Bevacizumab-induced isolated oculomotor nerve palsy in glioblastoma multiforme.

INTRODUCTION: Bevacizumab, a monoclonal antibody against the vascular endothelial growth factor receptor, is the standard treatment of recurrent glioblastoma multiforme. In addition to common systemic side effects of bevacizumab, there are rare cases of cranial nerve palsy. CASE REPORT: We report a case of transient oculomotor nerve palsy after systemic administration of bevacizumab. Twenty-four hours after the systemic infusion of bevacizumab, transient oculomotor nerve palsy developed in a 49-year-old male patient. In the cranial MRI, there was no malignancy-related progression. MANAGEMENT AND OUTCOME: Bevacizumab treatment was discontinued. Methylprednisolone was started considering that bevacizumab increased the inflammatory response. Oculomotor nerve palsy resolved in 14 days. DISCUSSION: There are many side effects of bevacizumab whose mechanisms of action have not been fully explained. Cranial nerve involvement is rarely reported. Our case is the first reported case of bevacizumab-induced oculomotor nerve palsy.

Acute intractable headache and oculomotor nerve palsy associated with nicorandil: A case report.

Acute non-traumatic headaches with neurological deficits alarm emergency department (ED) physicians. Typically, a sudden headache with oculomotor nerve palsy involving a pupil indicates the possibility of a subarachnoid hemorrhage (SAH) due to an aneurysm originating from the posterior communicating artery. For the ED physician, thinking beyond the possibility of an SAH can be crucial. Here, we report on a 59-year-old woman who presented to the ED with an intractable headache and right ptosis. She had previously received nicorandil for paroxysmal atrial fibrillation in the cardiology clinic. Her vital signs were stable upon ED arrival. Neurological examination revealed a mild anisocoria with a sluggish response to light stimuli in the right eye. Adduction, supraduction, and infraduction were also limited in the right eye. Nuchal rigidity was not apparent. An urgent brain magnetic resonance image (MRI) with angiography was requested to assess for possible SAH, but revealed no aneurysm. Cerebrospinal fluid analysis was also unremarkable. The patient's headache and oculomotor nerve palsy improved completely after discontinuation of nicorandil for 3 days. To the best of our knowledge, this is the first case report on side effects of nicorandil presenting as a severe headache with reversible oculomotor nerve palsy involving a pupil, symptoms which mimicked a possible SAH due to aneurysm.

Oculomotor nerve palsy caused by imidacloprid at initial diagnosis: A case report.

RATIONALE: Amid the pervasive deployment of imidacloprid, the incidence of poisoning from this compound has risen markedly. Those afflicted with imidacloprid poisoning typically exhibit symptoms ranging from headaches, dizziness, nausea, and abdominal pain, to impaired consciousness and breathlessness, yet instances of ocular paralysis induced by this toxin have not previously been documented. PATIENT CONCERNS: When the pesticide spray inadvertently made contact with the patient's eyes, they were seared with a burning sensation and discomfort. Subsequent to this incident, on the second day, the individual began to experience diplopia in the right eye and found it arduous to elevate his eyelids, indicating a challenge in achieving full extension. DIAGNOSES: Based on the medical history, symptoms, and signs, the patient was diagnosed with oculomotor nerve palsy caused by imidacloprid. INTERVENTIONS: The treatment involved intravenous dexamethasone to reduce inflammatory response in the eye tissue; oral pantoprazole enteric-coated tablets to suppress acid production and protect the stomach; Xuesaitong administered intravenously to improve blood supply to the eye and promote metabolism of toxins; vitamin C, cobamamide, and vitamin B1 for nerve nutrition and antioxidant effects; local application of tobramycin-dexamethasone eye drops for anti-inflammatory purposes; and repeated flushing of the conjunctival sac with saline. Finally, the patient improved and was discharged. OUTCOMES: After active treatment, the patient finally improved diplopia and ptosis. LESSONS: This report marks the first documentation of oculomotor nerve palsy induced by imidacloprid, featuring diplopia, and blepharoptosis without substantial limitation of ocular motility. Following therapeutic intervention, the patient showed marked improvement and was discharged from the hospital, providing a point of reference for the treatment of analogous cases in future clinical practice. It also serves as a reminder for the public to take appropriate precautions when using imidacloprid.

Cranial Nerve Disorders Associated With Immune Checkpoint Inhibitors.

