----start----- more neuro stuff dr vite?? clinical evaluation of animals with brain disease the cranial nerve exam you already heard about basic neuro exam and PNS; today we'll discuss the CN exam. remember - this isn't much different from the PNS exam; now we're moving into the area of peripheral nerves that come directly from the brain, is all. We've had a lot of neuroanatomy before. it's important to know from the standpoint of neurologists that you do not need to know the name and location of every CN nucleus in order to be a veterinarian, but you need some neuroanatomy. here is what you need to know: 1. when talking about brain, split into three parts a) cerebrum, cerebral hemispheres: what makes you you, helps you pass or fail a test, gives you emotions b) brainstem: diencephalon, midbrain, and pons/medulla. this is an extension of the spinal cord cranially. (note the pituitary gland beneath the diencephalon) c) cerebellum: fine motor ability, playing piano, typing, knitting. coordinates activity if you know those three anatomical parts, you're halfway there. one more step: functional separation of parts: the diencephalon (relay center for higher functions) is glommed with the cerebrum functionally the midbrain and pons/medulla are the functional brainstem the cerebellum is still the cerebellum :) now. there are 12 cranial nerves and you have to memorize them: OOOTTAFAGVAH, right? olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, auditory/vestibulocochlear, glossopharyngeal, vagus, accessory, hypoglossal all cranial nerves originate at the level of the brain stem except for CN I the olfactory nerve. all act like a network of electrical wires; all exit the skull ventrally and criss cross the head and select body parts CN I: olfactory nerve function: smell signs of dysfunction: may be unobserved; may lose ability to follow scent (working dogs, drug dogs, etc) testing: response to food, alcohol, cloves - don't use bleach or ammonia, those will irritate nose lining and affect the trigeminal; electro-olfactogram associated with old part of brain - rhinencephalon - not brainstem. CN II: optic nerve function: vision, sensory portion of PLR (pupillary light response) clinical signs of dysfunction: blindness, mydriasis (based on where lesion is - if bilateral and in certain spot see mydriasis, dilation of pupil) testing: menace response, obstacle course, visual placing, ERG or VEP (electrical tests of retina or higher centers) video: menace response - lightly move hand toward dog face, watch for blink - be careful not to move enough air to irritate the cornea and cause blink. can throw cotton ball on floor and see if dog sees it and chases it. placing response - approach table, see if dog places feet on the table. dogs and cats who are blind walk a little funny - this cat runs into things and has almost a dysmetric gait, walking with a long stride, as if reaching forward to see what is in front of him. this is typical of blind animals. also we have to understand a little bit about what the retina looks like - remember the optic disk is in the middle, vessels coming off, bright part is the tapetum lucidum; if there is disease, you may see retinal hemorrhages (associated with hypertension, other) which can cause blindness; effusions - may lift retina away from eye surface, looks like water drops, bullous lesions. visual pathway: light hits retina. optic nerve carries electrical impulse to optic chiasm. impulse crosses over to the contralateral optic tract (white matter). synapse at thalamus in the lateral geniculate nucleus; then carried by optic radiations to the visual cortex (occipital cortex). if you destroy left retina, left eye is blind. if you destroy visual cortex on right side, left eye is blind. once you reach thalamus, lesions produce contralateral blindness. remember that. also remember the menace response - a good way to see if one or two eyes are blind. if you get no menace response in left eye, you could have any part of the optic system damaged. could be a blind eye; could have a defect in the facial nerve causing inability to blink; could have a demented animal who doesn't percieve this as a menacing gesture; puppies/kittens do not develop menace response until 12 weeks of age. also, output from occipital cortex could be damaged - goes via cerebellum, cerebellar disease can prevent blink in response to menace response. bilateral mydriasis is produced by disease in optic chiasm CN III: oculomotor nerve function: constricts pupil; moves the globe of the eye; elevates the eyelid clinical signs of dysfunction: dilated, nonresponsive