Oscillopsia, Nystagmus, Saccadic Oscillations, and Intrusions

2014 ◽  
pp. 373-412
Author(s):  
Shirley H. Wray
Keyword(s):  
Saccadic Eye Movement ◽  
Vestibular Nystagmus ◽  
Paraneoplastic Encephalitis ◽  
Ocular Flutter ◽  
Slow Drift ◽  
Close Observation ◽  
Pendular Nystagmus ◽  
The Central Nervous System ◽  
Upbeat Nystagmus ◽  
Cancer Of The Lung

Nystagmus, defined as an involuntary repetitive, rhythmic to-and-fro movement of the eyes initiated by a slow drift that shifts an image off the fovea, is discussed in detail. The steps to take in evaluating nystagmus are emphasized , including the importance of close observation with the patient supine, prone, and lying on either side Central vestibular nystagmus due to disease of the central nervous system is covered fully and case studies include patients with upbeat nystagmus and with acquired pendular nystagmus.. When a saccadic eye movement takes the eye away from fixation (saccadic intrusion), a variety of saccadic oscillations can occur, in particular multidirectional saccades without an intersaccadic interval, which is diagnostic of opsoclonus; ocular flutter; or the two oscillations combined. . Two paraneoplastic syndromes illustrate these disorders , a case of ocular flutter associated with paraneoplastic encephalitis and cancer of the lung, and an infant with opsoclonus as the herald syndrome of a neuroblastoma.

Management of opioid poisoning

2016 ◽  
Author(s):  
Alison L. Jones
Keyword(s):  
Respiratory Depression ◽  
Opioid Antagonist ◽  
Arterial Oxygen ◽  
Opioid Use ◽  
Analgesic Tolerance ◽  
Medication Misuse ◽  
Acute Withdrawal ◽  
Close Observation ◽  
The Central Nervous System ◽  
Long Acting

Opioids are ‘morphine like’ substances that have actions at specific opioid receptors (especially µ receptors) in the central nervous system (CNS). Tolerance of respiratory depression develops at a slower rate than analgesic tolerance, placing patients with a long history of opioid use at particular risk for respiratory depression. If chronic users abruptly stop taking opioids, they develop an acute withdrawal syndrome. Most opioid toxicity is the result of inadvertent overdosage during recreational use or in self-harm, but it can also be due to medication misuse and drug errors. It is characterized by three main clinical features (all may not be consistently present); depressed respiratory rate (the sine qua non of opioid poisoning) and respiratory volume, and reduced arterial oxygen desaturation, CNS depression, and small or pin-point pupils. Opioid-poisoned patients require early clinical assessment, appropriate administration of intravenous naloxone (competitive opioid antagonist) and meticulous respiratory supportive care, with close observation. Because of the longer half-life of opioids than naloxone, repeated doses may be needed for long-acting opioids or large doses of shorter acting opioids. If opioid antagonists are given to regular opioid users in excess, they can precipitate acute withdrawal symptoms. The need for ITU admission usually occurs as a result of a complication of the opioid toxicity.

scholarly journals Brainstem angiocentric glioma: report of 2 cases

2017 ◽  
Vol 20 (4) ◽  
pp. 347-351 ◽  
Author(s):  
Kristin J. Weaver ◽  
Lexi M. Crawford ◽  
Jeffrey A. Bennett ◽  
Marie L. Rivera-Zengotita ◽  
David W. Pincus
Keyword(s):  
Cerebral Hemispheres ◽  
Third Ventriculostomy ◽  
Pathological Features ◽  
First Case ◽  
Close Observation ◽  
Pontine Lesion ◽  
The Central Nervous System ◽  
Angiocentric Glioma ◽  
Initial Description