OBJECTIVE: To describe the spectrum, treatment, and outcome of cranial nerve disorders associated with immune checkpoint inhibitor (Cn-ICI). METHODS: This nationwide retrospective cohort study on Cn-ICI (2015-2019) was conducted using the database of the French Refence Center. In addition, a systematic review of the literature (MEDLINE, Scopus, and Web of Science) for records published between 2010 and 2019 was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines using the search terms cranial nerve or neuropathy or palsy and immune checkpoint inhibitors. RESULTS: Among 67 cases with ICI-related neurologic toxicities diagnosed in our reference center, 9 patients with Cn-ICI were identified (7 men, 78%, median age 62 years [range 26-82 years]). Patients were receiving a combination of anti-cytotoxic T-lymphocyte antigen 4 and anti-programmed cell death 1 (PD-1)/PD-1 ligand (n = 5, 56%) or anti-PD-1 antibodies alone (n = 4, 44%). Cn-ICI involved optic (n = 3), vestibulocochlear (n = 3), abducens (n = 2), facial (n = 2), and oculomotor (n = 1) nerves. Two patients had involvement of 2 different cranial nerves. Treatment comprised corticosteroids (n = 8, 89%), ICI permanent discontinuation (n = 7, 78%), plasma exchange (n = 2, 22%), and IV immunoglobulin (n = 1, 11%). Median follow-up was 11 months (range 1-41 months). In 3 cases (33%), neurologic deficit persisted/worsened despite treatment: 2 optic and 1 vestibulocochlear. Among cases from the literature and the present series combined (n = 39), the most commonly affected cranial nerves were facial (n = 13, 33%), vestibulocochlear (n = 8, 21%), optic (n = 7, 18%), and abducens (n = 4, 10%). Trigeminal, oculomotor, and glossopharyngeal nerves were less frequently affected (total n = 7). CONCLUSION: Cranial nerve disorders can complicate treatment with ICIs. Approximately one-third of the patients had persisting deficits, most frequently involving hearing and vision loss.

Ocular ischemia and ischemic oculomotor nerve palsy after vascular embolization of injectable calcium hydroxylapatite filler.

A healthy 25-year-old man who received a calcium hydroxylapatite filler injection for nose augmentation by a dermatologist suddenly developed blepharoptosis and orbital pain on the right side, associated with progressive visual disturbance of the right eye. Patchy necrosis at the nose and glabella, limitations of extraocular movements, and anterior segment ischemia, as evidenced by conjunctival injection, chemosis, corneal edema, dilated pupil, hyphema, and hypopyon, were noted. Orbital CT demonstrated linear deposits of a similar density to bone in the right medial orbit and eyelid, suggestive of multiple emboli along the conjunctival vessels. A provisional diagnosis of ocular ischemia and ischemic oculomotor nerve palsy secondary to vascular embolization was made. After 3 months, visual acuity, all intraocular inflammation, oculomotor nerve palsy, and skin necrosis resolved completely except for a dilated pupil.

Unilateral blindness with third cranial nerve palsy and abnormal enhancement of extraocular muscles on magnetic resonance imaging of orbit after the ingestion of methanol.

Methanol is generally known to cause visual impairment and various systemic manifestations. There are a few reported specific findings for methanol intoxication on magnetic resonance imaging (MRI) of the brain. A case is reported of unilateral blindness with third cranial nerve palsy oculus sinister (OS) after the ingestion of methanol. Unilateral damage of the retina and optic nerve were confirmed by fundoscopy, flourescein angiography, visual evoked potential and electroretinogram. The optic nerve and extraocular muscles (superior rectus, medial rectus, inferior rectus and inferior oblique muscle) were enhanced by gadolinium-DTPA on MRI of the orbit. This is the first case report of permanent monocular blindness with confirmed unilateral damage of the retina and optic nerve, combined with third cranial nerve palsy after methanol ingestion.

Ischemic oculomotor nerve palsy due to hyaluronic acid filler injection.

Hyaluronic acid (HA) is the most popular agent today for intradermal injections to improve wrinkles and other cosmetic defects. Ischemic necrosis due to injection of HA is one of the serious complications. Because there are many vascular branches around the nose, caution and care should be given during facial filler injection. Although the incidence is rare, blindness and permanent visual loss may occur. We describe a 29-year-old woman presented with painful erythematous swelling with violaceous patch on right periocular area and glabella after HA filler injection. After injecting the filler, she felt pain and dizziness, and her vision became blurred. She immediately received hyaluronidase around the HA filler inject area and during hospitalized for 10 days, she was successfully treated with systemic steroid, vasodilator, prophylactic antibiotics, and LLLT (low-level laser therapy) without any defects.

