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ACVIM General - Imp stuff > Neurology > Flashcards

Neurology Flashcards

1
Q

Where would the lesion be with a LMN bladder? Causes? Clinical sings?

A

Lesion: sacral SC or pelvic nerve

Causes: IVDD, cauda equine syndrome, congenital malformation of the sacrum (manx cats), SI luxations, sacrococcygeal fractures, spinal tumors, LS disease

Clinical signs: Urine scalding, UTIs, overflow incontinence

Large, turgid bladder that is easily expressed

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2
Q

Where would the lesion be with a UMN bladder? Causes? Clinical sings?

A

Lesions: lesions above the sacral spinal cord. Incomplete reflex detrusor contraction and spasticity of the EUS incomplete emptying

Causes: IVDD, tumors, trauma

Clinical Signs:
Large turgid bladder
Impaired stream of urine
Overflow incontinence
Automatic bladder: involuntary micturition when threshold capacity of the bladder is reached
Concurrent paresis/paralysis

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3
Q

What’s second line tx for status epilepticus in dogs

A

Keppra- IV
Phenobarbital - IV or CRI –> superior in dogs
Fosphenytoin - IV

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4
Q

What are the 4 stages of status epilecticus?

A
  1. Impending – neurotransmitter release, ion channel opening/closing –> 1st line tx
  2. Established – GABA R decrease, internalization of GABA R units, NMDAR and AMPAR up-regulation –> 2nd line tx
  3. Refractory – excitatory and inhibitory neuropeptides release/imbalance, +/- BBB drug transporters unregulated –> 3rd line tx
  4. Super refractory – gene expression alterations –> likely minimally to non-responsive
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5
Q

When can electroencephalogram be useful?

A

Non convulsive status epilepticus

Seizure termination would be - epileptiform discharged

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6
Q

Define status epilepticus

A

Continuous seizure activity or >1 sequential seizure without full recovery of consciousness in between with a duration >30mm

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7
Q

Best non-IV tx of SE in DOGS

A

Intranasal midazolam

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8
Q

What are the steps to follow for 3rd line seizure management

A

3rd line - anesthetic medications used for controlling seizure activity

  1. Ketamine IV bolus, followed by CRI
    If ketamine doesn’t work – dexmedetomidine IV bolus and CRI
  2. Propofol IV bolus, possibly followed by CRI – CAUTION in cats
  3. Anesthetic barbiturates (pentobarbital or soium thiopental) IV bolus and CRI
  4. Inhalation anesthesia
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9
Q

What’s the MOA of dexmedetomidine? How is it neuroprotective?

A

MOA: alpha2 adrenoreceptor agonist –> decreased excitatory neurotransmitters via suppression of sympathetic NS + NE release in amygdala, hippocampus and cerebral cortex

Neuroprotective – decreasing cerebral metabolic and oxygen demands, decreasing brain edema via VASOCONSTRICTION and contributing to maintaining normal mean arterial pressure

SE: decreased resp, bradycardia, cardiac arrhythmias, hypothermia

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10
Q

MOA of ketamine and SE

A

MOA: NMDA-receptor antagonist –> reduced release of glutamate
Also increased blood pressure

SE: vomiting, vocalization, salivation

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11
Q

MOA of propofol and SE

A

MOA: potentiates GABA by decreasing rate of dissociation of GABA from its receptors –> prolonged binding = influx of Cl –> hyperpolarization of postsynaptic cell membrane
-Interacts with glycine (agonist) and NMDA (antagonist) receptors as well as Ca channels

SE: CV and resp depression, pain at injection site, loss of gag reflex

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12
Q

Why do we have to be cautious with cats and propofol

A

Can cause Heinz body anemia

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13
Q

MOA and SE of anesthetic barbiturates (pentobarbitone and sodium thiopentone)

A

MOA: GABA receptor agonists
-Neuroprotective effect by decreasing intracellular Ca and Na, glutamate release and cerebral oxygen consumption

SE: resp and CV depression, hypotension, hypothermia, cardiac toxicity (sodium thiopentone), vocalizations and seizure-like movements in recovery

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14
Q

Tx for patients with supra refractory seizures

A

Hypothermia
IV magnesium and allopregnanolone

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15
Q

MOA of Mg for anti seizure

A

MOA: inhibit NMDA receptor and Ca channels, increase cerebral blood flow via vasodilation

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16
Q

Use of hypothermia for seizures

A

Decreases excitatory neurotransmittets, Ca, glutamate-induced excitotoxicity, cerebral metabolic rate
Normalizes ICP

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17
Q

What retrogene mutation is associated with TL IVDD is chondrodystrophic breeds?

A

FGF-4 on chromosome 12 –> leads to early chondrioid metaplasia, degeneration, mineralization of nucleus pulpous

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18
Q

How can MRI help with prognosis of TL IVDD?

