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ACVIM Specialty 2023 > Neurology COPY > Flashcards

Neurology COPY Flashcards

1
Q

What creates the resting membrane potential of a neuron?

A
  • Na/K ATPase pumps: exchange 3 Na+ ions out of the cell in exchange for 2 K+ ions
  • Creates a more negative potential inside the cell compared to the outside
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2
Q

What is the resting membrane potential difference of a neuron (in mV)?

A

-65 to -70 mV

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3
Q

What triggers opening or closing of the ion channels in a neuron?

A

Membrane voltage or a neurotransmitter binding to a receptor linked to the channel

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4
Q

When a neuron depolarizes past -55 mV, what channels open to begin the action potential?

A

Voltage gated Na+ channels

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5
Q

As Na+ diffuses into the cell, it further depolarizes the membrane until it approached the equilibrium potential for Na+. What is this (in mV)?

A

59 mV

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6
Q

The depolarization of the membrane from Na+ influx triggers the opening of voltage-gated K+ channels. What occurs?

A

K+ diffuses out of the cell to its equilibrium potential of -90 mV

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7
Q

How do toxins such as pyrethrins cause tremors and seizures?

A

Block sodium channel inactivation, increasing action potential generation

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8
Q

What two factors influence the speed at which action potentials travel down an axon?

A
  • Axonal diameter
  • Myelin
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9
Q

Ions flow directly between neurons in what types of synapses?

A

Electrical synapses or gap junctions

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10
Q

What causes the release of neurotransmitters into the synapse?

A
  • Action potential depolarizes the nerve terminal => opening of voltage gated Ca++ channels
  • Ca++ flows into the cell and activates synaptic vesicle proteins that allow the vesicle to dock and fuse with the cell membrane => release of the neurotransmitter into the synaptic cleft
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11
Q

Name 3 families of ionotropic receptors

A
  1. Nicotinic acetylcholine, gamma-amino butyric acid (GABA) and glycine
  2. Glutamate
  3. ATP or purine P2X receptors
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12
Q

What occurs when acetylcholine binds to nicotinic receptors?

A

The nicotinic pore becomes permeable to cations => Na+ diffusion into the cell => depolarization of the post-synaptic neuron

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13
Q

What enzyme in the synaptic cleft breaks down acetylcholine to choline and acetic acid?

A

Acetylcholinesterase

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14
Q

What causes myasthenia gravis?

A

Autoantibodies against the alpha1 subunit partially block the acetylcholine receptor in the neuromuscular junction

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15
Q

What is the major inhibitory neurotransmitter? What occurs when the receptor is stimulated

A
  • GABA
  • The GABA-A receptor becomes permeable to Cl-, leading to diffusion of Cl- into the cell
  • Leads to hyperpolarization of the cell and an inhibitory post-synaptic potential
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16
Q

What is the mechanism of action of diazepam and phenobarbital?

A

Bind to the extracellular sites on the GABA-A receptor - do not open the channel, but they alter the kinetics so that it stays open longer after GABA binds. Makes it harder to depolarize the cell and cause seizures

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17
Q

What is the major excitatory neurotransmitter in the CNS? What are the two receptors it binds to?

A
  • Glutamate
  • AMPA and NMDA - must bind both receptors to produce an effect
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18
Q

What happens after glutamate binds AMPA and NMDA?

A
  • Binding to AMPA partially depolarizes the membrane and releases a Mg++ ion that was blocking NMDA
  • Binding to NMDA then leads to additional Na+ and Ca++ conductance
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19
Q

What causes excitotoxicity?

A

Excessive NMDA receptor activation, leading to accumulation of intracellular Ca++ => cell death

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20
Q

A system of microtubules is utilized for transporting proteins, vesicles, etc from the neuronal cell body to the axon and back. What are the names of these microtubules?

A
  • Kinesins - transport from the cell body to the axon terminal
  • Dyneins - transport from the terminal back to the cell body
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21
Q

What is temporal summation?

A

Several action potentials from the same pre-synaptic neuron summate to depolarize the post-synaptic neuron

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22
Q

What is spatial summation?

A

Several action potentials from multiple, different pre-synaptic neurons summate to depolarize the post-synaptic neuron

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23
Q

What is the reticular activating system?

A
  • Monoaminergic and cholingeric neurons in the brainstem and basal forebrain send large projections to activate the forebrain and mediate consciousness, attention, etc.
  • Lesions within these projections can lead to stupor or coma
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24
Q

A head or body turn typically localizes disease to what region?