Envenomation by Montpellier snake (Malpolon monspessulanus) with cranial nerve disturbances.

The Montpellier snake (Malpolon monspessulanus) is an opisthoglyphous snake rarely implicated in human envenomation because the anatomy of its venom apparatus is generally unsuitable for venom delivery to large mammals. The authors report one case of human envenomation by the Montpellier snake in Southern France. Envenomation occurred under exceptional circumstances (finger of patient inserted deeply into the mouth of the reptile). The clinical picture was dominated by neurological symptoms (ptosis, oculomotor paralysis). The patient recovered in 6 days with symptomatic treatment.

[Oculomotor anomalies from medications]. / Les anomalies oculomotrices dues aux médicaments.

Many medicines, mainly with neurological purpose, interfere with the oculomotricity. The biochemistry of the oculomotor systems and thus, the mechanisms of action of these drug interferences are not completely clarified. Most medicines impair the eye movements at the level of their fine adjustment by feed-back loops implying the cerebellum. Quite often, the interferences remain asymptomatic, restricted to a saccadic pursuit, hypometric saccades or an end-point nystagmus. Sometimes however, symptoms of dizziness or oscillopsia appear, due to loss of the vestibulo-ocular reflexes efficiency. A diplopia or a blurred vision by double outline could be suggestive of an ocular motor paresis or a loss of the binocular fusion due to drugs action.

Triptans and third nerve paresis: a case series of three patients.

PurposeThe aim of this report is to increase awareness of a possible association between cranial nerve paresis and the use of sumatriptan in migraine sufferers, particularly in patients who have additional vascular risk factors.Patients and methodsWe describe a series of three cases where third nerve paresis developed in patients who were treated with the oral form of sumatriptan. All of the patients had a clear history of repetitive migraine headache and none of them had previous third nerve paresis.ConclusionAmong a variety of medications for the treatment of migraine, there are some drugs with vasoconstrictive effects, particularly triptans. These drugs may be a contributing factor for microvascular damage of the cranial nerves and other organs.

Paresia unilateral do terceiro nervo após uso de Metronidazol oral / Unilateral third nerve palsy after use of oral Metronidazole

Resumo Paciente do sexo feminino, 19 anos, com queixa de diplopia, náusea e vômito de início súbito. Ao exame físico, a paciente apresentava rotação da cabeça para a esquerda e limitação da adução do olho direito, sugerindo paresia do músculo reto medial. Ausência de ptose palpebral ou paresia de outra musculatura ocular extrínseca e sem outras alterações na avaliação oftalmológica. Foi relatado pelo paciente o uso de Metronidazol, duas doses de 500 mg, no mesmo dia em que os sintomas começaram. A ressonância magnética do crânio foi solicitada. O resultado mostrou um cisto da glândula pineal, estando os outros aspectos dentro da normalidade. A paresia do músculo reto medial e diplopia persistiram por 14 dias, mesmo após a suspensão do antibiótico, optando, assim, por iniciar a corticoterapia oral, evoluindo com boa resposta clínica, melhora dos sintomas e regressão da paresia muscular.

Abstract Female patient, 19 years old, with a complaint of diplopia, nausea and vomiting of sudden onset. Upon physical examination, the patient presented herself with the head position rotated to the left and limitation of adduction of the right eye, suggesting paresis of the medial rectus muscle. Absence of palpebral ptosis or paresis of other extrinsic musculature of the eye, and without other alterations in the ophthalmological evaluation. It was reported by the patient the use of Metronidazole, two doses of 500 mg, the same day the symptoms started. The magnetic resonance imaging of the skull was requested. The result showed a cyst of the pineal gland, the other aspects being within normality. The paresis of the medial rectus muscle and diplopia persisted for 14 days, even after the antibiotic was discontinued, thus opting to initiate oral corticosteroid therapy, evolving with good clinical response, improvement of symptoms and regression of muscular paresis.

Pupil-sparing third nerve palsy associated with sildenafil citrate (Viagra).

