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Small Animal Med > Exam 3 Spring (Neuro) > Flashcards

Exam 3 Spring (Neuro) Flashcards

1
Q

Spinal Cord Segments in Dogs & Cats

A

o 7 cervical vertebrae BUT 8 spinal cord segments
o 13 thoracic
o 7 lumbar
o 3 sacral
o ~5 caudal

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2
Q

Patellar Reflex

A

o Monosynaptic
o L4-6 spinal cord segments & nerve roots
o Femoral nerve
o Innervates the quadriceps for extension of the stifle

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3
Q

Withdrawal Reflex

A

o Polysynaptic
o Pelvic limb -> L6-S1 -> Sciatic nerve
o Thoracic limb -> C6-T2 -> multiple nerves
o Innervates muscles for flexion of the limb
o Does not signify ability to feel

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4
Q

Cutaneous Trunci Reflex

A

o Start at hips
o Pinch dermatome
o Both lateral thoracic nerves
o C8-T1
o Bilateral cutaneous trunci contraction
o If there is cutoff: lesion is 1-2 spinal cord segments cranial
o If absent on one side: efferent problem on that side

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5
Q

CN II

A

o Optic Nerve
o Sensory for vision

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6
Q

CN III

A

o Oculomotor
o Motor to extraocular muscles, levator palpebrae
o Constricts pupil

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7
Q

CN IV

A

o Trochlear
o Motor to dorsal oblique

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8
Q

CN V

A

o Trigeminal

Opthalmic
 Sensory to eye & medial canthus

Maxillary
 Sensory to maxilla

Mandibular
 Sensory to mandible
 Motor to muscles of mastication

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9
Q

CN VI

A

o Abducent
o Motor to lateral rectus & retractor bulbi

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10
Q

CN VII

A

o Facial

Sensory
 middle ear,
 head blood vessels,
 palate,
 rostral 2/3 tongue

Motor
 ears,
 eyelid (orbicularis oculi),
 cheeks,
 lips,
 rostral digastricus (skeletal)
 mandibular / submandibular salivary glands
 lacrimal glands
 nasal glands (smooth - parasympathetic)

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11
Q

CN VIII, CN IX, CN XII

A

CN VIII
 Vestibulocochlear
 Hearing

CN IX
 Glossopharyngeal
 Sensory to carotid body, caudal tongue, rostral pharynx
 Motor to pharyngeal muscles & parotid salivary gland

CN XII
 Hypoglossal
 Motor to tongue

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12
Q

CN X

A

 Vagus

Sensory
* Aortic body
* Sinus
* Pharynx
* Larynx
* Thoracic & abdominal cavity

Motor
* Pharynx
* Larynx
* Esophagus
* Organs of the throax & abdomen

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13
Q

CN XI

A

 Accessory

Internal Branch
* Motor to everything vagus is

External
* Motor to trapezius, sternocephalicus, brachicephalicus

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14
Q

Menace Response Pathway

A

o Optic nerve(CN2) ->
o optic chiasm ->
o cross over ->
o optic tract ->
o thalamus (lateral geniculate) ->
o visual / occipital cortex ->
o motor / frontal cortex ->
o cross back over ->
o descending tracts
o cerebellar influence ->
o Facial nerve (CN 7)

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15
Q

PLR Pathway

A

o Optic nerve ->
o Optic chiasm ->
o Cross over ->
o Optic tract ->
o Pretectal area ->
o Bilateral oculomotor nerve
o Direct constriction stronger than indirect

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16
Q

Which Nerves does the Oculovestibular Reflex Test

A

o CN 8
o MLF
o CN 3
o CN 4
o CN 6

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17
Q

Ocular Sensation Reflex Pathway

A

o Touch eye ->
o CN 5 (ophthalmic branch) ->
o CN 7 – blink
o CN 6 – eyeball retraction & elevation of 3rd eyelid

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18
Q

Palpepbral Reflex Pathway

A

o Touch canthus of eyes ->
o CN 5 (maxillary & ophthalmic) ->
o CN 7 blink

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19
Q

Facial Reflex Pathway

A

o Touch different spots on face ->
o CN 5 (ophthalmic, maxillary, mandibular) ->
o CN 7 ->
o Blink & twitch

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20
Q

Facial Response Pathway

A

o Cover eyes and put hemostats in nostril ->
o CN 5 (ophthalmic) ->
o Cross over ->
o Thalamus ->
o Somatosensory/parietal cortex ->
o Motor cortex ->
o Move head away from stimulus

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21
Q

Which Nerves do Jaw Tone, Facial Symmetry, Gag reflex, and the Tongue Test

A

Jaw Tone
o CN 5 (mandibular)

Facial Symmetry
o CN 5 & 7

Gag Reflex
o CN 9 & 10

Tounge
o CN 12

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22
Q

Perineal Reflex

A

constriction of the anus (anal tone)
o pudendal nerve -> S1-3

flexion of tail
o caudal spinal cord segments

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23
Q

Localizing UMN or LMN Lesions

A

Front Limb
 UMN - Anything before C6
 LMN - At C6-T2

Hind Limb
 UMN – Anything before L4
 LMN – At L4-S1

Decreased patellar reflex & normal withdrawal
 L4-L6

Increased Patellar & decreased withdrawal
 L6-S1

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24
Q

Nerves with Parasympathetic Function

A

o 3
o 7
o 10
o 11

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25
Q

UMN VS LMN Signs

A

UMN
 Normal to increased spinal reflexes
 Normal to increased muscle tone
 increased step distance
 Disuse muscle atrophy

LMN
 Decreased to absent spinal reflexes
 Decreased to absent muscle tone
 decreased step distance
 Neurogenic muscle atrophy

