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Lecture 7&8,14&15: Lesion Localization 1-4 Understand how to perform a neurologic exam Observation Behavior changes: pacing, head pressing, circling, aggressive, blind, obsessive, incontinence, distant, seizures Due to a forebrain lesion Head pressing: red nucleus within the midbrain is the...

Lecture 7&8,14&15: Lesion Localization 1-4 Understand how to perform a neurologic exam Observation Behavior changes: pacing, head pressing, circling, aggressive, blind, obsessive, incontinence, distant, seizures Due to a forebrain lesion Head pressing: red nucleus within the midbrain is the main gait generator, with a forebrain lesion, the inhibitory effects of the forebrain are no longer present on the red nucleus (disinhibition), red nucleus takes over and causes animal to walk. Lack of higher cognition from the forebrain, so when animal gets to the wall, it does not know what to do and head presses/continues to go Circling: animal with forebrain lesion will circle towards the side of the lesion because of hemineglect Mentation: level of conscious a patient is Obtunded: abnormal response to stimulus and not fully aroused Can be secondary to diffuse forebrain lesion or from a brainstem lesion Stuporous: patient only responsive to strong or noxious stimulus Secondary to a brainstem lesion affecting the ARAS Comatose: patient has a heartbeat, may or may not be breathing, and is not responsive to any stimulus Secondary to a brainstem lesion affecting the ARAS, *forebrain lesions can cause stupor or comatose but only if they affect the brainstem (herniation) Ascending reticular activating system is responsible for keeping a patient alert and is located in the brainstem Have to rule out systemic disease causing animal to be lethargic Gait Ataxia: without order Proprioceptive (spinal, sensory) ataxia: cross limbs, scuff and knuckle paws, often UMN component, paresis Vestibular: patients drift towards one side, usually head tilt and nystagmus, secondary to damage to cerebellum or vestibular system Cerebellar: dysmetria, hypermetria, secondary to damage to cerebellum Paresis: difficulty initiating movement, often used synonymously with weakness Paraparesis: T3-L3 or L4-S3 Tetraparesis: C1-C5 or C6-T2 or diffuse lower motor neuron If reflexes absent in all limbs: diffuse lower motor neuron If reflexes absent in thoracic limbs only: C6-T2 If reflexes present in all limbs: C1-C5 Paralysis/plegia: absence of movement Ambulatory vs non ambulatory: able to take 10 unassisted steps Have to be ambulatory to be ataxic Tetra/quadra: all four limbs Para: pelvic limbs only Hemi: only one side of the body Mono: only one limb Lameness vs ataxia Orthopedic disease is more common, more regular/predictable, and will have pain localized to limb Ataxic patients usually have other neurological deficits When describing gait, ambulatory? Paretic or plegic? Ataxia/type? What limbs? Posture Decerebrate: patient is rigid in all limbs, often with opisthotonus, generally stuporous to comatose Lesion in the brainstem (midbrain) Decerebellate: patient is rigid in the thoracic limbs, may have opisthotonus, but has flexed pelvic limbs, generally alert to obtunded Lesion in the cerebellum or cerebellar peduncles Head turn: head is no longer along the longitudinal axis Lesion is in forebrain Head tilt: head is no longer level along the horizontal axis Lesion is in vestibular system Torticollis: flexion of neck/malformation of cervical vertebrae, contracture/flexion of cervical muscles; hard to differentiate from head turn, but is rare Opisthotonus: head in dorsal extension, star gazing Lesion is intracranial or cranial cervical, not helpful for localization Schiff sherrington: thoracic limbs have increased extensor tone (spasticity), pelvic limbs are paretic to plegic Lesion is T3-L3 myelopathy Differentiate from decerebtrate/decerebellate by getting animal up, can walk with front legs normally and no sign of brainstem or cerebellar disease Risus sardonicus: facial contracture, pulls muscles back so much animals can barely see, caused by tetanus Spasticity: secondary to upper motor neuron lesion except in cases of Schiff sherrington If all 4 limbs are spastic: C1-C5 myelopathy If pelvic limbs are spastic: T3-L3 lesion