Why is pupillary response important

It receives input from cerebral structures and projects to brain stem and spinal cord structures to regulate the balance of sympathetic and parasympathetic input to the organ systems of the body.

The main pathways for this are the medial forebrain bundle and the dorsal longitudinal fasciculus. The hypothalamus then uses this visual system input to drive the pupillary reflexes. If the retina is activated by high levels of light, the hypothalamus stimulates the parasympathetic response. If the optic nerve message shows that low levels of light are falling on the retina, the hypothalamus activates the sympathetic response.

Output from the hypothalamus follows two main tracts, the dorsal longitudinal fasciculus and the medial forebrain bundle Figure 2. Along these two tracts, the hypothalamus can influence the Eddinger—Westphal nucleus of the oculomotor complex or the lateral horns of the thoracic spinal cord.

These two tracts connect the hypothalamus with the major parasympathetic nuclei in the brain stem and the preganglionic central neurons of the thoracolumbar spinal cord. The hypothalamus also receives input from other areas of the forebrain through the medial forebrain bundle.

The olfactory cortex, the septal nuclei of the basal forebrain, and the amygdala project into the hypothalamus through the medial forebrain bundle. These forebrain structures inform the hypothalamus about the state of the nervous system and can influence the regulatory processes of homeostasis.

A good example of this is found in the amygdala, which is found beneath the cerebral cortex of the temporal lobe and plays a role in our ability to remember and feel emotions. The amygdala is a group of nuclei in the medial region of the temporal lobe that is part of the limbic lobe Figure 3. The limbic lobe includes structures that are involved in emotional responses, as well as structures that contribute to memory function. The limbic lobe has strong connections with the hypothalamus and influences the state of its activity on the basis of emotional state.

For example, when you are anxious or scared, the amygdala will send signals to the hypothalamus along the medial forebrain bundle that will stimulate the sympathetic fight-or-flight response.

The hypothalamus will also stimulate the release of stress hormones through its control of the endocrine system in response to amygdala input.

Figure 3 The Limbic Lobe. Ecker, J. Melanopsin-expressing retinal ganglion-cell photoreceptors: cellular diversity and role in pattern vision.

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The average size is mm Bersten et al, The pupils should be equal in size. Pupil shape should be ascertained. It should be round; abnormal shapes may indicate cerebral damage; oval shape could indicate intracranial hypertension Fairley, The pupils should be identical in shape. Pupil reaction to light should be brisk and after removal of the light source, the pupil should return to its original size.

There should also be a consensual reaction to the light source, that is the opposite pupil also constricts when the light source is applied to one eye Jevon, Pupil reaction should be documented as per local policy, for example B brisk , S sluggish or N no reaction. An involved pupil will be dilated and minimally reactive, but could be only partially involved and show a partially dilated and sluggishly responsive pupil. CN III palsy due to compression tumor, aneurysmal is likely to be pupil involving because the pupillary fibers are superficial in the cranial nerve, whereas ischemic CN III palsies typically are pupil sparing.

Pupil involvement due to compression will result in lost direct, consensual and near responses in the affected eye. Aberrant regeneration may occur over several months and may lead to light-near dissociation, with the near response arising from misdirected innervation from the medial rectus. Pupil-involving cases require emergent evaluation because it is likely to be associated with an aneurysm see case report.

Emergent imaging, preferably MRI and MRA, should be ordered to rule out aneurysm in acute pupil-involving presentations of CN III palsy and in patients with no vasculopathic risk factors, particularly young patients. In pupil-sparing cases, where microvascular ischemia is the probable offender if the patient history includes vasculopathy e.

Daily observation is recommended for the first 5 days to monitor for delayed pupil involvement, then every 4 to 6 weeks thereafter. Improved function is expected within about 3 months. Aberrant regeneration takes time, so is most often congenital or associated with a history of trauma or a slowly expanding aneurysm or mass, but is not associated with microvascular CN III palsy.

Pupil-sparing CN III palsies can also be related to giant cell arteritis, so in applicable patients, this must also be ruled out.

Physiologic anisocoria. Notice approximately equal amounts of anisocoria in bright top and dim bottom lighting. The pupil is typically abnormally dilated, exhibits minimal or no response to light, but maintains a sluggish near response with slow redilation. The consensual pupillary response is also typically absent or sluggish. Accommodative tonicity may be similar, with a slow relaxation of the ciliary body after near focusing. The retained near response is likely due to more neural fibers controlling the near than light pupillary reflex.

There may also be some aberrant regeneration of accommodative fibers redirecting to the iris sphincter, thus leading to this light-near dissociation.

The affected, miotic pupil will have an intact light and near pupillary reflex, but due to an inactive pupillodilator muscle, the pupil will slowly dilate due to passive sphincter release in the dark. Note, however, that alpha-receptor upregulation takes several days to develop, so apraclonidine testing may not be useful in acute cases.

There is no way to differentiate first- from second-order neuron lesions with topical ophthalmic pupillary testing. If the patient has any recent history of trauma or if there is any head, neck or chest pain associated, emergent MRA or CTA should be obtained to rule out an internal carotid artery or aortic dissection; concomitant MRI or CT of the rest of the sympathetic chain should also be acquired. Unless the patient history or testing has better isolated an area of concern, the imaging should include the entire sympathetic chain — the head and neck extending down to at least T2 to rule out an apical lung mass.

Light-near dissociation is a hallmark finding with an Argyll Robertson pupil, where the pupil reacts poorly to light but maintains a brisk near response. In addition to light-near dissociation, an Argyll Robertson pupil is typically miotic and irregularly shaped; this tends to be bilateral, but certainly can be asymmetric. Of importance, vision must be intact for this pupillary reaction to be described as an Argyll Robertson pupil.

An Argyll Robertson pupil is seen as a manifestation of neurosyphilis, but light-near dissociation itself can also be seen with other problems. Because of the anatomic arrangement of the fibers that cause the light and near reflexes, with those causing the near reflex being located more anteriorly, the near reflex may remain intact with lesions that affect the more posterior light reflex fibers.

Note right ptosis, right miosis and heterochromia in the top photo. The bottom photo was taken after the instillation of apraclonidine.

Note reversal of anisocoria and improvement of right ptosis. In addition to an Argyll Robertson pupil and aberrant regeneration after a CN III palsy, both previously described above, light-near dissociation can also be found in several other diseases involving midbrain pathology, including neoplasms particularly pinealomas , brainstem strokes, midbrain hemorrhages, arteriovenous malformations, alcoholic midbrain degeneration, encephalitis, hydrocephalus and trauma.

Dorsal midbrain Parinaud syndrome, which often results from direct or compressive injury to the dorsal midbrain, often from pinealomas, includes bilaterally mid-dilated pupils with light-near dissociation and is also associated with eyelid retraction, supranuclear upgaze paralysis and convergence retraction nystagmus.

The patient was asymptomatic, with no pertinent systemic symptoms. The patient underwent 0.