Neurolocalization

Vestibular system

** Three anatomical components: ** 1) Peripheral vestibular system (CN VIII in inner ear) 2) Central vestibular system (4 vestibular nuclei in rostral medulla) - receive info from IPSILATERAL CN VIII + Flocculonodular lobe - project IPSILATERAL: A) spinal cord: medial / lateral vestibular tracts = excitation ipsilayeral limb/neck extensors (to catch when falling) B) RAS / Medial longitudinal fasiculus MFL: to nuclei CN III, IV, VI = coordinates eye/head, movement; physiologic nystagmus C) V+ center (normally inhibit motion sickness), D) floc. lobe cerebellum (coordinate body/head movement - cerebellum TONES DOWN ipsilateral vestibular system) E) somatosensory center - consciousness of balance - in cortex so processed by contralateral side (e.g. yoga) 3) Flocculonodular lobe of cerebellum and caudal cerebellar peduncle - refer to neurophysiology cards for details Brain takes information from both sides and processes relative to each other • Increase in activity (firing rate) from one side could alternatively be considered a relative decrease in activity from the other side • Loss of activity from one side could alternatively be considered a relative increase in activity from the other unaffected side Need NON-vestibular signs to help localize b/w peripheral/central

Signs associated with cerebellar disease?

- Anisocoria = sign people miss the most; with deep cerebellar nuclei lesions (often asked on multiple choice) Other classics: - hypermetria (and hypometria) - absent menace - truncal sway - wide-based stance - head tilt if floculonodular lobe

Deciphering Vestibular Exam

1. Confirm vestibular disease by observing 4 Hallmark Signs 2. Determine peripheral or central A. Postural reaction deficits? i. If no, then lesion is peripheral** ii. If yes, then: - Are the postural reactions ipsilateral to the head tilt? ** If yes, then lesion is in central vestibular system affecting rostral medulla ** If no, then lesion is in the cerebellum, leading to paradoxical vestibular disease, and the lesion is ON THE SIDE OF THE POSTURAL REACTION DEFICITS

Neuroanatomic localizations

1.Spinal cord and spinal nerve localizations a. Spinal cord localizations (Myelopathies) i) C1-C5 ii) C6-T2 iii) T3-L3 iv) L4-caudal •L4-L6 (femoral) •L7-S1 (sciatic) •S1-S3 (pelvic, pudendal) b. Spinal nerve localizations i) Single nerve affected ii) Diffuse neuromuscular 2.Brain and cranial nerve localizations a. Brain localizations i) Prosencephalon ii) "Caudal fossa" + central vestibular iii) Cerebellum b. Cranial nerve localizations i) Single CN affected (ex. peripheral vestibular syndrome)

Sensory gait abnormalities - ataxia

3 types •General proprioceptive ataxia --> nonspecific •Vestibular ataxia --> localizes to the vestibular system •Cerebellar ataxia--> localizes to the cerebellum A note on lameness: Lameness can be orthopedic OR due to a nerve root signature (sciatica is an example of a nerve root signature). If you observe lameness, perform an orthopedic exam. If no abnormalities found, suspect nerve root signature.

Spinal cord functional anatomy

A lower motor neuron lesion implies a lesion affecting lower motor neurons •LMNs are the final common pathway to muscle innervation •Loss of LMN à decreased LMN activity = •LMN paresis or plegia •Decreased tone •Decreased/absent reflexes An upper motor neuron lesion implies a lesion affecting upper motor neurons •UMNs are generally inhibitory to the LMNs they synapse with •Loss of UMN à increased LMN activity = •UMN paresis or plegia •Increased tone "Hyperreflexia"/increased reflexes

Withdrawal reflex - thoracic limbs

C6-T2 All thoracic limb nerves All flexor muscles

Cutaneous trunci

C8-T1 Sensory : segmental spinal nerves (usually 2 vertebrae in front of cut off where lesion localizes) Motor: lateral thoracic nerve Cutaneous trunci m

Paradoxical vestibular disease

Central lesion affecting caudal cerebellar peduncle, cerebellar flocculonodular lobe** - INHIBITORY to vestibular tracts - Lose the inhibition = disinhibition Meanwhile, the unaffected side still has a functional cerebellum that is continuing to inhibit its side of the vestibular system Contralateral head tilt fast phase TOWARD lesion Postural reactions on OPPOSITE SIDE head tilt / circling*** but IPSILATERAL LESION