A

Rostral brainstem or cerebral disease

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25
Q

A plantigrade stance localizes disease to what?

A

Peripheral neuropathies

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26
Q

Describe decerebrate rigidity. Where does this localize disease to?

A
  • Opisthotonus with rigid extension of the neck and all four limbs
  • Midbrain or rostral cerebellar lesions
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27
Q

Describe decerebellate rigidity. Where does this localize disease to?

A

Opisthotonus with extension rigidity of the limbs BUT the hips are flexed or intermittently flexed
- Severe cerebellar lesions

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28
Q

A short, choppy, stilted gait is often indicative of what type of paresis?

A

Lower motor neuron

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29
Q

A long-striped, spastic gait with proprioceptive ataxia is indicative of what type of paresis?

A

Upper motor neuron

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30
Q

What causes general proprioceptive ataxia?

A

Disruption of the spinocerebellar tracts and conscious proprioceptive pathways that relay the anatomic location and degree of muscle contraction to the brain

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31
Q

Describe what general proprioceptive ataxia looks like

A
  • Crossing the limbs
  • Scuffing or dragging the digits
  • Standing or landing on the dorsal aspect of the paws
  • Delay in the swing phase of the gait
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32
Q

What causes vestibular ataxia?

A

Loss of orientation of the head with respect to the eyes, neck, limbs, and trunk

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33
Q

Describe what vestibular ataxia looks like

A
  • Tendency to drift, lean, or fall in one direction
  • +/- head tilt or nystagmus
  • Normal strength and proprioception with peripheral lesions, may be abnormal with central lesions
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34
Q

Describe what cerebellar ataxia looks like

A
  • Hypermetric gait with sudden bursts of motor activity
  • Overflexion of the limbs on protraction
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35
Q

What must be intact for a pet to perform postural reactions?

A

All major sensory and motor (UMN and LMN) components of the CNS and PNS - using postural reactions to evaluate conscious proprioception is a misnomer, because all postural reactions rely on BOTH motor and proprioceptive systems

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36
Q

What is the prosencephalon?

A

Cerebrum and thalamus

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37
Q

Unilateral prosencephalic lesions (cerebrum and/or thalamus) will result in postural reaction deficits on what side? They are usually accompanied by what other changes?

A
  • Contralateral side to the lesion
  • Often accompanied by contralateral menace deficit, contralateral sensory deficits, or changes in mentation/behavior
  • Gait is usually normal but may circle or pace
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38
Q

Describe the characteristic physical exam findings with a T3-L3 lesion

A
  • Postural reaction deficits in the pelvic limbs with normal thoracic limbs
  • Paraparesis with GP ataxia
  • UMN in the pelvic limbs: normal to exaggerated muscle tone and spinal reflexes
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39
Q

Describe the characteristic physical exam findings with a C1-C5 lesion

A
  • Tetraparesis with GP ataxia
  • Postural reaction deficits in all four limbs
  • UMN signs in all four limbs - normal to exaggerated spinal reflexes and muscle tone
    +/- Horners syndrome
    +/- respiratory difficulty
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40
Q

Describe the characteristic physical exam findings with a C6-T2 lesion

A
  • Thoracic limbs: LMN signs - flaccid paralysis or paresis, short choppy gait, reduced withdrawal reflexes and muscle tone
  • Pelvic limbs: UMN signs/GP deficits - long strided gait, normal to exaggerated spinal reflexes and muscle tone
  • +/- Horners with T1-T3 lesions
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41
Q

What mediates the patellar reflex?

A

Femoral nerve through the spinal cord segments L4-L7

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42
Q

In the thoracic limbs, the nerves responsible for the withdrawal reflex arise from what spinal cord segments?

A

C6-T2

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43
Q

In the pelvic limbs, the nerves responsible for the withdrawal reflex arise from what spinal cord segments?

A

Mediated by the sciatic nerve through L6-S1

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44
Q

With spinal cord lesions, where will the cutaneous trunk reflex stop?

A

Typically it is preserved for 1-2 vertebral bodies caudal to the level of the lesion

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45
Q

Deficits in cranial nerve III will lead to what clinical signs?

A

Oculomotor nerve = motor to the extraocular muscles and parasympathetic to the pupil
- Ventrolateral strabismus
- Diminished to absent PLRs with dilated pupils

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46
Q

Deficits in cranial nerve IV will lead to what clinical signs?

