Isolated Oculomotor Nerve Palsy Research Articles

Etiological distribution of isolated oculomotor nerve palsy: analysis of 633 patients and literature review.

The etiological distribution of oculomotor nerve palsy has varied amongst the studies. This study aimed to define the clinical features and underlying etiologies of isolated oculomotor nerve palsy by recruiting patients from all departments in a referral-based university hospital. The medical records of 672 patients who had a confirmed diagnosis of isolated oculomotor nerve palsy at all departments of Seoul National University Bundang Hospital, Seongnam, South Korea, from 2003 to 2020 were reviewed. A proportion of the etiology of isolated oculomotor nerve palsy was also compared with that of patients pooled from the previous studies that were searched on PubMed in May 2022. The most common etiology was microvascular (n = 168, 26.5%), followed by vascular anomalies (n = 110, 17.4%), neoplastic (n = 86, 13.6%), inflammatory (n = 79, 12.5%), idiopathic (n = 60, 9.5%) and traumatic (n = 53, 8.4%). Neurologists were mainly involved in the management of microvascular and inflammatory oculomotor nerve palsies whilst ophthalmologists mainly participated in the care of idiopathic, neoplastic and traumatic palsies. Neurosurgeons mostly took care of oculomotor nerve palsy due to vascular anomalies. The proportion of etiologies of isolated oculomotor nerve palsy may differ according to the specialties involved in the management. The results of previous studies on the etiological distribution of isolated oculomotor nerve palsy should be interpreted with this consideration.

Complete Recovery of Herpes Zoster-Associated Isolated Oculomotor Nerve Palsy without Systemic Steroids

Complete Recovery of Herpes Zoster-Associated Isolated Oculomotor Nerve Palsy without Systemic Steroids

Internal carotid artery aneurysm with incomplete isolated oculomotor nerve palsy: a case report

BackgroundOculomotor nerve palsy is a common and well-described disease with diverse etiologies. Clinicians should quickly and correctly diagnose and treat oculomotor nerve palsy according to its characteristics and the accompanying symptoms and signs. Intracranial aneurysm is an important and frequent cause of oculomotor nerve palsy. Considering the catastrophic consequences of rupture, the possibility of an urgent, life-threatening disease should always be considered.Case presentationA 63-year-old Chinese woman presented with intermittent left ptosis and diplopia and painless incomplete oculomotor nerve palsy without pupil involvement. She manifested no mydriasis or extraocular muscle weakness, and the light reflex was normal. Other cranial nerves and somatosensory and somatomotor examinations were normal. The neostigmine experiment and electromyography were normal, so the diagnosis of myasthenia gravis was excluded. Brain magnetic resonance angiography showed a 4-mm aneurysm located at the cavernous segment of the left internal carotid artery. Unfortunately, the patient refused digital subtraction angiography and was discharged home without further treatment.ConclusionNeuroimaging must be performed to exclude intracranial aneurysms in oculomotor nerve palsy regardless of whether the pupils are involved, as aneurysm rupture carries substantial morbidity and mortality.

COVID-19 and isolated oculomotor nerve palsy: Clinical features and outcomes

AimThis study aims to describe the clinical characteristics of patients with isolated oculomotor nerve palsy from COVID-19 infection, and provide guidance on their treatment and management. MethodsWe performed a systematic review and retrospective analysis on the clinical features and outcomes of patients with isolated oculomotor nerve palsy from COVID-19 reported in literature over the past three years. ResultsWe analyzed a total of 11 cases; 9 identified in literature from January 2020 to September 2022, together with our two patients. Their median age was 46 years (range 2–65), and three were children. More than half (6/11, 55 %) were without medical history. Oculomotor nerve palsies tended to occur early (longest interval of 16 days), but they can also occur concurrently (2/11, 18 %) or before the appearance of COVID-19 symptoms (1/11, 9 %). COVID-19 symptoms tended to be mild (8/11, 73 %). Oculomotor nerve palsies, however, displayed neither a clear gender predilection, nor consistent clinical features in terms of the severity of extraocular weakness and the involvement of pupillary light responses. Nearly two-thirds (7/11, 64 %) received no pharmacological treatment. Regardless, recovery was complete in nearly all (9/10, 90 %), with most occurring within a month (8/9, 89 %) ConclusionIsolated oculomotor nerve palsies are early but uncommon complications of COVID-19. They affect patients with mild infections, and can be the first symptom. Prognosis is excellent, with recovery being often complete and early. Early discharge and outpatient clinical review, with or without short courses of oral steroids, are reasonable treatment measures.