Flaccid: secondary to lower motor neuron lesion, can be diffuse, or at the intumescence of the spinal cord Neck guarded: looking down, secondary to cervical pain Kyphosis: arched back, secondary to thoracolumbar pain, abdominal pain, or malformation Hands on (see below) Tools: surface with traction, plexor, hemostats, transilluminator, fundic exam lens, cotton ball Understand terminology related to the neurologic exam Central nervous system: brain and spinal cord Peripheral nervous system: nerves and muscles Intumescence: widening of the spinal cord where the nerves come out Decussation: everything in the forebrain crosses over, before going to the rest of the body (lesion on right side causes signs on contralateral side) Brainstem and spinal cord are ipsilateral (lesion on right side causes signs on same side) Encephalopathy: lesion to the brain Myelopathy: lesion to the spinal cord Lesions to PNS: radiculopathy, neuropathy, myelinopathy, junctionopathy, myopathy Autonomic nervous system: originates in the hypothalamus, ventral part of the diencephalon Sympathetic NS: norepinephrine is main neurotransmitter, effector organ receptors are alpha or beta Nerves arise from C8-L4 Parasympathetic NS: acetylcholine is main neurotransmitter, effector organ receptors are muscarinic (PNS) or nicotinic (CNS) Nerves arise from cranial nerves III, VII, IX, X, and sacral spinal cord (S1-S3) Horner’s syndrome: lack of sympathetic innervation to head and neck Lesion locations: hypothalamus, cervical myelopathy, cranial thoracic cavity, neck trauma, middle ear/guttural pouch Horses: sweating occurs in neck above lesion Upper motor neuron: cells that arise from the forebrain, brainstem, or cerebellum Lower motor neuron: cells that arise from spinal cord segments Ventral nerve roots are formed by the axons of the LMN Nerve roots combine with other nerve roots to form named nerves Spinal cord segments vs vertebrae 8 cervical spinal cord segments and only 7 cervical vertebrae Lesion localization corresponds to spinal cord segment/nerve root In cervical region, nerve root exits cranial to respective vertebrae In thoracic and cranial lumbar regions, spinal cord segment lines up with vertebrae In caudal lumbar and sacral regions, spinal cord segments are cranial to vertebrae, but nerve roots exit caudal to numbered vertebrae (cauda equina) Hemineglect: animal will ignore one side of their world because it no longer exists, because of decussation, will only acknowledge world to the side of the lesion Nystagmus: involuntary side to side or circular motion of the eyes Dysmetria: inability to control the distance, speed, and range of motion necessary to perform smoothly coordinated movements Hypermetria: overflexion and overextension of the limb Localize neurologic deficits to specific neuroanatomic regions CNS vs PNS Lesions within the CNS often have mixed motor and sensory (proprioception and/order nociception) deficits Lesions to PNS are often sensory, or more commonly, motor Ex: cat with diffuse weakness in all legs but no proprioceptive deficits most likely has a lesion in the PNS, while a cat with diffuse weakness in all legs with severe proprioceptive deficits most likely has a CNS lesion Upper motor neuron vs lower motor neuron: assess reflexes and tone of limbs Reflexes: do not involve brain Lower motor neurons are spastic/hyperexcitable in abscense of upper motor neuron influence Upper motor neuron lesion Normal to increased reflexes and tone in the affected legs Disuse atrophy can be seen with UMN lesions, chronic, mild atrophy, takes days to weeks to develop Lower motor neuron lesion Decreased to absent reflexes and tone in affected legs Neurogenic atrophy, acute and severe C1-C5 lesion: upper motor neuron inj ury in all limbs (normal to increased tone/reflexes) C6-T2 lesion: lower motor neuron signs thoracic, upper motor neuron pelvic limbs T3-L3 lesion: thoracic limbs are normal with the exception of schiff sherrington, upper motor neuron pelvic L4-S3: thoracic limbs are normal, decreased to absent pelvic Intracranial Forebrain Cerebrum (telencephalon) Thalamus (diencephalon) Cerebellum (dorsal metencephalon) Brainstem Midbrain (mesencephalon) Pons (ventral metencephalon) Medulla (myelencephalon) Vestibular system Central: cerebellum, myelencephalon