Neuro 13/14 PDF

Neuro 13/14 Cranial nerves - Some entirely sensory, some entirely motor, some both - 12 pairs that og from specific area of brain and innervate head or sometimes body. - Unique function(s) including special functions like taste, smell, hearing, balance, vision - Has motor, sensory or bot...

Neuro 13/14 Cranial nerves - Some entirely sensory, some entirely motor, some both - 12 pairs that og from specific area of brain and innervate head or sometimes body. - Unique function(s) including special functions like taste, smell, hearing, balance, vision - Has motor, sensory or both axons - Nerve cell bodies for somatic motor fibers in CN are found within nuclei in brian itself. Considered lower motor neurons with the nerve cell bodies in the CNS - Nerve cell bodies for the somatic sensory neurons (not special senses) are in ganglia outside the CNS. - CN nerves are considered part of the PNS and CNS (nuclei) Terminology is confusing… General somatic afferent = sensory, pain and temp to the face General somatic efferent = motor (muscles for chewing or facial movement) Special Somatic afferent = sensory fibres, vision, hearing, balance, has special afferent function Special Visceral Afferent = taste and smell General Visceral Efferent = motor fibers from the ANS (PARA) that innervate smooth muscle e.g., innervation of gut by vagus nerve Special Visceral efferent = innervates larynx, pharynx and part of the esopahgus to control swallowing and respiration But just know if they are motor, sensory or mixed and whether its Autonomic (Para) fibers CN I: Olfactory nerve Function: is sensory only, responsible for the conscious perception of smell. Anatomy: chemoreceptors in the nasal mucosa that detect odours and transmit sensory info to the axons in CN I. Receptors that bind to chemicals, different chemicals = smell perceived. The nucleus for this nerve is found in the olfactory bulb (in the The rhinencephalon) and anterior olfactory nucleus in the forebrain. Clinical exam: sense of smell difficult to evaluate, not really examined at OVC. Remember if a animal sniffs, it does not necessarily perceive odours. Examples: Anosmia -absent sense of smell, hyposmia- decreased sense in smell (humans after viral infections) CN II: Optic nerve Function: for sensory visual perception (VISION) and the sensory component of the pupillary light reflex. Anatomy: light entering the retina activates photoreceptors which generate AP, which are relayed via retinal ganglion cells which form the axons in the optic nerves. The optic nerves form each eye converge at the optic chiasm, there is some decussation, and the optic tracts are formed by the continuation of the axons. Optic nerve and retina are part of the CNS actually! Piece of brain evolved to make the eye. Tract outside of the brain. - Cell body of neurons in the retina: ganglion cells - Axons finish in both brainstem and thalamus - Conscious (response and vision pathway): lateral geniculate nuclei (80%) - used for Menace response - Subconscious (reflex pathway): pretectal nuclei (mesencephalon, aka midbrain that makes a part of brainstem 20%) - used in PLR So, 1. Retinal Ganglion cells → form optic nerve → leaves eye and goes to optic chiasm → some decussation → nerve fibres are now the optic tract → most to the fibres end in the LGN of the thalamus → info passed onto visual cortex Damage to optic nerve: - Before optic chiasm, blindness in the eye supplied by damaged optic nerve - Damage at optic chiasm, blindness partial (outside) in both eyes - Optic tract is damaged, partial blindness too Clinical exam used for CN II and III 1. The Pupillary Light Reflex (PLR) a) Direct PLR - Shine light into the eye and observe for pupillary constriction in the same eye - Abnormal result is lack of constriction. Also test oculomotor nerve (CN III) on the same side b) Indirect (Consensual) PLR: shine light into one eye, and observe the other eye for pupillary constriction. Abnormal result is lack of constriction. This also tests the oculomotor nerve CN III of the opposite side. Lesion at brainstem? - Might not see constriction, as pretectal nuclei (mesencephalon, aka midbrain that makes a part of brainstem) is used