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26
Q

Types of Muscle Atrophy

A

Disuse
 evolves more slowly,
 less severe

Neurogenic
 Fast (10-14 days)
 severe

Primary Myopathic
 variable

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27
Q

Stuporous Vs Comatose

A

Stuporous
 Responds to deep pain only

Comatose
 Non-responsive even to deep pain

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28
Q

Decerebrate Rigidity; Signs, Lesion

A

Signs
 Opisthotonos
 Extensor rigidity of all limbs
 Stupor or coma
 +/- respiratory problems
 +/- HR & BP problems

Lesion
 Midbrain

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29
Q

Decerebellate Rigidity; Signs, Lesion

A

Signs
 Opisthotonos
 Extensor rigidity of thoracic limbs +/- pelvic limbs
 Awar of environment
 Other cerebellar signs

Lesion
 Cerebellar

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30
Q

Schiff Sherrington; Signs, Lesion

A

Signs
 Extensor rigidity of thoracic limbs

Lesion
 Acute, severe spinal cord injury of T3-L3

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31
Q

Head Turn Vs Tilt

A

Head Turn
o Supratentorial lesion
o Head toward side of lesion

Head tilt
o Cerebellar or vestibular
o USUALLY toward side of lesion (vestibular)
o Away from side of lesion can be w/ cerebellar lesion

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32
Q

Cerebellar Vs Vestibular Signs

A

Cerebellar
 Intention Tremor
 Menace deficit but visual
 Decerebellate rigidity
 Weird eye things
 Increased urination
 NO concious proprioception deficits

Vestibular
 Head tremors & eyelid contraction secondary to nystagmus
 Positional nystagmus
 May have concious proprioception deficits

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33
Q

Vestibular; Central or Peripheral

A

Central
 Vertical nystagmus
 Changing nystagmus
 CN deficits other than 7 & 8
 conscious proprioception deficits

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34
Q

Localizing Lesion w/ Head tilt

A

If there is hemiparesis/paresis/weakness
o lesion is central & on side of paresis

If no paresis
o lesion on side of tilt

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35
Q

Circling

A

o Always circle to side of lesion

Tight circles
 Cerebellar / vestibular (infratentorial)

Bigger circles
 Supratentorial

Hugging wall
 Usually blind in that side

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36
Q

Reasons for Ventral Neck Flexion

A

o Neck pain
o Myopathy / neuropathy
o Thiamine deficiency
o Myasthenia gravis
o Hyperthyroidism
o Organophosphate toxicity
o Ethylene glycol toxicity
o K, Na, Ca, phosphate abnormalities

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37
Q

Nerve Root Signature

A

o Dogs that are walking, stop, and hold one paw up
o Sign of a problem with the nerve root
o Can be infection but often tumor
o C6-T2 or L4-S3

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38
Q

Types of Ataxia

A

Vestibular
 Falling & leaning

Cerebellar
 Hypermetria (walking on hot rocks)
 Cerebellum or spinocerebellar tracts of spinal cord

Proprioceptive/Sensory
 Wide-based stance
 Crossing over
 Swaying

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39
Q

2 Engine Gait

A

o Decreased step distance in front
o Increased step distance in pelvic
o Lesion at C6-T2

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40
Q

Paresis; Definition, Types, Clinical Presentation

A

o Weakness at gait &/or supporting weight

Types
 Para – pelvic limbs
 Tetra – all 4 limbs
 Hemi – front & hind limbs on one side
 Mono – 1 limb
 Classified as ambulatory or non

Clinical Presentation
 Slow/shuffling gait
 Dragging/knuckling paw
 Collapse/falling
 Exercise intolerance
 Unable to support weight
 Difficulty rising
 Etc

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41
Q

Plegia

A

o No voluntary motor movement

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42
Q

Central Cord Syndrome

A

o CP deficits in front limbs only
o Due to lesion in central spinal cord

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43
Q

Signs of Problem w/ CN3

A

o Ptosis (droopy upper eyelid)
o Ventrolateral resting strabismus
o Mydriasis due to parasympathetic dysfunction

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44
Q

Horner’s Syndrome

A

o Miosis (anisocoria)
o Elevated 3rd eyelid
o Ptosis (droopy upper eyelid)
o Enopthalmos

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45
Q

Anisocoria; Causes of Miosis Vs Mydriasis

A

Miosis
 Increased parasympathetic due to drugs or cerebrocortical dz
 Decreased sympathetic due to horner’s
 Corneal ulcer
 Uveitis
 Spastic pupil syndrome in FeLV/FIV cats

Mydirasis
 Decreased parasympathetic due to atropine or CN3 dysfunction
 Increased sympathetic due to phenylephrine
 Blindness
 Glaucoma
 Iris atrophy
 Cerebellar dz

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46
Q

Strabismus

A

CN 3, 4, 6 dysfunction
o resting strabismus

CN 8 dysfunction
o positional strabismus

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47
Q

Decreased Facial Sensation & reflex

A

o CN5 & CN 7 dysfunction
o Contralateral cortex dysfunction

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48
Q

CN 5 Mandibular Branch Dysfunction

A

o Atrophy of temporal muscle on affected side
o Drop jaw = bilateral dysfunction
o Neurotropic keratitis due to reduced blinking & lack of corneal nutrition

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49
Q

CN7 Dysfunction

A

o Paralysis = drooping of face on affected side
o Hemifacial spasm = contraction of face on affected side