A

Trochlear nerve = motor to the dorsal oblique muscle
- Dorsomedial strabismus

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47
Q

Deficits in cranial nerve V will lead to what clinical signs?

A

Trigeminal = motor to the muscles of mastication, sensory to the face
- Masticatory muscle atrophy, dropped jaw if bilateral
- Decreased or absent facial sensation

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48
Q

Deficits in cranial nerve VII will lead to what clinical signs?

A

Facial = motor to muscles of facial expression, parasympathetic to lacrimal glands, taste
- Inability to close the eyelid, move ear, or retract lip
- Hemifacial tetany
- Dry eye

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49
Q

Deficits in cranial nerve VIII will lead to what clinical signs?

A

Vestibulocochlear = balance, hearing
- Head tilt, vestibular ataxia, nystagmus
- Deafness

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50
Q

Deficits in cranial nerve IX will lead to what clinical signs?

A

Glossopharyngeal = sensory and motor to the pharynx
- Diminished gag reflex, dysphagia

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51
Q

Deficits in cranial nerve X will lead to what clinical signs?

A

Vagus = sensory and motor to the pharynx, larynx, and viscera
- Diminished gag reflex, dysphagia
- Laryngeal paralysis
- Megaesophagus

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52
Q

The menace response may be absent until what age in puppies and kittens?

A

10-12 weeks

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53
Q

What must be intact for the menace response to occur?

A
  • Functional optic nerve (CN II)
  • Optic tract (diencephalon)
  • Optic radiation up to the occipital cortex
  • Functional cerebellum
  • Efferent pathway to the facial neurons (CN VII)
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54
Q

Deficits caudal to the optic chiasm will result in an absent menace on what side?

A

Contralateral side

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55
Q

What must be intact for a pupillary right reflex to occur?

A
  • Functional optic nerve (CN II)
  • Intact optic tract (thalamus)
  • Optic radiation up to the occipital cortex
  • Functional oculomotor nerve (CN III)
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56
Q

If a patient has an absent direct PLR but a positive indirect PLR in one eye, where is the lesion?

A

In the eye itself or the optic nerve on that side

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57
Q

What must be intact for palpebral reflex to occur?

A

CN V and VII

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58
Q

What must be intact for physiologic nystagmus to occur?

A
  • Vestibulocochlear (CN VIII) relays impulses to the brainstem
  • Abducent (VI) and oculomotor (III) neurons => abduction and adduction of the eyeball
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59
Q

What is Schiff-Sherrington sign? It occurs with lesions in what portion of the spinal cord?

A
  • Spastic paraplegia in the thoracic limbs with either UMN signs or paradoxical LMN signs in the pelvic limbs
  • Occurs with T3-L3 lesions
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60
Q

What gene leads to dramatically accelerated intervertebral disc degeneration in chondrodystrophic breeds?

A

Expression of fibroblast growth factor 4 (FGF4) on chromosome 12

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61
Q

In Hansen type I IVDE, what changes occur in the nucleus pulposus that lead to failure of the intervertebral disc unit and extrusion of mineralized material into the vertebral canal?

A

Early chondroid metaplasia, degeneration, and mineralization

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62
Q

What is the nucleus pulposus?

A

The highly hydrated central portion of the disc

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63
Q

What is the annulus fibrosis?

A

The ligament that makes up the periphery of the disc and attaches to the vertebral endplates

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64
Q

What characterizes Hansen type II IVDE?

A

Protrusion of the annulus fibrosis - fibroid metaplasia leads to slow protrusion of the disc into the spinal canal. Annulus remains intact (nucleus pulposus does not extrude out)

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65
Q

Compare the signalment and presentation of dogs with type I vs type II IVDE

A

Type I: younger dogs (3-6 yrs), often chondrodysplastic breeds, present for acute onset signs

Type II: older (5-12 yrs), more common in large dogs (GSD, Labs), causes slowly progressive myelopathy

66
Q

Which imaging modality can provide prognostic information about locomotor outcome and risk of progressive myelomalacia in dogs with IVDE?

A

MRI- consider in paraplegic, deep pain negative dogs rather than a CT

67
Q

When performing MRI for IVDE, what images should be acquired at minimum?

A
  • T2 weighted sagittal and transverse images at minimum
  • HASTE may be helpful for prognostic info
68
Q

In young to middle aged, chondrodystrophic dogs with suspected acute TL-IVDE, what imaging modality can be recommended first-line?

