The pupils should be the same size and the should have a round shape. Reactivity: Begin with the eyelids closed. The assessment of reactivity is a 4 - step assessment using the "swinging flashlight" technique. Begin by shining light into one eye we will begin with the right for ease of explanation.
When pupillary dilation or loss of reactivity occurs as a result of CN III compression, both direct and indirect light reflex response is impaired in the same eye e.
If direct light reflex is lost but indirect light reflex is preserved, true CN III compression is less likley. This suggests an afferent defect is affecting the side with the loss of direct response.
Example: the pupillary reflex is absent in the right eye when light is shone into the right eye, but the right pupil constricts in response to light directed into the left eye. This suggests a problem with the sensory input to the right eye called an afferent defect.
Diabetes, vascular conditions or eye diseases may cause afferent defects. Observe for the following: The eyes should move in the same direction in tandom. This is called "conjugate gaze".
When the eyes separate or move in different directions, the patient has disconjugate gaze. An awake individual with disconjugate gaze will have double vision called diplopia. Downward gaze toward the nose is CN IV. Top Stories. Getting the data on homelessness. Hospital News. MRT Week has started: Let's celebrate and recognize this essential role in health care. Ensuring patients and Essential Care Partners are heard in palliative care.
Donor Impact. Miracle Treat Day is Thursday October 28! The latter activation leads to an increase in sympathetic outflow in general, including cardiovascular activity, and increased sympathetic stimulation of the iris manifesting as pupil dilation [see Figure 9 in 44 ]. Activation of the wake-promoting neurones in the LC leads to activation of the cerebral cortex, both directly via the coeruleo-cortical pathway 41 , 44 , and indirectly via shifting the overall activity of the subcortical sleep-arousal network in the direction of wake-promotion 6.
Interestingly, cortical activation may involve areas associated with processing non-luminance-related information, such as cognitive load. As these cortical areas are known to project to the LC 58 , 59 , , their activation would provide reinforcing positive feedback to luminance-evoked LC activation.
Collaterals from spinothalamic tract. Pain signals are carried, via the somatosensory nucleus of the thalamus, to the somatosensory area of the cerebral cortex, by the spinothalamic , and trigemino-thalamic pathways for review, see Both pathways send collaterals to the LC, as demonstrated in the cat and monkey Figure 2.
Pain signals increase LC activity, as shown in the rat by recording the electrical discharge of LC neurones , , expression of cFos , and noradrenaline release Figure 5. Species-specific effects of noxious stimulation on the pupil. Conventions are as in Figure 3. Pain signals arising from noxious painful stimulation are conveyed to the LC via collaterals from the spinothalamic tract. However, the mechanisms are different.
On the other hand, in diurnal animals pain signals stimulate sympathetic premotor neurones in the LC, leading to a sympatho-excitatory effect. See text Collaterals From Spinothalamic Tract for details.
In rabbits, another diurnal species, the noxious stimulus used was electrical stimulation of the sciatic nerve Therefore, reflex dilation in the rabbit, like in man, is likely to be mediated by sympathetic excitation originating in sympathetic premotor neurones in the LC.
In contrast to diurnal species, in nocturnal animals, reflex dilation seems to reflect parasympathetic inhibition rather than sympathetic stimulation Figure 5. Reflex dilation in cats crepuscular animals and rats was studied extensively by Michael Koss and his colleagues in the s 40 , 78 , , They concluded that noxious stimulation in cats and rats activated a noradrenergic pathway inhibiting the EWN, leading to a reduction in parasympathetic outflow, appearing as pupil dilation 40 see Collaterals From Spinothalamic Tract.
The differential effect of noxious stimulation on the noradrenergic control of pupil function in diurnal and nocturnal animals suggests that while in diurnal animals pain signals may preferentially activate excitatory sympathetic premotor neurones in the LC, in nocturnal animals they may activate mainly inhibitory parasympathetic premotor neurones projecting to the EWN Figure 5. Moreover, it has been proposed that the inhibitory noradrenergic pathway to the EWN may originate from the LC, and that the LC could exert dual influence on pupillary activity via an excitatory output to the IML and an inhibitory output to the EWN 63 This model of the dual noradrenergic control of pupillary activity by the LC is elaborated further in the present review.
