Cranial Nerve Palsy and Risk of Kidney Cancer: A Nationwide Population-Based Study.

Background and Objective: Understanding whether cranial nerve palsy (CNP) acts as an independent risk factor for kidney cancer could have important implications for patient care, early detection, and potentially the development of preventive strategies for this type of cancer in individuals with CNP. This study aimed to examine the risk of kidney cancer following the onset of ocular motor CNP and assess whether CNP could be considered an independent risk factor for kidney cancer. Materials and Methods: A population-based cohort study was conducted using data from the National Sample Cohort (NSC) database of Korea's National Health Insurance Service which was collected from 2010 to 2017. Follow-up was until kidney cancer development, death, or 31 December 2018. Cox proportional hazard regression analysis was performed to determine hazard ratios (HRs) for kidney cancer according to CNP status. Participants aged 20 years or more diagnosed with CNP from 2010 to 2017 were included. Exclusions comprised individuals with specific pre-existing conditions, inability to match a control group, and missing data, among others. CNP patients were age-sex matched in a 1:5 ratio with control cases. The primary outcome was incidence of kidney cancer during the follow-up period. Results: This study comprised 118,686 participants: 19,781 in the CNP group, and 98,905 in the control group. Compared to the control group, participants with CNP had a higher risk of kidney cancer (adjusted HR in model 4, 1.599 [95% CI, 1.116-2.29]). After a 3-year lag period, the CNP group had a significantly higher risk (adjusted HR in model 4, 1.987 [95% CI, 1.252-3.154]). Conclusions: Ocular motor CNP may be an independent risk factor for kidney cancer, as indicated by a higher incidence of kidney cancer in CNP patients. Further research is needed to elucidate the underlying mechanisms and explore potential preventive measures for kidney cancer in patients with ocular motor CNP.

Proteinuria and risk of ocular motor cranial nerve palsy: a nationwide population-based study.

Understanding the association between dipstick-detected proteinuria and oculomotor cranial nerve palsy (CNP) could have significant implications for understanding the mechanism of CNP development and for developing preventive strategies against CNP development in patients with proteinuria. This study aimed to determine the relationship between dipstick-determined proteinuria and ocular motor CNP using National Sample Cohort (NSC) database from Korea's National Health Insurance Service (NHIS). A nationwide population-based cohort study was conducted using data from the NSC database of Korea's NHIS. These data were collected from 2009 to 2018. A one-year time lag was established to prevent a situation in which the causal link was inverted. Participants aged 20 years or more who were diagnosed with proteinuria in 2009 were included. Individuals with specific pre-existing CNP, missing data, and those who were newly diagnosed with CNP or who died within one year of being tested were excluded. The study population was classified into six groups according to the degree of proteinuria (negative, trace, or between 1 + and 4 +) based on the urine dipstick test. A Cox proportional hazard regression analysis was performed to determine the linkage between the degree of proteinuria and ocular motor CNP. A total of 5,807 (0.14% of subjects) with ocular motor CNP were assigned to the ocular motor CNP group and 4,047,205 subjects were assigned to the control group. After full adjustment of comorbidities, hazard ratios (HRs) for 1 + , 2 + , 3 + and 4 + proteinuria groups were 1.449 (95% confidence interval [CI] 1.244-1.687), 2.081 (1.707-2.538), 1.96 (1.322-2.904), and 3.011 (1.507-6.014), respectively, for developing ocular motor CNP compared to the proteinuria-negative group. In subgroup analysis, the HR of patients with proteinuria for the development of ocular motor CNP was higher in the younger age group (less than 40 years) (P = 0.0242) and the group with DM (P = 0.04). Our population-based cohort study demonstrated a significant association between proteinuria and the incidence of CNP, suggesting that urine protein level could be a new clinical marker for predicting the development of CNP.

Recurrent Painful Ophthalmoplegic Neuropathy with Unilateral Oculomotor and Trochlear Nerve Palsy in an 8-year-old Girl.

