Possibilities of prismatic correction in the treatment of congenital horizontal nystagmus

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

Un caso di vertigine a esordio acuto/subacuto in un adolescente

The most common forms of paediatric vertigo are usually represented by benign causes. The occurrence of vertigo may nonetheless represent the onset of an underlying neurological disease, even without other neurological signs. The paper presents the case of a teenager with acute/subacute onset of vertigo and nausea; the examination revealed horizontal nystagmus with clinical features suggesting a peripheral form and minimal coordination defect. However, the clinical picture and persistence of symptoms led to perform brain imaging (MRI), which showed inflammatory demyelinating lesions with no signs of chronicity. These signs allowed a clinically isolated syndrome belonging to the spectrum of multiple sclerosis related disorders to be diagnosed.

Millard-Gubler Syndrome Associated with Cerebellar Ataxia in a Patient with Isolated Paramedian Pontine Infarction – A Rarely Observed Combination with a Benign Prognosis: A Case Report

Isolated pontine infarction accounts for 7% of all ischemic strokes. Millard-Gubler syndrome is a clinical syndrome which occurs following lesions involving the ventral portion of the caudal pons, resulting in classic clinical features such as ipsilateral abducens and facial nerve palsy and contralateral hemiparesis. We report the case of a 55-year-old male patient having presented to the Yehuleshet Specialty Clinic 6 years back with sudden-onset dysarthria and appendicular ataxia of 10 days duration. He reported having right hemibody weakness and blurred vision, which have significantly improved since then. He had a history of smoking of 30 pack-years. However, he quit smoking 8 years ago. There was no history of prior stroke, transient ischemic attack, diabetes, hypertension, head trauma, or dyslipidemia. On examination, he had horizontal left gaze palsy with horizontal nystagmus suggesting left-sided 6th cranial nerve palsy. He had mild left-sided facial palsy causing dysarthric speech. Right upper limb dysmetria was observed during examination; otherwise, motor, sensory, fundus, and gait examination results were normal. He had low serum vitamin D. Brain magnetic resonance imaging examination showed a 25 × 10 mm segmental lesion in the left median pons involving the basis pontis and tegmentum section. The lesion had T2 and T1 abnormal prolongation with no diffusion restriction, suggesting a subacute pontine infarct. The patient was managed with aspirin 325 mg, atorvastatin 80 mg, physical therapy, and vitamin D supplementation, and advised on behavioral risk factors. Six years after his isolated pontine infarction, the patient is fully recovered from dysarthria, facial palsy, hemiparesis, right-sided appendicular ataxia, and horizontal nystagmus, and the follow-up brain MRI showed radiological evidence of chronic paramedian pontine perforator infarction. Millard-Gubler syndrome may present with cerebellar ataxia if the paramedian pontine infarction area slightly extends laterally, affecting the middle cerebellar peduncles. Isolated pontine infarction may have a good prognosis if diagnosed and managed early.

Ataxic syndrome in a chronic phenytoin user

Introduction: Phenytoin is an anticonvulsant used routinely for about eight decades. However, depending on the dose and plasma concentration, its use may be associated with side effects due to toxicity, such as ataxic syndrome. Case report: We attended a 37-year-old patient, epileptic since childhood, who had been using Divalproate Sodium 250mg 8 / 8h, Phenobarbital 150mg once a day and Phenytoin 100mg 8/8 for a long time. He denied smoking and drinking. He was admitted due to acute rotational vertigo, nausea, motor incoordination and impaired speech and gait, progressing for 7 days. Neurological examination revealed drunken dysarthria, pendular patellar reflexes, signs of axial and appendicular incoordination and ataxic gait. Cranial nerves: there was decomposition of the eye movement and hypometric saccades to the vertical upward look, horizontal nystagmus with alternating phases to the extreme looks. Laboratory exams, cranial tomography with and without contrast, brain magnetic resonance with gadolinium): within the normal range. Given the above, our diagnostic hypothesis was Phenytoin Poisoning. After gradually replacing it, there was a progressive improvement in the neurological condition. His serum level was not determined due to the unavailability of this test in our service. Conclusion: In view of its routine use, excluding other etiologies, this diagnosis should always be remembered.

Nystagmus characteristics of healthy controls

BACKGROUND: Healthy controls exhibit spontaneous and positional nystagmus which needs to be distinguished from pathological nystagmus. OBJECTIVE: Define nystagmus characteristics of healthy controls using portable video-oculography. METHODS: One-hundred and one asymptomatic community-dwelling adults were prospectively recruited. Participants answered questions regarding their audio-vestibular and headache history and were sub-categorized into migraine/non-migraine groups. Portable video-oculography was conducted in the upright, supine, left- and right-lateral positions, using miniature take-home video glasses. RESULTS: Upright position spontaneous nystagmus was found in 30.7% of subjects (slow-phase velocity (SPV)), mean 1.1±2.2 degrees per second (°/s) (range 0.0 – 9.3). Upright position spontaneous nystagmus was horizontal, up-beating or down-beating in 16.7, 7.9 and 5.9% of subjects. Nystagmus in at least one lying position was found in 70.3% of subjects with 56.4% showing nystagmus while supine, and 63.4% in at least one lateral position. While supine, 20.8% of subjects showed up-beating nystagmus, 8.9% showed down-beating, and 26.7% had horizontal nystagmus. In the lateral positions combined, 37.1% displayed horizontal nystagmus on at least one side, while 6.4% showed up-beating, 6.4% showed down-beating. Mean nystagmus SPVs in the supine, right and left lateral positions were 2.2±2.8, 2.7±3.4, and 2.1±3.2°/s. No significant difference was found between migraine and non-migraine groups for nystagmus SPVs, prevalence, vertical vs horizontal fast-phase, or low- vs high-velocity nystagmus (<5 vs > 5°/s). CONCLUSIONS: Healthy controls without a history of spontaneous vertigo show low velocity spontaneous and positional nystagmus, highlighting the importance of interictal nystagmus measures when assessing the acutely symptomatic patient.

Nystagmus goggles: how to use them, what you find and what it means

A fundamental characteristic of peripheral vestibular nystagmus, in particular horizontal nystagmus, is that it is suppressed by visual fixation. This means that a patient with a vertigo attack of peripheral vestibular origin might have no obvious spontaneous nystagmus on clinical examination. Goggles that reduce or remove visual fixation allow the cliniican to observe nystagmus in this situation. Nystagmus goggles are essential for any clinician dealing with dizzy patients. Here, we discuss why this is so and how easy it is to acquire and use them.