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Background: Opsoclonus is a rare disorder characterized by conjugate multidirectional, horizontal, vertical, and torsional saccadic oscillations, without intersaccadic interval, resulting from dysfunction within complex neuronal pathways in the brainstem and cerebellum. While most cases of opsoclonus are associated with autoimmune or paraneoplastic disorders, infectious agents, trauma, or remain idiopathic, opsoclonus can also be caused by medications affecting neurotransmission. This review was prompted by a case of opsoclonus occurring in a patient with Multiple System Atrophy, where amantadine, an NMDA-receptor antagonist, appeared to induce opsoclonus., Methods: Case report of a single patient and systematized review of toxic/drug-induced opsoclonus, selecting articles based on predefined criteria and assessing the quality of included studies., Results: The review included 30 articles encompassing 158 cases of toxic/drug-induced opsoclonus. 74% of cases were attributed to bark scorpion poisoning, followed by 9% of cases associated with chlordecone intoxication. The remaining cases were due to various toxics/drugs, highlighting the involvement of various neurotransmitters, including acetylcholine, glutamate, GABA, dopamine, glycine, and sodium channels, in the development of opsoclonus., Conclusion: Toxic/drug-induced opsoclonus is very rare. The diversity of toxics/drugs impacting different neurotransmitter systems makes it challenging to define a unifying mechanism, given the intricate neuronal pathways underlying eye movement physiology and opsoclonus pathophysiology., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

Background: The benefits of intraarterial thrombolytic treatment (IATT) in reversing hyaluronic acid (HA)-related visual deficits remain unclear. This study aimed to report a 5-year experience in the treatment of visual deficits resulting from HA embolization by IATT in a tertiary medical center., Methods: From December of 2015 to June of 2021, the medical records of consecutive patients with HA-related visual deficits who underwent IATT were reviewed retrospectively. The demographics, clinical features, imaging data, treatment details, and follow-up results of the patients were analyzed., Results: A total of 72 consecutive patients were analyzed, including five men (6.9%) men and 67 women (3.1%), aged 29.3 ± 7.6 years (range, 17 to 50 years). Thirty-two patients (44.4%) showed preserved visual acuity, and 40 (55.6%) exhibited no light perception on admission. Ocular motility disorders were detected in 63 patients (87.5%), ptosis was detected in 61 patients (84.7%), and facial skin changes were detected in 54 patients (75%). The technical success rate of IATT was 100%, with successful recanalization of the occlusive artery. No procedure-related complications were detected, and all skin injuries, ptosis, and ocular motility disorders were healed. Improved visual acuity was detected in 26 cases (36.1%). In the binary logistic regression model, only preoperative preserved visual acuity was independently associated with a good outcome., Conclusions: IATT for selective patients with HA-related visual deficits is efficient and safe. Preoperative preserved visual acuity was independently associated with a good outcome after IATT., Clinical Question/level of Evidence: Therapeutic, IV., (Copyright © 2023 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the American Society of Plastic Surgeons.)

Competing Interests: Competing interests: None declared.

An oculogyric crisis is a tonic conjugated deviation of the eyes, usually upward. We present two cases with a drug induced oculogyric crisis. The differential diagnoses should include epilepsy, a functional neurological movement disorder, ocular tics, ocular dyskinesia or ocular bobbing. Typically, in an oculogyric crisis the patient's awareness is intact; accompanied signs can be blepharospasm, neck flexion, jaw opening with or without tongue protrusion and autonomic symptoms. The underlying pathophysiology seems an imbalance between cholinergic and dopaminergic pathways. Most frequently an oculogyric crisis is caused by antidopaminergic medications, for example neuroleptics and metoclopramide. Treatment of medication-induced oculogyric crisis with parenteral anticholinergics typically leads to a fast remission of symptoms. Consider tocontinue anticholinergic therapy orally for a few days.