Liu et al. This finding is also consistent with the existence of a direct link between the LC and the EWN, and thus has bearing on a controversy regarding the connection between the LC and the EWN Nieuwenhuis et al. An example is the projection from the retina to the DRN: both a direct and an indirect connection have been described see Retinal Inputs to the Dorsal Raphe Nucleus, and Figure 6.
Figure 6. Connections of the light-stimulated serotonergic pathway. Connections are shown by arrows: red-excitatory; blue-inhibitory putative. The DR receives both a direct and an indirect input from the retina; the indirect connection involves hypothalamic orexinergic neurones.
Apart from sending an inhibitory output to the EWN, the LC also inhibits other parasympathetic preganglionic brainstem nuclei salivatory nuclei, vagal nuclei Electrical stimulation of the lateral hypothalamus in experimental animals leads to pupil dilation due to inhibition of the EWN via an inhibitory noradrenergic input The central nucleus of the amygdala sends an excitatory peptidergic projection to the LC; the neuropeptide involved is corticotrophin-releasing factor CRF Both the amygdala and the LC have been implicated in the generation of anxiety.
Furthermore, there is likely to be a synergistic interaction between these two nuclei in mediating anxious responses: stress-induced activation of the central amygdala is transmitted to the LC by a CRF-containing output from the amygdala , Anxious states amenable for experimental study can be generated by the paradigm of fear conditioning: pairing of a noxious stimulus e.
Using this paradigm, it was possible to modulate two physiological reflexes, the acoustic startle reflex and the pupillary light reflex, by the anticipatory anxiety associated with the procedure Interestingly, the two reflexes are changed in opposite directions: the acoustic startle reflex is potentiated, whereas the pupillary light reflex is inhibited by conditioned fear. The activation of the amygdala by stressful stimulation is transmitted to the LC, leading to potentiation of the noradrenergic facilitation of striated muscle contraction, in the startle reflex paradigm, and enhancement of the noradrenergic inhibition of the EWN, leading to inhibition of the light reflex The sensitivity of the accompanying mydriasis to antagonism by dapiprazole would indicate the associated involvement of the sympathetic output, probably arising from the activation of sympathetic premotor neurones in the LC.
Collaterals from the spinothalamic tract project to parasympathetic premotor neurones in the LC in nocturnal animals, such as rats 40 , , , and in crepuscular animals, such as cats 40 , WPN are active during wakefulness and quiescent during sleep, whereas SPN display the opposite pattern of activity.
Each nucleus in the network is defined by its connections and the neurotransmitter used. WPN neurones use glutamate, the neuropeptide orexin, acetylcholine, and the monoamines noradrenaline, dopamine, serotonin 5-hydroxytryptamine [5-HT] , and histamine. The LC is in the hub of this network. The LC has a two-way, mutually antagonistic relationship with the VLPO of the hypothalamus, a major sleep-promoting nucleus.
Examples of drugs indirectly influencing LC activity and thus leading to alterations in the level of arousal are the stimulant modafinil and the sedative drug pramipexole.
Modafinil increases dopaminergic excitation of LC neurones via blocking the uptake of dopamine into dopaminergic nerve terminals, leading to stimulation of excitatory postsynaptic D 2 dopamine receptors 67 , whereas pramipexole reduces LC activity by attenuating the dopaminergic activation of LC neurones via stimulating inhibitory D 2 dopamine autoreceptors on the dopaminergic neurones Consequently, alterations in the level of arousal are transmitted to the pupil.
In general, an increase in alertness is associated with an increase in sympathetic output and pupil dilation, whereas sedation is linked to a decrease in sympathetic output and pupil constriction. During transition from wakefulness to sleep drowsiness or sleepiness , there is likely to be instability between opposing excitatory wake-promoting and inhibitory sleep-promoting inputs impinging on the LC, leading to fluctuations in LC activity.
Due to the close association between LC activity and pupillary diameter see Noradrenergic Pathway , the drowsiness-related fluctuations of LC activity are transmitted to the pupil, leading to fluctuations in pupil diameter.