PMON96 A Curious Case of Isolated Oculomotor Nerve Palsy From a Non-Functional Gonadotroph Adenoma

Abstract Introduction Pituitary adenoma typically presents with signs and symptoms of hormone hypersecretion and only 30% of cases present clinically as nonfunctioning adenomas. Furthermore, amongst these less than 5% are associated with ocular nerve palsies. We report a rare case of isolated, unilateral oculomotor nerve palsy due to a non-functional gonadotroph adenoma expanding into the left cavernous sinus. Case 48 years old male with a pertinent medical history of Type 2 Diabetes Mellitus presented to the ER with 3 days of intractable generalized headache associated with double vision, nausea, and increased lethargy. On initial examination, he had findings of oculomotor nerve palsy on the left eye (ptosis, the eye being down and out, and non-reactive pupil to direct or consensual light stimulation) while the rest of his examination was normal. His initial blood work was non-revealing and normal. He underwent extensive imaging including an initial CT scan showing a pituitary macroadenoma, followed by a pituitary-focused MRI brain revealing a hyperplastic pituitary lesion measuring 17.8 mm×22.5 mm in axial axis and 16.4 mm×14.4 mm in sagittal axis with extension into the left cavernous sinus. Biochemical workup was done to evaluate the pituitary function and it revealed a low total testosterone level (95 ng/ml) with a suppressed LH (2.1IU/l) and FSH (1.76 mIU/ml), a low fT4 (0.58 ng/dl) with a suppressed TSH (0.68 mIU/l), low cortisol (1.2 mcg/dl) with a suppressed ACTH of < 5 pg/ml and normal IGF-1 and prolactin levels. He was given stress dose steroids and underwent transsphenoidal resection of the pituitary mass. Pathology of the specimen showed immunoreactivity for SF1 and ASU which was suggestive of a gonadotroph adenoma. The patient showed no signs or symptoms of diabetes insipidus post-operatively, however, was managed for secondary adrenal insufficiency, hypothyroidism, and hypogonadism. He was discharged home on hydrocortisone, levothyroxine, and metformin. He followed up at the Neuroendocrine clinic within a week of discharge and maintained a regular outpatient follow-up where he showed gradual improvement in his symptoms. Conclusion Visual impairment from a non-secreting pituitary adenoma is usually from chiasmal compression. Very rarely, pituitary macroadenoma expands laterally into the cavernous sinus and compresses the oculomotor nerve causing signs and symptoms of third nerve palsy. This case highlights the importance of recognizing different presentations of nonfunctional pituitary adenoma early as this could improve both the morbidity and mortality associated with them. Reference Choong, K., Lee, S L. Pituitary Macroadenoma with invasion into the cavernous sinus, cranial nerve palsies (Endocrine Today) Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

Isolated Oculomotor Nerve Palsy Caused by Onodi Cell Sinusitis

Onodi cell sinusitis is a rare cause of isolated oculomotor nerve palsy. The sphenoid sinus and Onodi cell mucocele or invasive fungal sinusitis are often associated with multiple cranialnerve symptoms simultaneously. However, isolated cranial nerve palsy due to simple sinusitis is rare. Sinus disease associated with cranial nerve palsy is difficult to diagnose based on patient history or physical examination alone; CT and MRI help in correctly assessing these lesions. Here we report a case of Onodi cell sinusitis observed in a patient who presented with isolated oculomotor nerve palsy. The patient underwent endoscopic sinus surgery and recovered completely at 2 months postoperative.

Silent killer presenting as isolated oculomotor nerve palsy

Head trauma can result trivial to life threatening manifestations to a person. Subdural hemotoma is characterised by accumulation of blood in subdural space, in most cases it is a serious condition and requires prompt diagnosis and treatment for the same to provide good outcome. Large collection, mid line shift, brain herniation associated with subdural hematoma is associated with increased morbidity and mortality. However, if the collection is minimal or is places like tentorium cerebelli may not have the typical presentation and if it’s picked up using the subtle signs the devastating sequelae can be prevented. We report a 19 years old male with head trauma presenting with features of right-side isolated oculomotor nerve palsy who eventually found to have tentorial subdural hemotoma in imaging which has been intervened and complications were avoided.

Bevacizumab-induced isolated oculomotor nerve palsy in glioblastoma multiforme

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. 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. Bevacizumab treatment was discontinued. Methylprednisolone was started considering that bevacizumab increased the inflammatory response. Oculomotor nerve palsy resolved in 14 days. 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.