Objectives: Oculogyric crisis is a dystonic movement disorder characterized by continuous contraction of the ocular muscles and spasmodic movements of the pupils in a fixed position, usually upward., Methods: In this case report, an early-stage acute oculogyric crisis due to low-dose olanzapine in a 15-year-old adolescent boy is presented., Results: To the best of our knowledge, this is the first report showing that acute oculogyric crisis can develop with low-dose olanzapine administration., Conclusions: Even though second-generation antipsychotics are safer than conventional antipsychotics in terms of extrapyramidal adverse effects, this possibility should always be taken into consideration through this case report., Competing Interests: Conflicts of Interest and Source of Funding: The authors have no conflicts of interest to declare., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

The caudal fastigial nuclei (cFN) are the output nuclei by which the medio-posterior cerebellum influences the production of saccades toward a visual target. On the basis of the organization of their efferences to the premotor burst neurons and the bilateral control of saccades, the hypothesis was proposed that the same unbalanced activity accounts for the dysmetria of all saccades during cFN unilateral inactivation, regardless of whether the saccade is horizontal, oblique, or vertical. We further tested this hypothesis by studying, in two head-restrained macaques, the effects of unilaterally inactivating the caudal fastigial nucleus on saccades toward a target moving vertically with a constant, increasing or decreasing speed. After local muscimol injection, vertical saccades were deviated horizontally toward the injected side with a magnitude that increased with saccade size. The ipsipulsion indeed depended on the tested target speed but not its instantaneous value because it did not increase (decrease) when the target accelerated (decelerated). By subtracting the effect on contralesional horizontal saccades from the effect on ipsilesional ones, we found that the net bilateral effect on horizontal saccades was strongly correlated with the effect on vertical saccades. We explain how this correlation corroborates the bilateral hypothesis and provide arguments against the suggestion that the instantaneous saccade velocity would somehow be "encoded" by the discharge of Purkinje cells in the oculomotor vermis. NEW & NOTEWORTHY Besides causing dysmetric horizontal saccades, unilateral inactivation of caudal fastigial nucleus causes an ipsipulsion of vertical saccades. This study is the first to quantitatively describe this ipsipulsion during saccades toward a moving target. By subtracting the effects on contralesional (hypometric) and ipsilesional (hypermetric) horizontal saccades, we find that this net bilateral effect is strongly correlated with the ipsipulsion of vertical saccades, corroborating the suggestion that a common disorder affects all saccades.

Background: Lithium salts have been commonly used for prophylaxis and treatment of bipolar disorder and have numerous side effects. However, there has been no report of skew deviation and downbeat nystagmus associated with lithium. Herein, we report the first case of lithium-induced skew deviation and downbeat nystagmus., Case Presentation: A 39 years-old woman presented with intermittent vertical diplopia and dizziness within 1-2 months. Ophthalmologic examination revealed downbeat nystagmus and 6 prism diopters of right hypertropia. Funduscopic examination showed mild incyclotorsion on right eye. However, ductions and versions were within normal range. Other neurological examinations were also normal. She had a history of bipolar disorder treated with daily 600-900 mg of lithium for past 6 years, and 2 months before the first visit, daily dose of lithium was increased to 1200 mg. We referred the patients to psychiatrist. Although the serum level of lithium was within the normal therapeutic range, her daily dose of lithium was reduced to 600 mg and then stopped. 6 days after cessation of lithium, down beat nystagmus and right hypertropia were completely resolved and symptoms did not recur over a year., Conclusion: Even within a normal therapeutic range, downbeat nystagmus and skew deviation can occur as side effect of lithium. Dehydration may contribute to the neurotoxicity of lithium.

Purpose of Review: To summarize the visual and oculomotor outcomes in children with prenatal opioid exposure and review the effects of opioids on the developing central nervous system., Recent Findings: Animal models and imaging studies in children suggest that prenatal opioid exposure may affect neuronal survival and result in delayed maturation of white matter tracts and decreased volumes in certain brain areas. Visual evoked potential testing in children demonstrates delayed maturation of the afferent visual system in opioid-exposed groups compared with controls, though 'catch-up' development is seen with longitudinal follow-up. Strabismus and nystagmus are also more common in exposed children, and these findings appear to persist., Summary: As rates of opioid dependence and prenatal opioid exposure continue to increase, it is important to evaluate the short-term and long-term effects of opioids on the developing visual system. An understanding of these risks is important when counseling the parents or guardians of opioid-exposed children, though larger studies with more long-term follow-up will improve our prognostic abilities.

