Exam 3 Flashcards

Question

Forelimb Withdrawal reflex What nerves/spinal cord?

Answer 1

Test objective: "Cutaneous trunci is absent caudal to ...?"

Answer 2

Nerve evaluated -Pudendal (S1-S3) -Perineal (S1-S3)

Answer 3

-CNI and CN XI -Most test are reflex arcs -Some are responses: implication that requires cortex 1. Menace response 2. Nasal sensation **Consistency order is key**

Answer 4

1. Menace Response CN II, VII - Cortical, cerebellum -Move hand toward one eye, opposite eye is covered -Blinking is the normal response -Not present in puppies and kittens until about 3 mts **Requires contralateral cortical input** 2. Palpebral Reflex & Facial Sensation CN V, VII - Cortical -Medial cantos of the eye -Afferent: CN V (ophthalmic branch) -Efferent: CN VII 3. Pupillary Light Reflex CN II, III

Answer 5

Nasal sensation test the ophthalmic brach +/- maxillary -Contralateral, so cortex somatosensory test too.

Answer 6

Afferent: CN II (optic n) Efferent: CN III (oculomotor nn) Assessment of the pupil size and symmetry Swinging light test: Direct PLR = what is happening in the ipsilateral eye Indirect = what is going on in the opposite eye

Answer 7

-Oculocephalic Reflex & Oculovestibular Reflex Test for connection of MLF which is the connection between CN VIII, CN III, IV, VI. Afferent: CN VIII (Vestibulocochlear) - Gravity Efferent: CN III, IV, VI Abnormal signs -Spontaneous (resting) -Positional (inducible) Orientation -Horizontal -Rotary -Vertical Direction -Of the FAST PHASE

Answer 8

Gag Reflex Caudal Brainstem Afferent: IX, X Efferent: IX, X, (XI), (XII) back of the throat Abnormal: no jaw tone usually Jaw Tone From Trigeminal nerve Lesions: atrophy of temporals/masseter muscles, loss of jaw tone, dropped jaw (bilateral) Tongue From CN XII (Hypoglossal nn) General Somatic Efferent

Answer 9

Spinal Palpation -Hyperesthesia = increased sensitivity to stimulation -Perform from caudal to cranial -Vertebral column (start at L7) -Press spinous process and epaxial muscles -Gently flex and extend neck -Squeeze transverse process

Answer 10

Evaluated by -Cranial nerves -Spinal reflexes -Propioceptive positioning -Spinal palpation Still to be evaluated: superficial pain and deep pain Perform if needed and always last

Answer 11

-Perception of noxious stimuli Afferent information. -Heat, pain, pressure, chemical -Often difficult to differentiate from superficial and deep pain perception **Pain is a conscious, emotional sensation which means it requires input from the brain** Perform test -Use the least noxious stimulus possible -Fingers before hemostats -Skin/webbing between toes, nailed, or last digit -Normal response indicates deep pain perception. Withdrawal of limb (unless LMN location) -Behavioral response: anxiety, vocalization, attempt to escape -Turning head, attempt to bit -Increase in respiration or pupil dilation -withdrawal of the limb only does NOT indicate pain perception -If voluntary movement in its limbs = 99% of the time will have nociception -Do not unduly harm the animal by crushing its toes

Answer 12

1. Mentation 2. Paw placement +/- reflexes 3. Menace response +/- PLR, palpebral reflex

Answer 13

Identify key points from neurological case history Assimilate exam findings Assign a neurolocalization based on all findings Generate a brand differential list based on sign-time graph

Answer 14

1. Congenital/anomalous 2. Neoplastic 3. Degenerative 4. Inflammatory, Toxic 5. Traumatic, vascular

Answer 15

Forebrain disease? 1.Mental status: QAR 2.Walking in circles: no 3.Seizures: No seizures 4.Central blindness: No central blindness 5.Decreased facial expression: (contralateral) No 6.Postural reaction deficits: proprioceptive ataxia both rear limbs. Moderate to severe paraparesis. Normal postural reactions in front limbs. Very delayed paw replacement and hopping bilaterally in rear. Gait -Forelimbs: normal -Rear limbs: exaggerated patellar reflexes bilaterally. Cutaneous trunci absent bilaterally caudal to L1 -CN: normal -Spain pain elicited on palpation at thoracolumbar junction **Arched back, walking as if drunk** Conclusions -Gait affected: midbrain or caudal to it because forebrain does not cause gait abnormalities -Lesion location: caudal to foramen magnum bc mentation normal -Caudal to T2 bc forelimbs normal -Lesion is T3-L3 Dx: -Intervertebral Disc Herniation -Degeneration

Answer 16

Gait -Affected rear limbs -1 year history of wobbly rear limbs -No improvement steroids, pain meds. -Absent paw replacement and hopping bilaterally -Rear normal patellar reflexes bilateral, normal withdrawal bilaterally. -Cutaneous trunci absent caudal to T13 Conclusions -Location: T3-L3 -Degenerative: chronic, progressive, non-painful thoracolumbar myelopathy in an old-aged dog. -Degenerative, Neoplastic, Infectious. -DX: Fluid accumulation in Spine "diverticulum"

Answer 17

-6 yo beagle -No history of trauma -Screamed and reluctance to move -Screams when approached Neuro PE -Ambulatory with mild tetra paresis and proprioceptive ataxia 4 limbs -Slightly delayed paw replacement and hopping 4 legs -All spinal reflexes normal -Marked pain and hyperesthesia elicited on gentle flexion of the neck Conclusions: -Lesion location: C1-C5, caudal to foramen magnum bc mentation was normal -Acute onset, painful disease resulting in cervical myelopathy in a middle-aged dog -DX: IVD herniation

Answer 18

Signalment: 6 yo, female spayed west highland white terrier History -Recumbent in backyard 4 days earlier, unable to walk -Static over past 4 days -Left thoracic and pelvic limbs: voluntary movement PE -Urine scald in inguinal region -No other significant abnormalities Neuro PE -Dog falls to the right when placed on feet -No motor function seen on right -Absent proprioception right front and hind, slightly delayed on left rear and front -Reflexes: most significant 0-1 withdrawal right thoracic limb -No pain on spinal palpation or neck flexion Conclusion -Lesion location: C6-T2 -Acute onset, non-progressive, non-painful, asymmetrical. -DX: Stroke, Ischemic myelopathy

Answer 19

Signalment History: fallen down stairs, depressed PE: collapsing trachea and locating patellas typical for breed Neuro exam: anxious, inappropriate, slow to respond to stimuli. -Paced around always to the right. -Rt side: normal postural reactions -Lft side: delayed to absent paw placement and hopping -All spinal reflexes normal Central blindness phenomenon -Absent menace response (CN VII, CN II) OS, normal OD -Normal palpebral (CN V, VII) and pupillary light reflexes (CN II, III) UO -Nasal sensation blunted (CN V, CN I, CN VII) left, normal right. -Normal oculi-vestibular movements -Normal gag reflex. Conclusions -Lesion: Intracranial -Circling and compulsive to the right: forebrain right side affected -Acute onset behavioral changes. Progressively more severe despite medication -DX: Meningioencephalitis, Asymmetrical Brain, Right-sided.