Angiocentric glioma is a rare tumor that was recognized by the WHO Classification of Tumours of the Central Nervous System as a distinct clinicopathological entity in 2007. Since this initial description, the vast majority of cases of angiocentric glioma reported in the literature have involved tumors of the cerebral hemispheres. To date, only 1 case of angiocentric glioma arising from the posterior midbrain has been reported. The authors present the cases of 2 pediatric patients who were found to have brainstem angiocentric gliomas. The clinical course, radiological and pathological features, treatment, and follow-up are described. The first case is one of a 5-year-old girl who presented with double vision, headache, and nausea and was found to have a midbrain lesion with pathological features consistent with angiocentric glioma. She was treated with resection and endoscopic third ventriculostomy (ETV), followed by close observation and serial neuroimaging. The second case is one of a 6-year-old boy who presented with progressive mouth drooping and problems with balance. He was found to have a pontine lesion with pathological features consistent with angiocentric glioma. This patient was treated with ETV, followed by close observation and serial neuroimaging. This report includes 6 and 1.5 years of follow-up of the patients, respectively. While there are limited data regarding the prognosis or long-term management of patients with brainstem angiocentric gliomas, the cases described in this report suggest an indolent course for this tumor, similar to the course of angiocentric gliomas located in the cerebral hemispheres.

Autoimmune Dementia

2018 ◽  
Vol 38 (03) ◽  
pp. 303-315 ◽  
Author(s):  
Justin Long ◽  
Gregory Day
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Impairment ◽  
Relevant Information ◽  
Paraneoplastic Encephalitis ◽  
Immune Mediated ◽  
Paraneoplastic Disease ◽  
Chronic Complication ◽  
The Central Nervous System ◽  
Diagnostic Framework

AbstractDementia refers to an acquired syndrome of intraindividual cognitive decline that ultimately interferes with an individual's ability to manage their usual duties at work or home. As experience with the diagnosis and management of patients with autoimmune and paraneoplastic encephalitis (AE) has expanded, it has become increasingly apparent that dementia may arise as a subacute or chronic complication of immune-mediated injury to the central nervous system. Progressive memory and thinking problems may represent the first (or only) sign of an underlying autoimmune or paraneoplastic disease. Accordingly, there is a need to routinely consider the diagnosis of AE in patients with dementia, and to evaluate patients recovering from AE for clinically meaningful cognitive impairment. We review and summarize the available evidence concerning the diagnosis and care of AE patients with associated cognitive impairment, herein referred to as autoimmune dementia (AiD). Relevant information is used to propose a novel diagnostic framework that may be applied to improve recognition, and facilitate the expedited evaluation and treatment of patients with AiD.

scholarly journals Saccadic eye movement related potentials

2007 ◽  
pp. 707-713
Author(s):  
F Jagla ◽  
M Jergelová ◽  
I Riečanský
Keyword(s):  
Eye Movement ◽  
Sensorimotor Integration ◽  
Saccadic Eye Movements ◽  
Saccadic Eye Movement ◽  
Cognitive Mechanisms ◽  
Neuropsychological Disorders ◽  
Related Potentials ◽  
The Central Nervous System ◽  
Attention Level ◽  
Insight Into

The saccadic eye movement related potentials (SEMRPs) enable to study brain mechanisms of the sensorimotor integration. SEMRPs provide insight into various cognitive mechanisms related to planning, programming, generation and execution of the saccadic eye movements. SEMRPs can be used to investigate pathophysiological mechanisms of several disorders of the central nervous system. Here we shortly summarize basic findings concerning the significance of SEMRP components, their relationship to the functional brain asymmetry and visual attention level as well as changes related to certain neuropsychological disorders.

Upbeat Nystagmus

2011 ◽  
pp. 118-121
Author(s):  
Matthew J. Thurtell ◽  
Robert L. Tomsak ◽  
Robert B. Daroff
Keyword(s):  
Common Type ◽  
Wernicke’S Encephalopathy ◽  
Wernicke's Encephalopathy ◽  
Vestibular Nystagmus ◽  
Visual Symptoms ◽  
Upbeat Nystagmus

Upbeat nystagmus is a less common type of central vestibular nystagmus that is often transient. However, it can be persistent and responsible for visual symptoms. We review the characteristics and causes of upbeat nystagmus in this chapter. We also discuss the management of upbeat nystagmus occurring in the setting of Wernicke’s encephalopathy.