These oscillations increase as the level of arousal decreases. The Pupillographic Sleepiness Test PST provides quantitative measures of the oscillations that can be used as indices of the degree of sedation , Indeed, the two measures of pupil diameter fluctuations generated by the PST total power, Pupillary Unrest Index , correlate with electroencephalographic and subjective measures of sedation , The PST has also been used to assess the sedative and alerting properties of centrally acting drugs 74 , , , — , and the PST measures correlate well with other measures of alertness, such as critical flicker fusion frequency CFFF and visual analog scales.
It would be expected that drug-induced changes in arousal would affect both pupillary indices of alertness: in the case of sedation, an increase in sleepiness waves would be paralleled by miosis, and in the case of stimulation, a decrease in sleepiness waves would be paralleled by mydriasis.
Although this prediction has been confirmed in the case of some drugs e. Examples of a dissociation between the effects of sedation on pupillary oscillations and pupil diameter are two highly sedative drugs: diazepam and pramipexole. While both drugs enhance pupillary oscillations in darkness, and display sedative effects on CFFF and visual analog scales, diazepam-induced sedation is associated with no change in pupil diameter , whereas pramipexole-induced sedation is accompanied by mydriasis Such extraneous actions may either compromise the transmission of sympatho-excitatory signals from the LC to the SCG, or change the balance between sympathetic and parasympathetic outputs to the iris, by interfering with the parasympathetic output.
However, the resultant decrease in LC activity is not passed on to the pupil by the sympathetic output from the LC. The possibility that diazepam may alter the relationship between the sympathetic and parasympathetic outputs to the iris has been excluded: it does not affect the parameters of the light reflex response or the diameter of the pupil dilated by the cholinoceptor antagonist tropicamide, applied topically Preganglionic sympathetic neurones in the IML integrate inputs from supraspinal premotor neurones, including those in the LC, and an intricate network of intraspinal interneurones GABA receptors have been identified on bulbospinal neurones, projecting to sympathetic preganglionic neurones in the IML, on presynaptic terminals of such neurones, and on interneurones in the IML Indeed, GABAergic neurotransmission plays an important role in controlling sympathetic outflow Benzodiazepines may increase the activity of sympathetic preganglionic neurones via disinhibiting some of their excitatory inputs, and this increase in activity may mask the effect of the sedation-induced reduction in the excitatory input from the LC However, further experimental work would be needed to confirm this hypothesis.
It is highly sedative due to inhibiting an excitatory input to the LC from dopaminergic neurones located in the VTA. As expected, pramipexole-induced sedation is associated with enhancement of pupillary sleepiness waves. However, paradoxically, this is paralleled by mydriasis, rather than miosis , This paradoxical effect of pramipexole may be due to the unexpected finding that it attenuates the pupillary light reflex response.
As pramipexole has no affinity for cholinoceptors, a central mechanism has been postulated. Consistent with this model, it has been shown that amisulpiride, a D 2 dopamine autoreceptor antagonist, evokes an effect opposite to that of pramipexole: it potentiates the light reflex Therefore, in the case of pramipexole-induced sedation, miosis resulting from a reduction in sympathetic outflow to the iris, as a consequence of reduced LC activity, may have been superseded by mydriasis, due to parasympathetic inhibition.
As discussed above see Functional Organization of Noradrenergic Premotor Autonomic Neurones in the Locus Coeruleus , there is evidence supporting the view that sympathetic and parasympathetic premotor neurones in the LC form separate populations, and, in many situations, operate independently.
However, the sympathetic and parasympathetic divisions of the autonomic nervous system do not function in isolation. Examples of cross-talk between the two divisions have been described in the medulla oblongata and the PVN in the hypothalamus There is also evidence of cross-talk between the two populations of premotor autonomic neurones in the LC.
The anatomical basis of such cross-talk may be the gap junctions between LC neurones, through which cells can communicate with each other via eletrotonic transmission Electrotonic coupling of LC neurones has been implicated in the synchronization of spontaneous firing and the generation of endogenous rhythmic activity , An alternative mechanism may be the activation of noradrenergic parasympathetic premotor neurones from recurrent excitatory axon terminals of sympathetic premotor neurones.
Indeed, such a mechanism has been described to operate in the LC Light is a powerful activator of sympathetic activity, consistent with light-evoked stimulation of sympathetic premotor neurones in the LC see Dorsomedial hypothalamus. However, in addition to its sympatho-excitatory effect, light has also been reported to evoke a parasympatholytic effect 55 , The possible mechanism for this dual effect of light on autonomic outflow, affecting both divisions of the autonomic nervous system, may be the simultaneous activation of both sympathetic and parasympathetic premotor neurones in the LC.