A 19-year-old female was seen at the emergency department following an auto-intoxication. An oculogyric crisis (ogc) was observed, in the absence of other extrapyramidal symptoms (eps). In a second anamnesis, patient indicated that she had taken risperidone 3 mg (an atypical antipsychotic). This particular case description of an isolated ogc shows that care providers should be attentive to the occurrence of ogc, even if the most frequent eps are absent. This case also emphasizes the importance of a complete history in order to efficiently and timely guide the care provider to the correct diagnosis.

Ictal gaze deviation and oculogyric crisis (OGC) can show identical clinical manifestations. We report a case of repeated drug induced OGCs in a 38 year old patient with secondary progressive multiple sclerosis. He was referred to our center for treatment of "intractable" epilepsy manifesting as episodic eye and head deviations with apparent unresponsiveness. In the epilepsy monitoring unit, ten typical spells were captured without epileptiform electroencephalographic correlates, but we discovered chronic exposure to metoclopramide. A diagnosis of OGC was suspected and Metoclopramide was stopped. This robustly improved the frequency of his spells. In a setting of usage of antidopaminergic medications and/or pontomesencephalic lesions, a low threshold should be kept for the diagnosis of oculogyric crisis, thus avoiding seizure diagnoses and inappropriate treatment of the phenomenon. Video-EEG monitoring is essential for teasing apart epilepsy and OGC., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Upgaze or sustained elevation of the eyes, is an alteration of ocular motility initially described in hypoxic coma. We report a 65-year-old woman admitted with hypotension and alteration of sensorium due to the ingestion of 9.5 g of Bupropion. She presented two seizures of short duration, without epileptic activity on the EEG. She had a persistent asynchronous myoclonus in extremities, tachycardia and prolonged Q-t. She suffered a cardiac arrest caused by asystole, which recovered quickly in five minutes. At that moment, upgaze appeared, associated with a persistent ocular opening, which persisted for days, but finally disappeared, without remission of coma. A magnetic resonance imaging done at the eighth day, showed hyperintensity of the oval center and corpus callosum which disappeared in a new imaging study done 30 days later, where images of hypoxia in the basal nuclei and cortex appeared. The patient died forty seven days after admission. Up-gaze is an ominous oculomotor alteration linked to an important but incomplete damage in the cerebral cortex, a condition that perverts some sequences of the ocular opening, reversing the Bell phenomenon and producing eyelid retraction.

FK506 (tacrolimus) is an immunosuppressive drug and more potent than cyclosporine. FK506 is widely used for immunosuppression in the prevention and treatment of graft-versus-host disease after allogeneic bone marrow transplantation and solid organ transplantation. Neurotoxicity is a recognized complication of FK506 therapy, but ptosis and weakness of eye abduction unilaterally has not been reported in association with FK506 administration to date. We discuss a 13-year-old male patient who developed ptosis and weakness of eye abduction unilaterally 90 days after transplantation with bone marrow from an unrelated donor, for acute lymphoblastic leukemia in this case report. FK506 therapy was administered for graft-versus-host disease prophylaxis and CMV infection was treated with ganciclovir. The physical examination findings completely resolved 72 to 96 hours after concomitant FK506 and ganciclovir treatment were terminated.

Background: Oculogyric crises are involuntary movements of the eyeballs and can occur due to different etiologies., Phenomenology Shown: This video abstract shows a man with oculogyric crises due to side effect of neuroleptics., Educational Value: Oculogyric crises are easy to recognize if once seen., Competing Interests: Funding: None. Conflicts of Interest: The authors report no conflict of interest. Ethics Statement: The patient that appears on video has provided written informed consent; authorization for the videotaping and for publication of the videotape was provided.