A

CT scan - mineralized discs show up well, low likelihood of missing a compressive lesion, shorter scan time and lower cost compared to MRI

69
Q

Ambulatory dogs can be managed medically for IVDE. However, they have a higher risk of what compared to dogs managed surgically?

A

Recurrence 80% positive outcome with medical management vs 93-98% with surgery

70
Q

What percent of paraplegic deep pain positive dogs recover with medical vs surgical management?

A

60% medical, 93% surgical

71
Q

What percent of paraplegic deep pain negative dogs recover with medical vs surgical management?

A

21% medical, 60% surgical

72
Q

Surgery should be considered for what cases of ambulatory IVDE?

A
  • Young, active dog with multiple mineralized disc, particularly with recurrence
  • Progressive, unimproved neurologic signs
  • Persistent pain despite medical management
73
Q

Surgery is always recommended for dogs with what clinical signs of IVDE?

A

Non-ambulatory paraparetic or paraplegic, deep pain positive OR negative dogs

74
Q

What are the core components of medical management for IVDE?

A
  1. Activity restriction
  2. Pain management
  3. Treatment of retention incontinence
  4. Prevention and treatment of skin damage and decubital ulcers
75
Q

How long should activity be restricted in dogs medically managed for IVDE?

A

At least 4 weeks - crate or small room, no off leash walking, jumping, or stairs

76
Q

What class of anti-inflammatory medication is recommended for IVDE? What is not recommended?

A
  • NSAIDs
  • Glucocorticoids not recommended for acute TL-IVDE - associated with poor outcome and decreased QOL, higher rate of recurrence
77
Q

How long should NSAIDs be used for acute IVDE cases?

A

5-7 days - if the dog remains painful despite activity restriction beyond this point, consider surgery

78
Q

What adjunctive treatment has a low level of evidence for improving outcome in TL-IVDE dogs compared to medical management alone?

A

Electroacupunture

79
Q

What surgical procedure may improve outcome and lessen the risk of PMM in dogs with severe neurologic signs?

A

Durotomy

80
Q

What is prophylactic fenestration?

A

Removing disc material in situ with the goal of preventing future extrusion
- Usually performed at the site of extrusion along with decompression to lessen further extrusion through the ruptured annulus in the postoperative period
- May also be performed at the adjacent disc spaces

81
Q

Is fenestration recommended?

A
  • At the risk of the herniated disc - yes. Minimizes risk of recurrence
  • Prophylactically at other disc sites - should be considered, especially in dachshunds and Frenchies
82
Q

When is fenestration NOT recommended?

A

L4-L5 and more caudal sites
T10-11 and cranial

83
Q

How long can pain persist after hemilaminectomy?

A

Up to 6 weeks, smaller percent (15%) develop chronic neuropathic pain

84
Q

What pain management protocol should be used following surgical correction of IVDE?

A
  • IV or SC opioids for 24-48 hours (longer if needed)
  • Fentanyl patch for 3-5 days
  • NSAIDs for 7 days
  • Gabapentin (q8) or pregabalin
85
Q

Normal bladder function lags behind the initial appearance of voiding and can be suboptimal for how long after motor recovery?

A

6 weeks

86
Q

In dogs in which the bladder cannot be manually expressed, what medications should be administered?

A

Alpha adrenergic antagonist +/- diazepam

87
Q

Is intensive rehabilitation useful post-operatively in dogs with IVDE?

A

Safe, but failed to improve the rate or extent of recovery of walking compared to dogs only receiving basic PROM and assisted walking

88
Q

How soon can rehabilitation be started in dogs post-operatively?

A

24 hours post-op - earlier initiation of rehab may improve likelihood of deep pain negative dogs recovering ambulation

89
Q

What rehabilitation exercise are recommended in dogs post-operatively?

A

Cryotherapy, PROM, massage, assisted standing and walking

90
Q

What is progressive myelomalacia (PMM)?

A

Clinical syndrome characterized by progressive necrosis, ischemia, and hemorrhage of the spinal cord that expands cranially and caudally from the initial site of insult

91
Q

When does PMM develop after an acute IVDE injury?

A

24 hours to 14 days

92
Q

What are the risk factors for PMM?

A
  • Most important = Injury severity: paraplegic deep pain negative dogs most at risk
  • Location: lumbar intumescence disc extrusion more at risk
  • Frenchies (but also have a high rate of lumbar intumescence)
93
Q

When should anti-epileptic drugs be started?

