conducted a complete analysis of the visual and oculomotor function in several researches with MS patients conducted in the last 4 years, obtaining a characterization of some visual aspects of the patient with MS. Concerning the binocular function, several alterations have been detected in MS patients, with divergence at near distance and stereopsis the most affected parameters. Likewise, MS patients with previous optic neuritis present worse binocular vision. Symptomatology compatible with convergence insufficiency measured with the CISS (Convergence Insufficiency Symptom Survey) is frequently reported by MS patients, but not supported by signs that show clear trend to esophoria at near. This discrepancy between the signs and symptoms could be due to the peculiarities of the CISS questionnaire, including items that are also related to the cognitive function and other ocular abnormalities.Oculomotor alterations have been reported also in patients with multiple sclerosis (MS), especially saccadic dysfunctions. The indirect analysis of horizontal saccades with the Developmental Eye Movement (DEM) and King‐Devick tests shows that are affected by MS, with more level of alteration if there has been a previous episode of optic neuritis. Similar findings have been also reported by other authors using objective eye tracking or video‐oculographic systems. Specifically, the most reported saccadic alterations in advanced MS and clinically isolated syndrome (CIS) are saccadic dysmetry (41.7%) and impaired smooth pursuit (42.3%), which relates to prolonged saccadic latency, no matter if they have suffered or not optic neuritis or internuclear ophthalmoplegia (INO). An increase in saccadic latency has been even found in children with MS. Saccadic initiation time (SI time) and average inter‐saccadic intervals (ISI) are also higher in patients with MS. Furthermore, the first cause of acquired pendular nystagmus is MS.Finally, macular sensitivity measured by microperimetry has been found to be altered in MS patients, especially in eyes with previous optic neuritis. Likewise, a fixational instability characterized also my microperimetry is present in MS patients with optic neuritis, with more increase of the vertical axis of the fixation area than of the horizontal. The ratio of the disease also affects the patient fixation pattern.

Teaching Video NeuroImage: Dramatic Response to Topiramate in Acquired Pendular Nystagmus From Multiple Sclerosis.

Teaching Video NeuroImage: Dramatic Response to Topiramate in Acquired Pendular Nystagmus From Multiple Sclerosis.

Pendular Seesaw Nystagmus: Disappearance With Monocular Occlusion

We report a case of pendular seesaw nystagmus caused by bitemporal hemianopia; the nystagmus disappeared while in darkness as previously described, but it also disappeared with monocular occlusion, which indicates the pivotal role of binocular vision in the pathogenesis.

Pendular nystagmus in cattle

This datasheet on pendular nystagmus in cattle covers Identity, Hosts/Species Affected, Diagnosis.

Horizontal gaze palsy with progressive scoliosis syndrome in a paediatric patient

Abstract Rationale: Horizontal Gaze Palsy and Progressive Scoliosis syndrome (HGPPS) is a very rare autosomal recessive disorder that has been reported mainly in consanguineous families. Our aim was to describe a rare case of HGPPS in a pediatric patient. Patient concerns: A 3-year-old male child was referred to our pediatric ophthalmology clinic because of squint since he was 6 months old. His parents were concerned that both eyes gradually became more esotropic over the past year. In addition, the child was unable to walk independently and was undergoing physiotherapy for mobility issues. Diagnoses: Skeletal examination revealed scoliosis. The child was unable to stand without any support. Orthoptic assessment revealed bilateral horizontal gaze palsy with abduction deficit, convergent squint, and pendular nystagmus. Vertical eye movements were preserved. Convergence was also preserved. Magnetic resonance imaging revealed bilateral hypoplastic sixth nerve nuclei with brainstem hypoplasia, the presence of a deep midline pontine cleft, and a butterfly shaped medulla. The child was referred to the genetic clinic, and mutation in the ROBO 3 gene was confirmed. The patient was diagnosed with HGPPS. Interventions: The esotropia was corrected with prisms, and no other surgical intervention was attempted due to the child's general poor health. Outcomes: To date, the esotropia has remained stable around 35 to 40 diopters, and its control with prism has been adequate. The total follow-up time from the presenting appointment in our clinic until the most recent appointment was approximately two years. Lessons: HGPPS is a rare autosomal recessive syndrome characterized by clinical and radiological findings. Our main learning point is that the diagnosis of HGPPS should be included in the differential diagnosis in children who present with combined symptoms of squint and skeletal abnormalities.

Nystagmus: Diagnosis, Topographic Anatomical Localization and Therapy.