Oculogyric crisis (OGC) describes the clinical phenomenon of sustained dystonic, conjugate and typically upward deviation of the eyes lasting from seconds to hours. It was initially observed in patients with postencephalitic parkinsonism, but since then a number of conditions have been associated with OGC. These include drug-induced reactions, hereditary and sporadic movement disorders, and focal brain lesions. Here, we systematically review the literature and discuss the spectrum of disorders associated with OGC in order to aid clinicians place this rare but distinctive clinical sign into the appropriate diagnostic context. We also provide a brief synthesis of putative pathophysiological mechanisms, as well as therapeutic recommendations based on the literature and our own experience., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Extrapyramidal symptoms are an uncommon but well-recognized side effect after the administration of general anesthesia in patients without a significant neurologic history. Several case reports implicate propofol as the likely causative agent producing these symptoms, which include ballismus, dystonia, choreoathetosis, and opisthotonus. Currently, there is no clear consensus on first-line treatment of these symptoms. In each of the published cases, anticholinergic medications and benzodiazepines were central to initial management, although the speed and extent of symptom resolution were variable. Here we present a case of a 17-year-old boy with ulcerative colitis who presented with ballismus, torticollis, tongue thrusting, and oculogyric movements after colonoscopy under general anesthesia with propofol. The patient responded promptly to treatment with diphenhydramine. This is the first reported case in which diphenhydramine was successfully used as the primary treatment of severe extrapyramidal symptoms in a pediatric patient after propofol administration., (Copyright © 2017 by the American Academy of Pediatrics.)

Case Report: We present the case of an 11-year-old boy with acute diplopia in near vision secondary to transient convergence palsy, possibly in relation to amoxicillin., Discussion: Convergence palsy is an uncommon eye disorder. The causes are reviewed, and amoxicilin is identified as presumptive etiologic agent. This is the first case reported., (Copyright © 2016 Sociedad Española de Oftalmología. Publicado por Elsevier España, S.L.U. All rights reserved.)

Oculogyric crisis (OGC) is an often recurrent dystonic adverse effect of antipsychotic treatment characterized by a sustained fixed upward gaze lasting minutes to hours. The risk of OGC has not been established. We prospectively estimated the incidence rate of OGC in an early intervention service for psychosis and provided details regarding the antipsychotics implicated, clinical presentation, and long-term outcomes of OGC. The Nova Scotia Early Psychosis Program provides comprehensive, team-based care to youth and young adults with schizophrenia spectrum disorder. For 6 years (April 2008 to March 2014), 452 new patients were admitted to the program and participated in an individualized program of care. Eight patients (4 females; mean age, 19.8 years) developed recurrent episodes of OGC after 3 months to 2 years of treatment with 1 or more second-generation antipsychotics, yielding an incidence rate of 1.8% (95% confidence interval, 0.9%-3.4%). Risperidone or olanzapine (alone or in combination with a second antipsychotic) seemed causative in each case. Also implicated in the onset or recurrence of oculogyric episodes were ziprasidone, quetiapine, clozapine, aripiprazole, and the first-generation antipsychotic loxapine. Follow-up ranged between 2 and 7 years. Episodes stopped after switching antipsychotic treatment in 4 cases and after stopping antipsychotic treatment in 2 cases. In the other 2 cases, recurrences were ongoing at last follow-up 2 and 6 years after onset with antipsychotic treatment continuing. We observed a high rate of tardive-onset, recurrent, and potentially chronic ocular dystonias in patients with first-episode psychosis caused by the use of second-generation antipsychotics.

A 60-year-old woman reported horizontal "shimmering" movement while reading crossword puzzles when using fluvoxamine, bupropion, quetiapine, lithium, and levothyroxine. This visual disturbance, likely oscillopsia, started after the fluvoxamine was added and waned as the fluvoxamine was tapered, disappearing after the drug was discontinued. Genetic testing to explore how the patient metabolizes these medications combined with YouScript® interaction analysis suggest that she may have had abnormally high plasma concentrations of fluvoxamine during this time. Oscillopsia may be a novel dose-dependent side effect of fluvoxamine. Genetic testing combined with YouScript has the potential to discover novel drug side effects, elucidate drug interactions and guide future prescribing decisions.