Parasympathetic premotor neurones may have been activated either directly or indirectly, via the spread of sympathetic premotor neuronal activity to parasympathetic premotor neurones via electorotonic transmission or recurrent axon collateras. Monoamines are accumulated in synaptic vesicles of the nerve terminals by an active membrane pump, the vesicular monoamine transporter VMAT. Drugs that inhibit VMAT2 in noradrenergic nerve terminals, such as reserpine and tetrabenazine, lead to depletion of noradrenergic neurones of noradrenaline These drugs are not selective for either sympathetic or parasympathetic premotor neurones in the LC: they deplete both populations of noradrenergic premotor neurones of noradrenaline.
Depletion of noradrenaline of sympathetic premotor neurones leads to a sympatholytic effect sedation, miosis, hypotension , whereas depletion of noradrenaline of parasympathetic premotor neurones results in a parasympathomimetic effect potentiation of the light reflex response, increase in salivation The parasympathomimetic effect is likely to be due to removal of the noradrenergic inhibition of the EWN by the LC.
Noradrenaline reuptake inhibitors, including a number of antidepressants, enhance the effect of released noradrenaline, by blocking its reuptake into noradrenergic nerve terminals They, like the VMAT inhibitors, are not selective for either population of pre-autonomic noradrenergic neurones in the LC, and potentiate the effects of noradrenaline at all the different targets of noradrenergic projection. The antidepressants desipramine, reboxetine, and venlafaxine enhance both the sympatho-excitatory and parasympatholytic effects mediated by noradrenergic autonomic outputs.
These drugs cause mydriasis and shortening of the recovery time of the light reflex response, due to potentiation of noradrenergic stimulation of preganglionic sympathetic neurones in the IML and of the dilator pupillae muscle in the iris. They also attenuate the pupillary light reflex response and reduce salivary output, due to potentiation of the noradrenergic inhibition of preganglionic parasympathetic neurones in the EWN and the salivatory nuclei — It should be noted that while the parasympatholytic effect of desipramine could be due to the blockade of cholinoceptors in the iris, this explanation cannot be applied to the parasympatholytic effects of venlafaxine and reboxetine since these drugs have little affinity for cholinoceptors The basis for this selectivity is likely to be a difference in the baseline activities of sympathetic and parasympathetic premotor neurones.
Sympathetic premotor neurones are likely to have high baseline activity due to their stimulation by light via an input from the retina see Dorsomedial hypothalamus , whereas the baseline activity of parasympathetic premotor neurones is likely to be low. It is likely that in these cases the baseline activity of parasympathetic premotor neurones was high enough to allow autoreceptor stimulation to be converted into an observable response.
The baseline activity of parasympathetic premotor neurones may have been raised by the spread of activity from the sympathetic premotor neurones to the parasympathetic premotor neurones via electronic transmission through gap junctions. This pathway is displayed in Figure 6. The hub of the serotonergic pathway is the dorsal raphe nucleus DRN which contains serotonergic neurones, some of which function as sympathetic premotor neurones.
These neurones send an excitatory projection to preganglionic neurones in the IML where it stimulates 5HT 2A receptors. The premotor autonomic neurones in the DRN contain inhibitory 5HT 1A receptors: the stimulation of these receptors by serotonin, released from recurrent serotonergic axon terminals, inhibits the activity of the serotonergic neurones.
The existence of parasympathetic premotor neurones has been postulated: these neurones, via an inhibitory output to the EWN, would inhibit the light reflex. However, although the DRN inhibits the parasympathetic output to the pupil, this is likely to be via an indirect route see 5-HT1A Receptors, below. Serotonin 5-hydroxytryptamine, 5-HT is one of the major monamine neurotransmitters that, like noradrenaline, is involved in the regulation of both arousal 6 , and autonomic function , Serotonergic neurones are located in nine nuclei B1—B9 in the midline raphe of the brainstem, and project widely throughout the neuraxis , Largest of these nuclei is B7, corresponding to the DRN, that is responsible for the serotonergic control of arousal Several serotonergic nuclei are involved in autonomic regulation, including the DRN and a number of caudal raphe nuclei.