Iatrogenic CNS demyelination in the era of modern biologics

2019 ◽  
Vol 25 (8) ◽  
pp. 1079-1085 ◽  
Author(s):  
Neha Kumar ◽  
Hesham Abboud
Keyword(s):  
Checkpoint Inhibitors ◽  
Complete Response ◽  
Tnf Alpha ◽  
Paraneoplastic Encephalitis ◽  
The Past ◽  
The Central Nervous System ◽  
Cns Demyelination ◽  
Term Monitoring ◽  
Necrosis Factor

The number of reported cases of iatrogenic demyelination of the central nervous system (CNS) is on the rise. This is, in part, related to the recent expansion in the use of biologics. Review of literature from the past decade suggests that in addition to vaccines, tumor necrosis factor (TNF)-alpha inhibitors and checkpoint inhibitors are the most frequently cited inducers of central inflammation. About one-third of demyelinating cases in the setting of TNF-alpha inhibitors evolve into full-blown multiple sclerosis. In addition to demyelination, checkpoint inhibitors may also cause accelerated paraneoplastic encephalitis and other antibody-mediated conditions. Luckily, the overall prognosis of iatrogenic central inflammation is favorable, with most cases having partial or complete response to steroids and discontinuation of the offending agent. Long-term monitoring and initiation of maintenance immune-modulating therapy may be necessary in some patients. In this article, we provide an updated review of biologic-induced inflammation of the CNS.

Radiological Correlate of Ocular Flutter in a Case with Paraneoplastic Encephalitis

2011 ◽  
Vol 23 (2) ◽  
pp. 251-253 ◽  
Author(s):  
Christopher R. Newey ◽  
Aarti Sarwal ◽  
Guiyun Wu
Keyword(s):  
Paraneoplastic Encephalitis ◽  
Ocular Flutter

Bárány’s Life in Uppsala and His Work with Lorente de Nó

2016 ◽  
Author(s):  
Robert W. Baloh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Eye Movements ◽  
Reticular Formation ◽  
Slow Phase ◽  
Vestibular Nystagmus ◽  
Cortical Control ◽  
Abducens Nucleus ◽  
The Central Nervous System ◽  
Voluntary Eye Movements

Lorente de Nó came to Uppsala, Sweden, in 1924 to work with Robert Bárány, with the goal of studying the central nervous system pathways of the vestibular nystagmus response. Bárány’s 1907 book described a patient with a lesion involving the reticular formation of the pons close to the abducens nucleus who could generate only the slow phase of nystagmus. With stimulation, the patient’s eyes slowly deviated to one side and became pinned. The patient also had a loss of voluntary eye movements. Bárány concluded that there must be separate centers in the brainstem for the production of the slow and fast phases of nystagmus. He speculated that the center for generating fast phases was in the reticular substance next to the abducens nucleus and that this component was under the influence of cortical control. Nó would go on to perform studies of these central pathways for generating nystagmus in rabbit.

Upbeat Nystagmus

2019 ◽  
pp. 151-154
Author(s):  
Matthew J. Thurtell ◽  
Robert L. Tomsak
Keyword(s):  
Medical Treatment ◽  
Clinical Features ◽  
Treatment Options ◽  
Common Type ◽  
Imaging Findings ◽  
Vestibular Nystagmus ◽  
Wernicke Encephalopathy ◽  
Common Cause ◽  
Upbeat Nystagmus ◽  
Symptoms And Signs

Upbeat nystagmus is a less common type of central vestibular nystagmus that is often transient. It is a vertical jerk-waveform nystagmus with downward slow phases and upward quick phases. In this chapter, we begin by reviewing the clinical features of upbeat nystagmus. Since it can be produced by lesions in a variety locations in the brainstem and cerebellum, we next describe the symptoms and signs that can help to localize the causative lesion. We list the causes of upbeat nystagmus. We then discuss the clinical and imaging findings in Wernicke encephalopathy, which is a common cause of upbeat nystagmus, and we review the management of Wernicke encephalopathy. Lastly, we briefly discuss the medical treatment options for persistent upbeat nystagmus.

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