A
  • Identifiable structural lesion present or prior history of brain disease/injury
  • Acute, repetitive seizures: 3 or more generalized seizures within a 24 hours period
  • Status epileptics: ictal event >5 minutes
  • 2 or more seizures within a 6 month period
  • Prolonged, severe, or unusual post-ictal periods
94
Q

Where is the majority of phenobarbital metabolized and what enzymes does it induce?

A
  • In the liver
  • Auto-inducer of hepatic microsomal enzymes (p450 system) - can decrease elimination half life with chronic dosing - can enhance clearance of other drugs (levetiracetam, zonisamide, etc)
95
Q

What two anti-epileptic drugs have been shown to reduce seizures by >50% for more than 6 months and are highly recommended as monotherapy?

A

Phenobarbital
Imepitoin

96
Q

What is primidone?

A

Precursor drug to phenobarbital - less effective AND less tolerated that just giving phenobarbital - no advantage to it, the consensus statement does not like it haha

97
Q

When should serum phenobarbital concentrations be measured?

A
  • At 2 weeks and 6 weeks after starting the drug
  • Then every 6 months, if the pet has >2 seizures in 6 months, and every 2 weeks after a dosage change
98
Q

When should phenobarbital levels be obtained?

A

In the morning, before dosing, in a fasted dog (trough levels)

99
Q

What is the safe and effective therapeutic serum concentration range for dogs treated with phenobarbital?

A

15-35 ug/mL

100
Q

When should potassium bromide serum concentrations be measured?

A
  • Between 6-12 weeks after starting the drug
  • Then annually, unless the patient has >3 seizures in the year or is having signs of toxicity
101
Q

When should potassium bromide serum concentrations be measured?

A

At any time point >2h after dosing

102
Q

Should levetiracetam serum levels be measured?

A
  • Not if used as mono therapy - wide therapeutic index
  • Yes if used with phenobarbital, as phenobarbital can alter the pharmacokinetics of levetiracetam (may need to increase dosing)
103
Q

When should serum zonisamide levels be measured?

A
  • 1-2 weeks after starting the drug, then with dosage adjustment or if seizure frequency increases
104
Q

What are the dose dependent CNS effects of anti-epileptic drugs?

A

Sedation, ataxia, imbalance, cognitive impairment

105
Q

What idiosyncratic reactions can occur with phenobarbital use? When and how often do they occur?

A

Immune mediated anemia, neutropenia, thrombocytopenia
- All rare - 4% of cases in one study
- Usually occur in the first 6 months
Acute, idiosyncratic hepatoxicity
Superficial necrolytic dermatitis

106
Q

How does phenobarbital affect testing for hypothyroidism?

A

Causes low serum total and free T4

107
Q

What idiosyncratic reactions can occur with zonisamide use?

A
  • KCS and polyarthropathy (reported in 1 dog)
  • Acute toxic hepatopathy
  • Renal tubular acidosis (reported in 1 dog)
108
Q

When should a second anti-epileptic drug be started?

A

Based on seizure frequency and severity (duration, cluster activity, postictal effects)

109
Q

When selecting a second anti-epileptic drug, what factors should be considered?

A

Select a drug with:
- Different mechanism of action
- Minimal drug-drug interactions
- Avoid additive toxicity

110
Q

What are movement disorders?

A

Involuntary movements without changes in consciousness
- Includes tremors, myoclonus, paroxysmal dyskinesia, etc

111
Q

What is canine paroxysmal dyskinesia?

A

Subtype of movement disorder in which there are recurrent episodes of abnormal, involuntary movement - either a lack of movement (hypokinetic) or excessive movement (hyperkinetic). Usually self-limiting

112
Q

What portion of the telencephalon is vital to the control of movement?

A

The basal nuclei

113
Q

Dopaminergic projections to the caudate and putamen are the overriding control of the basal nuclei. What does stimulation of D1 dopamine receptors do? D3 dopamine receptors?

A

D1 = increased glutamatergic activity
D2 = decreased glutamatergic activity

114
Q

What is dystonia?

A

Sustained, involuntary muscle contraction that produces an abnormal posture or twisting movement - can be generalized, segmental, or focal

115
Q

What causes dystonia?