A

Presence and extent of intramedullary T2 hyper intensity, T2 hypo intensity, and attenuation of CSF signal on HASTE/T2 sequences – associated with worse locomotor outcome and development of myelomalacia

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19
Q

What’s the sensitivity of CT for IVDD? What makes it less accurate

A

81-100% sensitivity for cchondrodystrophic dogs w mineralized disks
Distinguishes between chronically extruded material

Less accurate if >5yo and <7kg

Does not provide insight on severity of parenchymal injury

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20
Q

When would CT be the first line advanced imaging in TL IVDD

A

Suspect acute TL-IVDE - low likelihood of missing compressive surgical lesion

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21
Q

Fenestration at which sites is not recommended for IVDD?

A

Routine fenestration of L4-5 and more caudal sites
Fenestration at T10-11 or above - not recommended due to low rate of disk extrusion at these sites

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22
Q

What medications can be used to aid in urination post op TL surgery

A

Alpha receptor antagonists - prazosin, phenoxybenzamine, alfuzosin, tamsulosin or centrally acting muscle relaxant (diazepam)

bethanecol use not recommended - unwanted cholinergic effects

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23
Q

What are clinical findings in a dog with suspected progressive myelomalacia

A

Ascending paralysis
Hypoventilation
Loss of segmental spinal reflexes
Cranial migration of CTR caudal border
Decreased abdominal tone
Horners syndrome
Diffuse pain
Thermodysregulation
Malaise

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24
Q

Lesions where in the SC are more likely to develop myelomalacia

A

Lumbar intumescensce

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25
Q

Name clinical biomarkers for evaluation of progressive myelomalacia

A

Serum pNfn - increases
Myelography - diffuse intraparenchyman constrast
SSTSE CSF:L2 ratio >7.4 – sensitivity 100%, specificity 75%

26
Q

What nerve(s) affected with medial strabismus

A

CN VI

27
Q

What nerve(s) affected with ventrolateral strabismus

A

CN III

28
Q

Menace CN involved

A

CN II - afferent
CN VII - efferent

29
Q

What nerve(s) affected with dropped jaw

A

Bilateral CN V

30
Q

What nerve(s) affected with ptosis

A

CN III

31
Q

What nerve(s) affected with diminished to absent PLRs

A

CN III

32
Q

What nerve(s) affected with atrophy to trapezius

A

CN XI

33
Q

What nerve(s) affected with masticayoty muscle atrophy

A

CN V

34
Q

What nerve(s) affected with dorsomedial strabismus in a cat

A

CN IV

35
Q

What nerve(s) affected with atrophy of the tongue

A

CN XII

36
Q

What nerve(s) affected with deviation of the nasal philtrum (contralateral)

A

CN VII

37
Q

CN responsible for PLR

A

CN II - response to light

38
Q

CN responsible for pupil constriction

A

CN III (oculomotor)

39
Q

Name neuro signs associated with cerebellar disease

A

-Intention tremors of head, neck, eyes
-Opisthotonus and extensor rigidity of all limbs with hips flexes
-Truncal sway
-Head tilt
-Hypermetria/spastic gait
-Spinal reflexes: normal to exaggerated
-CN: menace deficit (ipsilateral), anisocoria (rare)

40
Q

Neuro signs associated with prosencephalic disease

A

-Mentation: seizures, abnormal behavior, propulsive activity, depression to coma
-Posture/gait: head turn, normal gait (unless parachute lesion), propulsive circling (ipsilateral to lesion), aimless wandering, head pressing
-Posture rxns: contralateral deficits
-Contralateral hypalgesia
-CN contralateral menace deficits with normal or abnormal PLRs

41
Q

Neuro signs associated with. mid to caudal brainstem disease

A

-Mentation: depression-coma
-Posture/gair: UMC tetraparesis/plagia and GP deficits; vestibular ataxia, opisthotonos (BS lesion)
-Postural reactions: ipsilateral deficits (pons, medulla), contralateral deficits (rostral midbrain)
-Muscle mass, spinal reflexes: normal to increased x4
-CN: anisocoria (III), dropped jaw, atrophy of muscles mastication (CN V), facial hypalgesia (V), head tilt (VIII), resting or positional nystagmus (VIII), dysphagia (IX, X), tongue paresis/paralysis (XII)
Resp or cardiac abnormalities

42
Q

Describe what you would see in pelvic limbs, thoracic limbs, other in a C1-C5 lesion

A

Postural reactions: delayed to absent x4
Thoracic limb: UMN paresis; GP deficits, normal withdrawal
Pelvic limb: UMN paresis; GP deficits, normal to increased spinal reflexes
Severe lesions: Spastic tetraplegia, horners syndrome (ipsilateral miosis), resp complications

43
Q

Describe what you would see in pelvic limbs, thoracic limbs, other in a C6-T2 lesion

A

Postural reactions: delayed to absent x4
Thoracic limb: LMN paresis (short and choppy gait); reduced withdrawal
Pelvic limb: UMN paresis; long stranded gait, normal to exaggerated spinal reflexes
Severe lesions: Flacid LMN paralysis in TL, spastic paraplegic HL, horners syndrome (T1-T3), resp complications