Answer 20

PE -Noticeably decreased muscle tone and moderate muscle atrophy Neuro exam -QAR -Lateral recumbency -Flaccid paralysis/tetraplegia with absent muscle tone -Unable to bark, can move mouth -Can move head slightly -Absent postural runs and spinal reflexes in all 4 limbs -CN normal Conclusion -DX: diffused LMN or neuromuscular disease 1. Absent spinal reflexes in all 4 limbs 2. Widespread flaccid paralysis with muscle atrophy 3. Aphonia (inability to bark) **Acute, idiopathic polyradiculoneuritis, AKA Coonhound paralysis** -Ddx: tick paralysis, coral snake bite, botulism, fulminant myasthenia gravis

Answer 21

Conclusion -Orthopedic disease

Answer 22

signalment: 8mt old female intact Yorkshire terrier -Thin 3/9 -Innapropriate mental behavior -Normal gate -Paces -Propioception delayed, hopping delayed in all four limbs -spinal reflexes normal -CN: absent menace (CN II, CN VII), normal palpebral and PLR OU. Conclusion -Insidious onset, minimally progressive disease showing forebrain signs in a young, toy-breed. -Lesion: forebrain (cerebrum) -Ddx: degenerative, anomalous, metabolic, nutritional, infectious. -DX: Congenital Hydroencephalus

Answer 23

History -Slowly progressive gains abnormality since 2.5 yo. (3.5 yo Golden retriever) Neuro exam -Truncal sway -Intention tremors -Cerebellar ataxia (marked) -No paresis noticed -Hyperactive reflexes -No cranial nerve abnormalities Conclusion -Slowly progressive onset of severe cerebellar deficits in a young, mature dog -Cerebellum dysfunction/deficits -DX: Neosporosis (neospora caninum). Degenerative, infectious

Answer 24

DX: Clot older dog, Disk herniation with compression of caudal equine L7-S1 -Slow, insidious onset of hair abnormalities in an older dog, large breed -Pain elicited when tail elevated -Location: L4-S3 -Decreased withdrawal bilaterally hind limbs = caudal to T2 -slightly increased patella reflexes bilaterally: means L4-L6 Femoral ok. -L7-S1: SCIATIC problem

Answer 25

Old German Shepherd DX: degenerative myelopathy Slow insidious onset of gait abnormality in al older large-breed dog. No pain elicited -Hip dysplasia history -PE: normal -Neuro exam: wide based stance in pelvic limbs. Truncal ataxia, thoracic limbs appear normal. Severe paraparesis with marked proprioceptive ataxia. Paw replacement absent in both hind limbs. Hemiwalking pelvic. -Cutaneous trunci absent caudal to T13 -Location: T3-L3 -Patellar reflex normal (L4-L6 Ok)

Answer 26

Understand what conditions can mimic seizure activity Compare different types of seizures and epilepsies Develop a clear understanding of how to diagnose primary (idiopathic) epilepsy Describe what aspects of epilepsy management need to be expressed to clients

Answer 27

1. Clinical manifestation of excessive and or hyper synchronous neural activity -originate from forebrain (cerebrum/thalamus) Types A. Generalized B. Focal 2. Seizures are NOT -syncope -Narcolepsy/cataplexy -Acute vestibular dysfunction -Animals sleeping/dreaming -Tremors (can be confusing) -Movement disorders

Answer 28

1. Prodrome: before onset of seizure -Changes in behavior, anxiousness, seeking attention, hiding -Can last several days 2. Aura: initial manifestation of seizure -Drooling, vomiting, pacing, whining, barking, -Seconds to minutes in duration prior to full seizure 3. Ictus: actual phase event per EEG. -Seconds to minutes in duration 4. Postictal phase: abnormal behavior, disorientation, deep sleep, weakness, confusion, blindness, sensory and motor dysfunction. -Minutes to 48 hours 5. Interictal period: Time between seizures

Answer 29

1. 2 or more seizures within 24 hours 2. Seizures lasting more than 5 minutes -Repeated without full return to consciousness in between -Associated with worse prognosis 3. Hyperthermia, hypoventilation, hypoxia, hypertension, possible neurotoxicity, neuronal cell death, increased ICP

Answer 30

-The entire brain is involved -Tonic/clonic most common: bilateral compulsive tonic and clonic muscle contractions. -Reflects involvement of both cerebral hemispheres: motor manifestations are bilateral -Impaired consciousness +/- autonomic signs Common complications -Urination/defecation/hypersalivation -vocalization due to pain but inability to control it -Biting tongue -Head trauma -Aggression

Answer 31

-Abnormal activity in one specific area of the forebrain -Motor, autonomic, or behavioral signs all possible Simple - if consciousness not altered, can respond to stimuli Complex -If consciousness is impaired: fear aggression, whining, appearance of hallucinations Arise from FOCAL AREAS of FOREBRAIN -Paroxysmal changes in motor function: facial-muscle twitching, single-limb movements (Contralateral cerebrum) -Paroxysmal changes in vegetative or sensory function: fly biting, licking, bug-hunting, anxiety, restlessness. Excessive unmotivated vocalization, autonomic signs.

