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The Neurologic Disorders in Film
Published in Eelco F. M. Wijdicks, Neurocinema—The Sequel, 2022
What is currently known about the disorder is that after a flu-like illness, patients with encephalitis lethargica develop marked sleepiness, ocular movement disturbances, and fever. Abnormal posturing (dystonia) was not initially part of the manifestation, and stupor (hence, the word lethargic) was most prominent and persistent. Some patients could become immediately alert; others had more cyclic responsiveness, with sleep during the day and wakefulness during the night. In earlier descriptions, paralysis of eye muscles was very common, but very often, other cranial nerves were involved. Oropharyngeal dysfunction could lead to early demise. This combination of upper cranial nerve involvement and stupor now, in retrospect, would fit well with an upper brainstem lesion, and indeed, the mesencephalon showed necrosis and perivascular lymphocytic infiltrate. In some patients, the hypothalamus was involved. Many of these patients either developed a catatonic state or recovered with narcolepsy. The parkinsonian manifestations occurred often after a period of years after the infection, but more than 50% of the survivors developed parkinsonian symptoms within 5 years and 80% within 10 years. Oculogyric crisis was a common manifestation.
Von Economo’s encephalitis
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Oculogyric crises occurred in 15%–20% of patients at the height of the epidemic [69]. Incidence of approximately 30% were reported to the 1960s [1]. Following the introduction of l-dopa in the treatment of postencephalitic Parkinsonism, the incidence approached 100% [1]. It lasted seconds to hours; typically resulted in tonic deviation of the eyes upward or upward and laterally, often with spasmodic deviation of the head. These crises could be precipitated by emotions. During the spell, consciousness was preserved, but the patient was incapable of voluntarily moving his eyes except momentarily with strong effort. The frequency of the oculogyric crises varied from individual to individual. At times, the crises were accompanied by movement disorders, e.g., dystonic posturing, typically of the head and neck, or by verbal utterances or coprolalia [70–72]. Sometimes, forced thoughts of sexual and violent nature, other compulsions, or religious rituals accompanied the oculogyric crises [70–72]. Oculogyric crises were virtually unknown prior to the epidemic of encephalitis lethargica [73]. Other ocular abnormalities observed included slight ptosis, impaired pupillary reaction and Argyll Robertson pupils, nystagmus, squint, impaired convergence and extraocular muscle palsies.
Neurology
Published in Shibley Rahman, Avinash Sharma, A Complete MRCP(UK) Parts 1 and 2 Written Examination Revision Guide, 2018
Shibley Rahman, Avinash Sharma
Oculogyric crisis is an acute dystonic reaction of the face/eyes and is usually a consequence of typical neuroleptic drugs such as haloperidol and chlorpromazine but is unusual with newer agents such as olanzapine anad clozapine.
Neuro-ophthalmology of movement disorders
Published in Expert Review of Ophthalmology, 2018
The most common simple motor ocular tic is increased frequency of blinking, sometime leading to transient blepharospasm [81]. Oculogyric tics and transient intermittent blepharospasm are examples of dystonic tics observed in 28% and 11%, of patients with Tourette syndrome, respectively [82]. Oculogyric dystonic tics should not be confused with oculogyric crises that are the involuntary spasmodic eye movements into a fixed position that can be quite painful and last for minutes or even hours. Etiology of oculogyric crisis is usually exposure to dopamine-receptor blocking medications. Oculogyric dystonic tics have characteristic features of tics such as premonitory urge and supressibility.
Oculogyric Crisis with Downward Deviation – A Photo Essay
Published in Neuro-Ophthalmology, 2018
Hüseyin Nezih Özdemir, Neşe Çelebisoy
Oculogyric crisis (OGC) describes the clinical phenomenon of sustained dystonic, conjugate and typically upward deviation of the eyes, although a few cases with downward or lateral deviations were described.1,2 OGC was first described in patients with encephalitis lethargica, but is most commonly seen in the present day in patients exposed to neuroleptics.3 Although the pathophysiology of acute dystonic reactions is still unclear, it is believed to be due to a deficit in central dopamine transmission resulting in overactive striatal acetylcholine release.4 The spectrum of conditions associated with OGCs is wide and encompasses three main categories of disorders: (1) drug-induced disorders, (2) hereditary and sporadic movement disorders and (3) disorders related to focal brain lesions.1 Sixty-eight per cent of all reported patients with drug-induced OGCs we could identify were due to neuroleptics.1 Both typical and atypical neuroleptics induced OGCs; however, the use of typical neuroleptics and OGCs was more commonly reported.1 Patients who have experienced a single episode of acute dystonic reaction are at higher risk for future dystonic reactions when exposed to other dopamine receptor blocking agents.5 It is commonly reported as an acute disorder.1 Clinical presentation may vary from very brief and subtle eye deviation as an isolated symptom to more severe and even painful forms accompanied by neck flexion, jaw opening, blepharospasm, tongue protrusion and autonomic signs, such as perspiration, pupillary dilation, increases in blood pressure and heart rate.1 The common basis of these disorders is a metabolic, anatomical or functional disruption of the nigrostriatal pathway, mainly of dopamine metabolism.
Common systemic medications that every optometrist should know
Published in Clinical and Experimental Optometry, 2022
Dystonia, an involuntary muscle contraction, is referred to as oculogyric crisis when involving the extraocular muscles.55 Oculogyric crisis has been shown to occur secondary to psychogenic drugs, including antipsychotics, carbamazepine, topiramate, and SSRIs.56 During an oculogyric crisis, any form of gaze paralysis can occur. The symptoms of oculogyric crisis commonly occur early in the course of treatment or shortly after dosage is increased. The onset is often acute, and can be successfully reversed with anticholinergic, antihistaminergic, and other drugs.57 Patients taking benzodiazepines should be warned of their effects on eye movements. These drugs can serve a safety risk when operating machinery such as automobiles due to their effects on saccadic and smooth pursuit eye movements.58,59 Benzodiazepines may also contribute to acquired nystagmus which is fortunately readily treatable with clonazepam, with one study of five cases showing 100% efficacy in nystagmus management.60 Lithium use has been associated with downbeat nystagmus in multiple case studies. In each case, cessation of the nystagmus followed discontinuation of the drug.61–63 Carbamazepine, an anticonvulsant, has been shown to cause a number of ocular movement disorders, including diplopia, downbeat nystagmus, and oscillopsia.64 Although not clinically significant, gaze-evoked lateral nystagmus can occur in 25% of patients taking carbamazepine.65 Finally, topiramate can induce nystagmus in high doses.66 Optometrists can monitor for gaze paralysis and other ocular motility issues with observation of EOM movements, clinical observation, and history of present illness discussion. As eye care providers observe short- and long-term ocular motility defects from psychogenic medications, pronounced defects may warrant discussion of a lower drug dose or discontinuation.