Polyneuropathy

DDX: - Metabolic polyneuropathy = DM, hypothyroidism, paraneoplastic - Inflammatory/Infectious: 1) Acute polyradiculoneuritis * acute ascending flaccid tetraparesis * ddx = NMJ diseases (tick paralysis, botulism, fulminant MG) 2) Protozoal polyradiculoneuritis = neospora >> toxo; both clindamycin 3) Idiopathic neuropathies - trigeminal, facial, vestibular

NMJ Disorders

DDX: 1) Tick paralysis = neurotoxin of female tick salivary glands; interfers with ACH release from pre-synatic terminal via Ca+-mediated mechanism - Dermacentor (US) - Ixodes (AUS) - 5-9 days post tick attachment - rapid ascending flaccid paresis to tetraplegia in 12-72 hours; uncommon CN deficitis except fiacial/asticatory weaknes, dysphonia 2) Botulism = acute diffuse LMN from exposure to neurotixns produced by C. bostulinum bacterium (gram + anaerobe ubiquitous); block release of ACH at pre-synaptic termainl in BOTH skeletal muscle + cholinergic autonmic synapsis - irreversibley binds SNARE proteins (docking synaptic ACH vesicles to presynaptic membranes to allow release of ACH) - ileus, tachy/bradycardia, mydriasis, urinary retention - CN = decreased palpebral reflex, mageasophagus, diminished PLR 3) Acquired MG = autoimmune disorder against nicotinic AChR on post-synaptic muscle terminal - generalized vs. focal vs. severe fulminant forms - fatiguable palpebral reflex is classic but not always present; otherwise exercise induced tetraparesis, megaesophagues - thymoma 4) Congenital MG = deficiency of AChR Not NMJ disease, but similar clinical signs: 1) Exercise-induced collapse of Labs = autosomal recessive protein dynamin 1 (DNM1) - fatigue, flaccid para/tetraparesis during/after strenuous activity - normal mental status - specific loss of patellar reflex during collapse episode - dynamin = maintains synaptic vesicle function during sustained neurotransmission

Horner Syndrome

Due to loss of sympathetic******* innervation of the eye Sympathetic innervation to eye: •Pupil dilation •Eyes positioned rostrally in orbit •Eyelids wide •Loss of sympathetic innervation to eye = Horner syndrome 1) Miosis 2) Enophthalmos 3) Ptosis 4) Elevation of 3rd eyelid First order neuron = UMN in the rostral brainstem --> travels down cervical spinal cord to synapse on 2nd order Second order neuron = preganglionic neurons; cell bodies in T1-T3 --> course up vagosympathetic trunk to synapse on 3rd order neurons Third order neuron = post-ganglionic neurons; in cranial cervical ganglion --> project to eye/adenxa Phenylephrine testing: mydriasis within 20 minutes indicates POST ganglionic lesion - quicker because of deinnerativon hypersensitiviy, body upregulates receptors when lack of neurotransmitter from post-ganglionic

** Four hallmark signs of vestibular disease **

EITHER peripheral or rostral medulla function 1) Head tilt - towards affected side (unopposed extensor neck muscles other side) 2) Vestibular ataxia - fall/circle towards affected side (other side extensors still working) 3) Spontaneous nystagmus - relative increase in activity from unaffected side, brain thinks head circling in this direction so fast phase away from lesion 4) Positional strabismus ipsilateral - eye passively falls on affected side

Postural Observation

Head tilt: eyes are not parallel to floor = Vestibular localization Head turn: entire head facing one direction* = Prosencephalon localization *Can sometimes affect entire body, leading to body turn called torticollis Wide-based: generally indicates issue with balance = Vestibular or cerebellum •Kyphosis: arched back, indicates back pain •Lordosis: sunken back •Low head carriage, indicates neck pain •Decerebrate rigidity = Severe brainstem lesions - Cerebrum is disconnected from brainstem •Decerebellate rigidity = Cerebellum severely affected •Schiff-Sherrington = Severe thoracolumbar spinal cord injury (usually T13-L1) •ASCENDING UMNs from PLs to TLs are lost --> loss of UMNs to TLs - front limbs stiff and side, hind limbs paralysis

Patellar Reflex

L4-L6 Femoral nerve Extensor mms

Withdrawal reflex - pelvic limbs

L6-S1 Sciatic nerve Flexor mms

4 year M outdoor mixed breed hound with acute onset of vomiting, progressive ascending weakness, bradycardia, increased respiratory effort, and collapse NE: Depressed mentation Flaccid tetraplegia Absent CP x 4 Decreased/asbsent reflexes x 4 with intact pain sensation Facial nerve paralysis and decreased gag reflex