These nuclei project to the IML of the spinal cord , where they are likely to stimulate excitatory 5HT 2 receptors on sympathetic preganglionic neurones There is also a population of serotonergic interneurones in the IML Serotonin interacts with a large array of presynaptic auto and postsynaptic receptors that can mediate both excitatory and inhibitory effects.
Inhibitory 5-HT 1A autoreceptors on serotonergic neurones play an important role in the regulation of serotonergic neurotransmission These species include the rat — , the mouse ; the Mongolian gerbil , , , and the Chilean degus It has been shown that stimulation of this pathway by light can modulate the expression of cFos, an index of neuronal activity, in the DRN Furthermore, stimulation of the DRN by light can lead to alterations in complex behaviors, such as affective and defensive behaviors.
It has been shown that both conventional and melanopsin-containing retinal ganglion cells project to the DRN The majority of retinal ganglion cells projecting to the DRN are conventional alpha-like ganglion cells with Y-like physiological properties , Orexinergic neurones may be directly light-sensitive via an input from the retina , or may be activated indirectly by light via the SCN For the role of the orexinergic system in pupillary control, see Latero-Posterior Hypothalamus.
Serotonergic neurones in the DRN operate via stimulating serotonin receptors both in the DRN and the targets innervated by it. The role of these receptors in controlling pupil function has been explored using selective 5-HT 1A receptor agonists and 5-HT 2 receptor antagonists.
The stimulation of these receptors on sympathetic premotor neurones would mediate a sympatholytic effect by switching off the activity of these neurones, and thus attenuating their excitatory influence on sympathetic preganglionic neurones Postsynaptic 5-HT 1A receptors also play a role in autonomic regulation: by inhibiting sympathetic premotor neurones in the RVLM they mediate a sympatholytic effect on cardiovascular function In diurnal species, these drugs evoke miosis, whereas in nocturnal animals they cause mydriasis.
As in man, the buspirone-induced miosis was unaffected by the topical application of the cholinoceptor antagonist homatropine, it was concluded that the miotic response was likely to be due to sympathetic inhibition Miotic responses to buspirone and lesopitron were also light-dependent: responses were larger in light than in darkness.
The light-dependence of the miotic responses to the 5-HT 1A receptor agonists is consistent with the operation of a serotonergic light-stimulated sympathetic pathway. The pupillary responses could be antagonized by not only 5-HT 1A receptor antagonists e. These observations argue against the existence of a direct serotonergic inhibitory input to the EWN operating via 5-HT 1A receptors Figure 6.
Indeed, an intricate neuronal network has been proposed to operate within the LC modulating the firing of noradrenergic neurones. In this network, the noradrenergic neurones may be under tonic inhibition by GABAergic interneurones that in turn may be inhibited by a serotonergic input operating via inhibitory 5-HT 1A receptors.
Therefore, disinhibition of the noradrenergic neurones by 5HT 1A receptor stimulation could lead to an increase in noradrenergic neuronal firing An ascending output from the DRN to the cerebral cortex stimulates excitatory 5-HT 2A receptors, and thereby increases arousal 6 , and a descending output to the sympathetic preganglionic neurones in the IML stimulates 5-HT 2A receptors, leading to sympathetic stimulation Figure 6.
It has been shown that the 5-HT 2 receptor antagonists ICI , and ICI , have dose-dependent miotic and sedative effects in man , , consistent with the attenuation of 5-HT 2 receptor-mediated functions. The dose-dependent miosis suggests that the 5-HT 2 receptors in the IML may mediate a tonic sympatho-excitatory effect on the pupil. Light has robust effects on the autonomic control of the pupil: it stimulates the parasympathetic output and inhibits the sympathetic output.
While the mechanisms underlying the light reflex have been the subject of intensive investigation, especially since the discovery of the role of melanopsin-containing retinal ganglion cells in its initiation , there has been relatively less interest in the sympathetic control of the pupil by light.
While the inhibitory effect of light on the sympathetic output to the pupil was demonstrated in the s and s, little experimental work has been done since then.