Peripheral: vestibular apparatus and CNVIII Spinal cord C1-C5: cranial cervical spinal cord C6-T2: cervicothoracic intumescence T3-L3: thoracolumbar L4-S3: lumbosacral intumescence Understand what the overall parts of the nervous system are that a lesion may be localized to and the typical neurologic signs seen with disease in those regions Intracranial Forebrain Behavior changes (head pressing, circling) Mentation changes (obtunded) Seizures Narcolepsy Head turn Opisthotonus Abnormal paw placement Mildly delayed hopping Cerebellum Ataxia (cerebellar and vestibular) Head tilt (vestibular) Decerebellate (cerebellum or cerebellar peduncles) Opisthotonus Absent hopping Brainstem Mentation changes (obtunded, comatose, stupor) Decerebrate (midbrain) Opisthotonus Abnormal paw placement Delayed to absent hopping/wheelbarrowing Vestibular system Ataxia (vestibular) Head tilt Opisthotonus No extensor postural thrust Spinal cord C1-C5 Tetraparesis with reflexes present in all limbs Opisthotonus Spasticity in all 4 limbs Respiratory depression (phrenic nerve from C5-7) C6-T2 Tetraparesis with reflexes absent reflexes in thoracic limb Horner syndrome (sympathetic nerves exit caudal cervical spine) Nerve root signature (lift leg when standing, abnormal pain sensation) Absent cutaneous trunci Absent withdrawal reflex in thoracic limb, usually bilateral T3-L3 Paraparesis Schiff Sherington Spasticity in pelvic limbs Spinal shock Cutaneous trunci cutoff L4-S3 Paraparesis Abnormal anal tone Flaccid tail L4-S1: absent withdrawal reflex in pelvic limb, usually bilateral L4-L6: absent patellar reflex, usually bilateral Sacral: absent perineal All spinal cord Abnormal paw placement Delayed to absent hopping Peripheral nervous system (motor unit disease) Decreased to absent reflexes and tone Tetraparesis Abnormal paw placement Absent hopping/wheelbarrowing/extensor postural thrust Absent withdrawal reflex, usually unilateral Absent myotatic reflexes, usually unilateral Assess severity of neurologic deficits and the implications to prognosis Modified glasgow coma scale: can help determine prognosis (grave, guarded, good) Discuss the hands on portion of the neurological examination and identify neurologic deficits (vs normal responses) Cranial nerves: graded 0 (absent), 1 (decreased), and 2 (normal) Olfactory I Typically not assessed because difficult to do Avoid irritating substances like alcohol because that triggers nociceptors and CN V Hide food under cups, but animals may be nervous and not willing to do behavior If worried about obstruction, put cotton ball by nose to detect air flow Optic II Retina → axons from rods and cones form optic nerve → may or may not cross at optic chiasm → formation of optic tract → fibers synapse on lateral geniculate nucleus (vision relay center in thalamus) → ascending projections to the occipital cortex through optic radiations Communication between frontal cortex and occipital lobe allows for visual recognition and behavior responses Menace response (CN II and CN VII): learned response, not a reflex, most learn by 12 weeks of age Afferent pathway: same as vision (CN II) Efferent pathway: motor cortex → pons synapses in pontine nucleus → cerebellum another synapse → CN VII nucleus → orbicularis oculi muscle to cause the eyelid to blink Do not assume animal is blind if only sign is no menace (can be CN VII) Hand moves quickly towards patients eye, stop before touching hair Cover one eye to assess each eye individually Watching patient navigate unfamiliar environment Blindfold one eye at a time Table test: with eyes open, lift animal close to edge of table and see if they lift paws before hitting edge of table (with eyes closed tests proprioception) Cotton ball test: throw cotton ball into field of vision and look for response, does not make sound when hitting ground Pupillary light reflex (CN II and CN III) Direct: look at eye shining light on, should constrict Consensual: look at other eye not shining light on, should also constrict Pathway: optic nerve → optic chiasm → optic tract → through thalamus → pretectal nucleus in midbrain → decussates → parasympathetic nucleus of CN III → pupillary constrictor muscle Not all fibers decussate again, causes consensual changes No direct or consensual response → optic