Answer 32

1. Idiopathic (primary) epilepsy -No recognized underlying metabolic or structural cause -Most common -Genetic or hereditary possible 2. Symptomatic (secondary) epilepsy -Metabolic or structural brain disorders 3. Probably symptomatic (cryptogenic) epilepsy -Metabolic or structural brain disorders that are present yet undetectable 4. Reactive seizures -disturbances in systemic metabolism or toxicosis Ex: hepatic encephalopathy, xylitol, or chocolate toxicity. -No structural brain disease -Not considered a true epilepsy

Answer 33

-Spontaneous seizures, most often during rest/sleep. -Quick and uneventful recovery -Initial frequency: q 4-6mts -Increase in frequency and severity over time if untreated -Stressors are very common in humans **NORMAL interictal period and NORMAL neurological exam** -Border collies, Australian shepherd, Labrador Retriever, Pitbull, Boxers, etc. -onset ~1-5 yo (6 months to 6 years) -Usually generalized tonic-clonic: may be focal that proceed to generalized tonic/clonic

Answer 34

Signalment History: very important -Vaccination, travel, trauma, exposure to toxins? -Medical, surgical history Seizure description -Onset -Frequency -Duration -Characteristic of poetical phase PE and Blood pressure -Heart murmurs, other sigs of cardiac disease (syncope) -Hypertension -Minimum database: CBC, CHEM, UA, BP -BG, Creatinine -Other lab tests: bile acids, rule out PSS, liver disease. T4, ACTH stim. -Addison's (hypoglycemia) Cushing's (Increased BP, hypercuagulable) Imaging -Thoracic radiographs, Abdominal, Ultrasound abdomen Testing for brain disease -MRI, CT -CSF -Infectious disease tests -EEG

Answer 35

1. Maintenance: control of the seizures. Decrease in severity, duration, frequency. Maintain quality of life for pet and owner -Surgery: cortical resection vs. corpus collasum division -Vagal nerve stimulation: expensive and limited data -Acupuncture -Ketogenic diet -Cannabidiol (CBD) 2. Emergency tx: stop the seizure Treatment recommended when -Symptomatic epilepsy -Seizures occurring more than once every 2-3 mts -Status or cluster seizures -Prolonged postictal periods -If the client can not deal with it Client Education -Treatment is lifelong -Anticonvulsants daily -Periodic monitoring -Emergencies will happen -Keep seizure log -Drugs have cost and side effects -Do not alter drug doses -Be cautious of other drugs/supplements Management Mistakes -Failure to obtain diagnosis -Insufficient drug doses -Owner non-compliance -Use of wrong drug -Setting unrealistic expectations

Answer 36

1. Idiopathic epilepsy -Most respond well to combination therapy -Small % may be refractory even with multiple medications -If seizure free for >1yr: weaned slowly -Diazepam (oral): NEVER CATS Anticonvulsants -Phenobarbital -Bromide -Zonisamide -Levetiracetam -Topiramate -Diazepam: short half life and tolerance -Clonazepam: short half life and tolerance Others -Gabapentin: usually used as pain medication. binds to alpha2 subunit of Ca channels -Pregabalin -Felbamate: inhibits excitatory transmission (NMDA) start slow -Carbamazepine: voltage gated Na channels

Answer 37

-Diazepam injectable, PR -Midazolam injectable, PR -Additional dose of patient's daily med -Clorazepate course: 1 mg/kg BID until seizure free for 24hrs

Answer 38

Recognize the individual components of the vestibular system Explain the normal function of the vestibular system in regards to coordinated limb and eye movements Differentiate the common signs associated with peripheral vs. central vestibular disease Understand just how paradoxical vestibular disease occurs List the most causes of peripheral and central vestibular disease

Answer 39

Functions -Maintain balance (general proprioception, visual system) -Stabilize images during head movement -Coordinate posture, movements, and ocular position with respect to the influence of gravity Abnormalities C/S -Head/body posture -Gait -Occular movements Anatomy -Labyrinth -Bony - perilymph: the bone -Menbranous - endolymph: inside the bone 1. Macula of saccule: vertical 2. Macula of utricle: horizontal 3. Cristae of SCC: rotational Provide continuous tonic input Stimulation of one side = inhibition of the other

Answer 40

1. Distal Portion -CN VIII receptors to vestibular portion -Within petrous temporal bone 2. Proximal portion -Travels through acoustic meatus with CN VII -Enters brainstem on rostral medulla -Very close to CN V on pons and CN VII on medusa

Answer 41

1. Vestibular nuclei 2. Cerebellar components Others -Other CN nuclei -Medial longitudinal fasciculus: pathway from vestibular nuclei to LMNs in motor nuclei of CN III, IV, and VI. Coordinate, conjugate eye movements as the head changes. -Descending spinal cord tracts -Vomiting center: less of a problem in vet med -Conscious perception of orientation: thought to ascend through thalamus to temporal bone

Answer 42

1. Spinal cord 2. Rostral brainstem 3. Cerebellum: projects continuous inhibitory impulses back to vestibular nuclei. Helps maintain position of head, trunk, and limbs when body moves -Crucial fo "paradoxical vestibular syndrome" Vestibulospinal tract -Travels to all segments of ipsilateral spinal cord, including cervical Causes: -Fascilitation of ipsilateral extensor mm. -Inhibition of ipsilateral flexor mm. -Inhibition of contralateral extensor mm.

Answer 43

VS helps stabilize image on retina -Information from semicircular canals -Movement of head induces compensatory eye movement -Vestibular neurons - motor nuclei CN III, CN IV, and CN VI. Normal: Turning the head to the RIGHT -Contraction of Left lateral rectus and Right medial rectus "slow phase" -Reset is the "fast phase" and it is controlled by higher centers not the vestibular system. Pathologic: Lesion on left inner ear -Left neuronal input abolished -Right input remains -Nystagmus has the FAST PHASE to the RIGHT -Stimulates right vestibulospinal tract: increases tone on right -Head and body tilt or lean LEFT **Asymmetry of input, Rt side overdoing it**

Answer 44

1. Nausea +/- 2. Head tilt: due to unilateral loss of antigravity muscle tone. Usually ventrally deviated ear is the side of the lesion 3. Pathologic nystagmus: Distinct fast as slow phase "jerk" -Described by direction of the fast phase. Ex: rotary nystagmus with fast phase to the right -Can be spontaneous or induced (positional) -Always try to induce it -Quickly compensated for a. Horizontal b. Rotary c. Vertical 4. Positional strabismus -Ventrally or ventrolaterally deviated globe when head/neck is extended -Loss of CN III, IV, VI innervation -Ipsilateral to lesion 5. Vestibular ataxia -Wide-based stance, leaning, listing, tight turning circles, falling, rolling -Asymmetric input to vestibular tracts -No paresis