A

Cocontraction of agonist and antagonist muscles with spread from the origin to extraneous muscles

116
Q

Define tremors

A
  • Involuntary, rhythmic, oscillatory movements of a body part caused by alternating contractions of agonist and antagonist muscles
  • Occurs in a regular cycle - the rhythmical character differentiates from other disorders
  • Only occur while awake, stop during sleep
117
Q

What is the difference between a “rest tremor” and an “active tremor”?

A
  • Rest tremor - observed when the affected body part is not being actively supported against gravity (laying down) - not voluntarily activated
  • Active tremor - observed when the muscles are active. Can be postural (orthostatic) what occurs when standing or kinetic that occurs with voluntary movement
118
Q

A kinetic, active tremor is typically indicative of disease where?

A

Cerebellar disease

119
Q

Idiopathic head tremors would be classified as what type of tremor?

A

Postural (orthostatic), active tremor

120
Q

What is myokymia?

A
  • Bursts of single motor unit potentials firing at 5-150 Hz
  • Results from abnormal potassium channel function
  • May be benign or indicative of pathology
121
Q

What is neuromyotonia?

A
  • Higher frequency (150-300 Hz) bursts of motor unit potentials that originate in motor axons
  • Abrupt onset and offset
122
Q

What makes myokymia and neuromyotonia unique among movement disorders?

A

Persist during sleep and general anesthesia, unless given a neuromuscular blocking agent

123
Q

What are tetanus and tetany? Name 2 causes

A
  • Sustained muscle contractions without relaxation
  • Results from disinhibition of extensor motor neurons
  • Can results from the disease tetanus (clostridial neurotoxin tetanospasm) or hypocalcemia
124
Q

What is “spinal walking”?

A
  • Acquisition of involuntary motor function in paraplegic animals without pain sensation (complete TL spinal cord lesion)
  • Reflex gait
125
Q

In paraplegic, deep pain negative dogs that underwent intensive rehabilitation, what percent achieved spinal walking? How long did it take?

A
  • 59%
  • 75 days
126
Q

In paraplegic, deep pain negative dogs that underwent intensive rehabilitation, what factors were associated with achieving spinal walking?

A

Younger age, earlier start of physiotherapy, light weight

127
Q

What is syringomyelia?

A
  • Fluid filled cavities within the central spinal cord
  • Develops as a consequence of obstruction of CSF, most commonly from Chiari-like malformations
128
Q

What are the clinical signs of syringomyelia?

A
  • Vocalization (65%), spinal pain (55%), reduced activity/stairs/jumping, touch aversion, sleep disturbances, head scratching/rubbing,
  • Phantom scratching, scoliosis, weakness only seen in the largest (>4mm)
129
Q

In a retrospective study, what clinical sign was inversely associated with syrinx size?

A

Head scratching/rubbing

130
Q

What is the underlying cause of acquired myasthenia gravis?

A
  • Complement fixing autoantibodies against the nicotinic acetylcholine receptors at the post-synaptic membrane (against the main immunogenic region of the alpha chain)
131
Q

Seronegative myasthenia gravis occurs in what percent of dogs with the generalized form?

A

2%

132
Q

How is myasthenia gravis treated?

A
  • Anticholinesterase drugs - increase the half life of acetylcholine in the synaptic cleft to increase binding
    +/- Immunosuppressives
133
Q

What percent of dogs with myasthenia gravis achieved complete remission (able to be off all drugs and symptom free 4 weeks later) with low antibody levels?

A

31%

134
Q

What percent of dogs with myasthenia gravis did not improve with treatment?

A

30%

135
Q

What factors were associated with clinical remission in dogs with myasthenia gravis? With lack of remission?

A

Remission: younger age, comorbid endocrine disease
Lack of remission: higher initial AChR antibodies, regurgitation

136
Q

What is the most common cause of unilateral masticatory muscle atrophy?

A

Neoplasia of the mandibular branch of the trigeminal nerve - nerve sheath tumor&raquo_space; lymphoma, etc

137
Q

Primary CNS histiocytic sarcoma causes what changes on CSF tap?

A
  • Marked inflammation
  • Neoplastic cells detected in 52%
138
Q

What was the MST for CNS histiocytic sarcoma?

A

No treatment <1 day
Palliative intent radiation: 5 days
Definitive intent: 44 days

139
Q

In dogs with lesions that neurolocalize to the brain or cervical spinal cord, where should CSF be collected from? Thoracolumbar lesions?