BACKGROUND: Recurrent painful ophthalmoplegic neuropathy (RPON) is a rare disorder with a unilateral headache accompanied by ipsilateral episodes of painful ocular cranial nerve neuropathy, which typically occurs in childhood. CASE REPORT: We report an 8-year-old female with four episodes of RPON involving unilateral third and fourth cranial nerves. Right eye exotropia and complete ptosis were detected on examination. Brain MRI images revealed right third nerve enhancement where it exits from the brainstem. She completely recovered after 5 weeks with the administration of prednisolone and indomethacin. DISCUSSION AND CONCLUSION: Due to the rarity of this condition in children, recurrent painful ophthalmoplegic neuropathy should be considered as a differential diagnosis of unilateral or bilateral painful ophthalmoplegia, particularly with a history of migrainous headache. Since it is a treatable entity, and repeated attacks may lead to permanent sequela, early intervention is crucial.

Systemic Lupus Erythematosus and Third Nerve Palsy: Unusual Presentation and Review of the Literature.

We report the case of a young female with pyrexia of unknown origin, cutaneous macules and an incomplete third cranial nerve palsy, that led to the diagnosis of systemic lupus erythematosus (SLE) with neurological manifestations. Her visual acuity was normal. Fundus examination showed cotton wool spots in both eyes. Neuroimaging was also normal. Systemic work up revealed pancytopaenia, hypocomplementaemia, and the presence of multiple autoantibodies including anti-double stranded deoxyribonucleic acid and lupus anticoagulant. She was effectively treated with intravenous pulsed corticosteroid therapy, cyclophosphamide, and oral hydroxychloroquine. This case highlights the uncommon involvement of cranial nerve mononeuropathy in SLE, the importance of systemic examination and autoimmune workup in young patients with such a presentation.

Liver enzymes and risk of ocular motor cranial nerve palsy: a nationwide population-based study.

This study aimed to assess the associations between liver enzymes including γ-glutamyl transferase (GGT) and the development of ocular motor cranial nerve palsy (CNP) using the National Sample Cohort database from Korea's National Health Insurance Service. We analyzed data from 4,233,273 medical screening examinees aged 20 years or more in 2009. Study participants were followed up until December 31, 2018. A Cox proportional hazard regression analysis was performed for quartiles of liver enzymes to determine the linkage between each value and ocular motor CNP using quartile 1 as a reference after adjusting for potential confounders. A total of 5,807 (0.14%) patients developed ocular motor CNP during the follow-up period of 8.22 ± 0.94 years. The incidence of ocular motor CNP gradually increased as the GGT levels increased. The highest quartile of the GGT group had hazard ratio (HR) of 1.245 (95% confidence interval [CI], 1.136-1.365). Regarding alanine aminotransferase (ALT), the highest quartile of the ALT group had HR of 1.141 (95% CI, 1.049-1.241). However, the incidence of ocular motor CNP did not gradually increase as the ALT levels increased. The coexistence of the increased level of GGT, metabolic syndrome, and obesity showed a stronger association with ocular motor CNP development (HR, 1.331; 95% CI, 1.173, 1.511) compared to having a single factor or two factors. In conclusion, our population-based cohort study demonstrated a significant association between serum GGT level and the incidence of ocular motor CNP, suggesting that GGT could be a new clinical marker for predicting the occurrence of ocular motor CNP.

Unilateral diplopia and ptosis in a child with COVID-19 revealing third cranial nerve palsy.

We report the case of a 10-year-old boy with acute-onset diplopia and ptosis in the right eye. CR was positive for SARS-CoV-2. The patient was managed successfully with corticosteroids. We highlight the need for heightened suspicion of occult COVID-19 infection among children presenting with unusual III nerve palsy.

Disseminated lymphoblastic lymphoma revealed by an isolated third cranial nerve palsy.

Dysfunction of the third cranial nerve can be provoked by a number of different conditions. An isolated cranial neuropathy as a first clinical sign of a non-Hodgkin lymphoma is very infrequent. We represent here an atypical case of lymphoblastic lymphoma revealed by an isolated third cranial nerve palsy. The patient was managed by alternating cycles of cyclophosphamide, vincristine, and prednisone. She made a full recovery with a complete resolution of the symptomatology.

Myasthenia Gravis Mimicking Third Cranial Nerve Palsy: A Case Report.