pupil; ventrolateral strabismus; ptosis (droopy lid) testing: PLR, physiological nystagmus, observing position of eye for strabismus (abnormal eye position at rest), pilocarpine response testing which will let the pupil constrict if it can. sometimes muscles are stuck and it can't. slide: dog as seen from the end of his own nose. remember if you shine light into one eye, both pupils should constrict. video: cat showing physiological nystagmus while being spun around in a chair. as you move the head the eyes move with slow phase, quick phase, slow, quick, etc. it's important also that the animal can look around the room by itself - that it has volitional control. hold head still while waving piece of food around and you will see that the eyes move to follow the food. with oculomotor nerve paralysis, won't be able to move the eye medially. as you rotate the head, the eyes won't ever move medially. pathway of PLR: light hits retina travels down optic nerve crosses in optic chiasm goes down contralateral optic tract then jumps off tract goes to pretectile, to midbrain, shoots back up to eye to cause constriction of the pupils. this bypasses the visual cortex. so where in this system do lesions cause blindness and loss of PLR? anywhere from optic tract forward. this dog has normal left PLR. he has no right PLR when left eye is covered. so right eye's pupil *can* constrict if light is perceived by the left eye. but when left eye is covered, right eye doesn't percieve light, so there is no reflex. this eye, then, must also be blind. damage must be in retina, optic nerve, or optic chiasm (not optic tract??) CN IV: trochlear nerve function: rotates dorsal part of the globe medially signs of dysfunction: rotational strabismus - but you can't really tell in animals with round pupils like dogs and people, but in cats or cattle with different shapes to their pupils you can see it. testing: physiologic nystagmus, observation of eye or retina to tell if it is in a normal position. this nerve comes off dorsally from midbrain then crosses. CN VI: abducent nerve function: moves globe laterally, retracts the globe signs of dysfunction: strabismus (convergent, crosseyed), inability to retract globe - important for testing. testing: physiologic nystagmus, observation of eye, globe retraction LR6, DO4 eh? comes off medulla about midway. good test question: what three nerves are responsible for eye position? III, IV, VI. damage to those produces strabismus. eye looking ventrolaterally: damage to III eye looking rotationally strabismoid: damage to IV eyes with convergent strabismus: damage to VI sympathetic innervation to the eye: remember CN III constricts the eye sympathetic innervation to the eye or to the head causes pupillary dilation (as in fear response, etc). the clinical signs of dysfunction are horner's syndrome: miosis, ptosis (drooping lid), enophthalmosis (sunken eye). testing: sympathomimetic drugs - use epinephrine, pseudephedrine, something in the eye. see if pupil dilates. the pathway is: sympathetic nerves originate in thoracolumbar cord - the efferent comes out by sympathetic chain ganglia. remember home of autonomic nervous system is the hypothalamus - where emotion, sympathetic tone come from. so your nerves start there, go through brainstem, cord - exit at T1-T3, then goes up through vagosympathetic trunk along lateral neck, with synapse at cranial cervial ganglia, then runs through the tympanic bulla, and up to the eye. this pathway is important for your board exam - they want to know what 3 lesions most commonly cause horner's syndrome. what are they? 1. spinal cord lesion at T1-T3, brachial plexus disease, disc disease, etc. 2. mediastinal masses 3. tympanic bulla disease (middle ear disease) (guttural pouch in horse) remember sympathetic tone to whole face is affected, so the ipsilateral side of the face will feel warmer - loss of sympathetic tone causes vasodilation and warmth of skin. (due to loss of sympathetic vasoconstriction) CN V: trigeminal nerve function: sensation over the face, motor to muscles of mastication signs of dysfunction: loss of sensation over the face, inability to close mouth testing: corneal reflex, palpebral blink reflex, stimulation of face, muscle palpation/jaw tone, electromyography video: testing trigeminal nerve. touching medial and lateral canthus. there are three main branches of the trigeminal nerve - maxillary, ophthalmic and mandibular. note that if there is a motor response that also tests facial nerve. with disease of trigeminal often dog can not close his mouth - it just hangs open - can be due to trigeminal