Lesion localization = Generalized LMN Possible etiologies? - Botulism, acute fulminating MG, tick paralysis, rabies Diagnostic plan: MDB, thoracic radiographs Electrodiagnostics Myasthenia titer, Tensilon test Sample vomitus, feces, serum to look for botulinum toxin Supportive care Results: - Stress leukogram, chemistry abnormalities consistent with dehydration - CXR demonstrate mild aspiration pneumonia - Tensilon test negative - EMG/NCV: reduced nerve conduction velocity and amplitude; no decremental response - Serum, vomitus positive for botulinum toxin Presumptive diagnosis: Botulism Prognosis is favorable given supportive care and time

6 yr M Weimeraner with progressive lethargy and stiffening gait over 6 months. No response to steroids or antibiotics NE: Depressed mentation Stiff, stilted gait; shuffles all 4 feet when walking Normal postural reactions Diminished withdrawal and patellar reflexes pelvic limbs Decreased palpebral reflex, facial mm on the left

Lesion localization: - Polyneuropathy vs. myopathy secondary to metabolic/endocrine disease Possible etiologies? - Metabolic disease, endocrine disease, immune-mediated disease, toxicosis, infectious disease Results: - Elevated ALKP, ALT, CPK, cholesterol, triglycerides - Thyroid panel consistent with hypothyroidism Presumptive diagnosis: - Peripheral neuropathy or myopathy secondary to hypothyroidism Multiple endocrine diseases may cause secondary neuropathies/myopathies to develop, but hypothyroidism in particular has been associated with generalized LMN disease Prognosis for weakness associated with hypothyroidism is good to excellent with treatment

Neuromuscular disease

Localization: - Normal mentation usually - Paresis/weakness, but NOT ataxic - short-strided, elephant on ball, quickly fatigue - Hyporeflexia - Normal CPs*** sensory is not affected (but can fatigue eventually) - Decreased muscle tone/mass - cervical ventroflexion in cats (MG, ddx: hypokalemia, thiamine deficiency, polymyosititis, polyneuropathy, ethylene glycol toxicity) - only CNs possibly affected = VII (polyradiculoneuritis, hypothyroidism), X (laryngeal polyneuropathy) - if multiple CNs = botulism, tick paralysis, diffuse polyneuropathy DDX: - Primary neuropathy: 1) Polyradiculoneuritis 2) infectious 3) endocrine (DM, hypothyroidism, insulinoma) 4) Neoplastic (nerve sheath tumor) 5) Paraneoplastic (immune-mediated, insulinoma) 6) Electrolyte disturbances 7) Toxic 8) Breed-related / degenerative - NM junction specifically: 1) M.G. ** 2) Botulism 3) Tick Paralysis 4) Electrolyte disturbances (calcium, tetany) - Primary myopathy: 1) Infectious, Inflammatory (immune-mediated) 2) Inherited 3) Metabolic, endocrine, toxic, electrolyte disturbances

5 yr F Pomeranian with progressive tetraparesis of 4 weeks duration NE: Alert, normal posture, tetraparesis, generalized muscle atrophy (most severe in masticatory, supra-, and infraspinatus mm) Normal postural reactions Decreased withdrawal reflex in all 4 limbs Diminished menace response OU, diminished facial mm reflex and palpebral reflex bilaterally Mild cervical hyperesthesia

Localization: generalizaed LMN disorder Possible etiologies? - Polymyositis, polyneuritis, myasthenia gravis, botulism, polyradiculitis, meningitis, cervical disk herniation Diagnostic plan: - MDB with CK - assess general health, evaluate muscle - CXR - screen for megaesophagus - Electrodiagnostics (EMG/NCV) +/- biopsies - Advanced imaging of cervical spine, CSF tap Results: CPK - 1026 EMG - scattered areas of fibrillations in cervical and shoulder musculature NCV - normal nerve conduction velocities, no decremental response Radiography - no abnormalities Muscle biopsy - small multifocal mononuclear cellular infiltrates Presumptive diagnosis: Polymyositis (immune-mediated vs. infectious) Follow up with infectious disease titers and full immunologic evaluation Prognosis variable depending upon cause

Bilateral peripheral vestibular disease

Occasionally, animals can develop bilateral peripheral vestibular disease • Most commonly in cats with bilateral otitis media interna Result: • Wide, sweeping movements of head from one direction to the other • Normal gait and posture (no vestibular ataxia or head tilt) • Lack of physiologic nystagmus

