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Pupillary abnormalities range from benign isolated findings to harbingers of significant, even life‐threatening, conditions. A complete understanding of the neuroanatomy underlying the innervations to the antagonistic pupillary sphincter and dilator muscles is essential to detecting, and discerning the importance of, a particular pupillary abnormality. The sphincter muscle receives neuronal input from the parasympathetic division of the autonomic nervous system, whereas the dilator muscle receives input from the sympathetic division. Afferent input carrying light information to the brain is transmitted by retinal ganglion cell axons via the optic nerves, chiasm, and tracts. The parasympathetic innervation to the pupil originates in the Edinger‐Westphal nucleus in the midbrain. The sympathetic innervation to the pupil consists of a three‐neuron pathway originating in the hypothalamus. Important pupillary disorders include physiologic anisocoria, relative afferent pupillary defect, amaurotic pupil, Argyll Robertson pupils, cranial nerve III palsy, pharmacologic mydriasis, tonic pupil, and Horner syndrome. Key Concepts: Examination of the pupil is an important part of the physician's neurological and ophthalmological evaluation of a patient. The size of the pupil is controlled by the actions of antagonistic muscles located within the iris: the pupillary sphincter and dilator. Constriction of the pupils is mediated by the parasympathetic nervous system, whereas dilation of the pupils is mediated by the sympathetic nervous system. Pupillary constriction to light occurs via an involuntary reflex arc. Retinal ganglion cell axons involved in carrying light information for the pupillary light reflex exit the optic tract (proximal to the lateral geniculate nucleus) to synapse in the midbrain pretectal nucleus. The parasympathetic output controlling pupillary constriction originates in the Edinger‐Westphal nucleus in the midbrain and terminates at the pupil sphincter muscle. Pupillary dilation involves a ‘three‐neuron’ sympathetic pathway, which originates in the posterolateral hypothalamus and terminates at the pupil dilator muscle. A relative afferent pupillary defect is caused by a decreased amount of light information from the affected eye reaching the pretectal nuclei in the midbrain and is most commonly a sign of ipsilateral optic nerve pathology. Damage to cranial nerve III can result in injury to the parasympathetic fibres travelling to the pupillary sphincter muscle, thus disrupting the efferent arc of the pupillary light reflex, resulting in deficient pupillary constriction on the involved side. Horner syndrome, characterised by miosis, ptosis, and facial anhidrosis, results from disruption of the oculosympathetic pathway.
Pupillary abnormalities range from benign isolated findings to harbingers of significant, even life‐threatening, conditions. A complete understanding of the neuroanatomy underlying the innervations to the antagonistic pupillary sphincter and dilator muscles is essential to detecting, and discerning the importance of, a particular pupillary abnormality. The sphincter muscle receives neuronal input from the parasympathetic division of the autonomic nervous system, whereas the dilator muscle receives input from the sympathetic division. Afferent input carrying light information to the brain is transmitted by retinal ganglion cell axons via the optic nerves, chiasm, and tracts. The parasympathetic innervation to the pupil originates in the Edinger‐Westphal nucleus in the midbrain. The sympathetic innervation to the pupil consists of a three‐neuron pathway originating in the hypothalamus. Important pupillary disorders include physiologic anisocoria, relative afferent pupillary defect, amaurotic pupil, Argyll Robertson pupils, cranial nerve III palsy, pharmacologic mydriasis, tonic pupil, and Horner syndrome. Key Concepts: Examination of the pupil is an important part of the physician's neurological and ophthalmological evaluation of a patient. The size of the pupil is controlled by the actions of antagonistic muscles located within the iris: the pupillary sphincter and dilator. Constriction of the pupils is mediated by the parasympathetic nervous system, whereas dilation of the pupils is mediated by the sympathetic nervous system. Pupillary constriction to light occurs via an involuntary reflex arc. Retinal ganglion cell axons involved in carrying light information for the pupillary light reflex exit the optic tract (proximal to the lateral geniculate nucleus) to synapse in the midbrain pretectal nucleus. The parasympathetic output controlling pupillary constriction originates in the Edinger‐Westphal nucleus in the midbrain and terminates at the pupil sphincter muscle. Pupillary dilation involves a ‘three‐neuron’ sympathetic pathway, which originates in the posterolateral hypothalamus and terminates at the pupil dilator muscle. A relative afferent pupillary defect is caused by a decreased amount of light information from the affected eye reaching the pretectal nuclei in the midbrain and is most commonly a sign of ipsilateral optic nerve pathology. Damage to cranial nerve III can result in injury to the parasympathetic fibres travelling to the pupillary sphincter muscle, thus disrupting the efferent arc of the pupillary light reflex, resulting in deficient pupillary constriction on the involved side. Horner syndrome, characterised by miosis, ptosis, and facial anhidrosis, results from disruption of the oculosympathetic pathway.
Objective The presence of aura is rare in cluster headache, and even rarer in other trigeminal autonomic cephalalgias. We hypothesized that the presence of aura in patients with trigeminal autonomic cephalalgias is frequently an epiphenomenon and mediated by comorbid migraine with aura. Methods The study retrospectively reviewed 480 patients with trigeminal autonomic cephalalgia in a tertiary medical center for 10 years. Phenotypes and temporal correlation of aura with headache were analyzed. Trigeminal autonomic cephalalgia patients with aura were further followed up in a structured telephone interview. Results Seventeen patients with aura (3.5%) were identified from 480 patients with trigeminal autonomic cephalalgia, including nine with cluster headache, one with paroxysmal hemicrania, three with hemicrania continua, and four with probable trigeminal autonomic cephalalgia. Compared to trigeminal autonomic cephalalgia patients without aura, trigeminal autonomic cephalalgia patients with aura were more likely to have a concomitant diagnosis of migraine with aura (odds ratio [OR] = 109.0, 95% CI 30.9–383.0, p < 0.001); whereas the risk of migraine without aura remains similar between both groups (OR = 1.10, 95% CI = 0.14–8.59, p = 0.931). Aura was more frequently accompanied with migraine-like attacks, but not trigeminal autonomic cephalalgia attacks. Interpretation In most patients with trigeminal autonomic cephalalgia, the presence of aura is mediated by the comorbidity of migraine with aura. Aura directly related to trigeminal autonomic cephalalgia attack may exist but remains rare. Our results suggest that aura may not be involved in the pathophysiology of trigeminal autonomic cephalalgia.
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