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50
Q

Idiopathic Geriatric Vestibular Dz

A

o Older dogs
o Acute onset of peripheral vestibular signs
o Mild head tilt to severe imbalance / rolling (usually unilateral)
o Improve rapidly, although can take 2-3 wks for complete recovery
o Can have residual head tilt or relapse
o can happen in cats but at any age (rare)

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51
Q

Supratentorial; Location, Clinical Signs of Lesion

A

o Forebrain
o CN 1 & 2

Clinical Signs
 Contralateral paresis
 Contralateral CP deficits
 Contralateral menace deficits
 Contralateral facial response deficits
 Contralateral hemi-neglect
 Ipsilateral circling
 Ipsilateral head turn
 Seizures
 Behavioral changes

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52
Q

Infratentorial; Location, Clinical Signs of Lesion

A

o Hind brain
o CN 3-12

Clinical Signs
 Ipsilateral paresis
 Ipsilateral CP deficits
 Ipsilateral CN deficits (contralateral CN 4)
 Cerebellar / vestibular signs
 Decerebrate & decerebellate rigidity
 Abnormal respiration
 Severe altered mental status

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53
Q

Intracranial Degenerative Dz

A

o Slowly progressive signs
o Non-painful
o Multifocal or widespread signs
o May have organomegaly if storage dz

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54
Q

Congenital Hydrocephalus; Clinical Signs, Diagnosis, Treatment

A

o Often due to stenosis of mesencephalic aqueduct
o Often toy breeds

Clinical Signs
 Dome shaoed head
 Persistent fontanels
 Ventral/lateral strabismus
 Poor learners
 Visual deficits
 Circling
 Seizures

Diagnosis
 Ultrasound, CT, MRI
 CSF analysis to rule out inflammatory dz

Treatment
 Pred to decrease CSF production
 Acetazolamide or mannitol
 Omeprazole to decrease CSF production (lifelong)
 Ventricular CSF shunting

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55
Q

Hydrancephaly

A

o Cerebral hemisphere reduced to fluid filled sac
o Meninges & ependyma intact
o Associated w/ panleukopenia in kittens

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56
Q

Lissencephaly; Basics, Clinical Signs

A

o Smooth brain = minimal sulci/gyri
o Abnormal cerebral cortical neuronal migration during fetal development

Clinical Signs
 Seizures
 Poor learning
 Blindness
 Typically non-progressive or lethal

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57
Q

Cerebellar Hypoplasia;

A

o Congenital & rare abnormal development of cerebellum
o Cats: panleukopenia virus exposure in utero
o Dogs: Maybe herpes or parvo exposure in utero
o Incoordination & CP deficits
o Non-progressive & may learn to compensate over time

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58
Q

Caudal Occipital Malformation Syndrome; Signalment, Pathophysiology

A

Signalment
 Small breed dogs
 Cavalier King Charles especially prone

Pathophysiology
 Malformation of caudal occipital area overcrowds caudal fossa ->
 Cerebellar compression & herniation ->
 Focal meningeal hypertrophy at foramen magnum ->
 Increase CSF pressure ->
 Hydrocephalus ->
 Concurrent syringohydromyelia

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59
Q

Caudal Occipital Malformation Syndrome; Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
 Scratching at head
 Spinal pain
 Paresis/paralysis
 CP deficits
 Diminished menace
 Seizures
 scoliosis

Diagnosis
 MRI w/ occipital defect & fluid around spinal cord

Treatment
 Prednisone
 +/- omeprazole
 +/- gaba for pain
 Surgical foramen magnum decompression if does not improve w/ meds

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60
Q

Hepatic Encephalopathy; Pathophysiology, Clinical Signs, Diagnosis

A

Pathophysiology
 Liver failure or shunt ->
 GABA, aromatic acid, mercaptans, skatoles, ammonia not filtered out of blood ->
 Demyelination of white matter
 Ischemic necrosis of grey matter ->

Clinical Signs
 Obtundation
 Abnormal behavior
 Head pressing
 Visual deficits
 Ptyalism in cats
 Signs can worsen after meals

Diagnosis
 Widened sulci on MRI
 Lentiform nuclei light up on MRI

61
Q

Hypoglycemia; Mechanism, Neuro Signs

A

Mechanims
 Neuroglycopenia ->
 Sympathetic nervous system stimulation

Clinical Signs
 Coma
 Irritability
 Pupillary dilation
 Seizures
 Tremors
 Weakness
 Visual defects

62
Q

Na Abnormalities; Consequences of Correcting too Fast; Safe Correction

A

Too rapid correction of hypernatremia
 Cerebral edema

Too rapid correction on hyponatremia
 Thalamic myelinolysis
 Brain cell dehydration
 Hemorrhage

Safe correction
 < 0.5meq/L/hr

63
Q

Hypothyroidism; Neuro Signs,

A

 CN 5, 7, 8 deficits
 Decreased facial sensation
 Facial paralysis
 Vestibular dysfunction
 Lar par and/or megaesophagus due to CN 10 dysfunction
 Appendicular neuropathy
 Myasthenia gravis
 Hypertension -> atherosclerosis -> stroke
 Myopathy
 Myxedematous stupor/coma (rare)

64
Q

Hyperthyroidism; Neuro Signs

A

o Restlessness, irritability, aggressiveness
o Wandering, pacing, circling
o Stroke due to hypertension
o Tremors
o ventral neck flexion

65
Q

Hyperadrenocorticism; Neuro Signs

A

 Myopathy type II – muscle atrophy & myotonia
 Neuropathy
 Systemic hypertension & stroke
 hydrocephalus
 Seizures 7/or blindness due to space occupying tumor

66
Q

Thiamine Deficiency; Basics, Brain Areas Affected, Clinical Signs, Treatment

A

o All fish diet in cats (thiaminase)