in this reflex pathway. Retina → optic nerve → optic chiasm → optic tract → pretectal area of midbrain → interneurons → EW nucleus or Para moto nuclei of CN III(oculomotor) on both sides of the brain → AP down a preganglionic PARA fiber in CN IIII → ciliary ganglion to synapse with a post ganglionic fiber→ goes to constrictor muscles of the iris Notes: - Bilateral events because of crossover events at the optic chiasm (II) and the pretectal area (interneurons to III) - Also bilateral SYM (autonomic) control of pupillary dilation from T1 to T2 spinal segments, however SYM response is not changed by light. PLR useless for SYM response Example lesions: 1. Lesion at left optic nerve CN II? No info being received, NO constriction on left and right side  2. Lesion at optic chiasm? Will still see constriction Clinical exam fro II and VII 2. The Menace Response - While covering one eye, make a threatening gesture at the uncovered eye, looking for a blink in response. And possibly an aversive head movement. - In order for the blink to be produced, the following structures must be intact: retina, CN II, LGN, path to/through visual cortex, cerebellum, CN ViII) - Response NOT a reflex because cortex is involved - Examples of clinical disease: blindness total or partial, observed by absence of MR and PLR Pathway: II in → processing at LGN of thalamus → processing at cortex and cerebellum → VII out Break the pathway down… Visual Pathway: CNII retina → optic nerve → optic chiasm → contralateral optic tract → LGN---> optic radiation → visual cortex Motor Pathway: visual cortex impulses→ motor cortex → facial motor nucleus → facial muscles around the eye e.g. orbicularis oculi and levator palpebrae muscles - Response is modified by the cerebellum, coordinating incoming sensory and outgoing motor response for a blink Lesion at cerebellum? Should also see other signs like cerebellar ataxia. CN III: oculomotor nerve Function: motor control of iris constrictor muscles (PARA, ANS - pupillary constriction). Somatic motor innervation (aka somatic nucleus) of some medial rectus and retractor bulbi muscle. Anatomy: originated from nuclei in the rostral (anterior) ventral area of the midbrain (there are 2 nuclei on each side, 1 for eye movement, 1 for iris constriction), Fibers that control the pupillary sphincter and ciliary muscles, og in the Edinger-Westphal nucleus Leave midbrain → along the way they separate to control different extraocular muscles → for PS and CM og in EWN and travel with oculomotor nerve Clinical exam: - Look at eye and PLR Damage to CN III motor part or nerve: - If nerve of somatic nucleus is damaged = ventrolateral strabismus results (down and out, side and downwards), ipsilateral damage (muscles nerves are damaged) Damage to CN III nerve or EW nucleus: - Abnormal PLR - an inappropriate lack of constriction of the pupil. Possible anisocoria Side note: horner’s syndrome can also cause anisocoria (nothing to do with CN III, still output, SYM issue) CN IV: trochlear nerve Function: motor innervation of the dorsal oblique muscle of the eye- this muscle helps to keep the visual world “steady” by counter-rotating the eye head tilts to the side. The horizon…rotation of the eye… Eye movements, motor. Anatomy: motor nucleus located caudally in the mesencephalon (midbrain), present on both sides. Clinical exam: difficult to diagnose in dogs (fundoscope?). In species with slit-like pupils, a dorsolateral rotation of the affected eye can be observed. - Mild dorsolateral strabismus - Abnormal movements of eyes when head is moved or gaze shifts lateral - Rotation of fundus via ophthalmoscope CN V: Trigeminal Nerve Function: motor and sensory components.  - Sensory portions innervate the face (pinnae, eyelids, cornea, oral cavity, mucosa of the nasal septum) - Motor innervates the muscles involved with mastication Anatomy: the nuclei (sensory and motor) are located/og in the pons. - Sensory component has 3 branches. 