A
  • Brain/cervical: may be benefit to collecting from both locations - TP, RBC, and TNCC differed between locations, pathologist interpretation differed in 67%
  • Thoracolumbar: lumbar tap only, CM tap not representative
140
Q

In a study comparing intranasal and IV midazolam for status epilepticus, which route was superior for cessation of seizure activity?

A

Both were effective (stopped seizures in 76% IN and 61% IV) BUT the time it took to place a catheter made IN much faster (100 vs 270 seconds)

141
Q

How long did intranasal and IV midazolam take to stop seizures in dogs with status epilepticus?

A

IN 33 sec, IV 64 sec after administration

142
Q

In dogs <15 kg, the incidence of IVDD on TL MRI was 95%. In dogs >15kg, it was only 58%. What other diseases were more likely in dogs >15kg?

A

Neoplasia (12 times more likely than little dogs) and fibrocartilaginous embolic myelopathy (7 times more likely than little dogs)

143
Q

What is congenital myasthenic syndrome?

A

Heterogenous group of inherited disorders of neuromuscular transmission. Can be presynaptic, synaptic, or post-synaptic

144
Q

What are the clinical signs of congenital myasthenic syndrome?

A
  • Progressive muscle weakness, worsened by exercise that starts after weaning
  • Megaesophagus is NOT a common feature
145
Q

Congenital myasthenic syndrome has been observed in what breeds? What are the mutations associated?

A
  • COLQ mutations in Labs and Goldens
  • CHRNE mutations in Jack Russel Terriers and Heideterriers
146
Q

What anti-epileptic drug has been shown to be an excellent treatment for noise phobia in dogs?

A

Imepitoin - GABA agonist

147
Q

What breeds are most commonly affected by idiopathic head tremor syndrome?

A

Dobermans, Bulldogs, Boxers, Labs

148
Q

What is the clinical appearance of idiopathic head tremor syndrome?

A

Sudden onset of short episodes with horizontal or vertical rhythmical tremor like movements of the head - no loss of consciousness or responsiveness, can usually be interrupted with distractions

149
Q

What anti epileptic drug was NOT effective for the treatment of idiopathic head tremors?

A

Imepitoin

150
Q

What is acute or idiopathic polyradiculoneuritis?

A
  • Most common acute, generalized neuropathy worldwide
  • Sudden onset of LMN signs - typically develop in the pelvic limbs and rapidly ascend to involve the thoracic limbs
  • Flaccid LMN tetraparesis or plegia
151
Q

What causes idiopathic polyradiculoneuritis?

A
  • Immune mediated disorder affecting the ventral spinal nerve roots more severely with minimal dorsal nerve root involvement
152
Q

What percent of patients with idiopathic polyradiculoneuritis have cranial nerve involvement? What nerve is most commonly involved?

A

80% - most commonly affects the vagal nerve => dysphonia

153
Q

What antibodies have been identified in dogs with idiopathic polyradiculoneuritis?

A

anti-GM2 ganglioside antibodies - very similar to human Guillain-Barré syndrome

154
Q

What are the risk factors for developing idiopathic polyradiculoneuritis?

A
  • Recent vaccination
  • Upper respiratory and GI infections - in particular, Campylobacter is found in 40% of patients 1-2 weeks before hand and is associated with consumption of raw chicken
155
Q

In a study of 8 cats with acquired myasthenia gravis and no evidence of a cranial mediastinal mass, what percent achieved remission within 6 months of diagnosis?

A

100% - 4 did not receive any treatment and resolved. Wild.

156
Q

What is myotonia?

A

Delayed muscle relaxation after muscle activation
- Usually improves with continuous activity (warm up phenomenon)
- In paradoxical myotonia, it worsens with repeated activity/exercise and improves with rest

157
Q

Paradoxical pseudomyotonia has been described in what two breeds?

A

English Springer Spaniel and Cocker Spaniel

158
Q

Border terriers have an inherited form of what movement disorder? What is it characterized by?

A

Paroxysmal dyskinesia - dystonia, muscle fasciculations, falling over while retaining consciousness

159
Q

Antibodies against what antigens have been identified in the CSF of dogs with MUE?

A

Neuronal cell surface antigens - NMDAR1, GFAP

160
Q

What factors can precipitate seizures in dogs with idiopathic epilepsy?

A

Stressful situations, sleep deprivation, weather, hormonal factors (estrus) - more likely to trigger focal seizures vs generalized

ACVIM Specialty 2023 (38 decks)

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