Reader Response: Pearls & Oy-sters: Isolated Oculomotor Nerve Palsy due to Pituitary Apoplexy Missed on CT Scan

I enjoyed reading this interesting case report by Marzoughi et al.1 As explained by the authors, medial lesions of the cavernous sinus can spare other neighboring cranial nerves and present as isolated oculomotor nerve palsy such as in the reported case. However, the authors do not relate to the innervation of the pupil. Their patient had briskly reactive pupils to light and accommodation, that is, the parasympathetic fibers were spared. Pupillary sparing in third nerve palsy has been described in cavernous sinus lesions that save the superior and lateral aspect of the nerve where pupillary parasympathetic fibers are concentrated. Nevertheless, the right pupil was larger than the left. The anisocoria became worse in bright light vs dim light, which indicates a parasympathetic lesion and is in discrepancy with the finding of brisk reaction to light. Could the mild dilatation of the right pupil be due to an irritative lesion of the sympathetic fibers to the right pupil? If this was the case, signs of lesion of the ophthalmic branch of the trigeminal nerve—which contains sympathetic pupillary fibers—should be present. Finally, a physiologic anisocoria could account for mild pupil differences but should not differ in dim vs bright light. Since this is a teaching article, I would be grateful for an explanation.

Reader Response: Pearls & Oy-sters: Isolated Oculomotor Nerve Palsy due to Pituitary Apoplexy Missed on CT Scan

We read with interest the case presented by Marzoughi et al.1 describing a patient with pituitary apoplexy and isolated oculomotor nerve palsy. This case demonstrated that pituitary apoplexy was an important differential diagnosis for acute headache and cranial nerve palsies, with which we totally agree. Meanwhile, there are several tips we think would be helpful to pile on. First, for patients with acute headache and cranial nerve palsy, a negative CT scan cannot rule out the possibility of subarachnoid hemorrhage (SAH). Previous studies confirmed the superiority in detecting SAH by susceptibility-weighted imaging (SWI) than CT.2 In addition, uniform and consistent blood from lumbar puncture can help with the diagnosis.3 Second, previous studies reported that a negative CT angiography (CTA) or even digital subtraction angiography (DSA) cannot rule out the possibility of intracranial aneurysm.4 Besides, the guidelines recommended that for SAH patients with negative DSA, a repeated DSA was still recommended.5 Back to this case, if the CT/MRI did not show the abnormality in pituitary, it is still possible for the patient to have SAH and intracranial aneurysm, even with negative CT/CTA/MRI.

Author Response: Pearls & Oy-sters: Isolated Oculomotor Nerve Palsy due to Pituitary Apoplexy Missed on CT Scan

We appreciate the comments and helpful tips by Dr. Zhang et al. on our paper.1 We agree with their comment that a negative CT scan cannot rule out the possibility of a subarachnoid hemorrhage (SAH) or apoplexy, which makes having a low threshold for follow-up scanning with MRI imperative. Had the MRI scan also been unremarkable, we agree that it would have been reasonable to consider a lumbar puncture to explore a possible bleed in the context of a severe headache and focal neurologic signs before attributing it to other, less-serious etiologies. Interestingly, some subarachnoid hemorrhages may be due to non-aneurysmal events of venous origin, particularly in the perimesencephalic areas and not necessarily due to missed aneurysms.2 Finally, it is important to note that a critical take away from this case is that pituitary apoplexy can mimic a subarachnoid hemorrhage presenting with a third nerve palsy, and it is, therefore, important to have on the differential diagnosis of patients presenting with thunderclap headache, in addition to the typically considered diagnosis of SAH.

Author Response: Pearls & Oy-sters: Isolated Oculomotor Nerve Palsy due to Pituitary Apoplexy Missed on CT Scan

We appreciate Dr. Pollak's comments about our paper.1 Indeed, although our patient's pupil ipsilateral to his third nerve palsy seemed briskly reactive at the bedside, this does not mean the parasympathetic pathway was intact. The anisocoria that we reported—with the right pupil larger than the left, especially in bright light—indicated parasympathetic pupillary dysfunction—i.e., failure of the right pupil to constrict appropriately to bright light—with this function being mediated by the parasympathetic fibers of the oculomotor nerve.2 This was exactly why we did not call this a pupil-sparing third nerve palsy. We agree with Dr. Pollak that the pupillary finding was not explained by physiologic anisocoria owing to the difference in bright vs dim light. There were no signs of trigeminal ophthalmic branch involvement in our patient.