1. Ophthalmic branch - innervates the ocular region and the medial canthi 2. Maxillary branch - innervates the nasal region and lateral canthi 3. Mandibular branch - innervates the bucca area and ear - Sensory component has a large ganglion called the trigeminal or Gasserian ganglion which contains primary nerve cell bodies for the sensory component of the nerve - Motor fiber not connected to trigeminal ganglion Clinical exam for sensory portion: - Observe for blink response by checking palpebral reflex - Look for symmetrical response to stimulation of the nasal mucosa (use cotton bud to touch nasal mucosa on each side of nasal septum - maxillary branch). Palpebral reflex (test CN V and VII) - Stimulate the medial canthus (ophthalmic branch) and lateral canthus (maxillary branch) or skin over mandible (mandibular branch) and look for a blink (normal) - Ophthalmic = medial canthus - Maxillary = lateral canthus - Mandibular = ear or jaw Method: touch the medial canthus, the lateral canthus of the eye, and the skin near the external ear. Observe a reflex blink and possibly a withdrawal of the head. V in, VII out. Sensory portion of CN V sensory receptors on the skin of the face to branch of CN V(ophthalmic, maxillary and mandibular branches) → sensory nucleus of CN V(in the pons, trigeminal ganglion?) → impulse to the motor nucleus of VII (for the reflex) and to the sensory cortex (for the behavioural response) Motor due to CN VII (reflex blink only not head movement) After receiving the impulse from the sensory nucleus of CN V → motor nucleus of CN VII generates impulse that travel → motor component of CN VII to the muscles of the eyelid Damage to right CN V, touch right eye = no blink response in either side (no sensory input) Damage to right CN VII and touch right eye = no blink response in right eye, but blink in left Sensory loss: absent palpebral reflex, lack of sensation in face - Feel with V, close eyelid with VII Clinical exam for motor portion: - Check jaw tone Motor loss: masseter, temporalis muscle wasting, loss of jaw tone, long time = muscle atrophy CN VI: Abducens Nerve Function: MOTOR - innervates the lateral rectus and retractor bulbi muscles (also innervated bu oculomotor nerve) Anatomy: nucleus is located in the dorsal medulla (brainstem) Clinical exam: examine the position and movement of the eyes, look for the eye to be retracted, allowing the third eyelid to be extruded Example of disease - Medial strabismus and loss of lateral gaze - Inability to retract globe CN VII: facial nerve Functions: motor and sensory components. Motor branches innervate the facial muscles. Sensory branches innervate the palate and cranial two thirds of the tongue (tast, pain/proprioception). Also, PARA(ANS) innervation of glands (submandibular salivary, lacrimal) Anatomy: multiple specific nuclei are in medulla. Innervation to the muscles and glands, eyelids, lips, sensory fibers from tongue. More than one nucleus, all in brainstem. Clinical exam: - Observe facial asymmetry, droopy eyelids, lips, inability ot blink properly - Observe menace response and palpebral reflex: able to blink in response to a threatening gesture (also tests II) or touch of the facial skin (also tests V)  - Palpebral closure: brus finger across the palpebral commissure, observe how tightly the animal is able to close its eye. - Sensory and PARA aren’t really tested Lesion: facial paralysis CN VIII: Vestibulocochlear nerve Function: two branches. The cochlear, or auditory, nerve has sensory function in hearing. The vestibular nerve is involved in orienting the head and body. Anatomy: - Vestibular portion consists of the vestibular nerve and four vestibular nuclei in the brainstem(medulla). Responsible for the normal posture and coordination of the eye, head, neck trunk and limbs - Vestibular info is projected to CN 3,4,6 via the medial longitudinal fasciculus (MLF) and also to the cerebellum. Proprioception. - The cochlear nerve travels together with the vestibular portion to the medulla. Auditory - Vestibular receptors in inner hear, sense head movement and change in head position - Info transmitted to vestibular nuclei in medulla and cerebellum - Begins at the membranous labyrinth????? Clinical exam: 1. Oculocephalic reflex test - Tests the vestibular system - Tests for normal and physiological nystagmus - Move head laterally from side to side and observe symmetrical, coordinated eye movement (observe