PURPOSE: To report unilateral pupil-sparing third nerve palsy after use of sildenafil citrate (Viagra). METHOD: Case report. RESULTS: A 56-year-old man with a history of tobacco abuse was treated for erectile dysfunction. Viagra, 50 mg, was taken once without adverse effect. Three weeks later, the patient took a second dose of Viagra (50 mg); 36 hours later he experienced a complete pupil-sparing third nerve palsy. Erythrocyte sedimentation rate, blood glucose level, magnetic resonance imaging, and magnetic resonance angiography were normal. CONCLUSION: In a patient with microvascular disease, use of sildenafil may be associated with pupil-sparing third nerve palsy.

Apoplexy of a pituitary macroadenoma with reversible third, fourth and sixth cranial nerve palsies following administration of hypothalamic releasing hormones: MR features.

Pituitary apoplexy in patients with pituitary macroadenomas can occur either spontaneously or following various interventions. We present a case of a 71-year-old woman who developed third, fourth, and sixth cranial nerve palsies following administration of the four hypothalamic releasing hormones for routine preoperative testing of pituitary function. The MR examination showed interval tumor growth with impression of the floor of the third ventricle. There were also changes in signal intensity characteristics of the mass, suggestive of intratumoral bleeding. A transsphenoidal surgery with subtotal resection of the pituitary adenoma was performed. Microscopical examination revealed large areas of necrosis and blood surrounded by adenomatous tissue. Third, fourth, and sixth cranial nerve palsies completely resolved within 4 months. We conclude that MR imaging is useful in the demonstration of pituitary apoplexy following preoperative stimulation tests, but we suggest that these tests should be abandoned in patients with pituitary macroadenomas.

Adverse motor effects induced by antiepileptic drugs.

Cognitive effects of anti-epileptic drugs (AEDs) have been already extensively reported. In contrast, motor disturbances, frequently induced by these drugs, have not received similar attention. We review subjective and objective adverse motor effects of traditional and new AEDs. We discuss the methodological issues caused by the heterogeneous sources of information on drug adverse effects (controlled clinical studies, open studies, and case reports). We describe specific disturbances (vestibulocerebellar, dyskinesias, parkinsonism, tics, myoclonus, and tremor) as the effects of different AEDs on distinct motor circuitries. Finally, we summarize the role of sophisticated technical studies which provide a valuable insight into the specific or subtle effects of AEDs on the central nervous system.

[Vestibular and oculomotor changes in subjects treated with cisplatin]. / Alteraciones vestibulares y del sistema oculomotor en sujetos tratados con cisplatino.

Cisplatin is an agent used in the treatment of distinct oncologic diseases. We present the electrooculographic (EOG) findings of 6 patients which were seen at our Department under the diagnosis of chronic toxicity for cisplatin and associated vestibular alterations. Mean of age was 45 years. Three subjects were female (50%). The most frequent pathologic finding was ataxic pursuit tracking (100%). Additionally, spontaneous nystagmus, alterations in positional test, and vestibulo-ocular reflex suppression were also found. These results are discussed and the main literature concerning this matter is reviewed.

[Ophthalmic complications and local anesthesia. Pathophysiology and types of eye complications after intraoral dental anesthesia, and clinical recommendations]. / Ophthalmologische Komplikationen und Lokalanästhesie. Pathophysiologie und Formen der Augenkomplikationen nach intraoraler zahnärztlicher Lokalanästhesie und klinische Empfehlungen.

The present article reviews the different types of ophthalmologic complications following administration of intraoral local anesthesia. Since the first report by Brain in 1936, case reports about that topic have been published regularly in the literature. However, clinical studies evaluating the incidence of ophthalmologic complications after intraoral local anesthesia are rarely available. Previous data point to a frequency ranging from 0.03% to 0.13%. The most frequently described ophthalmologic complications include diplopia (double vision), ptosis (drooping of upper eyelid), and mydriasis (dilatation of pupil). Disorders that rather affect periorbital structures than the eye directly include facial paralysis and periorbital blanching (angiospasm). Diverse pathophysiologic mechanisms and causes have been reported in the literature, with the inadvertent intravascular administration of the local anesthetic considered the primary reason. The agent as well as the vasopressor is transported retrogradely via arteries or veins to the orbit or to periorbital structures (such as the cavernous sinus) with subsequent anesthesia of nerves and paralysis of muscles distant from the oral cavity. In general the ophthalmologic complications begin shortly after administration of the local anesthesia, and disappear once the local anesthesia has subsided.