Areas Affected
 Polioencephalomalacia
 Bilateral oculomotor
 Vestibular
 Lateral geniculate nuclei
 Caudal colliculus

Clinical Signs
 Acute & rapidly progressive
 Lethargy, anorexia
 Dilated pupils
 Vestibular signs
 Visual deficits
 Ventral neck flexion
 Coma
 Opisthotonos
 Death

Treatment
 Thiamine hydrochloride

67
Q

Meningioma; Basics, Clinical Signs, Diagnosis, Treatment

A

o Most common brain tumor in cats / dogs
o Arise from the arachnoid layer
o Usually histopathologically benign
o Extraneural metastasis rare
o Cats - well-encapsulated, firm, easily removable, can have multiple masses
o Dogs – usually solitary, meshwork of vessels internally, intimately attached to underlying tissue – more difficult to remove

Clinical Signs
 Supratentorial signs

Diagnosis
 MRI w/ contrast

Treatment
 Corticosteroids to decrease edema & inflammation
 Chemo
 Radiation
 Sx + radiation or chemo

68
Q

Meningioma; Prognosis

A

Cats
* w/ sx – 22-27mo
* may be curative

Dogs
* w/ sx 7mo
* w/ radiation 1-2yrs
* w/ sx + radiation 16mo – 3yrs

69
Q

Unilateral Muscle Atrophy

A

o tumor tumor tumor
o maybe infectious or trauma

70
Q

Nerve Sheath Tumor Treatment

A

 Sx but difficult to get clean margins
 Fractionated radiation therpay
 Radiosurgery if <2cm

71
Q

Pituitary Macroadenoma; Basics, Treatment

A

o Sella or suprasellar location
o >1 cm, expands into diencephalon
o Contrast enhancing

Treatment
 Fractionated radiation therapy
 Radiosurgery if <2cm
 Transsphenoidal hypophysectomy through hard palate (75% success)

72
Q

Canine Distemper Clinical Signs

A

 Hyperkeratotic foot pads
 Polioencephalomyelopathy & seizures in younger dogs
 Leukoencephalomyelopathy w/ cerebellar/vestibular signs in older dogs
 Myoclonus (repetitive muscle contraction)

73
Q

Rabies Clinical Signs

A

o Seizures
o Hypersensitivity to light & sound

Furious
 Aggression
 Forebrain signs
 More common in cats

Paralytic
 LMN to CNs signs
 Dropped jaw
 Swallowing deficit
 Hypersalivation
 More common in dogs

74
Q

Cryptococcus; Clinical Signs, Diagnosis, Treatment

A

o Multifocal symptoms

Diagnosis
 Round organisms w/ halo on CSF cytology

Treatment
 Fluconazole
 Cage rest
 Physical therapy

75
Q

Granulomatous Meningoencephalitis (GME); Basics, Clinical Signs, Signalment, Treatment, prognosis

A

o Granulomatous infiltration of lymphocytes, plasma cells & macrophages
o Primarily effects white matter
o Causes mass effect

Clinical Signs
 Optic neuritis
 Focal Brainstem signs
 Disseminated cerebrum, cerebellum, brainstem, & cervical spine

Signalment
 Young - middle age
 Small breeds

Treatment
 Corticosteroids
 Azathioprine
 Cyclosporin
 Cytosine arabinoside
 Procarbazine

Survival
 Weeks to years
 Can’t be cured & relapse will occur

76
Q

Encephalitis Protocol

A

o TMS
o Clindamycin
o Doxycycline
o Pred

Once infectious agents ruled out
 Discontinue antibiotics
 Increase pred to 2-4mg/kg/day
 +/- another immunosuppressive drug

77
Q

Necrotizing Leukoencephalitis (NLE); Signalment, Clinical Signs, Prognosis

A

Signalment
 Yorkies
 Juvenile – young adult

Clinical Signs
 Forebrain & brainstem signs
 White matter necrosis & cavitation

Prognosis
 Fatal w/in wks to months

78
Q

Necrotizing Meningoencephalitis (NME); Signalment, Clinical Signs, Prognosis

A

Signalment
 Pugs
 Maltese
 Juvenile to young adult

Clinical Signs
 Forebrain signs
 Seizures
 Grey & white matter necrosis & cavitation

Prognosis
 Fatal w/in wks to months

79
Q

Generalized Tremor Disorder; Clinical Signs, Signalment, Diagnosis, Treatment

A

Clinical Signs
 Diffuse, fine, whole body tremor

Signalment
 Small breeds
 Usually young

Diagnosis
 CSF w/ mild lymphocytic pleocytosis

Treatment
 Responds really well to pred but relapse possible

80
Q

Idiopathic Trigeminal Neuritis; Clinical Signs, Treatment, Prognosis

A

Clinical Signs
 Dropped jaw
 Masseter/temporalis atrophy
 Bilateral mandibular branch problem
 +/- sensory branch problem
 +/- Horner’s

Treatment
 Nutritional support
 PT

Prognosis
 Jaw function recovers in 4-6wks
 Persistent muscle atrophy

81
Q

Idiopathic Facial Paralysis; Clinical Signs, Treatment, Prognosis

A

Clinical Signs
 Unilateral/bilateral CN 7 palsy
 +/- CN 8 problem
 Exposure keratitis of eye

Treatment
 No specific
 Lubricate eyes

Prognosis
 Some never recover
 Can recover after 3-6 wks

82
Q

Pupil Abnormalities

A

Bilateral miotic (constricted) pupils
 Diffuse cerebrocortical dz

Unilateral mydriasis
 Unilateral caudal transtentorial herniation

Bilateral Mydriasis
 Bilateral caudal transtentorial herniation or foramen magnum herniation