neuritis which is self limiting, possible virus, goes away in 2-3 weeks. CN VII: facial nerve function: motor to muscles of facial expression, sensory to palate and tongue, motor to some salivary and lacrimal glands signs of dysfunction: inability to blink, facial drooping, deviation of nose, tragic facial expression testing: palpebral and corneal blink reflex, lip withdrawal, schirmer tear test. dog with facial nerve palsy - face droops, he drools, he can't blink on that side, whole side of face is droopy. video: tragic expression - can't close mouth, withdraw lip, feel sensation over face or nose, or blink. he's staring with mouth hanging open. trigeminal and facial nerves are affected. this is that polyradicular (sp) neuritis. came on rapidly in this case as is usual with this inflammatory disease. ---break--- T/Th 5-6 Vite office hours video: dog with head tilt to left, severe muscle atrophy on left side - masticatory, masseter and temporalis - unilateral trigeminal nerve disease. another thing to know that you must know is that when you look at animals with dropped jaws, do not shove your hand down their throats with no glove on, b/c rabies is a differential diagnosis for this. another thing that was asked during break was how come w/CN disease or facial nerve disease you do not often have a dry eye? the reason is the location of the lesion. most facial n. dz causes inability to move muscles but is distal to the branch that influences lacrimal apparatus - that is a very proximal piece. so most dogs with facial n. paralysis have adequate tear production and can "blink" with third eyelid. if there is dry eye, consider a lesion right up near the brain. CN VIII: vestibulocochlear function: hearing and equilibrium clinical signs of dysfunction: deafness, loss of balance, ataxia, head tilt, falling/rolling to one side, nystagmus, strabismus testing: behavioral for hearing - call dog, see if he comes - not good for unilateral though, BAER (brainstem auditory evoked response - electrical test for unilateral disease), physiological nystagmus, postrotatory nystagmus, vestibular righting. so even though III, IV, VI can cause strabismus, VIII coordinates how eyes move. remember - VIII tells your head which way is "up" and so your eyes and body move with respect to your head, to keep you in position and keep your visual field smooth. you need to know about this nerve b/c there are a lot of problems with it. unilateral lesion in cochlear nerve produces unilateral deafness. lesion in vestibular portion of nerve produces ataxia, head tilt toward side of lesion, rolling toward side of lesion, etc. cochlea, semicircular canals...brainstem...afferent inputs then control where head and eye position and body position will be - we call this balance. balance is controlled not only by vestibular system but also vision and feeling things around you, proprioception. you may feel off balance walking around in dark room. video: dr washabau spinning around then walking in a straight line with eyes open. now blindfolded and spinning around - can't walk in a straight line anymore. this was due to loss of vision. vision, proprioception, vestibular apparatus - loss of one results in loss of balance. video: dog showing us normal eye movements associated with head motion - eyes move with respect to position of head, coordinated by vestibular apparatus. dog showing us normal leg movement as he's pushed to the side - also in response to vestibular input. the spinning cat again - physiologic nystagmus - if this cat couldn't do this, it wouldn't have the "saccade" - the regular beat like motions of the eyes. (what is that word?) - this has a fast phase and a slow phase. slow to one side, then quick, the direction your are turning in has quick phase of saccade. the postrotatory nystagmus is due to inertia - usually four or five extra beats due to inertia of fluid in semicircular canals. dog showing left sided ventral strabismus - eye droop associated with left sided lesion. he has a bend - his whole body deviates to left. he can't appropriately respond when pushed to left, and he falls over. this dog has postrotatory nystagmus that goes on for too long - that's also abnormal. this bunny also has abnormal postrotatory nystagmus on one side. the other side is fine. only has unilateral vestibular disease. this cat has resting nystagmus. fast phase is to the left - usually away from side of lesion, so probably has lesion on right. remember - generally, head tilt is toward the side of the lesion; you fall and roll toward affected side; you have nystagmus at rest with fast phase going