Background: The most common pituitary adenoma presentation is a visual field defect and inappropriate pituitary hormone secretion. The compression of the optic chiasm causes visual impairment. Large pituitary adenomas can rarely cause diplopia and ptosis secondary to adenoma's lateral extension into the cavernous sinus. Myasthenia gravis is an autoimmune disorder involving neuromuscular junctions. It is characterised by skeletal muscle fatigability, commonly involving extraocular muscles, face and limbs. It is estimated that 75% of myasthenia gravis patients present with ptosis and diplopia. The association of myasthenia gravis with pituitary adenoma is very rare. Case Description: A 30-year-old lady presented with headache, diplopia and ptosis of the left eye for 2 months. She was diagnosed with acromegaly secondary to pituitary adenoma. Ptosis is a rare presenting feature in pituitary adenoma. Her case was discussed in a multidisciplinary meeting, and the consensus was that her ptosis is likely secondary to pituitary adenoma, which was involving the left cavernous sinus. She underwent transsphenoidal resection of pituitary macroadenoma. Three weeks post-surgery, she developed bilateral ptosis, dysarthria and dysphonia, which was diagnosed as myasthenia gravis. Clinical Implications: Ptosis is a rare manifestation of pituitary adenoma. Nonetheless, pituitary tumour patients presenting with ptosis should be evaluated for the neuromuscular disorder. A high index of suspicion is required for early diagnosis and prompt treatment of myasthenia gravis.

The Incidence and Etiologies of Third Cranial Nerve Palsy in Koreans: A 10-year Nationwide Cohort Study.

PURPOSE: This study aimed to determine the incidence, prevalence, and etiologies of third cranial nerve (CN3) palsy in Koreans. METHODS: Data were collected from the National Health Insurance Service-National Sample Cohort (NHIS-NSC) database of South Korea and analyzed. Incident CN3 palsy subjects in the cohort population were defined as cases occurring after the initial 4-year or longer washout period. The incidence and prevalence were analyzed by sex, age group, and year. The etiologies of CN3 palsy were evaluated using comorbidities. RESULTS: Of 1,108,253 subjects, 387 patients were newly diagnosed with CN3 palsy between 2006 and 2015. The incidence of CN3 palsy was 3.71 per 100,000 person-years (95% confidence interval, 3.35-4.09). The incidence of CN3 palsy increased with age and accelerated after the age of 60 years. The mean male-to-female incidence ratio was 1.16. The main cause was presumed to be vascular disease (52.7%), followed by idiopathic causes (25.8%), intracranial neoplasm (7.8%), unruptured cerebral aneurysm (5.4%), and trauma (5.2%). CONCLUSIONS: The incidence of CN3 palsy in Koreans increased with age and peaked between 75 and 79 years. The main cause of CN3 palsy was vascular disease.

Cause of acquired onset of diplopia due to isolated third, fourth, and sixth cranial nerve palsies in patients aged 20 to 50 years in Korea: A high resolution magnetic resonance imaging study.

AIMS: This study aimed to describe the etiologies of acquired onset of diplopia due to isolated third, fourth, and sixth cranial nerve palsies in young adults in Korea. METHODS: This retrospective study included 127 patients aged 20 to 50 years with acquired onset isolated third, fourth, and sixth cranial nerve palsies who received care at the Strabismus and Neuro-ophthalmology Department of Samsung Medical Center from 2013 to 2017. The etiologies of the palsies determined by clinical assessment, high-resolution magnetic resonance imaging (MRI) with three-dimensional constructive interference in steady state, and laboratory testing were analyzed. RESULTS: Fifty-nine patients manifested sixth cranial nerve palsy. Forty-six patients had fourth cranial nerve palsy and 22 patients had third cranial nerve palsy. The most common etiologies of the ocular motor nerve palsies were presumed inflammatory lesions (21.3%), followed by presumed microvascular causes (17.3%), and neoplasms involving the central nervous system (15.7%). Neoplasms were the most common cause of sixth cranial nerve palsy (25.4%). The most common cause of fourth cranial nerve palsy was presumed microvascular ischemia (28.3%), and presumed inflammatory lesions was the most common cause of third cranial nerve palsy (36.4%). Other non-traumatic causes included vascular lesions, ischemic brainstem stroke, intracranial hemorrhage, non-aneurysmal neuro-vascular contact, multiple sclerosis, and infection. CONCLUSION: A substantial proportion of young adult patients with ocular motor nerve palsies manifested pathologies other than presumed microvascular ischemia or idiopathic causes. Neuroimaging and laboratory tests have important roles in the evaluation of patients aged 20-50 years with acquired ocular motor nerve palsies.

Glioependymal cyst on the third cranial nerve: case report.