83
Q

Caudal transtentorial herniation or foramen magnum herniation; Clinical Signs

A

 Non-responsive mydriasis
 Seizures
 Respiratory changes
 Cushing’s reflex (hypertension + bradycardia)
 Brain heart syndrome (VPCs)

84
Q

Monroe-Kelli Doctrine

A

o 3 compartments w/in rigid skull
o If one increases, others have to decrease
o Cerebral perfusion pressure = mean arterial BP – Intracranial pressure
o Constricting vessels -> decrease ICP
o Lowering CO2 - > decrease ICP

85
Q

Traumatic Brain Injury; Stabilization, Surgery

A

Stabilization
 Treat hypovolemic shock
 Treat hypoxemia
 Mannitol (once hydrated) to decrease intracranial fluid
 Hypertonic saline to increase perfusion to brain
 Elevate head
 Monitor CO2
 Keep calm & quiet
 NO steroids

Craniotomy/ectomy
 If medical management is not working
 Open skull fractures
 Depressed skull fractures
 Foreign bodies
 Hematomas
 Must take images prior

86
Q

Physiology of a Seizure

A

o Glutamate causes excessive excitation
o GABA does not adequately inhibit

87
Q

Cluster Seizures Vs Status Epilepticus

A

Cluster Seizures
o 2 - more seizures w/in 24hrs
o Poor prognosis

Status Epilepticus
o 5 – more mins of continuous seizure
o Incomplete return to consciousness between seizures
o Guarded prognosis

88
Q

Focal Vs Generalized Seizures

A

Focal
o One hemisphere involved
o May or may not lose consciousness
o Lateralized or regional signs
o Can progress to generalized

Generalized
o Both hemispheres involved
o Typically lose consciousness
o Motor +/- autonomic
o Tonic/Clonic/Atonic/Myoclonic

89
Q

Reactive Seizures Vs Epilepsy

A

Reactive
 Response to transient disturbance
 Reversible when underlying disturbance is treated
 Metabolic/Toxic

Epilepsy
 Dz of brain predisposing to seizures
 2 – more seizures >24hrs apart
 Can be idiopathic or structural

90
Q

EEG; Basics, Methods to Perform

A

o Electroencephalography
o Distinguishes between seizures and other events
o Also useful for sleep disorders
o ]Ideally catch patient during an episode
o Can have false negatives

Sedated
 Looks for interictal activity
 Short

Ambulatory
 Longer, unsedated
 More likely to catch an episode

91
Q

When to treat Seizures

A

o ≥2 seizures in 6m
o Cluster seizures
o Status epilepticus
o Known structural brain disease
o Prolonged severe post-ictal periods

92
Q

Step 1 Emergency Seizure Control

A

o Benzo bolus to bind GABA
o Diazepam (IV, IN, PR)
o Midazolam (IV, IM, IN)

93
Q

Step 2 Emergency Seizure Control

A

o If benzo bolus unsuccessful

Benzo CRI
 Diazepam may bind to tubing
 Midazolam not useful after 6-12hr

Phenobarb or Keppra bolus
 Useful for clusters

Ketamine bolus
 Useful for status epilepticus
 Not useful for cluster

94
Q

Step 3 Emergency Seizure Control

A

o Propofol or inhalant anesthesia
o Works on GABA R
o Safe for refractory status epilepticus
o Must intubate
o Refer or call for consult

95
Q

Seizure Maintenance

A

o Balance between seizure control & side effects
o Pick one drug and use until maxed out dose
o Treat patient not levels

Goals
 >50% reduction in seizures
 1 seizure every 3m or less

96
Q

Phenobarbitol

A

o Binds to GABA R
o Increases Cl influx -> hyperpolarization
o Longest history & best efficacy seizure drug
o 1st line treatment in most species
o Inexpensive
o Highly bioavailable
o Hepatic metabolism
o Q12
o Reach stead state in 2wks

97
Q

Potassium Bromide

A

o Mimics Cl -> hyperpolarization
o Good efficacy
o 1st or 2nd line treatment
o NO cats
o Inexpensive
o Renal secretion
o SID
o Steady state at 3mo

98
Q

Levetiracetam (Keppra)

A

o Prevents neurotransmitter release
o Efficacy variable
o Rapid oral absorption
o Little hepatic metabolism
o Mostly excreted unchanged in urine
o “Honeymoon” period
o Often used as adjunct treatment
o Q8hr
o Steady state at <48hr

99
Q

Zonisamide

A

o Blocks Na channels -> hyperpolarization
o Carbonic anhydrase inhibitor
o Moderate efficacy
o Hepatic metabolism
o Q 12
o Narrow dose range
o “honeymoon” effect

100
Q

Misc Adjunct Seizure Therapies

A

o Oral benzos (stop working over time & contraindicated in cats)
o Ketogenic diet (sometimes works)
o CBD oil (no regulations, meh)
o Vagal nerve stimulation (questionable)
o Transcranial magnetic stimulation (questionable)

101
Q

Spinal Shock

A

o Sudden severe UMN injury
o Transient period of reduced excitability of spinal neurons distal to site of injury
o Initial Loss of Perineal (15mins), patellar (30min-2hr), & withdrawal (12+hr) reflexes
o Bladder reflexes may be affected longer
o NOT neurogenic shock

102
Q

White Matter of Spinal Cord

A

Ascending
 Sensory
 Dorsolateral
 Peripheral (less protected)

Descending
 Motor
 Ventrolateral
 Central (more protected)

