perksqert.blogg.se - Fixed dilated pupil differential diagnosis

Third-order neurons give rise to post-ganglionic axons, which leave the superior cervical ganglion and run along the course of the internal carotid artery through the cavernous sinus, where they meet up with the ophthalmic division of the trigeminal nerve (V1) and ophthalmic artery to travel to the eye. The second-order neuron leaves the spinal cord and passes over the apex of the lung to synapse at the superior cervical ganglion.

Originating in the posterior hypothalamus, the first-order neuron descends through the brainstem to synapse in the ciliospinal center of Budge between the levels of the eighth cervical and fourth thoracic vertebrae (C8-T4). Oculo-sympathetic innervation to the eye consists of a three-neuron arc. Efferent pupil fibers then travel with CN III back towards the orbit, where they synapse in the ciliary ganglion, with 3% of post-ganglionic fibers innervating the iris sphincter muscle (which allows for miosis) and the remaining 97% innervating the ciliary body (which allows for accommodation). This is also the reason why a lesion of the optic nerve or optic tract does not result in anisocoria, or difference in pupil size between the two eyes. For example, the direct response of the right eye (and consensual response of the left eye) indicates the integrity of the afferent pathway on the right side. Neutral density filters can be useful in grading relative afferent pupillary defects.īecause of this neuroanatomy, we are able to objectively measure the integrity of the afferent pathway by observing the direct and consensual light responses. 1 Pupil fibers synapse in the pretectal nuclei of the midbrain and travel to the two Edinger-Westphal nuclei of the oculomotor nerve (CN III), beginning the efferent pathway. The afferent pathway is responsible for transmitting the impulse of the incoming light via the photoreceptors of the retina, through the optic nerve to the chiasm and optic tract, then separate from the tract just anteriorly to the lateral geniculate body (LGN) before traveling to the mid-brain to bilaterally project to the pretectal nuclei. The pupillary light response consists of both an afferent and efferent pathway. The pupillary light and near responses are under parasympathetic innervation. Meaningful interpretation of pupillary findings requires a solid working knowledge of the anatomy of the light reflex and the autonomic innervation of pupillary responses. This article addresses the more commonly encountered pupil disorders and how clinicians can detect them through routine pupil testing. With careful clinical examination, this test can aid in the diagnosis and management of many of these conditions at the primary care level.

Coma or brain death: Severe brain damage may cause a change in the size and reactivity of the pupils.Pupil testing can reveal serious retinal and neuro-ophthalmic disease and therefore should be incorporated into every comprehensive eye examination.

Surgery: Eye surgery may result in alterations in pupil size, which can be permanent.

Seizure: Sometimes seizures (a disruption of electrical activity in the brain) can cause changes in the pupils, which may be equal or unequal.

Migraine: While it is not common, migraines can cause anisocoria.

Vision loss: Significant vision defects can affect pupil size and reactivity.

Increased intracranial pressure: This can result from a brain tumor, meningitis (inflammation of the fluid around the brain), or a stroke.

Trauma: An injury affecting the eye or the brain may cause the pupils to be unequal.

Inflammatory conditions, such as MS and sarcoidosis, also can do this. Inflammation: An infection affecting the eye or the cranial nerves can cause anisocoria.

Cranial nerve damage: This can occur due to a stroke (a blockage of blood flow or bleeding in the brain), brain aneurysm (defect in a blood vessel), or a brain tumor.Multiple sclerosis (MS): MS is a chronic neurological disorder that causes symptoms affecting vision, movement, sensation, and more.