Cranial+Nerves+I-VI

=**Cranial Nerves I-VI**=


 * 1. Describe how to examine each cranial nerve.**


 * **Nerve** || **Test** || **notes** ||
 * CN1 || Test each nostril separately with “scratch-n-sniff cards” or essential oils || Not usually done unless pt complains of anosmia ||
 * CN2 || Visual acuity (read a card), Visual Fields (count fingers), Fundoscopy, Pupilary Responses (swinging light) || see swingling light test and accommodation notes as well as lecture demos ||
 * CN3 || Eye is down and out, drooping eyelid, pupil is dilated || see Hankin’s Orbit lecture ||
 * CN4 || Not able to look down when eye is directed medially ||  ||
 * CN5 || test sensory for three branches plus motor function ||  ||
 * CN6 || inability to abduct eye ||  ||

__Swinging light test:__ Afferent loop: light in both eyes is sent to pretectal area (midbrain), synapses there, then to Edinger Westphal subnucleus (III). Efferent loop: parasympathetic fibers from EWN travel in III to ciliary ganglion, then to short ciliary nerves. Light in either eye causes consensual constriction. If there is an afferent loop lesion, less light detected in lesioned eye leads to “dilation on that side” In fact, both eyes constrict less, but you are looking at the lit eye efferent defect prevents constriction on that side but accommodation is stronger stimulus for constriction, often works partially when there is a III nerve lesion.

__Accomodation Reflex:__ 3rd n. somatic fibers activate both medial rectus muscles. Parasympathetic fibers from Edinger Westphal nucleus constrict pupillary sphincter constrictor muscle and activate ciliary muscle to relax suspensory ligament of lens. Smaller pupil, more convex lens allows close focus.

__Rules of Diplopia:__
 * 1) The false image is always the outer image.
 * 2) The false image always comes from the affected eye.
 * 3) Cover each eye to see which one generates the false (outer) image


 * 2. Localize cranial nerve or pathway lesions based on the functional deficits produced.**

__Stria medullaris__ thalami connects the olfactory areas to habenula __Stria terminalis__ connects the amygdala to the anterior hypothalamus and preoptic area __Medial Forebrain bundle__ connects olfactory areas to hypothalamus. Habenula and hypothalamus project to reticular formation, salivatory nuclei, Dorsal Motor Nucleus (DMN) of CN X for visceral responses
 * CN I**

Remember that the lens inverts images __Optic nerve__ Images are projected onto the opposite corner of the retina and are collected together with their matching part of the image at the optic chiasma. The right vision fields for each eye join and follow the left optic tract to the left lateral geniculate body and then to the primary visual cortex. Lesions of the optic nerve anterior to the chiasm cause monocular blurring, dimming or blindness. Lesion of the right optic tract (after the chiasm) causes a left hemifield visual loss. If loss is symmetrical in both eyes, it is called “homonymous”, hence this is a “left homonymous hemianopia” Midchiasm lesions cause bitemporal hemianopia (loss of outer images from each eye). __Parietal radiation__ carries fibers for inferior visual field __Meyer’s Loop__ carries fibers for superior visual field
 * CN II**

III nucleus is in medial midbrain ventral to cerebral aquaduct, above medial longitudinal fasiculus. Complex of multiple subnuclei with parasympathetics originating in Edinger Westphal n.
 * CN III**

Nucleus in midbrain, caudal to III, exits dorsal midbrain at level of inferior colliculus, crosses between post. cerebral and sup. cerebellar arteries, through dura between free and attached borders of tentorium, through cavernous sinus and superior orbital fissure above tendonous ring that suspends the eye rectus muscles.
 * CN IV**

__Sensory fibers__ synapse in trigeminal ganglion, sensory nucleus of V from midbrain to spinal cord __Motor nucleus of V__ in midpons, Motor input from motor cortex (volitional chewing), Sensory input from V, other cranial nerves (VIII, etc) __Ophthalmic n.__ travel in cavernous sinus exits skull at superior orbital fissure __Maxillary n.__ travel in cavernous sinus exits skull at foramen rotundum __Mandibular n.__ exits at foramen ovale – with motor branch __Mesencephalic nucleus__ has primary sensory neurons from branchial muscles (no synapse in trigem. gang.) mediating proprioception for reflex control of chewing __Pontine nucleus__ secondary sensory neurons for face __Nucleus of spinal tract of V__ merges with dorsal gray of spinal cord – mostly pain and temperature for face Upper Motor Neuron lesions: above the level of the motor nucleus, no effect due to bilateral cortical innervation Lower Motor Neuron lesions: involving the motor nucleus or the nerve, paralysis and atrophy of masseter on side of lesion
 * CN V**