Glioependymal cysts are a rare, congenital, and benign condition. The authors report a case of a 2-year-old female patient who presented with a large exophytic glioependymal cyst located in the left cerebral peduncle, which began with a history of deteriorating function of the left third cranial nerve (CN III). A left 3-piece fronto-orbitozygomatic approach and a microsurgical complete excision of the cyst were performed without complications by accessing the midbrain through the perioculomotor entry zone. The patient's CN III function completely recovered after 3 months. Because there are currently no widely approved and used classification systems for these cysts, their reporting, naming, and classification are quite confusing in the literature. Thus, their origin, classification, and most common locations warrant further investigation. In addition to reporting this case, the authors present their review of the literature.

Idiopathic third and sixth cranial nerve neuritis.

PURPOSE: To present cases with idiopathic third and sixth cranial nerve neuritis. STUDY DESIGN: Retrospective observational study METHODS: The results of high resolution pre- and post- cranial nerve magnetic resonance images (MRI) with three-dimensional sequences for visualizing cranial nerves in patients with third, fourth, and sixth cranial nerve palsies who were treated at the Neuro-ophthalmology Department of Samsung Medical Center were reviewed. Patients with cranial nerve enhancement confirmed by experienced radiologists were identified. The medical records of these patients were reviewed, and their demographics, clinical presentations, laboratory results, and clinical outcomes were analyzed. RESULTS: Of 265 patients with third, fourth, and sixth cranial nerve palsy, 60 were identified by high resolution MRI as having enhancement of the corresponding cranial nerve. Among these, 17 patients with infiltrative, granulomatous, or tumorous lesions were excluded. In addition, 28 patients with identifiable causes of cranial nerve palsy, such as Miller-fisher syndrome, virus infection, or radiation-induced neuropathy, as well as patients with vasculopathic risk factors, were also excluded. Ultimately, a total of 15 patients with idiopathic third and sixth cranial nerve neuritis were included in this study. The mean age of these patients was 43 ± 15 years. Eight patients had sixth cranial nerve palsy, six third cranial nerve palsy (two partial and four complete), and one patient with complete third and sixth cranial nerve palsy. Nine patients received steroid treatment. Eleven patients recovered fully within a period ranging from a few days to one year. Two patients were much improved up to 1 month after initial presentation, but were then ultimately lost to follow-up. Another patient was lost to follow-up after the initial work-up. The other patient lost to follow-up had partially recovered during the first 6 months. CONCLUSIONS: We present patients with idiopathic third and sixth cranial nerve neuritis. They tended to respond well to steroid treatment and to have good prognoses. In order to better understand the long-term prognosis of cranial nerve neuritis and possible association with other neurologic disorders, a larger scale and longer-term study is needed.

Combined Lateral Rectus Myectomy and Maximal Medial Rectus Resection in Complete Third Cranial Nerve Palsy.

This study was performed to describe lateral rectus myectomy and maximal medial rectus resection for correction of eye deviation in complete third cranial nerve palsy. A retrospective review of thirteen patients (fourteen eyes) with complete third cranial nerve palsy, who underwent lateral rectus myectomy and maximal medial rectus resection, was performed. These procedures were combined with superior oblique tendon transposition in nine patients with a large angle of exotropia (more than 60 prism diopters [∆]), or significant hypotropia (more than 5 ∆). Preoperative deviations were exotropia of 50 to 120 ∆ in thirteen cases and hypotropia of 5 to 25 ∆ in eight cases. Six months after the surgery, eleven patients were within 10 ∆ of orthotropia in primary position. Revision surgery was performed for two patients, eight and 18 months after the first operation. Eventually, five patients (38%) achieved orthotropia in the primary position, and seven patients (54%) had < 11 ∆ exotropia and < 6 ∆ vertical deviation. In conclusion, this procedure can be considered as an acceptable approach for treatment of strabismus in complete third cranial nerve palsy. This procedure is simple and can be easily performed even in very young children.

Weber syndrome secondary to brain stem tuberculoma.

This case report describes a rare presentation of presumed brain stem tuberculoma in a 28-year-old male who presented with acute onset of third cranial nerve palsy with contralateral hemiparesis (Weber syndrome) and upgaze palsy. Isolated midbrain tuberculoma is rare, presenting with varied clinical manifestations and radiological findings posing as a diagnostic dilemma. Weber syndrome is commonly caused by midbrain infarct secondary to occlusion of branches of the posterior cerebral artery and rarely from a tuberculoma. The patient is a case of disseminated tuberculosis with granuloma in midbrain causing pressure effect, thereby presenting with features consistent with Weber syndrome and upgaze palsy. The patient had good recovery with antitubercular treatment and systemic steroids.