103
Q

Order of Loss of Function w/ Spinal Cord Injury

A

o Ataxia + CP deficits +/- pain
o Ambulatory para/tetraparesis
o Nonambulatory para/tetraparesis
o para/tetraplegia w/ nociception (deep pain)
o para/tetraplegia No nociception (deep pain)

104
Q

Myelomalacia; Basics, Clinical Signs

A

o Spinal cord necrosis secondary to ischemia from injury
o Can occur up to 10 days after injury

Clinical Signs
 +-fever
 Hyperesthesia
 Decreased abdominal tone
 Reflex deficits
 Decreased anal tone
 Ascending cutaneous trunci reflex
 Decreased thoracic wall movement & dyspnea
 Eventual thoracic reflex deficits +/- horner’s
 Fatal

105
Q

IVDE: Intervertebral Disc Extrusion; Signalment, Pathophysiology, Clinical Signs, Diagnosis

A

Signalment
 Chondrodystrophic breeds (short legs/long back)
 Young
 Genetic defect in chromosome 12 and/or 18

Pathophysiology
 Degeneration of nucleus pulposus ->
 Compression & contusion of spinal cord

Clinical Signs
 Acute onset
 Progressive
 Painful
 Most commonly UMN T3-L3 signs
 Possibly cervical UMN signs

Diagnosis
 MRI w/ dark disks & spinal cord deviation

106
Q

IVDE: Intervertebral Disc Extrusion; Treatment

A

Medical
* If good motor function
* CRATE REST 4-6wks
* +/- analgesia & NSAIDs
* Avoid jumping
* Carry up stairs

Surgery
* Failed medical management or no motor function
* Still need 4-6wks crate rest post-op
* Deep pain (-) has poor prognosis

107
Q

IVDP: Intervertebral Disc Protrusion; Signalment, Pathophysiology, Clinical Signs, Diagnosis

A

Signalment
 Older
 Med-large breed dogs

Pathophysiology
 Chronic fibrosis & degeneration of entire disc ->
 Protrusion of entire disc

Clinical Signs
 Chronic
 Progressive
 Often non-painful
 T3-L3 UMN signs

Diagnosis
 MRI

108
Q

IVDP: Intervertebral Disc Protrusion; Treatment

A

Medical
* Preferred
* NSAIDs
* Rest
* PT
* Steroids if edema in cord

Surgery
* Rare
* May slow progression but not return fxn

109
Q

ANNPE: Acute Non-compressive Nucleus Pulposus Extrusion; Pathophysiology, Clinical Signs, Treatment

A

Pathophysiology
 Acute extrusion of disc fluid ->
 Spinal cord contusion but no compression

Clinical Signs
 T3-L3 UMN signs acutely after high activity
 +/- pain

Treatment
 Crate rest 4-6wks
 Physical therapy

110
Q

HNPE: Hydrated Nucleus Pulposus Extrusion; Basics, Diagnosis, Treatment

A

o Similar to ANNPE
o May not have inciting event
o Contusion & compression of spinal cord
o Most common in cervical region

Diagnosis
 MRI

Treatment
 Crate rest 4-6 wks
 Physical therapy

111
Q

Lumbosacral Stenosis (Cauda Equina Syndrome); Signalment, Pathophysiology

A

Signalment
 Older, Large breed
 Maybe young active dogs
 Maybe cats

Pathophysiology
 L7-S1 IVDP +
 DJD & proliferation of articular facets +
 Hypertrophic ligaments ->
 Narrowing of lumbosacral canal & foramen

112
Q

Lumbosacral Stenosis (Cauda Equina Syndrome); Clinical Signs, Diagnosis, Treatment, Prognosis

A

Clinical Signs
 Painful
 Marked nerve pain
 bunny hopping, tucked tail, short stride
 Pelvic Limb lameness
 pain on palpation
 +/- incontinence
 +/- pelvic limb reflex deficits
 NO ataxia

Diagnosis
 MRI (gold)
 CT
 Rads

Treatment
 Crate rest + steroids for 4-6wks
 Physical therapy
 Lean BCS
 Dorsal laminectomy if medical fails

Prognosis
 Poor if incontinent

113
Q

Degenerative Myelopathy; Basics, Diagnosis, Treatment

A

o Chronic, progressive
o T3-L3
o Middle aged – older
o German shepherds, corgis, etc
o SOD1 mutation

Diagnosis
 Genetic testing (shows risk not diagnosis)
 Degeneration of white matter on necropsy
 Diagnosis of exclusion

Treatment
 No real treatment
 May slow neuro decline w/ physical therapy

114
Q

Degenerative Myelopathy; Clinical Signs

A

Initial
* T3-L3
* Ataxia
* CP deficits
* Paraparesis
* Non-painful

Late
* Progression to paraplegia & LMN signs
* Progression to thoracic limbs
* Ascend to brainstem if ignored

115
Q

Osseus Associated Wobbler’s (Cervical Spondylomyelopathy); Basics, Clinical Signs, Diagnosis

A

 Young giant breeds
 Some large breeds
 Bony proliferation of vertebrae -> dorsolateral compression of spinal cord

Clinical Signs
* Chronic progressive
* Cervical pain
* Ataxia
* Tetraparesis
* +/- hypermetria
* Proprioceptive deficits
* +/-reflex deficits
* Pelvic often worse than thoracic

Diagnosis
* MRI (gold)

116
Q

Disc Associated Wobbler’s (Cervical Spondylomyelopathy); Basics, Clinical Signs, Diagnosis

A

 Middle aged large breed dogs
 Commonly dobies

Clinical Signs
* 2-engine gait

Diagnosis
* MRI

117
Q

Wobbler’s (Cervical Spondylomyelopathy); Treatment

A

Medical
* Crate rest 4-6 wks
* Gaba or pregabalin
* NSAIDs or steroids
* Physical rehab