Editors' Note: Pearls & Oy-sters: Isolated Oculomotor Nerve Palsy due to Pituitary Apoplexy Missed on CT Scan

Dr. Marzoughi and colleagues highlight the importance of personal visualization of neuroimaging and pursuit of advanced diagnostic testing in patients with severe headache and suspected intracranial lesions. In their case of an elderly gentleman with thunderclap headache and third nerve palsy, dedicated MRI with thin cuts through the sella identified pituitary apoplexy as the cause of the patient's symptoms. The fact that this patient exhibited brisk pupillary reactivity to light is somewhat atypical for a compressive third nerve palsy, as Professor Pollak comments. However, the authors indicate that the patient was anisocoric at presentation, with more pronounced asymmetry in bright light, meaning the ipsilateral parasympathetic pathway was dysfunctional. Furthermore, the pupillary fibers may be in a less vulnerable position in the cavernous sinus than in the subarachnoid space. Dr. Zhang et al. comment on other differential diagnoses for sudden, severe headache and cranial nerve palsies, which would include aneurysmal subarachnoid hemorrhage. In the absence of radiographic confirmation of a pituitary lesion—or other cause of thunderclap headache and cranial neuropathy (e.g., cavernous sinus thrombosis)—the clinician should pursue an occult aneurysm and/or subarachnoid hemorrhage as the cause of this patient's symptoms. Susceptibility-weighted and FLAIR MRI, conventional angiography, and lumbar puncture to evaluate for xanthochromia may be useful diagnostic tools when the cause of headache and cranial neuropathy(ies) remains elusive. Dr. Marzoughi and colleagues highlight the importance of personal visualization of neuroimaging and pursuit of advanced diagnostic testing in patients with severe headache and suspected intracranial lesions. In their case of an elderly gentleman with thunderclap headache and third nerve palsy, dedicated MRI with thin cuts through the sella identified pituitary apoplexy as the cause of the patient's symptoms. The fact that this patient exhibited brisk pupillary reactivity to light is somewhat atypical for a compressive third nerve palsy, as Professor Pollak comments. However, the authors indicate that the patient was anisocoric at presentation, with more pronounced asymmetry in bright light, meaning the ipsilateral parasympathetic pathway was dysfunctional. Furthermore, the pupillary fibers may be in a less vulnerable position in the cavernous sinus than in the subarachnoid space. Dr. Zhang et al. comment on other differential diagnoses for sudden, severe headache and cranial nerve palsies, which would include aneurysmal subarachnoid hemorrhage. In the absence of radiographic confirmation of a pituitary lesion—or other cause of thunderclap headache and cranial neuropathy (e.g., cavernous sinus thrombosis)—the clinician should pursue an occult aneurysm and/or subarachnoid hemorrhage as the cause of this patient's symptoms. Susceptibility-weighted and FLAIR MRI, conventional angiography, and lumbar puncture to evaluate for xanthochromia may be useful diagnostic tools when the cause of headache and cranial neuropathy(ies) remains elusive.

Case series of pituitary apoplexy presenting as isolated oculomotor nerve palsy and a review of literature with possible insight into underlying pathophysiology.

Case series of pituitary apoplexy presenting as isolated oculomotor nerve palsy and a review of literature with possible insight into underlying pathophysiology.

Pneumocephalus induced isolated oculomotor palsy :Case report and literature review

BackgroundDefined as the presence of air or gas in the cranial cavity, pneumocephalus is attributable to multiple etiologies, including trauma, infection, and neurosurgical procedures. While pneumocephalus-induced cranial neuropathy is extremely uncommon, particularly in the pediatric population, we report the first pediatric case of isolated oculomotor nerve palsy caused by iatrogenic pneumocephalus in the interpeduncular cistern. Case descriptionA 3-year-old girl diagnosed with a posterior fossa tumor underwent surgical resection, which was complicated by transient isolated oculomotor palsy. Imaging studies revealed pneumocephalus in the interpeduncular cistern. The patient was treated with high-flow oxygen and conservative measures that resolved the oculomotor palsy resolved within 6 h. ConclusionThis is the first case report of a pediatric patient diagnosed with pneumocephalus-induced oculomotor nerve palsy, a complication that may occur following cranial surgery. While a review of the literature revealed no similar case in pediatric populations, the present and previous reports suggest that pneumocephalus-induced oculomotor nerve palsy may resolve spontaneously with or without conservative treatment.

Clinical Prediction Score for Early Neuroimaging in Acquired Isolated Oculomotor Nerve Palsy.