Okada et al. The course of this pathway has not been investigated since then. However, review of the literature of experimental work investigating the connections of the pretectum to autonomic nuclei, allows filling in the missing gaps. This pathway overlaps with the pathway controlling melatonin synthesis, as sympathetic preganglionic neurones in the same segments C8-T2 of the IML innervate, via the SCG, both the pineal gland and the dilator pupillae muscle in the iris.
Although the role of this pathway in mediating the effect of light on the sympathetic control of melatonin synthesis is well established, its role in mediating the inhibitory effect of light on the sympathetic output to the pupil has not been studied experimentally. Light has a manifest sympatho-excitaroy effect on functions e. However, at the levels of C8-T2, the sympatho-excitatory effect of light may be superseded by its powerful inhibitory effect required for the operation of the light reflex and control of melatonin synthesis.
Therefore, pupil dilation resulting from the stimulation of the sympathetic output to the iris would be masked by the pupil-constricting effect of light. The latent mydriasis can be unmasked by drugs that modulate the activity of the hub nuclei. Drugs that inhibit LC activity e.
The light-stimulated sympathetic pathways, by attenuating light-evoked pupil constriction, may enable diurnal animals to function in daylight, when light may cause pinpoint pupils in nocturnal animals The activity of the light-stimulated pathways appears to be related to age.
The monotonic decline in pupil diameter with increasing age in humans — may reflect the gradual withdrawal of the activity of the light-stimulated sympathetic pathways since the decline in pupil diameter is paralleled by the age-dependent decline in the number of noradrenergic neurones in the LC The effect of age on the pupil is accentuated in Alzheimer's disease when the loss of noradrenergic neurones in the LC exceeds that seen in old age The noradrenergic light-stimulated sympathetic pathway has widespread connections via sympathetic and parasympathetic premotor neurones in the LC, and via these connections it is integrated into the wider central autonomic network 41 , Many drugs sedatives, stimulants, antidepressants, anxiolytics modify pupil function by actions via the noradrenergic light-stimulated sympathetic pathway.
Through its multiple inputs the noradrenergic light-stimulated sympathetic pathway is amenable to modulation by a wide range of physiological and psychological variables, and via its outputs it can transmit sympathetically and parasympathetically mediated alterations in pupil function.
There is a remarkable species difference in the operation of light-stimulated sympathetic pathways: diurnal animals respond differently from nocturnal animals to light, noxious stimulation, and autoreceptor agonist drugs e. Therefore autoreceptor agonists and pain signals may affect sympathetic premotor neurones preferentially, as compared to parasympathetic premotor neurones, in diurnal animals.
It has been shown in the monkey 58 , and in the mouse and rat 59 that cognitive load, applied using different paradigms, evokes fast transient changes in the firing rate and pattern of LC neurones. Furthermore, corresponding changes can be observed in neuronal firing in different areas of the cerebral cortex and colliculi. Unraveling the multiple sympathetic pathways controlling the pupil suggests that the sympathetic has roles beyond fading away in the background when the light reflex operates.
While the parasympathetic pathway mediating the light reflex has one robust dedicated function, the sympathetic pathways, through their connections, are multifunctional, integrating pupil function with a wide range of autonomic, neuroendocrine, physiological, and psychological functions. The author confirms being the sole contributor of this work and has approved it for publication.
They synapse at the superior cervical ganglion where third-order neurons travel through the carotid plexus and enter into the orbit through the first division of the trigeminal nerve. When performing a pupillary exam, it sometimes helps to illuminate pupils indirectly from the side, so you can actually see what is happening.
The variation should be no more than 1mm and both eyes should react to light normally. Can be dangerous if a manifestation Horner's syndrome e. Consider further workup such as imaging if anisocoria is suspected to be from a pathologic process. An RAPD is a defect in the direct response. It is due to damage inoptic nerve or severe retinal disease. It is important to be able to differentiate whether a patient is complaining of decreased vision from an ocular problem such as cataract or from a defect of the optic nerve.
If an optic nerve lesion is present the affected pupil will not constrict to light when light is shone in the that pupil during the swinging flashlight test.
However, it will constrict if light is shone in the other eye consensual response. The swinging flashlight test is helpful in separating these two etiologies as only patients with optic nerve damage will have a positive RAPD.
