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Clinical Examination in Neuro-Ophthalmology
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Selvakumar Ambika, Krishnakumar Padmalakshmi
Usually, the pupil size is equal in both eyes. Anisocoria occurs due to efferent dysfunction of pupils and is referred to when the difference in the pupil size of either eye is 1.0 mm. About 20% of normal individuals may have physiological anisocoria.
Cranial Neuropathies II, III, IV, and VI
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Tanyatuth Padungkiatsagul, Heather E. Moss
Horner's syndrome is characterized by mild ipsilateral ptosis, pupillary miosis, and facial anhidrosis. The syndrome can result from any lesion along these three-order neurons' circuit with postganglionic injuries lacking anhidrosis. Pupils in Horner's syndrome are unequal, called anisocoria, with affected eye being the smaller pupil, and degree of asymmetry is greater in dim light. Thus, anisocoria worse in dim light should prompt consideration of sympathetic pathway injury.
Neuro-ophthalmology
Published in Mostafa Khalil, Omar Kouli, The Duke Elder Exam of Ophthalmology, 2019
Anisocoria refers to the presence of asymmetrical pupillary size between the two eyes. It can be physiological or pathological. The normal pupil size is between 2–4 mm in light conditions and 4–8 mm in the dark (4).
Congenital alacrima
Published in Orbit, 2022
Zhenyang Zhao, Richard C. Allen
Autonomic dysfunction plays a central role in the ophthalmic features of AAAS. Alacrima is secondary to the disruption of the efferent parasympathetic arm of lacrimation. This is supported by lacrimal gland biopsy in these patients, which displays abnormal synapses devoid of neurotransmitter vesicles that activate the secretary process.61 Hypoplasia or absence of the lacrimal glands is observed in AAAS patients representing a process of denervation atrophy.20,21 This is consistent with animal studies showing a 50% decrease of the lacrimal gland size 7 days after postganglionic denervation.62 Mild to moderate keratoconjunctivis sicca is frequently observed secondary to tear deficiency. Severe corneal complications, such as corneal melt and ulceration, are rare in the AAAS patients likely due to the preservation of normal corneal sensation.61 Pupillary abnormalities are found in these patients ranging from a sluggish light response to anisocoria.22 Among these, tonic pupil with light near dissociation is the most common presentation, which is found in 83% of the patients in Houlden’s series of AAAS from 6 different families.23 Other ocular findings include optic nerve atrophy,22,23 relative afferent pupillary defect,24 and strabismus.22
Headache and intracranial hypertension in Guillain-Barré syndrome: a case report and literature review
Published in International Journal of Neuroscience, 2019
Tong Wang, Zhe Wang, Zhangyu Guo
However, her headache and limbs weakness got worse 1 month later. Then she was admitted to our hospital. The patient developed vomiting repeatedly 5 days later. Fundoscopic examination showed bilateral papilloedema. The antibodies of anti-GQ1b IgM, anti-GM1 IgG and anti-GM1 IgM in CSF were detected. An electrophysiological study was consistent with GBS. She was treated with intravenous gammaglobulin (0.4 g/kg/day for 5 days) and dehydration agent again. Disappointingly, her headache persisted and continued to increase in severity. In addition, she had a mild right sixth cranial nerve palsy and high blood pressure. We tested some immune-related antibodies and tumor markers in the serum. And these results were normal. No obvious abnormality was found in computed tomography (CT) (Figure 1A). Brain magnetic resonance imaging (MRI) (Supplementary Figure S1) and magnetic resonance venography (Supplementary Figure S2) excluded cerebral abnormalities. Three weeks after this admission, the patient complained of blurred vision. A repeat cerebral CT scan revealed enlargement of the third ventricle (Figure 1B). She developed the occipital pain and transient bilateral vision loss twice. Neurological examination showed bilateral anisocoria and unresponsive to light. In order to prevent the sharp increase of intracranial pressure causing brain hernia, she was operated with ventricular drainage + Ommaya capsule implantation. The headache was relieved immediately after the surgery and the CSF analysis was normal (Table 1). Two months later her muscle power had significant improved except for a mild degree of weakness.
Don’t Miss This! Red Flags in the Pediatric Eye Exam: Pupils
Published in Journal of Binocular Vision and Ocular Motility, 2019
Jennifer E. Lambert, Stephen P. Christiansen, Crandall E. Peeler
Pharmacologic blockage of or injury to one of the efferent pathways controlling pupil size results in pathologic anisocoria. In children with a history of amblyopia, it is not uncommon to see pharmacologic anisocoria as a result of atropine penalization of the better-seeing eye. Other medications, such as those used for pulmonary therapy, may also cause dilation of the pupil so it is important to consult with the parents of the child about any associated exposures.2 Pharmacologic anisocoria does resolve when the offending medication is withdrawn, though this may take up to a week in cases of atropine use. It is those patients who present with anisocoria with other neurologic red flags such as ptosis, strabismus, ophthalmoplegia, and/or light-near dissociation that require more careful examination and workup.