PurposeAn immediate neuroimaging investigation in patients with isolated oculomotor nerve palsy (ONP) remains controversial. We aimed to develop a clinical prediction score to determine whether or not acquired isolated ONP patients require prompt imaging.MethodsA retrospective study was performed. Demographic data and clinical presentations were collected to determine predictive factors favored for early brain imaging using multivariate logistic regression analysis.ResultsNinety-seven eyes of 96 patients diagnosed with isolated ONP were included. Forty-one eyes (42.3%) were caused by ischemia, while the other 56 eyes (57.7%) were caused by non-ischemic etiologies, namely aneurysm (n = 22), trauma (n = 18), inflammation (n = 5), tumor (n = 4), and others (n = 7). Eighty-two eyes (84.5%) had undergone neuroimaging study due to initially suspected non-ischemic causes. Only 36 (43.9%) revealed concordant diagnosis. The potential clinical predictors favored for neuroimaging using multivariate logistic regression analysis were age 10‒50 years (adjusted odds ratio [aOR] 9.01, 95% CI: 1.25‒64.8), age 51‒70 years (aOR 1.71, 95% CI: 0.46‒6.35), history of head trauma (aOR 7.14, 95% CI: 1.19‒42.9), absence of vascular risk factors (aOR 3.85, 95% CI: 1.23‒12.1), and poor pupillary response (aOR 6.96, 95% CI: 1.99‒24.3). The predictor scores with an area under the ROC curve of 0.852 were 4, 1, 4, 3, and 4, respectively. The optimum cut-point was 3 for a sensitivity of 96% and specificity of 44%.ConclusionPatients with acquired isolated ONP should be considered early neuroimaging studies when they are younger than 50 years old, have a history of head trauma, have no history of vascular risk factors, or have poor pupillary reaction.

Isolated Oculomotor Nerve Palsy in Takayasu Arteritis-A Rare Complication.

Isolated Oculomotor Nerve Palsy in Takayasu Arteritis-A Rare Complication.

Isolated Oculomotor Nerve Palsy in Mild Traumatic Brain Injury.

Isolated oculomotor nerve palsy is rarely encountered after mild traumatic brain injury. It is difficult to offer patients accurate management strategies or prognostic assessments because only a few reports have described the management of oculomotor nerve palsy. We performed a search for all clinical studies of isolated oculomotor nerve palsy after mild traumatic brain injury published up to July 9, 2019. We placed no restrictions on language or year of publication in our search, and we searched the following key words: traumatic brain injury, isolated oculomotor nerve palsy, mild head trauma, management, and prognosis. We identified 14 cases of isolated oculomotor nerve palsy after mild traumatic brain injury. In three cases, steroids were used to manage the oculomotor nerve palsy. Five patients who had underlying brain lesions underwent surgery, and seven patients were observed and followed up. The time to partial or complete resolution was 6.0 ± 5.3 mos with a range of 0.5-18 mos. This review includes a survey of surgical treatment for the management of traumatic brain injury that underlies oculomotor nerve palsies, steroid therapy to reduce related brain edema, and oculomotor rehabilitation with training eye movement behavior.

A Case of Isolated Oculomotor Nerve Palsy in Systemic Lupus Erythematosus

A Case of Isolated Oculomotor Nerve Palsy in Systemic Lupus Erythematosus

Clinical Significance of MRI Contrast Enhancement of the Oculomotor Nerve in Ischemic Isolated Oculomotor Nerve Palsy.

Background and PurposeContrast enhancement of the oculomotor nerve in MRI was recently noticed in patients with clinical ischemic isolated oculomotor nerve palsy (iIONP). The opinions about whether this is a sign of inflammation and whether or not to administer steroids vary between doctors. The study aimed to determine the associations between this enhancement and vascular-disease risk factors (VRFs) and inflammatory factors in iIONP patients.MethodsThe study recruited patients who had experienced iIONP during the previous 2 years. They were divided into groups A and B based on whether or not they exhibited an enhanced oculomotor nerve in MRI of the cavernous sinus using thin-section, fat-suppressed, and contrast-enhanced sequences. VRFs, inflammatory factors, and improvement scores were compared between the two groups.ResultsMost (71.1%) of the 45 included iIONP patients had enhanced oculomotor nerves in MRI. VRFs, periorbital pain, elevated C-reactive protein and erythrocyte sedimentation rate, the neutrophil-to-lymphocyte ratio, and the platelet-to-lymphocyte ratio were not significantly associated with the enhancement. Four of the five patients in group A exhibited an elevated cerebrospinal fluid (CSF) IgG synthesis rate. The improvement score of eight patients who received 80 mg of methylprednisolone in addition to the routine therapy was not significantly different from the scores of the other patients (p=0.485).ConclusionsMore than half of the iIONP patients had an enhanced oculomotor nerve in MRI. A few of them also had elevated CSF IgG synthesis rate, but no further evidence for inflammation was found. The administration of steroids seemed to have no benefit other than increasing the blood glucose level.