Answer 45

-Congenital anomaly of visual system -SIAMESE or HIMALAYAN cats -NOT a sign of vestibular dysfunction

Answer 46

1. Propioceptive deficits -Usually central 2. Altered mentation -Possible central 3. Head tilt -Peripheral -Central 4. Deficits other than CN VII or CN VIII -Not peripheral -Possible central 5. Nystagmus: both except -Vertical: central, not peripheral -Positional induced: Occasionally peripheral, but Yes central -Change in direction of fast phase: Central for sure 6. Horner's syndrome: both possible

Answer 47

-Lesions usually exert REGIONAL EFFECT -Vestibular nuclei, Ascending GP, Postural deficits -Descending UMN: Tetra/hemiparesis -ARAS: depressed consciousness -CN V-XII

Answer 48

-Caudal cerebellar peduncles -Flocculonodular lobes of cerebellum -Fastigial nucleus of cerebellar medulla **Remember cerebellum sends inhibitory impulses to vestibular nuclei at all times** Nystagmus: fast phase towards the lesion Head tilt: opposite to side of true lesion Ataxia (listing, falling, circling): opposite side of true lesion Postural reactions deficits: Ipsilateral to the lesion

Answer 49

-More common in cats -Usually peripheral in nature -Absence of head tilt -No pathologic nystagmus -No physiological nystagmus (absent oculo-cephalic reflex) -Crouched low to ground (can't feel gravity, but can feel ground) -Wide, lateral head excursions

Answer 50

1. Otitis media/interna: can see peripheral vestibular dysfunction VIII, facial nerve deficits, Horner's syndrome (eyelid affected) sympathetics -Most common cause -Unilateral or bilateral -Preceded by head shaking, pain, smell, or nothing -Common concurrent VII deficits and horner's syndrome -Otoscopy, bulla radiographs, advanced imaging. -Tx: myringotomy, C&S, flushing, appropriate antibiotics -VBO or TECA: ventral bulla osteotomy or total ear canal ableration 2. Idiopathic (dogs vs. cats) DOG -2nd most common -Geriatric -Unknown etiology -Usually >10 yo -Acute onset unilateral -Normal proprioception -Does NOT CN VII or Horner's syndrome -Signs stabilize in 2-3 days, resolution 2-3 weeks -Tx: Diazepam or Meclizine -Rare recurrence CAT -Any age -Summer and fall mts most common -Will occasionally be bilateral in nature -Etiology unknown 3. Inflammatory polyps (cats>dogs)

Answer 51

-Neurolocalization to central vestibular system is an indication for more advanced diagnostics -MRI, CSF, BAER test -Generally associated with rapid deterioration and death 1. Hypothyroidism -Change in CN VIII -Pathophysiology likely multifactorial -Increased cholesterol, triglycerides -Ischemic infarctions associated with atherosclerotic vascular disease -CNS demyelination 2. Neoplasia 3. Meningioencephalitis -Autoimmune -Otitis media/interna can result in abscess 4. Cerebrovascular accidents 5. Metronidazole toxicity -MOA unknown -Dose >60mg/kg/day -Cats show more forebrain signs

Answer 52

-Listing and circling to the right -Horizontal nystagmus fast phase to left -Manace absent on right -Follows cotton ball OU -PLR normal OU -Drooping right lip -Postural reactions all normal -Spinal reflexes all normal -No obvious pain or hyperesthesia Conclusions -Balance or vestibular dysfunction -CN VII involvement -Peripheral vestibular disease more likely -Right sided peripheral vestibular problem -Right sided CN VII problem: commonly affected with labyrinthine disease Ddx -Peracute, unilateral vestibular and facial nerve deficits in a middle aged cooker spaniel -Infectious, immune, idiopathic, traumatic, vascular DX: Idiopathic facial paralysis DX: Infectious Otitis media/interna

Answer 53

Horizontal nystagmus = peripheral but central disease is sneaky **Left ventrolateral strabismus when head elevated** Paw placement slightly delayed on left limbs

Answer 54

Create a proper differential list based on DAMMIT-V and the sign-time graph concept Understand the pathophysiology and clinical presentation of selected disease processes Outline general treatment plans and prognoses for selected disease processes

Answer 55

1. Degenerative -Cognitive dysfunction 2. Anomalous/structural -Hydrocephalus -Chiari-like malformations (COMS) 3. Metabolic -Hepatoencephalopathy 4. Nutritional -Thiamine deficiency 5. Neoplastic -Primary vs. secondary 6. Inflammatory -Infectious -Non-infectious 7. Traumatic -Head trauma -Hemorrhage 8. Toxic -Tremorgenic -Mycotoxins -Metronidazole 9. Vascular Disease -CVA and TIA -Feline Ischemic encephalopathy

Answer 56

In general -Time of onset can be young or old -Slow but steady progression without improvement -Signs of forebrain problems -Poor prognosis Pathophysiology -Uncertain, similar to Alzheimer's -Changes: cerebral vascular, meningeal thickening, gloss and ventricular dilation. -Progressive accumulation of protein B-amyloid, toxic, inhibits neuronal function -Intraneuronal accumulation of tau protein, precursor to neurofibrulary tangles C/S -Dogs >9 yo -Cats > 12 yo -Change in obedience/response to commands -Change in recognition of familiar people or pets -Frequent house soiling -Change in excitement for walks or outings -Frequency of waking in the night -Avoids being petted or touched Diagnosis -History: 1-2 years changes -Exclusion -MRI -CSF Tx -Pharmacologic: SLEGLINE -Diet, supplements, environment -Toys, environmental enrichment

Answer 57

General -Signs usually present shortly after birth -Signs remain static although many times they present after exacerbation -Treatments are aimed at reversing or managing nature.