Aim: To describe the presentation of an internuclear ophthalmoplegia (INO) associated with the use of anti-tumor necrosis factor α (anti-TNFα) medication., Methods: A case report of a woman, aged 27 years, who developed facial numbness, blurred vision, and diplopia on right gaze. She had a history of Crohn's disease, which was being treated by the anti-TNFα drug, adalimumab. On examination, a left INO was found., Treatment: The patient was prescribed a short course of corticosteroids and adalimumab treatment was discontinued., Results: Magnetic resonance imaging demonstrated typical demyelinating lesions including one responsible for the INO. Following a short course of corticosteroids and the discontinuation of the adalimumab treatment, the INO resolved, resulting in a swift improvement of ocular motility over a 2-week period., Conclusion: Anti-TNFα therapies have been associated with the development of demyelinating diseases. The presentation of a brainstem syndrome in a patient on anti-TNFα therapy should lead to investigation for central nervous system demyelination and cessation of the medication.

Background: An adolescent girl had isolated abnormal downward gaze and oculovestibular (cold caloric) testing during propofol administration, prompting concern for brainstem abnormality., Patient: An otherwise healthy 16-year-old girl presented after an intentional hanging. Brainstem reflexes were normal except that both eyes exhibited tonic downward gaze on initial examination. After propofol was suspended for 30 minutes in order to evaluate her level of responsiveness, her eyes normalized to midposition from tonic downward gaze. With reinitiation of propofol, the eyes returned to the former downward position. C-collar stabilization prohibited the usual oculocephalic (doll's eyes) evaluation. Right-sided cold water instillation resulted in right eye exodeviation to the right with minimal medial movement of the left eye to the right. After left-sided cold water instillation, the left eye deviated downward with minimal medial deviation of the right eye. She was extubated and off sedatives within 48 hours of admission, and normal ocular motility returned., Conclusion: This patient exhibited abnormal ocular motility and cold caloric response with single-agent propofol exposure. The remainder of her cranial nerve examination was normal, and her normal imaging studies and prompt resolution led us to suspect a propofol effect. Physicians should be aware of the pharmacologic alterations of ocular motility and cold caloric testing when propofol is administered., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Vigabatrin is an antiepileptic drug that results in higher gamma-aminobutyrate levels in the brain and retina. Vigabatrin-induced visual field defects are usually asymptomatic and only detectable by perimetry. Further, perimetry requires good cooperation, and children aged under 10 years cannot do it. Electroretinogram response amplitude to full-field 30-Hz flicker shine has been offered to be more specific in predicting visual field defects. This study is scheduled to investigate the vigabatrin-associated visual complications in 67 epileptic children taking vigabatrin using full-field electroretinogram. Electroretinographic surveys showed normal range parameters despite 3 months of vigabatrin treatment, and just 3 (4.47%) children had been visually impaired at the end of 6-month treatment. Among these 3 cases, 1 patient had persistent electroretinogram abnormality despite vigabatrin discontinuation. Our study suggests that vigabatrin is secure for short-term pediatric antiepileptic treatment, with few cases of visual impairments and that are often reversible., (© The Author(s) 2013.)

A 30-year-old woman with chronic foot pain after an orthopaedic surgery and chronic neck pain presented to the emergency department (ED) with a history of self-rotatory vertigo with unsteadiness. She had started low-dose pregabalin, 25 mg two times a day 9 months before experiencing symptoms with the dose gradually increased to 150 mg two times a day over this period. Clinical examination revealed difficulty performing eye pursuit with left eye and dysdiadochokinesia of the left arm. Owing to a suspicion of multiple sclerosis she underwent cerebral MRI, which was normal. Pregabalin was tapered over 2 months with a complete disappearance of the symptoms. We concluded that symptoms were due to pregabalin treatment.