Fixed strabismus

Only Motor: CN III, IV, or VI Result: normal pupil vector

Temporal muscle symmetry

Only motor n: CN V Result: symmetry (no atrophy) CC: Trigeminal mononeuropathies = mandibular motor dysfunction most common - acute onset flaccid paresis of mandibular nerve = dropped jaw - idiopathic trigeminal neuritis = most common - inflammatory/infections (neospora, toxoplasma, cryptococcus, rabies) - typically PERIPHERAL - e.g. neoplastic nerve sheath tumor; if central other severe

Lip tone/facial symmetry

Only motor n: CN VII Result: symmetry (no drooping) CC: Facial neuropathy/paralysis: acute inability to close palpebral fissure, droooping lip, drooling affected side - otitis media/interna, idiopathic (75% of dogs), metabolic (hypothyroidism), otic neoplasia/trauma, sulfonamide hypersensitivity - also part of neuromuscular diseases (polyrdiculoneuritits, tick paralysis, myasthenia gravis)

Localize: Monoparesis right forelimb, pinching first tow = elbow flexion / conscious response, pinching 5th toe does not; cutaneous trunic reflex present on left, absent on right when either left/right trunk tested; anisocoria with right pupil smaller than left

Right brachial plexus lesion aka avulsion usually - cranial part has been spared: musculocutaneous nerve (C6-7) intact with 1st toe pinch - caudal part lesion = radial nerve compromised, cannot sense 5th digit and importantly will never be able to weight bear b/c radius = extensors SNS to eye = T1-T3; fits with where this lesion is w/ brachial plexus Cutaneous trunic: C8-T1 = lateral thoracic nerve for MOTOR; sensory part comes off of spinal nerves all the way down - will not move on right if lesion in lateral thoracic nerve despite still being able to sense/move on the left

Localize: Normal mentation, gait, CPs with ophthalmoplegia, absent corneal reflex, absent response to palpation of nasal medium septum, fixed mid-sized pupil with normal menace response all OD

Right cavernous sinus syndrome III, IV, V (ophthalmic, maxillary), VI and SNS to eye all through this sinus - Cavernous sinus syndrome (CSS) is a condition caused by any pathology involving the cavernous sinus which may present as a combination of unilateral ophthalmoplegia (cranial nerve (CN) III, IV, VI), autonomic dysfunction (Horner syndrome) or sensory CN V1- CN V2 loss. Normal menace = normal VII, II Normal gait/mentation = CNS not involved

Localize: L-sided head tilt, ataxic gait, drifting to the left, hypermetric R-forelimb, normal CPs x4, opsoclonus

Right floculonodular lobe*** paradoxical vestibular opsoclonus = dancing eye movement = cerebellar vestibular signs

Anal sphincter tone

S1-S3 Caudal rectal External anal sphincter

Perineal reflex

S1-S3 Pudendal nerve

Match sensory organ with type of head movement detected: - Semicircular canal - Utricle - Saccule

Semicircular canal - rotational acceleration/deceleration Utricle - static position + horizontal linear acceleration Saccule - static position + vertical linear acceleration

PLR (pupillary light reflex)

Sensory nerve: CN II Motor nerve: CN III Result: Pupil constriction

Menace response

Sensory nerve: CN II + contralateral cerebral cortex + cerebellum Motor nerve: CN VII Result: Blink CC optic neuritis = acute onset vision loss, typically bilateral - mydriatic/unresponsive pupls - swollen optic disc/nerve visible = papilledema from intracranial hypertension OR optic nerve edema from glaucoma/uveitis - infectious (e.g. canine distemper, protozoal, viral) - immune-mediated (GME) - neoplasms of optic nerve/chiasm or cause compression (meningioma, glioma, pitutiary tumors) - ddx from SARDS (sudden acquired retinal degeneration syndrome) = also bilateral acute blindness w/ mydriatic pupils, but normal fundic and sluggish but present PLRS

Palpebral reflex

Sensory nerve: CN V Motor nerve: CN VII Result: Blink

Positional strabismus

Sensory only: CN VIII Result: Eyes track with head position

Gag reflex

Sensory: CN IX + X Motor: CN IX + X Result: Fast phase direction of head movement CC: Dysphagia, megaesophagus, laryngeal paralysis - primary myopathies, polyneuropathies, NMJ disoders (M.G., botulism), caudal brainstem lesions (encephalitis, neoplasia) - esophagus innervated by vagus + accessory nerves