Motor only, innervates lateral rectus __Abducens nucleus__ in dorsal pons, near midline __Axons of VI__ exits brainstem at pontomedullary junction, pierces dura lateral to dorsum sellae of sphenoid bone, sharp bend over apex of petrous temporal bone, enters cavernous sinus, travels between V1 and V2, passes through superior orbital fissure, tendonous ring to inervate LR. VI n. lesion causes lateral rectus weakness, diplopia on lateral gaze to the side of the lesion
 * CN VI**


 * Coordination of Lateral Gaze**
 * Lateral gaze is initiated in Brodmann’s Area 8, also known as “Frontal eye fields”
 * Fibers cross in pons, innervate lateral gaze center in pons at level of VI nucleus, Paramedian Pontine Reticular Formation (PPRF), also receives input from vestibular nuclei
 * PPRF sends excitatory input to ipsilateral VI nucleus, causes abduction of ipsilateral eye
 * PPRF sends excitatory input to contralateral III nucleus, causes contralateral eye to turn medially. Fibers travel in the median longitudinal fasciculus (MLF)

Saccadic System: Quick movements to a target Smooth pursuit System: Following a moving object Convergence System: Keeping a close object in focus Vestibular System: Keeping eyes directed while head moves
 * Eye movement control systems**


 * 3. Use your knowledge of cranial anatomy to solve neurological cases.**

__Case 1: The Bicyclist__ 1. What is the localization of the lesion? > //Evulsion of olfactory bulb// 2. Why couldn’t she smell anything? > //avulsion of olfactory bulb disrupted olfaction// 3. Why couldn’t she taste anything? > //Taste related to sense of smell// 4. What was the clear fluid? > //Blunt trauma and skull fractures can cause avulsion of bulb from cribriform plate and create CSF leak into nasal cavity Can diagnose CSF leak by testing fluid for glucose (higher in CSF than mucous).// 5. How do we examine for smell? Taste? > //See Objective 1.//

__Case 2: The photographer__ 1. What is the localization of the lesion? > //Likely demyelination of optic nerve fibers due to optic neuritis.// 2. Why did she have a hole in her vision? > //Central scotoma// 3. What is a “central scotoma”? > //A blind spot involving the macula where the greatest concentration of fibers originate// 4. Why was her retina pale? > //Eventual loss of retinal nerve fibers results in a pale retina// 5. What is the “swinging light test” > //see objective 1.// 6. Why did the right pupil constrict less? > //Loss of light sensation by the right retina results in an “afferent pupillary defect”//

__Case 3: The Gardener’s Headache__ 1. What is the localization of the lesion? > //Right oculomotor nerve (III)// 2. What caused the headache and stiff neck? > //The headache and stiff neck were due to a subarachnoid hemorrhage// 3. What caused the eye movement abnormalities? > //The III nerve lesion was due to an aneurysm of the posterior communicating artery pressing on III as it exits the midbrain// 4. What explains the pupil abnormality? > //The pupil is enlarged because efferent fibers from EW that travel in III to the ciliary ganglion are damaged by the pressure of the aneurysm.//

__Case 4: Cock-eyed Banker__ 1. What is the localization of the lesion? > //The lesion is in the right trochlear nerve, the lesion could also be caused by damage to the IV nerve nucleus on the left// 2. Why didn’t the med student find anything wrong? > //He didn’t isolate the SO, needed to look medially and down// 3. Why did she get double vision looking down? > //She gets double vision looking down (and left) because the right superior oblique is weak.// 4. Why did it get better when she tilted her head? > //To compensate for extorsion of globe (Head tilts away from nerve lesion, toward brainstem lesion).// 5. What was the cause of the lesion? > //Lesion is likely due to an infarct of the IVth nerve related to her diabetes//

__Case 5: The Pained Professor__ 1. What is the localization of the lesion? > //Trigeminal Neuralgia (usually maxillary)// 2. What is the cause of the pain? > //Cause unknown – may be due to pressure of brainstem arteries on V as it enters pons// 3. What is “tic douloureux” > //Trigeminal Neuralgia// 4. Why did the neurologist prescribe carbamazepine? > //Often controlled with anticonvulsants like carbamazepine that block excessive nerve discharges// 5. How do you examine CN V? > //See objective 1//

__Case 6: The Forgetful Shipper__ Loss of innervation to Lateral rectus due to retraction of CN VI during neuro surgery

__Case 7: The Cross-eyed Quarterback__ Internuclear Ophthalmoplegia: Lesion of medial longitudinal fasciculus prevents adduction of eye opposite to direction of gaze. Seen in multiple sclerosis, pontine infarcts, etc.