nerve lesion on the same side as eye you shined the light Direct response, but no consensual response → CN III lesion (opposite side) Horner syndrome (lack of sympathetic innervation) Miosis: small/constricted pupil Ptosis: drooping of upper eyelid Enophthalmos: sunken eye, causes protrusion of third eyelid Vasodilation Anisocoria: different pupil sizes Determine which one is normal (differentiate horner syndrome (miosis) from CN II or III lesion (mydriasis)) If in light, turn off lights → if miotic pupil is abnormal it will become more apparent and will not dilate as much If in dark, turn on lights → if mydriatic pupil is abnormal it will not change Dazzle reflex: similar to PLR, but bright light is introduced very quickly to the eye Involuntary aversion response (blink, third eyelid protrusion, head move) Fundic exam: CN II is the only nerve that can be visualized Sometimes eye must be dilated to perform a thorough fundic exam, should be done after PLR is assessed Oculomotor III, Trochlear IV, and Abducent VI Oculomotor nerve from midbrain Innervates dorsal, ventral, and medial rectus, ventral oblique, and pupillary sphincter Lesion = ventrolateral strabismus: ventral because of gravity, lateral because lack of innervation from medial rectus Will also have mydriasis because no innervation to pupillary sphincter Trochlear nerve from dorsal midbrain Innervates dorsal oblique Lesion = rotational strabismus Can only tell in goats with horizontal pupils and cats with vertical pupils Abducent nerve from medulla Innervates lateral rectus and retractor bulbi Lesion = medial strabismus (cross eyed) Can sometimes tell retractor bulbi has deficits when doing menace or palpebral reflex If CN VII paralysis, can tell abducent is still working because 3rd eyelid will elevate when doing palpebral reflex Trigeminal V Comes from the pons 3 branches that are sensory to the face Ophthalmic: medial canthus, cornea, medial nasal philtrum Maxillary: lateral canthus, maxilla Mandibular: mandible Only mandibular branch is motor to muscles of mastication Supplies temporalis, masseter, and digastricus which close the mouth and pterygoid which opens the mouth Both branches of mandibular nerve affected: dropped jaw Assess sensation to the face Palpebral reflex: no cortical input, just see if animal blinks when touch face Afferent: trigeminal nerve Medial canthus or cornea = ophthalmic Efferent: facial nerve Corneal reflex: same as palpebral but touch soft object to cornea Facial VII Originates from the medulla Motor to muscles of facial expression (blink) Sensory to inner ear pinna Parasympathetic for lacrimal/nasal gland secretions Assessing facial nerve Lack of menace or palpebral Facial nerve is efferent and other nerves are afferent, unlikely for both CN II and V to be affected at the same time, so if both menace and palpebral are decreased, it is likely facial Facial drooping (facial asymmetry, lift head up and look at lips) Lack of sensation to inner pinnae Neurogenic keratoconjunctivitis sicca (dry eye/nose) Vestibulocochlear VIII Originates from medulla Vestibular portion maintains posture and balance relative to the head, body, and limbs, detects acceleration and deceleration, coordinates eye movement Blind animal will still have normal eye position Vestibular deficit clinical signs Abnormal posture (head and limbs) Vestibular ataxia/incoordination Strabismus, usually lateral Nystagmus more common Assessing vestibular Evaluate posture Evaluate gait Oculocephalic reflex/physiologic nystagmus: normal fast pace of eye movement in the direction of head movement when the head is moved Evaluates VIII (sensory) and III, IV, VI (motor); does not assess vision! Assessing cochlear Animal generally has to be deaf in both ears Crude way to test for hearing is to clap loudly once, but animal may not care, so no response does not mean deaf More objective way to test is with brainstem auditory evoked response, electrodes with waves from cranial nerves Glossopharyngeal IX, Vagus X All originate from caudal medulla, nucleus ambiguus Innervate oropharynx, larynx, and esophagus Oropharynx Gag reflex Sensory: X Motor (cough): IX, X Animal usually licks after (tongue, XII) Swallowing Sensory: X Motor: shared by IX, X, and XII Larynx Recurrent laryngeal nerve (branch of vagus nerve) Accessory XI Spinal accessory is external branch of cranial nerve XI Supplies trapezius muscle, can rarely see atrophy Hypoglossal XII Most caudal, comes from medulla Assessing Inspect tongue for atrophy, asymmetry, or deviation Usually lick nose after gag reflex Watch patient drink water Proprioception: where limbs are in space, graded the same as cranial nerves Do paw placement and hopping on every animal Paw placement: flex foot so dorsal surface is on the floor, animal should return to normal position immediately Nerve from tip of toe to synapses at the brainstem, goes through thalamus to cerebrum Minimal strength required, but still needs some strength Pure cerebellar lesions do not affect Forebrain, brainstem, and spinal cord lesions can cause delayed to absent paw placement Hopping: one limb lifted off the ground, animal faces away from tester and is moved laterally, paw of limb on the ground should not cross midline and response should be quick and strong Synapse at various levels of the spinal cord, input from cerebellum, synapse in the thalamus Less input from forebrain Requires more strength Forebrain lesions can often have normal to delayed hopping, but absent paw placement Cerebellar lesions can have normal paw placement but absent hopping Brainstem and spinal cord lesions generally have delayed to absent hopping and paw placement Wheelbarrowing: done if paw placement and hopping do not reveal suspected deficit Lift animal at hips, and front limbs should move normally and easily Similar pathway to hopping Assess with head up and down Head up: proprioception tested, animal cannot compensate with vision Head down: strength is tested more than proprioception as head adds weight and they can compensate for proprioception with vision Extensor postural thrust: lift animal and support the thorax, lower pelvic limbs to the floor; animal should move limbs caudally in a walking movement Only performed in smaller animals because animal must become non weight bearing in the pelvic limbs Pathway similar to hopping Hemiwalking/hemistanding: lift thoracic and pelvic limb on one side so all weight is on opposite limbs, evaluate forward and lateral walking Rarely performed in larger animals; could hurt them, also should know proprioceptive deficits before this point (sometimes can pick up subtle lesions of forebrain) Should be roughly equal steps Paw placement/hopping pathway Table test: rarely done, difficult to interpret findings, some animals do not care Eyes covered to assess proprioception, animals should lift foot once it touches table Segmental spinal cord reflexes Must be other neurological abnormalities for reflexes to be reliable Ex: if animals has absent withdrawal reflex, then they should have paresis in that limb as well Generalized depression of reflexes may be seen in polyneuropathies or in abnormalities of the NMJ (botulism, tick paralysis) Animals that are tense and keep limbs in extension commonly have depressed or absent reflexes Graded 0-4: absent, weak, normal, exaggerated, and clonus Clonus: repetitive flexion and extension of the joint in response to a single stimulus, seen with chronic (weeks to months) loss of descending inhibitory pathways Motor response is what is evaluated, but afferent portion of reflex also has to be intact for a response Thoracic limb: brachial plexus, as move caudally in the intumescence, nerves go more distally in the limb Withdrawal or flexor** only reliable thoracic limb Animal in lateral recumbency, noxious stimulus applied to the foot, normal response is flexion of the entire limb Evaluate each joint (shoulder cranial intumescence, elbow mid, carpus caudal) Polysynaptic reflex: multiple synapses and interneurons (vs monosynaptic patellar reflex) Limb should be slightly extended and stimuli should be applied to dorsal (radial nerve) and ventral (ulnar nerve) sides Absence or depression, usually unilateral = peripheral nerve lesion Absence or depression, usually bilateral = C6-T1 lesion Crossed extensor and conscious perception of pain are also done at this time Myotatic reflexes: muscle contracts in direct response to stretch, not reliable in thoracic limb (absent or decreased should not be interpreted as abnormal) Monosynaptic: no interneurons Evaluate