The Neuro-ophthalmic Presentation of Intracranial Aneurysms

PURPOSE: To investigate the neuro-ophthalmic diagnosis and clinical manifestations of intracranial aneurysm. METHODS: A retrospective survey of 33 patients who were diagnosed with intracranial aneurysm and underwent neuro-ophthalmic examination from April 2008 to December 2016. Frequency of the first diagnosis of intracranial aneurysm in ophthalmology, neuro-ophthalmic diagnosis, location of intracranial aneurysm, examination of intracranial aneurysm rupture, and neurologic prognosis of Terson's syndrome patients were analyzed by image examination, neurosurgery, and ophthalmology chart review. RESULTS: Of the 33 patients, most patients (n = 31, 94%) were diagnosed with intracranial aneurysm at the neurosurgical department and only 2 patients were diagnosed initially at the ophthalmology department. Causes and association were: Terson's syndrome (n = 10, 30%), third cranial nerve palsy (n = 10, 30%), internclear ophthalmoplegia (n = 4, 12%), visual field defect (n = 3, 9%), optic atrophy (n = 3, 9%), sixth cranial nerve palsy (n = 2, 6%), and nystagmus (n = 1, 3%). The location of intracranial aneurysms were: anterior communicating artery (n = 13, 39%), medial communicating artery (n = 12, 36%), and posterior communicating artery (n = 5, 15%). Ten of 33 patients had Terson's syndrome, and 6 patients (60%) with Terson's syndrome had apermanent neurological disorder such as agnosia, gait disorder and conduct disorder. CONCLUSIONS: Third cranial nerve palsy was the most common neuro-ophthalmic disease in patients presenting with intracranial aneurysm. The neuro-ophthalmic prognoses for those diseases were relatively good, but, if Terson's syndrome was present, neurological disorders (agnosia, gait disorder, conduct disorder) were more likely to remain after treatment.

A Case Report: Consecutive Cranial Neuropathies Following the Use of Phosphodiesterase-5 Inhibitors.

We report a patient who suffered consecutive cranial neuropathies where each event was immediately preceded by the use of oral PDE-5 inhibitors. A discussion of the etiology of the events including possible interaction with other medications is included.

Third nerve palsy following carotid artery dissection and posterior cerebral artery thrombectomy: Case report and review of the literature.

BACKGROUND: Common causes of oculomotor nerve palsy are diabetes, aneurysmal compression, and uncal herniation. A lesser-known cause of third nerve dysfunction is ischemia, often due to carotid artery dissection. CASE DESCRIPTION: An 80-year-old man presented with an acute ischemic stroke with a National Institutes of Health Stroke Scale score of >20 from a high cervical internal carotid artery (ICA) dissection and a tandem ICA terminus embolic occlusion with extension of clot into the adjacent fetal posterior cerebral artery (PCA). We used a stentriever to perform selective PCA thrombectomy, with immediate postthrombectomy development of ipsilateral anisocoria. The anisocoria progressed into complete oculomotor nerve palsy over 8 h after the procedure. CONCLUSIONS: The clinical course described in this case is consistent with injury to the third nerve due to mechanical injury or occlusion of perforator supply to the nerve during thrombectomy. Oculomotor nerve palsy is a rare but known complication after ischemia; however, to our knowledge, this is the first case after thrombectomy for a PCA embolus.

Metastatic pancreatic carcinoma to the orbital apex presenting as a superior divisional third cranial nerve palsy.

Metastatic tumors to the orbit are rare, especially from a primary pancreatic carcinoma. A 59-year-old man presented with 4 weeks of right eye pain and eyelid swelling. There was right upper eyelid ptosis associated with a right supraduction deficit consistent with a superior divisional third cranial nerve (CN III) palsy. Magnetic resonance imaging revealed a right orbital apex lesion. A right orbital exenteration was performed for intractable and severe pain. Surgical pathology demonstrated a poorly differentiated carcinoma that was ultimately felt to be derived from the pancreas. In this report, we describe the clinical and neurological imaging findings of a superior divisional CN III palsy as the presenting manifestation of a presumed metastatic pancreatic carcinoma to the orbital apex, and review the neuroanatomy of CN III with particular emphasis on the anatomical bifurcation of the nerve into a superior and inferior division.