Answer 58

-Any increase in CSF volume within the ventricular system or SA space 1. Developmental 2. Acquired C/S -PE: dome shaped head, sunset eyes, +/- persistent fontanelle (fixed strabismus) -NE: Forebrain signs predominate, central blindness Diagnosis -Often presumptive based on exam -MRI > CT > Ultrasound Treatment -Corticosteroids (may decrease CSF production) Prednisone or Dexamethasone -Diuretics, but not sustainable for longterm -Carbonic anhydrase inhibitor -Proton pump inhibitor -Anticonvulsants Surgical -Ventriculoperitoneal shunt 75% successful improvement -Other procedures Prognosis -Guarded

Answer 59

-Usually from blockage of normal CSF flow

Answer 60

AKA CAudal Occipital Malformation Syndrome -Thought to be congenital occipital bone defect -Compression of cervicomedullary junction at foramen magnum -Variable degrees of syringomyelia Breeds: -Cavalier King Charles Spaniel most common -Brussels Griffon -Yorkshire terrier -French bulldog -Mini/toy poodle -Maltese -Pug dog -Pomeranian C/S -Highly variable -Problem is caudal fossa, so less forebrain -Cervical pain -Scoliosis "Phantom" scratching -Weakness and ataxia: C1-C5, or C6-T2 -Central vestibular signs -Seizures only rarely Diagnosis -Ddx for susceptible breeds -MRI -Occasionally incidental finding on MRI Treatment -Medical: mild to 1st time signs -Surgical: severe or recurrent signs -Gabapentin or Pregabalin: inhibits DORSAL HORN influx Ca++ -Tramadol: synthetic opiate -Amantadine: NMDA antagonist -Prednisone: lowest effective dose Surgery -Foramen magnum decompression -Reoperation rate high due to scarring within 5 years Prognosis -Overall fair to guarded

Answer 61

-Results from failure of liver to remove toxic substances -Commonly secondary to: Congenital/acquired portosystemic shunt End-stage chronic liver disease Acute, fulminant liver disease (LEPTO) C/S -Symmetrical -Depression -Dementia -Pacing -Head-pressing -Stupor -Coma -Seizures -Rarely cerebellar signs -Ptyalism (CATS) excessive secretion of saliva

Answer 62

1. Primary -Slow insidious onset 2. Secondary -Can cause thrombosis and infarction, or hemorrhage -Significant deficits relatively quickly 1. Primary Brain tumors -Brain parenchymal cells (neurons, glial cells) -Membranes (meninges, ependymal cells) -Vascular elements (choroid plexus) Signs caused by: -Invading effects -Peritumoral edema/inflammation -Ischemia -Obstructive hydrocephalus -Hemorrhage #1 Meningioma -Gliomas: Astrocytoma (GBM), Oligodendroglioma. C/S -Dogs >9 yo -Cats >10 yo -Dolichocephalic breeds = meningioma (Golden Retriever) -Brachycephalic breeds = Glioma (Boxer) -Cats = meningioma, better prognosis Dogs: seizures, behavioral change, circling, lethargy, visual deficits, and semi-inattention (neglect) syndrome Cats: behavioral change Dx -Suspicion -Susceptible breeds -BIOPSY only definitive surgical CT guided -Presumptive with imaging Tx -Surgery -Radiation -Chemotherapy

Answer 63

Many categories Variable onset and severity Disease will typically progress unless proper treatment is initiated General 1. Infectious meningoencephalitis: bacterial, viral, fungal, protozoal, rickettsial, verminous 2. Meningoencephalitis of unknown etiology MUE, thought to be autoimmune 3. Neoplastic -Diagnosis and treatment can be frustrating -Rarely get antemortem definitive diagnosis Sigs -Diffuse or multifocal encephalopathy -Forebrain or vestibular or cerebellar or all -Variable degrees of fever and neck pain Dx -Referral mostly -MRI/CT -CSF -Infectious disease testing Prognosis -Guarded

Answer 64

C/S -Concurrent neural signs -Hyperkeratosis -Enamel hypoplasia -GI disease -Mucopurulent Năsal discharge -Conjunctivitis -Choriorentinitis Pathophysiology -Paramyxovirus -Contact with secretions -Migrates via macrophages to lymph nodes and organs in 1st week -Immune response variable, can clear disease or progresses Forms 1. Young/Acute <1yo -Forebrain signs (seizures, blindness, behavioral) 2. Mature and Chronic >1yo -Leukoencephalomyelopathy: demyelinating in entire CNS. -Cerebello-vestibular, spinal cord dysfunction (myoclonus) difficulty walking 3. Adult/older >5 yo -Considered rare, mostly forebrain 4. Post vaccinal Dx -Frustrating -Lymphopenia common -MRI/CT -Multiple CDV, viral antigen, serum CSF Ab, urine RT-PCR. -Most consider results in light of patients c/s Treatment -Symptomatic not cure Prognosis -Most require euthanasia -Some recover, depends on immune response from patient

Answer 65

-Virulent type if feline enteric coronavirus (FECV) that hides in macrophages and forms immune complexes that deposit in a variety of tissues 1. Wet/effusive: immune complex 2. Dry: vasculitis and heavy accumulation of inflammatory cells Signs **The most common infection to affect CNS of cats** -Myelopathy -Persistent fever -Obtundation -Myriad of neurological signs -Cerebellovestibular, paraparesis, and seizures Dx -Serology -PCR -No test is perfect -MRI -CSF: very high protein -Diagnosis made at necropsy Prognosis -Usually fatal Vax questionable

Answer 66

Geographical -Cryptococcus neoformans: pigeon poop -Coccidioides immitus (Valley fever): SW USA -Blastomyces: usually systemic, affect eyes -Histoplasma: daily rare. Near river valleys -Aspergillus: more commonly causes discopondylitis. If meningeoencephalitis, likely fatal

Answer 67

-SRMA -GME -NME -NLE -Little White Shaker dog disease

Answer 68

-Likely immune mediated Breeds -Bernese MD, -Boxers -Beagles C/S -Acute onset spinal pain especially cervical -Minimal to no neurological abnormalities Pathology -Suppurative leptomeningitis with severe arteritis and fibrinoid necrosis of arterial wall Dx -Rule out other causes like IVDD, etc -CBC leukocytosis with mature neutrophilia (not toxic neuts) -CSF elevated protein, neutrophilic pleocytosis (mature) Tx -Pain medications -Immunosuppression -Predinosone, weaned slowly 4-6 mts -Elevated food water dish Px -Excellent but relapse possible