eye movements during and after the movement). - Known as Doll’s Eye Reflex - Normal nystagmus - Abnormal nystagmus = eyes move in a stationary animal, repeatedly back and forth, up and down, vertical or circles. Pathway: VIII (+II) in, III/IV/VI out Vestibulocochlear nerve (balance) and optic nerve (Vision) in Oculomotor nerve (eye movements, constriction), trochlear nerve (eye movements) and Abducens nerve (eye movements) out Sensory component: Primarily CN VII vestibulocochlear (some CN II) → vestibular input from semicircular canals in ear → vestibular nuclei in the medulla Relay component: Medial Longitudinal Fasciculus (MLF) MLF = tract in brainstem and SC which connects the vestibular nuclei with the nuclei of cranial nerves III, IV and VI. Coordinates vestibular proprioceptive info concerning the head and body with eye position so that the eyes can move appropriately and together Motor component: Motor nuclei of individual nerves that innervate extrinsic eye muscles, plus the nerves themselves: III/IV/VI Clinical exam continued: 2. Observe for vestibular = ataxia, stumbling, circling, head tilt (lesion on side of head tilt) 3. Hearing is not normally assed, noted in history as per o Lesion: head tilt, ataxia, circling, abnomal nystagmus CN IX: Glossopharyngeal nerve Function: motor and sensory. Motor innervation of the muscles of the pharynx. PARA (ANS, motor) innervation to the parotid Salivary glands. Sensory: tongue (caudal third), taste (caudal third), pharynx mucusa. Anatomy: its nucleic in the ventrolateral aspect of the medulla. Fibers run to pharynx and caudal tongue. Clinical exam: history of dysphagia, or regurg. Some Dr. Check GAG reflex (trauve to back of throat, but risk of getting bitten. CN X: Vagus nerve Function: motor and sensory. Innervation of the muscles of the pharynx, larynx, palate. Sense of taste (much overlaps with IX). Major function of the vagus is to supply PARA innervation to all the thoracic and abdominal vescaera and carry visceral sensory fibers from those tissues. Anatomy: largest nerve with multiple nucleic in medulla. Runs through vagosympathetic trunk to heart, lungs, viscera. Clinical exam: we don't really test it. But if needed I guess:  - GAG reflex - Oculocardiac reflex = pressure on eyeballs results in decreased HR Disease: dysphagia (difficulty swallowing), salvation (historical), regurg of undigested foods are potential signs. Chronic indigestion (vagus indigestion) in cattle particularly CN XI: Accessory nerve Function: motor. Innervation of muscles of neck like the trapezius muscle Anatomy: og from ventral roots of cervical segments and enters the skull through the foramen magnum before exiting through a foramen. Muscles innervated support then ck laterally along with the muscles innervated by C1-C4. Clinical exam: examine neck muscle atrophy or asymmetry. Examples of clinical disease: neck muscle atrophy- not often observed. CN XII: hypoglossal nerve Function: motor innervation of intrinsic and extrinsic muscles of the tongue Anatomy: originated in hypoglossal nucleus in medulla Clinical exam: observe the function and position of the tongue relative to the rest of the mouth. Examples of clinical disease: paralysis and atrophy of the tongue, uni or bilateral, sign of dysfunction. Lateral deviation of the tongue may be caused by damage to the nerve. Neuro 15 Using CN for neurological examinations - When the nerve OR their nucleus (nuclei in brain) is damages the function of the nerve is compromised - Or if it's part of reflex arc, reflex will be decreased or absent - Brain is also involved in consciousness, processing info to and from SC, cardiac and resp control, will see compromise of those function when the lesion is in the brain itself not the CN (PNS) Recall signs: Strabismus = CN III, IV, or VI damage Nystagmus = CN VIII Loss of tone = CN VII No PLR = CN II and III No menace response = CN II and VII Brain lesion? - Look at gait and mental status of the patient - Depressed and dull? ⇒ brain  - Behavioural change? ⇒ brain - Seizure? ⇒ brain - Multiple CN nerves affected ⇒ brain PNS CN lesion? - Mental status is normal, lesion outside of the brain - Single CN affected ? ⇒ not in brain