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An Approach to Oculomotor Anomalies in a Child
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
The presentation of an isolated oculomotor nerve palsy can vary from a complete palsy with the characteristic ptosis, mydriasis, and “down and out” appearance of the affected eye to a milder form, with any combination of affected muscles and any level of severity. When considering a third nerve palsy, a distinction is often made between a “complete” and “incomplete” palsy. A complete palsy is diagnosed when there is complete ptosis, a fixed pupil, and complete paralysis of the SR, inferior rectus, inferior oblique, and medial rectus. Historically, this distinction was thought to reflect the anatomical location of the causative lesion; however, it is now established that incomplete palsies can result from lesions anywhere along the pathway of the nerve.
Impairment of functions of the nervous system
Published in Ramar Sabapathi Vinayagam, Integrated Evaluation of Disability, 2019
A lesion in the oculomotor nerve results in oculomotor nerve palsy. The oculomotor nerve palsy manifests as diplopia due to paralysis of extraocular muscle namely superior rectus, inferior rectus, and inferior oblique muscles, ptosis due to paralysis of levator palpebrae superioris, and dilatation of the pupil due to paralysis of ciliary muscles and constrictor papillae.
Station 2: History Taking
Published in Saira Ghafur, Parminder K Judge, Richard Kitchen, Samuel Blows, Fiona Moss, The MRCP PACES Handbook, 2017
Saira Ghafur, Parminder K Judge, Richard Kitchen, Samuel Blows, Fiona Moss
What are the causes of an oculomotor nerve palsy? ‘Surgical’: These causes generally affect the pupil. Posterior communicating artery aneurysmSpace-occupying lesion in midbrain/sphenoid wing/near cavernous sinusHaemorrhage‘Medical’: These causes often do not affect the pupil. Causes of mononeuritis multiplexDemyelinationInfarction
Spindle cell oncocytoma of the neurohypophysis with metastasis to the sphenoparietal sinus and immunohistochemical negativity for S100 and epithelial membrane antigen (EMA)
Published in British Journal of Neurosurgery, 2023
Hanno M. Witte, Armin Riecke, Wolfgang Saeger, Carsten Hackenbroch, René Mathieu, Uwe Max Mauer, Chris Schulz
One year later, the patient developed complete oculomotor nerve palsy associated with the absence of the response of the right pupil to light and sixth nerve palsy on the left side. Contrast-enhanced MRI scans revealed a residual tumor in the region of the skull base which again showed marked progression and required repeat surgery. Transsphenoidal resection of the tumor was performed again two years after the initial presentation. By then, the SCO extended to the optic nerve on the right side and had led to a displacement of the pituitary stalk to the left with infiltration of both cavernous sinuses. In addition, MRI demonstrated tumor spread along the right sphenoparietal sinus. On the basis of this finding, the SCO was suspected to have metastasized, most likely via the hematogenous route (Figure 3). As a secondary finding, MRI showed areas of contrast enhancement in the region of the second cervical vertebra, which too were suspected to be metastases from the spindle cell oncocytoma of the hypophysis (Figure 4).
Oculomotor Synkinesis (Aberrant Reinnervation of the Third Cranial Nerve) Associated with Atypical Tolosa-Hunt Syndrome
Published in Neuro-Ophthalmology, 2020
Glenn R. Harris, Mark P. Breazzano, Irene Shyu, Sean P. Donahue, Patrick J. M. Lavin
A 70-year-old woman with history of systemic lupus erythematosus, controlled with 5 mg oral prednisone every other day for 14 years, presented with ophthalmoplegia, periorbital pain, and blurred vision. Initially, she presented to another facility with a rapid-onset right complete ptosis and periocular paraesthesia. Evaluation identified a pupil-involved right oculomotor nerve palsy. The left eye was normal. Brain MRI without contrast revealed an old small cerebellar infarct and nonspecific white matter changes. Computed tomographic angiography showed no evidence of a posterior communicating aneurysm. Her history, a normal sedimentation rate (15 mm/h), C-reactive protein (0.9 mg/L), and platelets of 200,000/mm3 excluded giant cell arteritis. An RPR was non-reactive, HIV was negative, and serum immunofixation electrophoresis was normal. An ANA performed at an outside institution was positive at 1:160 on low dose prednisone and hydroxychloroquine. Treatment with 60 mg prednisone daily for suspected THS was initiated, but she could not tolerate the subsequent agitation and hallucinations. Conventional contrast-enhanced MRI eight weeks after onset revealed diffuse thickening and enhancement of the right oculomotor nerve in the cavernous sinus and interpeduncular cistern (Figure 1). The ptosis and periorbital pain resolved after several months, but she continued to have binocular diplopia and sought a second opinion. Signs of oculomotor synkinesis were noted 14 weeks after our first evaluation, nine months after the onset of her ophthalmoplegia.
The Influence of Type 1 Diabetes Mellitus on Amplitude of Accommodation
Published in Current Eye Research, 2020
Ender Sırakaya, Bekir Küçük, Hatice Aslan Sırakaya
The accommodation reflex is controlled by a complex neural network and these pathways may be affected in patients with DM and consequently impaired accommodative functions. Although oculomotor nerve palsy is rarely observed in the general population, its incidence is relatively high among diabetic patients.25,26 For another indicator of accommodative dysfunction due to neuronal damage in such patients, Kim and Yu detected a reduction in ciliary body thickness in individuals with DM. The ciliary muscles, as a principal component of the ciliary body, have important functions in accommodation and are innervated by oculomotor nerves.27 Ischemic hypoxia associated with DM may cause the dysfunction of the ciliary muscles due to oculomotor nerve palsy and result in the malfunction of the accommodative reflex.11,13 Although patients with autonomic neuropathy were excluded from our study, subclinical inflammation may persist in those neural structures and cause accommodative dysfunction. In our study, RNFLs were thin in all quadrants among patients with DM compared to controls, albeit to a statistically significant degree only on average. Those results indicate the damage of ocular neural pathways among the patients.