Answer 69

-Fairly common idiopathic inflammatory CNS disease -Thought to be T-cell mediated hypersensitivity reaction C/S -Potential triggers of autoimmune attack include infections and vaccinations -Young to middle aged FEMALE SMALL BREED 1. Ocular 2. Focal 3. Multifocal/dessiminated: more common Pathology -Predilection for white matter and brain stem Signs -Largely dependent on location of disease -Common seizures and cerebella-vestibular dysfunction Hallmark: cytopath perivascular walls Dx -Histopath only definitive -Signs + suspicion + MRI + CSF + Negative infectious tests -Presumptive antemortem diagnosis -Mixed cell pleocytosis: macrophages/monocytes evidence of reactivity Tx -Multimoddal immunosuppression is recommended -Anticonvulsants if indicated -Corticosteroids: prednisone Adjunctive therapy -Cyclosporine -Cytarabine arabinoside -Azathioprine -Procarbazine -Mycofenolate mofetil -Lomustine -Leflunomide Px -Guarded -Patients with focal disease do better -Survival times are variable -Early intervention helps

Answer 70

Breeds -Pug - genetic marker -Maltese -Chihuaha -Shish Tzu -Pekingese -Papillon -Boston terrier -Non-infectious -Thought to be immune mediated -Potential triggers C/S -Acute to peracture onset of forebrain signs -Seizures predominate -Circling, visual impairment, head pressing, altered mentation Dx -Compatible signs -MRI/CT -CSF Tx -Same as for GME Px -Poor to grave -Therapy is unrewarding

Answer 71

Signs -Diffuse whole-body tumor -Rarely incapacitating only when severe Pathology -Mild lymphocytic meningoencephalitis Dx -MRI -CSF analysis Tx -Prednisone Px -Excellent

Answer 72

-Consider signalment -History and clinical course -Results of Neurologic exam -Rule out any strongly suspicious infectious causes -Discuss referral, pros/cons of empirical therapy -Initiate treatment (consider status of patient) -Closely monitor

Answer 73

-Acute onset of variable severe signs Common causes -HBC -Falls -Kicks -Penetrating wound -Bites Primary injury: concussion, contusion, laceration, bleeding Secondary injury: minutes to hours after initial insult. Driven by cerebral ischemia, results in an increase ICP C/S -Gait and posture: paresis, ataxia, circling. Opisthonus (spasms of muscles causing backward arching of the head, neck, spine) -Mental status: bright, depressed/obtunded, demented, stuporous, comatose -Vestibular signs -Pupils: size, symmetry, response to light -CV system -Respiratory rate and effort: Cheyne-Stoke's (occurs usually during sleep, a period of fast shallow breathing followed by slow heavier breathing and apneas), Kussmaul respirations (due to metabolic acidosis usually, rapid deep breathing at a consistent pace) -Cushing reflex: physiological nervous system response to acute elevations of intracranial pressure (ICP) resulting in Cushing's triad of widened pulse pressure (increased systolic, decreased diastolic) bradycardia, and irregular respiration. Reflex to brainstem ischemia seen in ICP increased.

Answer 74

Head Trauma Pupils and Prognosis

Answer 75

Medial Longitudinal Faciculus pathway assessment -dysfunction = lower score Treatment -Mannitol: indicated when Cushing response - high MAP with bradycardia -Hypertonic saline (7%): not if Na+ derangement present -Furosemide -Corticosteroids: CONTRAINDICATED (hyperglycemia) -Analgesia or anti=anxiety meds if indicated -Monitoring: serial neuro exams, recheck lab values -Supportive care: padded bedding, rotate, nutrition, eye lube, anti-convulsants if indicated

Answer 76

-Signs usually appear within minutes to hours after exposure -C/S do not tend to wax and wane once present Causes Mycotoxins -Penitrem A and -Roquefortine produced by fungi -Sources: garbage, moldy dairy products, walnuts, peanuts, bread and grains C/S -Tremors -Anxiety -Seizures -Polyuria -Elevated temp Dx -Degree of suspicion and compatible signs Tx -IV fluids, reduction of fever, and -Methocarbamol IV Px -Ecellent (signs abate in 2-3 days)

Answer 77

-Antibiotic and antiprotozoal ->60 mg/kg/day, though seen at lower doses MOA: bind GABBA-minergic receptor in cerebellum and vestibular sytem C/S -Head tilt, falling, cerebella-vestibular ataxia, vertical nystagmus, tremors, rigidity, rarely seizures. Tx -Diazepam -Initial IV dose -IV fluid therapy -Diazepam 3 days, response within 13.2 hrs, recovery 38.8 hrs

Answer 78

-Acute to parachute onset of c/s -Recovery ultimately depends on establishment of blood and oxygen and duration of tissue ischemia -Ischemia results in necrosis of neurons and glial cells -Once tissue dies it is called INFARCT -Penumbra: is the tissue around the infarct

Answer 79

Stroke -Abrupt onset of focal neurologic deficits resulting from an intracranial vascular event with clinical signs lasting <24 hrs Transient Ischemic attack -resolves within 24 hrs and no lasting signs 1. Hemorrhagic stroke -Less common -Neoplasia: most common -thrombocytopenia -Vasculitis -Hypertension -Idiopathic -Vascular malformation -DIC Dx -CFS may show hemorrhage -CT -MRI superior T2 Tx -Tincture of time -Underlying disease, anticonvulsants -Steroids controversial 2. Ischemic stroke -More common -Renal disease -Endocarditis -Neoplasia -D. immitis -Idopathic -Hyperadrenocorticism -Hypothyroidism, diabetes mellitus, hypercholesterolemia, chronic hypertension = Artherosclerosis Pathology -Hypoperfusion - anaerobic metabolism - reduced ATP - NA/K/ATPase failure - H2O into the cell - cytotoxic edema - cells depolarize - excitatory AA - Ca++ influx - Nitric Oxide and free radicals - cell death -release of inflammatory mediators. C/S -Forebrain -Area of infarction -Territorial: 3 cerebral arteries, 2 cerebellar arteries. -Lacunar: penetrating vessels Dx -MRI -CSF may be normal Prognosis -Ischemic > hemorrhagic -Idiopathic cases have fair to good prognosis

Answer 80

Cuterebra Larvae Tx -Supportive care with anticonvulsants -Unapproved and anecdotal tx -Ivermectin, etc.