44
Q

Describe what you would see in pelvic limbs, thoracic limbs, other in a T3-L3 lesion

A

Posture reactions: normal thoracic, delayed to absent hindlimb
Thoracic limbs: normal
Pelvic: UMN paresis, GP deficits, long strides gait, normal to exaggerated spinal reflexes
Severe: spastic paraplegic, schiff-sherrington in TL

45
Q

Describe what you would see in pelvic limbs, thoracic limbs, other in a L4-S3 lesion

A

Postural reactions: delayed to absent PL
Thoracic limbs: normal
Pelvic: LMN paresis (short and choppy), GP deficits, reduced patellar (L4-L6) or withdrawal reflexes (L6-S1)
Severe: flaccid paraplegia in PL - flaccid ants and tail with reduced to absent sensation to perineum

46
Q

Describe the pathway for Horners syndrome

A

1st order neurons originate in rostral brainstem –> cervical spinal cord —> (synapse with second order neurons - preganglionic) –> cell bodies in T1-T3 –>. course up the vagosympathetic trunk –> synapse with3rd order (post-ganglionic) in cranial cervical ganglion –> project to eye and adnexa

Summary: brainstem –> cervical SC (synapse–>preganglionic)–> T1-T3–>vagosymptathetic trunk–>postganglionic cranial cervical ganglion–>eye

47
Q

Describe CS of horners

A

Miosis
3rd eyelid prolapse
Ptosis
Enophthalmos

48
Q

What breed is predisposed to horners

A

goldens

49
Q

If you’re testing for horners with phenylephrine –> mydriasis within 20min. Where is the lesion?

A

Post ganglionic

50
Q

If you’re testing for horners with phenylephrine –> mydriasis after 20min. Where is the lesion?

A

Preganglionic

51
Q

Where are the majority of the idiopathic HS located

A

post ganglionic

most will resolve in 3-4months on its own

52
Q

Agent that causes botulism

A

Clostridium botulinum type C (dogs and cats)
Gram positive, motile, anaerobic spore forming bacilli

53
Q

Presentation of botulism

A

Rapidly progressive symmetric LMN paresis, +/- CN deficits
No sensory nerve deficits
No hyperesthesia
Parasympathetic system affected
Ascending paralysis
Cats can present with urinary incontinence and when the forelimbs are affected have spasm of the triceps muscle that results in caudal extension of the limb with carpal flexion (different than dogs)
Dogs can still wag their tails :)

54
Q

Mechanism of infection with botulism

A

Toxin ingested → survives in acid stomach conditions → absorbed into bloodstream from the SI → travels to peripheral cholinergic synapses → inhibits release of Ach → ascending symmetrical flaccid paralysis, megaesophagus, signs of autonomic dysfunction

Cleaves membrane associated SNARE proteins → type C toxin affects membrane, not vesicle SNARE proteins

Prevents release of Ach (pre-synaptic)

55
Q

Mechanism of acquired MG

A

Immune mediated destruction of POST synaptic ACH receptors
CD4+ T-cell activation of B-CellG

56
Q

Gold standard to diagnose MG

A

Ach receptor antibodies test
Diagnostic:
-Dog: >0.6
-Cat: >0.3

57
Q

Tx of MG

A

Anticholinestarase therapy. – pyridostigmine bromine (inhibits acetylcholinesterase)

58
Q

Where’s the toxin in tick paralysis

A

PRE synaptic
Prevents Ach release

59
Q

Causative agent of tetanus

A

Clostridium tetani - Gram positive, motile, anaerobic spore forming bacilli
Produced 2 toxins – toxin that causes problems is Tetanospasmin
Toxin for tetanus and botulism have similar composition: 2 polypeptide chains (heavy chain and light chain) joined by disulfide bond
Heavy chain attached to presynaptic nerve terminal
L chain is zinc-dependent matrix metalloproteinase

60
Q

Presentation for tetanus

A

Presentation: progressive muscle stiffness and rigidity
Facial muscle contraction, ears pulled towards each other
Stiff stilted gait, sew horse stance
Lockjaw
Laryngeal and pharyngeal involvement → dysphagia, dyspnea
⅓ of dogs have cryptogenic tetanus (no wound)

61
Q

Describe the pathophysiology of tetanus

A

Tetanospasmin toxin is released from C. tetani
Toxin enters into motor axon at NMJ → travel retrograde up to spinal cord → inhibits the inhibitory interneurons (Renshaw cells) in the spinal cord (level of the ventral horn) –> Toxin enters inhibitory interneurons in brain and spinal cord → interferes with GABA and glycine inhibitory neurotransmittersT

62
Q

Tx for Tetanus

A

Supportive care, nutrition, +/- tracheostomy
Clean wound
Abx recommended
Metronidazole - recommended as first line
Penicillin G - second line, as can antagonize GABA
Antitoxin has high risk of anaphylaxis

ACVIM General - Imp stuff (11 decks)

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