Nasal sensation

Sensory: CN V + contralaeral cerebral cortex Result: response to noxious stimuli

Physiologic nystagmus

Sensory: CN VIII Motor: CN III, VI Result: Fast phase direction of head movement

Spinal nerve* localization

Single nerve affected • Common scenarios: 1) Bilateral sciatic neuropathy 2) Brachial plexus avulsion - monoparesis, absent withdrawal / CPs, reduced muscle tone Diffuse neuromuscular - "affected x4 patient" • Affecting the final common pathway to the limb muscles - e.g. myasthenia • Loss of LMNs to thoracic and pelvic limbs - Flaccid tetraparesis/tetraplegia (x4) - Decreased to absent TL and PL reflexes (x4) - Decreased muscle tone x4 • Important *** - Neuromuscular disease does not affect ascending sensory projections --> postural reactions are intact x4 - NO ATAXIA, but weakness generalized

Localize: normal mentation, dramatic atrophy of muscles of mastication on the left, all other CNS normal and normal gait/CP

Specific to left trigeminal nerve, mandibular branch - Pure unilateral trigeminal motor neuropathy trauma? infection?

YOUNG ADULT DOG (bernese mountain dog, boxer, lab) presents w/ severe NECK PAIN, reluctance to move, acute relapsing fever, & neutrophilia that is GLUCOCORTICOSTEROID responsive. What do you suspect?

Steroid-responsive Menigitis-Arteritis (SRMA) - aka necrotizing vasculitis, juveline polyarteritis syndrome, aseptic suppurative meningitis - febrile, ypersthetic, cervical rigitidy, anorexia Increased levels of CSF and serum IgA** High CD11a expression on polymorphonuclear cells involved in enhanced passage of neutrophils into subarachnoid space leading tto meningitis / clinical signs DDX from GME, NME - SRMA = neutrophilic pleocytosis (NONdegenerative = ddx from bacterial meningitis) - GME, NME = mononuclear pleocytosis (macrophages, lymphocytes)

Localize" Paraplegic, normal patellar / withdrawal / perineal reflex, cutaneous trunci cut off at TL junction

T3-L3 Could localize further to 2 spinal segments before the TL cutoff if you have these signs with NORMAL cutaneous trunic, then can definitely localize to lumbar lesion

Cerebellum

Think of the cerebellum as the "downer" of the nervous system •Fine-tuning of movements •Inhibitory to the vestibular system •Cerebellar pathways are ipsilateral**

Paresis / plegia

Two forms of paresis or plegia: 1.Lower motor neuron (LMN) paresis/plegia -Short, choppy steps, crouched stance, look weak 2.Upper motor neuron (UMN) paresis/plegia -Long, lopey steps, exaggerated, look stiff

Spinal cord functional anatomy

White matter = axons • Dorsal white matter = ascending sensory projections • These are involved in postural reactions • Ventral white matter = descending motor projections • These are upper motor neurons Grey matter = cell bodies • Ventral horn cell bodies are lower motor neurons • C6-T2 contains LMNs to thoracic limbs • L4-caudal contains LMNs to pelvic limbs, tail, bladder

NON-vestibular signs pointing to CENTRAL vestibular (think what else is in rostral MEDULLA)

• General proprioceptive ataxia (spinocerebellar pathway) • Ipsilateral postural reaction deficits (ascendin sensory pathway to cortex) • Ipsilateral UMN hemiparesis** or tetraparesis if bilateral lesion (descending motor pathway) • Decreased mentation (RAS) • Ipsilateral CN reflex deficits attributable to CN V-XII

NON-vestibular signs pointing to PERIPHERAL vestibular

• Ipsilateral CN VII • Ipsilateral Horner syndrome

Cerebellar lesion findings

•Cerebellar ataxia- hypermetria •Intention tremor •Truncal sway •Postural reaction deficits •+/- paradoxical vestibular signs if FL lobe involved •Occasionally, ipsilateral menace deficit •Mentation normal**

Cranial Nerve Localization

•Cranial nerves are the lower motor neurons** and sensory neurons** of the head Common cranial nerve dysfunctions: - CN III: ophthalmoplegia --> dilated pupil +/- ventrolateral strabismus - CN V: trigeminal neuropathy --> unable to close jaw - CN VII: facial paresis/paralysis --> unable to blink, lip droop - CN VIII: peripheral vestibular disease --> hallmark signs of vestibular disease - CN IX/X: dysphagia

Brain and cranial nerve localization

•Distinguish between prosencephalon and caudal fossa •Cerebellum •Vestibular Some general principles: 1) Everything crosses at the midbrain A) Ascending sensory projections B) Descending motor pathways C) Cranial nerves 2) Seizures = Prosencephalon. Period. Always.