Answer 81

Intercapital ligament: T11, T12, T13 -Lacking ligament could be related to disks ruptures in those locations Intervertebral Disk -Annulus fibrosis (AF): made of collagen fibers. Attached to vertebral endplate on either side. Tough part that does not move -Nucleus pulposus (NP): jelly center, remnant of developing notochord. Absorbs shock. Eccentrically placed. AF much thicker ventrally

Answer 82

Hensen type I -Chondroid metaplasia of the NP -NP loses water binding capacity. -New Hayline cartilage calcifies and loses hydroelasticity C/S -3-6 yo but as early as 6mts -Presents as an ACUTE EXTRUSION of nuclear material out of disk Common sites -C2-C3 -T10-L3: is the danger zone -T11, T12, T13: have no inter capital ligament Hensen Type II -Fibroid metaplasia of the NP -NP replaced with fibrocartilage **NO calcification** -Micro tears in the AF, causes firm disc bulge C/S **Non-chondrodystrophic breeds, usually large breeds** ->5-7 yo -Chronic PROTRUSION of disk

Answer 83

-Anything with little twisted legs -Dachshund -Pekingese -Shih Tzu -Frenchie -Beagle -Basset hound, etc

Answer 84

-Spinal pain common -Reluctance to move -Abnormal posture Gait -Paresis and proprioceptive ataxia -Scuffing toes -Muscle spasms -Fasciculations, especially cervical -Bladder dysfunction (UMN vs. LMN) Dx -Neurolocalization is key -Plain radiographs: proper placement a must -CT better -MRI best Radiographs -Mineralization of disk confirms degenerative process -Narrowing or opacification in foramen -Narrowing or wedging of disk space -Overlapping of articular facets -NEVER for planning surgery Tx A. Cervical B. thoracolumbar 1. Conservative 2. surgical Order of loss of function with increasing damage 1. Propioception: outer most 2. Voluntary motor: next inner 3. Superficial pain 4. Nociception: Deep Pain, last inner most Pain Pathways (nociception) -Small, non-myelinated -Multisynaptic -Multi decussations -Loss of nociception: functional transection **If they can walk they should be able to fell deep pathways**

Answer 85

C2-C3 most common in small breeds C6-C7 in large breeds -Cervical hyperesthesia -Low head carriage -Neck guarding -Muscle fasciculations -Myelopathy

Answer 86

Conservative -Mildly affected patients -First time offenders -Cage confinement for 3-4 weeks (annulus must heal) -Gabapentin (MOA not fully understood, but binds to Alpha-delta units of voltage gated Ca++ channels, decreasing Ca influx, thus inhibiting release of excitatory neurotransmitters. -Predinisone questionable Px -Ambulatory patients very likely to respond -Reccurence 36% Surgical -Severely affected or chronic cases -Ventral slot decompression -Goal is to remove the perturbing material Px -Even tetraplegic dogs up to 83% full recovery -Small percentage have residual pain or deficits

Answer 87

Conservative treatment -Only grades 4-5 -First time offenders -Cons: recurrence likely -If absent nociception only 5% chance of recovery Tx -Strict confinement 3-4 wks -Medications: analgesics, Gabapentin, muscle relaxants -Do not admin dexamethasone = urinary tract infection more likely Surgical -Repeat offenders 0-3 grade -Cons: can not correct any functional damage to cord -Only relieving compression, can't fix neurological damage -Hemilaminectomy, dorsal laminectomy, pediculectomy, etc. Px - chance they can walk Henson Type I Intact nociception = 86-96% chondrodystrophic breeds. 78-85% non-chondrodystrophic breeds Henson type II -22-52% Absent nociception -Overall 0-76% chance of recovery

Answer 88

Review -Presence or absence of nociception is most prognostic indicator -Absent nociception: guarded to poor -Present nociception: 80-95% -Myelomalacia: 5-10% occurrence, grave prognosis Accessories -Slings, carts, diapers, etc

Answer 89

3 layers of smooth muscle 1. B-adrenergic and A-adrenergic receptors innervated by hypogastric nerve (SNS) 2. Cholinergic (PSNS) receptors innervated by pelvic nerve (contraction) 3. Stretch sensation in bladder wall transmit through pelvic nerve Urethra -Internal sphincter: A-adrenergic, stimulation = contraction, facilitates filling -External sphincter: innervated by pudendal nerve (somatic motor) cholinergic Filling phase Pointe Micturition Center -Hypogastric nerve: adrenergic = relaxation of bladder and contraction of internal sphincter -Inhibition of cholinergic cell bodies of pelvic nerve = relaxation of bladder -Pudendal nerve somatic efferents = contraction of external sphincter Evacuation -Pelvic nerve and pudendal nerve to the PMC -Threshold "on/off switch" -PMC will cause: inhibition of hypogastric nerve, facilitation of cholinergic in pelvic nerve, inhibition of pudendal nerve -DETRUSOR REFLEX

Answer 90

1. Detrusor reflex (local) 2. Brainstem influence 3. Cortical influence (conscious potty trained) can be consciously initiated or inhibited

Answer 91

-Occurs when lesion between Pons and L7 -Interfere with or abolish DEXTRUSOR REFLEX C/S -Hallmark: Increased sphincter tone (loss of inhibitory pudendal nerve) -Bladder feels turgid when palpated -Very difficult to express

Answer 92

-Occurs with any lesion of sacral spinal cord/nerve roots/pelvic plexus C/S -Hallmark: decreased bladder and sphincter tone -Easy to express -Constant dribbling

Answer 93

-Ischemic neuromyopahty "saddle thrombus" -Thrombus lodges in distal aorta inhibiting blood flow to the muscles and nerves of the pelvic limbs -Acute in cats, and insidious in dogs -Very commonly confused with disk disease, especially in dogs

Answer 94

-Occlusion artery/venous system that feeds the spinal cord -Embolizing fibrocartilage from NP -Exact mechanism unknown **Usually active, non-chondrodystrophic, large breeds** -Older cats #1 Miniature Schnauzer in small breeds -Acute onset, non-painful, and generally non-progressive after the first 24 hrs -BOXERS most commonly represented C/S -Signs and severity highly variable -Asymmetry -Dependent on location and distribution within the spinal cord Dx -Myelography and CT -MRI hyper intensity within cord representing edema Tx -Maintain spinal cord perfusion is key -Steroids contraindicated -Nursing care -Physiotherapy Px -Usually good -Lose of nociception, LMN signs, symmetry, owner compliance, no function at 2 weeks mark