away from side of lesion. slow phase is toward the lesion. strabismus - affected eye is on the side of the lesion. left sided disease gives left sided eye droop. this is in most cases. there are some exceptions. video; dog with right head tilt, ataxia and falling to the right side. right eye has ventral strabismus. nystagmus with fast phase to left. lesion is on the right side. vestibulocochlear disease occurs in ear or centrally. sometimes signs are more subtle - just a mild head tilt. can accentuate signs by blindfolding the dog. now the head tilt is worse, and the dog veers to the left side more when walking. could also put into spacecraft and take away proprioception but that would be rather extreme. other examples of important things - cochlea and semicircular canals have receptors for vestibular balance and hearing, in the inner ear, in the petrous temporal bone - hardest bone in body. when you look in the ear you see the eardrum - from pinna to drum is outer ear. opposite side of eardrum: hammer, stapes, and other bone that starts with A within the bulla - this is middle ear. then there is the round window. on the other side of that is inner ear. you have to have inner ear disease to have signs of vestibular dysfunction. but running through the bulla are two important nerves - facial nerve and sympathetic nerve - so if you see horner's syndrome, facial nerve paralysis, and vestibular dysfunction, disease is probably in middle and inner ear on that side. that's important b/c you could also get central vestibular dysfunction - medullary disease - lateral vestibular nucleus - wouldn't see facial nerve dysfunction with that. also, most common cause of disease at ear level is ear infection - can be treated. if you have a brainstem lesion, probably a tumor or encephalitis with much worse prognosis. vestibular dysfunction: CNS (medullary) or PNS disease (inner ear disease) loss of balance, head tilt, falling/rolling, nystagmus - see those with both but nystagmus with PNS disease is only horizontal or rotary. vertical or positional nystagmus is only seen with central disease. horizontal/rotary can also occur with central dz. strabismus occurs with both types horner's syndrome point to peripheral disease, not present with central other cranial nerve deficits: V through XII possible with central dz; VII could be peripheral disease cerebellar signs, mental depression, hemiparesis with ipsilateral postural defects all point toward central disease and are not present in peripheral disease. we see more vestibular dz in summer, b/c we see more ear dz then. CN IX: glossopharyngeal nerve function: motor to muscles of pharynx and palate; innervation of zygomatic and parotid salivary gland* (common board question); taste sensation to posterior 1/3 of tongue (facial to anterior 2/3) signs of dysfunction: difficulty swallowing testing: gag reflex, carotid sinus pressure video - gag testing - shouldn't be able to pull on epiglottis, that's not normal, should gag, pull away. carotid sinus pressure - should slow your heart CN X: vagus nerve function: normal swallowing, laryngeal function, parasympathetic innervation to heart signs of dysfunction: difficulty swallowing, regurgitation, altered vocalization, laryngeal paralysis testing: gag reflex, laryngeal reflex, oculocardiac reflex (pushing on eyes slows heart) remember the sympathetic nerve travels cranially along with the vagus. CN XI: spinal accessory nerve function: helps to swing the forelimb foward - not essential signs of dysfunction: atrophy of trapesius, sternocephalic, brachiocephalic mm tests: palpation, EMG CN XII: hypoglossal nerve function: innervation of tongue (motor i assume) signs of dysfunction: difficulty prehending and swallowing food, tongue deviates toward the injured side testing: observation of tongue, lack of tongue retraction what to do when presented with signs of CN dysfunction? 1. perform a full neuro exam 2. list dysfunctions which are (is) present: eg, paralysis of V, VII, and VIII on the left 3. localize the lesion: eg, suggests left brainstem lesion/mass 4. generate a ddx list: degenerative, anomalous, metabolic, neoplastic*, infectious, inflammatory, immune mediated, infarct, idiopathic *, trauma, toxin. note we seem some metabolic problems causing CN signs (hypothyroidism), mostly neoplastic, infectious, inflammatory. sometimes trauma to the head. toxins - the classic is metronidazole intoxication causing central vestibular signs. 5. perform tests to confirm or rule out ddxs. for the first 100 neurologically normal dogs you see, do a neuro exam! learn what normal is. ----end-----