Pethidine is an opioid that gains its popularity for the effective pain control through acting on the opioid-receptors. However, rapid pain relief sometimes brings about unfavourable side effects that largely limit its clinical utility. Common side effects include nausea, vomiting and hypotension. In patients with impaired renal and liver function, and those who need long-term pain control, pethidine may cause excitatory central nervous system (CNS) effects through its neurotoxic metabolite, norpethidine, resulting in irritability and seizure attack. On the contrary, though not clinically apparent, pethidine potentially causes inhibitory impacts on the CNS and impairs normal cerebellar and oculomotor function in the short term. In this case report, we highlight opioid's inhibitory side effects on the cerebellar structure that causes dysmetria, dysarthria, reduced smooth pursuit gain and decreased saccadic velocity.

The non-competitive N-methyl-D-aspartate receptor antagonist ketamine leads to transient psychosis-like symptoms and impairments in oculomotor performance in healthy volunteers. This study examined whether the adverse effects of ketamine on oculomotor performance can be reversed by the atypical antipsychotic risperidone. In this randomized double-blind, placebo-controlled study, 72 healthy participants performed smooth pursuit eye movements (SPEM), prosaccades (PS) and antisaccades (AS) while being randomly assigned to one of four drug groups (intravenous 100 ng ml(-1) ketamine, 2 mg oral risperidone, 100  ng ml(-1) ketamine plus 2 mg oral risperidone, placebo). Drug administration did not lead to harmful adverse events. Ketamine increased saccadic frequency and decreased velocity gain of SPEM (all P < 0.01) but had no significant effects on PS or AS (all P > or = 0.07). An effect of risperidone was observed for amplitude gain and peak velocity of PS and AS, indicating hypometric gain and slower velocities compared with placebo (both P < or = 0.04). No ketamine by risperidone interactions were found (all P > or = 0.26). The results confirm that the administration of ketamine produces oculomotor performance deficits similar in part to those seen in schizophrenia. The atypical antipsychotic risperidone did not reverse ketamine-induced deteriorations. These findings do not support the cognitive enhancing potential of risperidone on oculomotor biomarkers in this model system of schizophrenia and point towards the importance of developing alternative performance-enhancing compounds to optimise pharmacological treatment of schizophrenia.

Objective: To report our long-term experience with the local toxicity profile and ocular motility changes after treatment of intraocular retinoblastoma with subtenon topotecan chemotherapy., Design: Cross-sectional study., Participants: Ten eyes in 8 patients with retinoblastoma treated with subtenon topotecan., Methods: We assessed potential complications in ocular motility in eyes with retinoblastoma treated with subtenon topotecan using forced duction testing under general anaesthesia. Eyes subsequently enucleated because of treatment failure were examined histologically., Results: Ten eyes in 8 patients with retinoblastoma treated with 1 to 4 injections of subtenon topotecan were examined repeatedly, with a mean follow-up period of 37 months. Ocular motility remained normal in all eyes by forced duction, with no observed persistent conjunctival congestion, abnormal ocular motility, or enophthalmos in retained eyes 3 years after last injection. Histopathologic examination of the 2 enucleated eyes did not reveal signs of orbital tissue necrosis or fibrosis., Conclusions: Unlike subtenon carboplatin, subtenon topotecan therapy is not associated with long-term toxicity affecting ocular muscles or orbital soft tissue. No effect on ocular motility was observed., (Copyright © 2013 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved.)

Introduction: Oculogyric crises are considered to be a form of focal dystonia and can be observed as reactions to pharmaceuticals. The signs and symptoms may be confused with epileptic crises., Aims: To describe the clinical features and progress of patients with pharmaceutical-related oculogyric crises and to carry out a review of the topic., Case Reports: We conducted a retrospective, descriptive study of four patients evaluated in the neurology service due to oculogyric crises. The patients had been diagnosed with an associated conduct disorder requiring treatment with antipsychotic drugs. The episodes of oculogyric crises did not correlate with the findings in the electroencephalogram. They responded well to the reduction in dosage or to withdrawal of the apparent causing agent., Conclusions: The clinical picture does not present only in patients treated with antipsychotics but is also linked with other pharmaceuticals that are frequently used in daily paediatric practice. When oculogyric crises are the reason for visiting, differential diagnoses must be taken into account in order to avoid unnecessary studies and to carry out an appropriate therapeutic management.