Answer 95

-Unstable or malformed -AA joint the "no" joint results in excessive movement of AA joint -Ventral cord compression from cranial aspect of C2 -Transverse ligament injury most likely Pathophysiology & C/S -Young <2yo -Toy and small breed (yorkie) -Failure of normal development (dens, ligaments) -Predisposes to acute luxation from minor trauma -Can also become chronic (abnormal dens, stretching of ligaments, trauma) -Lesion: compression of spinal cord by axis C2 C/S -Acute neck pain -Reluctance to move -C1-5 myelopathy: Tetraparesis and ataxia 4 limbs (very likely is going to die due to respiratory dysfunction) -Postural deficits -UMN to all limbs -Animals resist flexion, DO NOT manipulate neck Dx -Radiographs: neutral view first, no flexion -Increased space between dorsal lamina C1 and spinous process C2 -Extreme caution when flexed views -Evaluate dens (CT better) -MRI for cord Tx -Conservative 60% success -External rigid splint/bandage for 6-8 weeks -Very labor intensive -Bandages sores/infections -Recurrence

Answer 96

-60-90% success -Eventual osseous fusion of AA joint -Immediate fixation Cons: invasive, expensive, implant failure, infection, migration

Answer 97

-Degenerative LS stenosis, cauda equina syndrome -Commonly affects adult, large breed dogs (GSD) Pathology -Chronic instability at LS joint (vertebral spondylosis) -Type 2 disk disease at L7-S1 -Subluxation of the sacrum under caudal aspect of L7 -Hypertrophy of interarcuate ligament -Facet/joint capsule hypertrophy C/S -Lumbosacral pain is an early indication -Spinal lordosis or tail flexion -Reluctance to rise, sit, climb stairs, jump. -Lameness resembles orthopedic disease. **Beware of concurrent hip dysplasia** L4-S4 myelopathy -Urinary/fecal incontinence -Decreased withdrawal reflexes especially at hock is common Dx -Radiography: may see LS spondylosis and articular facet hypertrophy -Myelography confusing due to anatomy -CT excellent for bony changes and MRI for soft tissue Tx Non-surgical -Forced exercise restriction -NSAIDs or steroid -Analgesics -Weight loss Surgical -Dorsal laminectomy at LS disk space +/- LS diskectomy Px -Non surgical: transient effectiveness or not at all -Surgical 55-87% success Pre surgical incontinence = poor post op outcome

Answer 98

-Slowly progressive -Non-inflammatory disease of spinal cord -Axonal degeneration +/- demyelination in TL cord Breeds -GSD -Pembroke Welsh corgi ~ 11 yo -Boxer -Chesapeake Bay -Retriever -Rhodesian Ridgeback -Rare in cats C/S -9 yo (8-14 yo) -Non-painful insidious onset, slowly progressive -T3-L3 myelopathy -Postural deficits in rear -Normal to hyperactive rear limb reflexes -Disuse atrophy -Progressive to bladder incontinence, paraplegia over 6-9 mts -Disease will proceed cranially in late stages Dx -Only histopath definitive -Exclusion of other diseases -DNA test? Tx -No effective treatment Px -Long term is poor

Answer 99

-Vertebral malformation Breeds -Labrador -Dalmatian -Giant breeds (great dane, mastiff) -Doberman pincher C/S -Any cervical spinal cord lesion can result in "wobbly" gait Giant Breed C/S -Ataxia and paresis begin ~1-2 yo -Overzealous nutrition? -Static Compression of spinal cord and/or nerve roots -Vertebral canal stenosis -Disk disease rarely involved

Answer 100

-6-8 yo -Slow progressive -Static or dynamic Path -IVD protrusion -Proliferation of annulus -Facet hypertrophy: joint capsule proliferation -Dorsal longitudinal ligament -Interarcuate ligament (yellow) C/S -Cervical pain -Low head carriage -Resistance to flexion **Caudal cervical spine most commonly affected** -Signs of c6-T2 myelopathy -Classic "2 engine gait" forelimbs are choppy, short, rear limbs are slow and clumsy Dx -Imaging radiographs to rule out other diseases -MRI preferred Tx -Conservative: exercise restriction, confinement 3-4 wks, NSAIDs, Gabapentin, Prednisone. -Neck brace -Improvement transient Surgical -Ventral slot and many others

Answer 101

-Both intracranial and spinal diseases associated -Fluid within spinal cord, central canal, or mixture -NOT CSF Sigs -Cervical pain -Phantom scratching -Myelopathy Dx -MRI only Tx -Prednisone -Gabapentin -Pain meds: Tramadol, Codeine

Answer 102

-Collection of signs that reflect sympathetic dysfunction, not a specific disease (loss of SNS tone) -Control of pupillary size is a tonic balance between Constriction and dilation Signs -Can be partial or complete -Unilateral or bilateral -Miosis: dilator pupillae and celiris mm. SNS = dilation -Ptosis: Orbital muscle: drooping of eyelid -Enophthalmos: orbital muscle retreats globe into socket -elevation of 3rd eyelid: orbital muscle -Possible stuffy/crusty nostril Conditions associated with Horner's syndrome -Brachial plexus damage -Neoplasia (thyroid, PNST) -Aggressive venipuncture -Otitis media/interna -CV accident stroke in the brains -Polyps -Mediastinal mass -Brain disease -Dysautonomia Golden Retriever = Idiopathic = 50% of canine cases Dx -Testing supposed to be able to distinguish where in the pathway the problem is -Unpredictable and unreliable -Best imaging of head and neck to check for structural lesions Pathway UMN from hypothalamus to T1-T3 (1st order) Preganglionic fibers from T1-T3 to CCG (2nd order) Postganglionic fibers to the eye (3rd order)

Answer 103

-Acute neuropathy of one or both facial nerves -Axonal loss of some demyelination but NO INFLAMMATION -Exact pathogenesis unknown "idiopathic" - analogue to Bell's palsy -Middle-aged to older animals Breeds #1 Crocker Spaniels C/S -Drooping ear, lip, and lower eyelid -Decreased to absent palpebral reflex and menace response -Can still see -Excessive salivation and history of dropping food/water -Corneal ulceration: blink and PS disruption -Rarely mild vestibular signs -Must rule out otitis media/interna and hypothyroidism Tx -Symptomatic treatment -Corticosteroids controversial, may be not indicated Px -Guarded for return to full function (unlike people) -Can go bilateral -Contracture of muscles possible in time

Exam 3 Flashcards

(134 cards)