Surgical
* Decompression
* Stabilization

118
Q

Atlantoaxial Instability; Basics, Pathophysiology, Clinical Signs, Diagnosis, Treatment

A

o Young Toy breed dogs
o Any breed w/ trauma

Pathophysiology
 Lack of ligaments + incomplete C1 ->
 Neck flexion ->
 Spinal cord compression

Clinical Signs
 Acute onset
 Cervical pain
 Ataxia
 Dullnes
 Tetraparesis
 +/- vestibular signs

Diagnosis
 Rads showing increased C1-C2 space or malalignment of C1-C2
 VERY careful w/ neck flexion for rads

Treatment
 Crate rest 6-8wks + neck brace
 Surgery (difficult)

119
Q

Vertebral Anomalies; Basics, Types

A

o Common in frenchies & pugs
o Usually incidental
o Block vertebrae (fused vertebrae)
o Hemivertebrae (major bend to spine)
o Butterfly vertebrae (type of hemi)
o Transitional vertebrae (vertabrea that developed partly into different type)

120
Q

Spina Bifida

A

o Bull dogs & manx cats
o Failure of closure of dorsal vertebral arch
o Lumbar/lumbosacral region
o Progressive T3-Cd signs
o Maybe incontinent
o May need sx

121
Q

Spinal Neoplasia; Extradural Vs Intradural Extramedullary Vs Intramedullary

A

Extradural
 Common
 Lymphoma, Chondrosarcom, osteosarcoma, hemangioma
 Maaaaybe nerve sheath tumors or meningiomas

Intradural Extramedullary
 Common
 Meningioma, nerve sheath tumors, nephroblastoma

Intramedullary
 Uncommon
 Hemangiosarcoma, glioma, ependymoma
 Maaaaybe nephroblastoma

122
Q

Spinal Neoplasia; Types In Dogs

A

Meningioma
* Common in older dogs
* C1-C5
* Often surgical

Nephroblastoma
* Young dogs
* T3-L3
* Often surgical

Peripheral Nerve Sheath Tumors
* Large breeds
* C6-T2
* Pain & lameness (nerve root signature)

123
Q

Spinal Neoplasia; Types In Cats

A

Lymphoma
* Young or old
* Extradural masses w/ infiltrate
* Thoracic spinal cord

Glioma

124
Q

Spinal Neoplasia; Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
 Pain
 lameness

Diagnosis
 thoracic & abdominal rads for mets
 spinal rads for vertebral lysis
 MRI for surgical planning

Treatment
 Pred to reduce spinal cord edema
 Sx
 Radiation (often w/ sx)

125
Q

Discospondylitis; Basics, Etiology, Agents

A

o Infection of disc & endplate
o Young -> middle aged large breed dogs
o Rare in cats
o Male > female

Etiology
 Migrating foreign body
 Penetrating wound
 Hematogenous
 Iatrogenic

Agents
 Most commonly
 E. coli
 Aspergillus (Germans)

126
Q

Discospondylitis; Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
 Pain
 +/- fever, anorexia, weightloss
 Myelopathy

Diagnosis
 Irregular/lytic endpaltes on rads
 Blood/urine culture
 Urine Asper testing
 RSAT fro Brucells
 +/- echo
 Maybe CT in early dz

Treatment
 Activity restriction
 Antibiotics based on C/S
 Empirically w/ Cephalexin or TMS
 +/- NSAIDs
 Treat for 6mo-1yr although pt will feel better in 1-2wks
 Recheck reds q2-3mo or at 6mo

127
Q

Granulomatous Meningoencephalitis/myelitis; Basics, Clinical Signs, Diagnosis, Treatment, Prognosis

A

o Usually small dogs
o Any age

Clinical Signs
 Acute, progressive
 May wax & wane
 Pain
 Lameness
 Hunched posture

Diagnosis
 CSF pleocytosis
 CSF culture
 PCR of CSF for infectious dz
 Histopathology post mortem (definitive)

Treatment
 Immune suppression w/ pred, cyclosporine etc

Prognosis
 Lifelong treatment

128
Q

Steroid Responsive Meningitis Arteritis; Basics, Clinical Signs, Diagnosis, Treatment

A

o Young large breed dogs
o Looks very similar to discopondylitis

Clinical Signs
 Acute, progressive
 May wax & wane
 Mostly cervical pain
 Dullness/lethargy
 Stiff gait
 Often febrile
 NO neuro deficits

Diagnosis
 Rule out other dz
 Neutrophilic pleocytosis & elevated protein on CSF

Treatment
 steroids

129
Q

Priorities During Spinal Trauma Emergencies

A

o ABCs

Brain
 Mentation
 pupil size
 PLR
 physiologic nystagmus

Spinal Cord
 Look for voluntary motor fxn
 Check reflexes
 Check deep pain
 DO NOT MOVE pt

130
Q

3 Compartment Model

A

o When looking at spinal trauma on CT
o Large dorsal – small middle – large ventral
o Trauma to >1 compartment = instabile

131
Q

Stable Vs Unstable Spinal Trauma

A

Stable
 No fractures or non-displace fractures
 Only 1 compartment effected
 More spinal cord contusion than bony compression
 +/- disc herniation

Unstable
 Visible vertebral fractures
 Subluxation or luxation
 Spinal cord compression
 +/- disc herniation
 May worsen w/ movement

132
Q

Spinal Trauma Treatment

A

o Strict crate rest 6-8wks
o External coaptation for cervical region
o Analgesia w/ fentanyl & NSAIDs
o Antibiotics if open wounds
o Surgery – faster recovery