Caudal fossa

•Medulla oblongata •Pons •Midbrain All components are ipsilateral • Crossing happens further rostral (between midbrain and thalamus) • So, deficits will be IPSILATERAL TO LESION • Cranial nerve deficits III-XII • Gait abnormalities • Postural reaction deficits Functional anatomy: • Reticular activating system • Ascending sensory projections • Descending motor projections • Nuclei for cranial nerves III-XII •III and IV: midbrain •V: pons •VI-XII: medulla •Anticipated deficits with caudal fossa lesion: 1) Abnormal mentation (obtundation, stupor, coma) - RAS 2) Proprioceptive ataxia - ascending sensory 3) Upper motor neuron tetraparesis - descending motor 4) Cranial nerve deficits •Reduced eye movements •Increased pupil size •Inability to close eyelids •Abnormal gag reflex

Spinal Reflexes

•Reflexes test a reflex arc •All reflex arcs have: 1.Peripheral sensory component 2.Central spinal cord component 3.Peripheral motor component •A lesion anywhere WITHIN the reflex arc will lead to decreased reflexes •A spinal cord lesion CRANIAL to a reflex arc can lead to increased reflexes*

Cranial nerve testing

•Reflexes test a reflex arc All reflex arcs have: 1. Peripheral sensory component 2. Central brain region processing 3. Peripheral motor component •Some cranial nerve tests evaluate responses, not reflexes •Response = learned •Cranial nerve testing evaluates: 1. Cranial nerves 2. Specific brain regions •Associations with brain regions: 1. Prosencephalon: CN I and CN II 2. Midbrain: CN III and CN IV 3. Pons: CN V 4. Medulla: CN VI-XII •All cranial nerves enter/exit their respective brain region IPSILATERALLY •Prosencephalon processes sensory information from CONTRALATERAL cranial nerves •Example: visual information from right eye processed by left cerebrum •General approach to interpreting CN testing abnormalities 1. If a single CN is affected, no other exam abnormalities, prioritize localizing to the CN 2. If multiple CN affected, + other exam abnormalities, prioritize central lesion affecting region(s) of brain associated with affected CNs

Prosencephalon

•Telencephalon (cerebrum) •Diencephalon (thalamus, hypothalamus, subthalamus, epithalamus, metathalamus •All deficits are CONTRALATERAL to affected side: • Ascending sensory projections CROSS between midbrain and thalamus • Cranial nerve II CROSSES at the chiasm • Sensory projections from cranial nerves --> contralateral cortex •Consciousness/Personality •Processing external world - Remember, contralateral! •Prosencephalon IS NOT involved in gait generation •NO GAIT DEFICITS with prosencephalic lesion •No paresis •No ataxia •Anticipated deficits with prosencephalic lesion: 1) Abnormal mentation 2) Normal gait, but circling toward lesion, head turn toward lesion 3) Contralateral deficits: •Postural reaction deficits •Cranial nerve deficits •Menace with normal PLR and normal palpebral reflex •Nasal hypalgesia 4) And remember: seizures = prosencephalon

Postural Reactions

•Testing kinesthesia: does the animal know where its limbs are in space? •Postural reactions = sensory test General pathway: 1. Sensory nerve --> spinal cord 2. Projection travels cranially through spinal cord, ipsilateral 3. Projection continues rostrally through medulla, pons, midbrain, ipsilateral 4. At junction between midbrain and thalamus, PROJECTION DECUSSATES ** 5. Projection then continues contralaterally through thalamus to the CONTRALATERAL cerebral sensory cortex A lesion anywhere along this pathway will lead to postural reaction deficit(s)

Mentation localization - abnormal

•is either a problem in the prosencephalon or the "caudal fossa" Prosencephalon: Telencephalon + Diencephalon •A lesion in the cerebrum or thalamus can lead to obtundation or dementia *rarely, can also lead to stupor or coma Caudal fossa: midbrain, pons, medulla •The reticular activating system (RAS) travels through these regions to keep the cerebrum awake •Lesion in caudal fossa can lead to obtundation, stupor, or coma