top limbs when in lateral recumbency Biceps: musculocutaneous nerve (C6-C8) Index finger on biceps, strike finger with plexor Elbow of dog is slightly extended at start, response is slight flexion of elbow/movement of biceps skin Triceps: proximal radial nerve (C7-T1) Elbow in flexion, triceps is struck just proximal to the olecranon Response is slight extension of the elbow or visible contraction of the triceps Extensor carpi radialis: distal radial nerve (C7-T1) Flexion of elbow and carpus, strike extensor carpi radialis just distal to elbow Response is slight extension of the elbow Pelvic limb Withdrawal or flexor** reliable: mostly sciatic nerve Same as thoracic, but both medial and lateral digits should be tested in each limb Testing for flexion, not response (nociception) Deep pain of medial digit is femoral nerve, but sensory to the rest of the toes is sciatic Hamstring atrophy, crouched stance, dropped hock, flinging limb forward when walking also signs of sciatic nerve deficits Can be caused by a lesion anywhere from L4-S1 Hock flexion: tibial nerve (caudal intumescence) Stifle flexion: sciatic nerve (mid intumescence) Hip flexion: femoral nerve (cranial intumescence) Myotatic reflexes: muscle contracts in direct response to stretch Patellar** only reliable: femoral nerve (L4-L6) Monosynaptic pathway: patellar tendon, golgi tendon organ, afferent nerve and dorsal nerve root, L4-6 spinal cord segments, ventral nerve root and efferent nerve, NMJ, quadriceps Animal in lateral recumbency, limb is supported under the femur with the left hand, patellar ligament struck by plexor Response is single, quick extension of the stifle Sciatic: sciatic nerve (L6-S1) Hit sciatic notch between the ischiatic tuberosity and the greater trochanter Results in extension of hip and possibly stifle and tarsus Gastrocnemius: tibial nerve Gastrocnemius tendon is struck with plexor just dorsal to the tibial tarsal bone, can strike fingers on fabellas Response is extension of the hock, contraction of caudal thigh muscles may occur Cranial tibial: fibular nerve Struck just distal to the proximal end of the tibia Response is flexion of the hock Cutaneous trunci reflex Afferent is each cutaneous branch from various spinal cord segments (T3-L5) Obvious cut off point suggests spinal cord lesion slightly cranial to the level of the cutoff Efferent is lateral thoracic nerve (C8-T1), goes to cutaneous trunci muscle Start caudally by wings of ilium and work cranially until response occurs Normal response is bilateral contraction of the cutaneous trunci Helpful for narrowing down location of lesion, but never change localization based on it Perineal reflex** reliable: pudendal nerve Elicited by light stimulation of the perineum Normal reaction is contraction of the anal sphincter and flexion of the tail Absence = sacral spinal cord or pudendal nerve lesion (not graded, yes or no) Babinski reflex (extensor toe): extension of toes when handle of plexor strokes caudolateral surface from the hock to the digits Normally absent in adults but present in newborns (not graded, yes or no) Crossed extensor reflex: may be observed when flexor reflex is elicited, extension of limb opposite the stimulated limb Flexor reflex sensory fibers send collaterals to interneurons on the opposite side of the spinal cord, which excite extensor motor neurons Generally considered abnormal except when animal is standing (to support body weight) In normal recumbent animal, extension response is inhibited through descending pathways Crossed extensor reflexes result from lesion in ipsilateral descending pathways, sign of UMN disease, likely chronic (not graded, yes or no) Hyperpathia: something that could be painful with enough force, not helpful localization Hyperesthesia: something that should not be painful but is Nociception (deep pain): conscious behavioral response (head movement, vocalization) to squeezing toes Determines prognosis for paralyzed patients Bladder function Lesion to S1-S3: damage to pelvic and pudendal nerve (LMN) → decreased tone of detrusor muscle and urethral sphincter → incontinence Lesion cranial to S1: UMN lesion → increased tone of detrusor muscle and urethral sphincter → firm bladder, urinary retention

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