Swing a light back and forth in front of the two pupils and compare the reaction to stimulation in both eyes. An RAPD is diagnosed by observing paradoxical dilatation when light is directly shone in the affected pupil after being shown in the healthy pupild to be from a pathologic process.
This decrease in constriction or widening of the pupil is due to reduced stimulation of the visual pathway by the pupil on the affected side. By not being able to relay the intensity of the light as accurately as the healthy pupil and visual pathway, the diseased side causes the visual pathway to mistakenly respond to the decrease in stimulation as if the flashlight itself were less luminous.
This explains the healthy eye is able to undergo both direct and consensual dilatation seen on the swinging flashlight test. The 25 The 25 Visit the Abraham Verghese Interviews Dr. Pathway s affected : You conclude that structures in the following reflex pathway have been affected. The Trigeminal Nerve. Section of the trigeminal nerve will eliminate somatosensory sensation from the face and the eye blink reflex e. However, light touch of the right cornea will elicit a bilateral eye blink.
The effect of sectioning the trigeminal nerve is to remove the afferent input for the eye blink reflex. The patient complains of pain in her left eye. Her left pupil appears dilated and is not reactive to light directed at either the left or right eye Figure 7.
The right pupil appears normal in size and reacts to light when it is directed in the right or left eye. Both eyelids can be elevated and lowered and both eyes exhibit normal movement. Touch, vibration, position and pain sensations are normal over the entire the body and face. Parasympathetic Innervation of the Eye. Section of the parasympathetic preganglionic oculomotor nerve or postganglionic short ciliary nerve innervation to one eye will result in a loss motor of both the direct and consensual pupillary light responses of the denervated eye.
Section of the left short ciliary nerve or a benign lesion in the left ciliary ganglion will result in no direct response to light in the left eye and no consensual response in the left eye when light is directed on the right eye a.
When the damage is limited to the ciliary ganglion or the short ciliary nerve, eyelid and ocular mobility are unaffected. The patient presents with a left eye characterized by ptosis, lateral strabismus, and dilated pupil. When asked to rise his eyelids, he can only raise the lid of the right eye.
When asked to close both eyes, both eyelids close fully. His left pupil does not react to light directly or consensually Figure 7. When asked to look to his right, his left eye moves to a central position, but no further.
The right eye is fully mobile. When the patient is asked to look straight ahead, you note his left eye remains directed to the left and depressed.
Observe the reaction of the patient's pupils to light directed in the left or right eye. The Oculomotor Nerve. Section of the oculomotor nerve produces a non-reactive pupil in the ipsilesional side as well as other symptoms related to oculomotor nerve damage e.
Section of the oculomotor nerve on one side will result in paralysis of the superior levator palpebrae, which normally elevates the eyelid. The parasympathetic preganglionic axons of the Edinger-Westphal nucleus, which normally travel in the oculomotor nerve, will be cut off from the ciliary ganglion, disrupting the circuit normally used to control the iris sphincter response to light. The patient complains of reduced vision in the left eye.
Pupil size in both eyes appears normal. However, both pupils do not appear to constrict as rapidly and strongly when light is directed into his left eye Figure 7. That is, compared to the response to light in the left eye, light in the right eye produces a more rapid constriction and smaller pupil in both eyes.
The Optic Nerve. Partial damage of the retina or optic nerve reduces the afferent component of the pupillary reflex circuit. The reduced afferent input to the pretectal areas is reflected in weakened direct and consensual pupillary reflex responses in both eyes a. Section of one optic nerve will result in the complete loss of the direct pupillary light reflex but not the consensual reflex of the blinded eye. That is, if the left optic nerve is sectioned, light directed on the left blind eye will not elicit a pupillary response in the left eye direct reflex or the right eye consensual response.
However, light directed in the right eye will elicit pupillary responses in the right eye and the left blind eye. The effect of sectioning one optic nerve is to remove the afferent input for the direct reflex of the blinded eye and the afferent input for the consensual reflex of the normal eye. Section of one optic tract will not eliminate the direct or consensual reflex of either eye as the surviving optic tract contains optic nerve fibers from both eyes.
However, the responses to light in both eyes may be weaker because of the reduced afferent input to the ipsilesional pretectal area.
A patient who is suffering from the late stages of syphilis is sent to you for a neuro-ophthalmological work-up. His vision is normal when corrected for refractive errors.
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