Nystagmus is defined as rhythmic, most often involuntary eye movements. It normally consists of a slow (pathological) drift of the eyes, followed by a fast central compensatory movement back to the primary position (refixation saccade). The direction, however, is reported according to the fast phase. The cardinal symptoms are, on the one hand, blurred vision, jumping images (oscillopsia), reduced visual acuity and, sometimes, double vision; many of these symptoms depend on the eye position. On the other hand, depending on the etiology, patients may suffer from the following symptoms: 1. permanent dizziness, postural imbalance, and gait disorder (typical of downbeat and upbeat nystagmus); 2. if the onset of symptoms is acute, the patient may experience spinning vertigo with a tendency to fall to one side (due to ischemia in the area of the brainstem or cerebellum with central fixation nystagmus or as acute unilateral vestibulopathy with spontaneous peripheral vestibular nystagmus); or 3.positional vertigo. There are two major categories: the first is spontaneous nystagmus, i.e., nystagmus which occurs in the primary position as upbeat or downbeat nystagmus; and the second includes various types of nystagmus which are induced or modified by certain factors. Examples are gaze-evoked nystagmus, head-shaking nystagmus, positional nystagmus, and hyperventilation-induced nystagmus. In addition, there are disorders similar to nystagmus, such as ocular flutter or opsoclonus. The most common central types of spontaneous nystagmus are downbeat and upbeat, infantile, pure torsional, pendular fixation, periodic alternating, and seesaw nystagmus. Many types of nystagmus allow a precise neuroanatomical localization: for instance, downbeat nystagmus, which is most often caused by a bilateral floccular lesion or dysfunction, or upbeat nystagmus, which is caused by a lesion in the midbrain or medulla. Examples of drug treatment are the use of 4-aminopyridine for downbeat and upbeat nystagmus, memantine or gabapentin for pendular fixation nystagmus, or baclofen for periodic alternating nystagmus. In this article we are focusing on nystagmus. In a second article we will focus on central ocular motor disorders, such as saccade or gaze palsy, internuclear ophthalmoplegia, and gaze-holding deficits. Therefore, these types of eye movements will not be described here in detail.

Возможности призматической коррекции при лечении врожденного горизонтального нистагма

Purpose. Analysis the effectiveness of prismatic correction in the treatment of congenital horizontal nystagmus. Material and methods. The study included 20 patients with congenital horizontal nystagmus. Depending on the type of nystagmus and compensatory mechanisms to reduce its amplitude, two groups were identified: 10 patients with pendular nystagmus and nystagmus blockage syndrome (mean age, M±sd, 5.8±1.9 years) and 10 patients with jerky nystagmus and abnormal head posture and a null zone (5.7±2.1 years). Fresnel prisms were used to select and prescribe prismatic correction. Patients were under dynamic control from 6 months to 2 years with an assessment of the results every 3 months. Results. During treatment (using prism correction), uncorrected visual acuity had a statistically significant increase of 1.8 and 1.5 times both in the first (p=0.004) and the second (p=0.001) group, respectively. A similar, and even more pronounced, change in visual acuity was observed for corrected visual acuity – in the first group it increased 3 times (p=0.001) and in the second group 2.2 times (p=0.001). Conclusion. Prismatic correction in pendular nystagmus and esotropia allows to simulate (eliminate) nystagmus blockage syndrome and, thereby, to improve the quality of vision of the patient. In its turn, prismatic correction in jerky nystagmus with abnormal head posture allows to move null zone into the primary position of gaze, increase visual acuity due to the optimal optical correction and improve the patient's quality of life. Key words: nystagmus blockage syndrome, convergence fusion, abnormal head posture, null zone, Fresnel prisms

Nystagmus – What's new?

Nystagmus is defined as to-and-fro oscillations of the eyes initiated by a slow drift of the eyes away from desired position and followed by either quick phases (jerk nystagmus) or slow drifts in the opposite direction (pendular nystagmus). There are a multitude of nystagmus types, etiologies, and mechanisms – each with different clinical implications and pharmacological treatments; thus, proper pattern identification of nystagmus is critical to accurate neurological diagnosis and effective therapeutic intervention. The most common acquired nystagmus types seen clinically that occur in central gaze and thereby may cause disabling oscillopsia (i.e., a subjective sense of visual motion) are acquired pendular nystagmus (APN) and pure vertical jerk nystagmus (upbeat = UBN, downbeat = DBN). The two most common forms of APN are horizontal/elliptical APN in multiple sclerosis and vertical/torsional APN with simultaneous spontaneous palatal movements in oculopalatal tremor. Oculopalatal tremor typically begins weeks to months after a brainstem stroke and is associated with hypertrophic degeneration of the inferior olive. UBN is most common with medullary lesions from multiple sclerosis or in the setting of Wernicke encephalopathy. DBN occurs with many pathologies affecting the cerebellum, especially the cerebellar flocculus/paraflocculus or nodulus/uvula. Recent updates to be highlighted include a slowly progressive form of oculopalatal tremor called progressive ataxia and palatal tremor (PAPT) and diagnostic insights to be gained from careful examination of the behavior of UBN and DBN in different gaze positions and following provocative maneuvers (e.g., head shaking, supine position).