Oculogyric crisis is a neurologic adverse event characterized by bilateral dystonic, usually upward, conjugate eye deviations. Cefixime is a third-generation cephalosporin and is widely used in clinical practice in childhood. Confusion, encephalopathy, coma, myoclonus, nonconvulsive status epilepticus, and seizures have been described with the use of cephalosporins. We presented a cefixime-induced oculogyric crisis in a 7-year-old boy during the treatment of urinary tract infection, and this is the first case of cefixime-induced oculogyric crisis whose ocular symptoms gradually disappeared within 48 hours after the drug was discontinued.

The authors experienced a case with ocular ischemia with hypotony following injection of a dermal filler for augmentation rhinoplasty. Immediately after injection, the patient demonstrated a permanent visual loss with typical fundus features of central retinal artery occlusion. Multiple crusted ulcerative patches around the nose and left periorbit developed, and the left eye became severely inflamed, ophthalmoplegic, and hypotonic. Signs of anterior and posterior segment ischemia were observed including severe cornea edema, iris atrophy, and chorioretinal swelling. The retrograde arterial embolization of hyaluronic acid gel from vascular branches of nasal tip to central retinal artery and long posterior ciliary artery was highly suspicious. After 6 months of follow up, skin lesions and eyeball movement became normalized, but progressive exudative and tractional retinal detachment was causing phthisis bulbi.

We report four patients with no preexisting movement disorders who developed oculogyric crises secondary to lamotrigine toxicity and had resolution of these crises after dose reduction. Episode numbers ranged from 1-20 per day and episode duration from 2 s to several hours. Mean plasma concentration of lamotrigine at the time of oculogyric crisis was 15.5 μg/mL, with a mean dose of 16 mg/kg per day., (Wiley Periodicals, Inc. © 2011 International League Against Epilepsy.)

Introduction: Eye movements convey important information about brain function. Neuropsychiatric conditions and medications may produce abnormal eye movements (EMs) in sleep. Serotonergic drugs are known to increase nocturnal EMs. Few studies have quantified sleep EMs due to technical complexity. We investigated the effects of serotonergic drugs on slow EMs in sleeping patients using an objective automated EM quantification tool., Methods: We studied patients who had polysomnograms for clinical assessment. We identified 5 sertraline, 7 citalopram, and 4 fluoxetine users who were not using other psychoactive medications. Controls were 10 age-matched patients on no medications. An automated objective EM detection tool was developed. The first and last 5 min of each sleep stage were assessed. ANOVA was used to assess the effects of time, stage, and medication., Results: No differences were noted between SSRI users and controls in demographics. Medications were associated with more slow EMs compared to controls (p<0.05). Among SSRI users, a non-statistical trend was noted for increasing slow EMs in the following pattern: sertraline

Objective: This study evaluated the utility of ocular motor measures in characterizing subtle cognitive changes after carbon monoxide (CO) poisoning., Background: Delayed onset of neurologic and psychiatric symptoms occurs in a number of patients with no apparent deficit immediately after CO poisoning. Although historically attributed to necrosis of the globus pallidus (GP), subsequent demyelination of the cerebral white matter has been proposed as the principal driver of these deficits. Here, we evaluate cognitive changes in a patient with structural deficits largely confined to the globus pallidus at 3 years post-CO poisoning, using ocular motor measures., Method: A battery of ocular motor tasks evaluated the basic metrics of movements, and the higher-order cognitive control processes governing movement., Results: Abnormalities were revealed across a broad range of saccadic measures, including latency, accuracy, and error rate, reflected impaired response inhibition, working memory, and attentional processes., Conclusions: These observations suggest subclinical deficits potentially reflecting damage to the GP. Furthermore, we have shown that ocular motor measures sensitively characterize cognitive deficits that may otherwise be overlooked after CO poisoning, and that may benefit from intervention.

Oculogyric crisis (OGC) is a dystonic and distressing side- effect which occurs immediately after the administration of high-potency antipsychotic drugs and is usually reported as a subtype of dystonia. We report a case of a young woman with schizophrenia who presented with tardive OGC related to amisulpride.