133
Q

Fibrocartilagenous Embolism; Pathophysiology, Clinical Signs, Diagnosis, Treatment, Prognosis, Recovery Rules

A

Pathophysiology
 Piece of dic embolizes in spinal cord vascular supply ->
 Ischemic injury

Clinical Signs
 Looks a lot like ANNPE
 Peracute onset
 Non painful
 Lateralized
 Non-progressive

Diagnosis
 Intrinsic lesion on MRI
 Pleocytosis +/- neutrophils on CSF
 Histo at necropsy

Treatment
 Support
 PT

Prognosis
 UMN good
 LMN guarded & may persist
 Loss of nociception (pain) grave

Recovery Rules of Thumb
 Want to see SOME improvement by 2wks
 Spinal cord should be mostly healed by 6wks

134
Q

Upper Motor Neuron Bladder; Injury, Pathophysiology, Clinical Signs, Treatment

A

o Spinal injury above S1-S3
o Usually T3-L3

Pathophysiology
 No detrusor contraction
 Increased filling
 Increased urethral tone
 Disruption of sensory input from bladder

Clinical Signs
 Large, distended turgid bladder
 Unable to urinate voluntarily
 Hard to express
 Bladder may overflow & result in dribbling
 Risk of atony

Treatment
 Prazosin for internal sphincter
 Diazepam for external sphincter
 Bethanechol for detrusor

135
Q

Lower Motor Neuron Bladder; Injury, Pathophysiology, Clinical Signs, Treatment

A

o Injury at S1-S3
o L4-S1
o Cauda equina

Pathophysiology
 No detrusor contraction
 Decreased urethral tone
 Disruption of sensory input from bladder

Clinical Signs
 Small or large flaccid bladder
 Poor urethral tone
 Dribbling urine
 May or may not express easily

Treatment
 Very difficult
 Poor prognosis

136
Q

Detrusor Atony; Stretch Vs Neurogenic

A

Stretch
 UMN
 Severe bladder distension
 Damage of tight junctions
 Obstruction of outflow
 DON’T express
 catheterize

Neurogenic
 LMN
 Bladder anatomy normal
 May recover if neuro issue treated
 Express or catheter

137
Q

Primary Detrusor Sphincter Dyssynergia

A

o Middle aged large breed male dogs
o Normal neuro
o Easy to catheterize

138
Q

Detrusor Overactivity; Basics, Treatment

A

o Usually underlying cystitis
o Occasionally idiopathic

Treatment
 Propantheline

139
Q

Urethral Sphincter Mechanism Incompetence; Basics, Treatment

A

o Female spayed dogs
o Most common cause of leaking urine
o Normal neuro

Treatment
 PPA
 Estrogens
 Testosterone in males

140
Q

Top 3 differentials for LMN dz

A

o Tick paralysis
o Botulism
o Polyradiculoneuritis (Coonhound paralysis)

141
Q

Tick Paralysis; Clinical Signs, Diagnosis

A

Clinical Signs
 Ascending paresis -> flaccid paralysis of all limbs in 12-72hrs

Diagnosis
 Find tick
 Response to tick med
 Should resolve in 12-48hrs

142
Q

Botulism; Clinical Signs, Treatment

A

Clinical Signs
 Pelvic paresis -> flaccid paralysis of all limbs

Treatment
 Support

143
Q

Polyradiculoneuritis; Clinical Signs, Treatment

A

o Auto-immune

Clinical Signs
 Pain
 Pelvic paresis -> flaccid paralysis of all limbs

Treatment
 Support
 If in need of ventilator -> poor prognosis

144
Q

Myasthenia Gravis; Types, Clinical Signs, Treatment

A

Types
o Congenital – lack of Ach receptor
o Acquired – Ach receptor antibody

Clinical Signs
 Short choppy gait worsens w/ activity
 Decreased palpebral reflex
 Megaesophagus
 Lar par or stridor
 Dysphagia
 Ventral neck flexion (cats)

Treatment
 Oral pyridostigme
 Feed elevated if have megaesophagus

145
Q

Myasthenia Gravis; Diagnosis

A

Tensilon test (not definitive)
* Edrophonium IV –> increase Ach at the NMJ
* Exercise patient to point of collapse
* See clinical improvement in gait and palpebral reflex within 30-60 seconds
* Effect lasts 5-10minutes
* Intubation & ventilation in case cholinergic crisis

 Muscle biopsy for congenital
 Ach receptor Ab titer for acquired

146
Q

Brachial Plexus Avulsion; Pathophysiology, Clinical Signs

A

o Traumatic abduction of limb -> C6-T2 stretched

Clinical Signs
 LMN
 Non painful

147
Q

Metronidazole Toxicity

A

 vestibular signs in dogs
 blindness & seizures in cats

148
Q

Masticatory Myositis; Clinical Signs, Diagnosis, Treatment

A

Clinical Signs
 Trismus (Lock jaw)
 Swollen, painful masseter & temporalis muscles
 Exophthalmos
 Highly elevated CK

Diagnosis
 2M antibody titer
 Muscle biopsy for prognosis

Treatment
 Must treat VERY quickly
 Immunosuppressive pred
 PT

149
Q

Tetanus; Clinical Signs, Treatment

A

Clinical Signs
 Sardonic grin & lock jaw
 Blepharospasm
 Extensor rigidity of limbs
 Exacerbated by excitement

Treatment
 Quiet environment
 Sedation
 Muscle relaxants
 Wound treatment
 Metronidazole & penicillin
 Maybe antitoxin (controversial)

Small Animal Med (10 decks)

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