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
2
Q
What is the resting membrane potential difference of a neuron (in mV)?
A
-65 to -70 mV
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
4
Q
When a neuron depolarizes past -55 mV, what channels open to begin the action potential?
A
Voltage gated Na+ channels
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
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
7
Q
How do toxins such as pyrethrins cause tremors and seizures?
A
Block sodium channel inactivation, increasing action potential generation
8
Q
What two factors influence the speed at which action potentials travel down an axon?
A
- Axonal diameter
- Myelin
9
Q
Ions flow directly between neurons in what types of synapses?
A
Electrical synapses or gap junctions
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
11
Q
Name 3 families of ionotropic receptors
A
- Nicotinic acetylcholine, gamma-amino butyric acid (GABA) and glycine
- Glutamate
- ATP or purine P2X receptors
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
13
Q
What enzyme in the synaptic cleft breaks down acetylcholine to choline and acetic acid?
A
Acetylcholinesterase
14
Q
What causes myasthenia gravis?
A
Autoantibodies against the alpha1 subunit partially block the acetylcholine receptor in the neuromuscular junction
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
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
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
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
19
Q
What causes excitotoxicity?
A
Excessive NMDA receptor activation, leading to accumulation of intracellular Ca++ => cell death
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
21
Q
What is temporal summation?
A
Several action potentials from the same pre-synaptic neuron summate to depolarize the post-synaptic neuron
22
Q
What is spatial summation?
A
Several action potentials from multiple, different pre-synaptic neurons summate to depolarize the post-synaptic neuron
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
24
Q
A head or body turn typically localizes disease to what region?
A
Rostral brainstem or cerebral disease
25
A plantigrade stance localizes disease to what?
Peripheral neuropathies
26
Describe decerebrate rigidity. Where does this localize disease to?
- Opisthotonus with rigid extension of the neck and all four limbs
- Midbrain or rostral cerebellar lesions
27
Describe decerebellate rigidity. Where does this localize disease to?
Opisthotonus with extension rigidity of the limbs BUT the hips are flexed or intermittently flexed
- Severe cerebellar lesions
28
A short, choppy, stilted gait is often indicative of what type of paresis?
Lower motor neuron
29
A long-striped, spastic gait with proprioceptive ataxia is indicative of what type of paresis?
Upper motor neuron
30
What causes general proprioceptive ataxia?
Disruption of the spinocerebellar tracts and conscious proprioceptive pathways that relay the anatomic location and degree of muscle contraction to the brain
31
Describe what general proprioceptive ataxia looks like
- 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
32
What causes vestibular ataxia?
Loss of orientation of the head with respect to the eyes, neck, limbs, and trunk
33
Describe what vestibular ataxia looks like
- 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
34
Describe what cerebellar ataxia looks like
- Hypermetric gait with sudden bursts of motor activity
- Overflexion of the limbs on protraction
35
What must be intact for a pet to perform postural reactions?
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
36
What is the prosencephalon?
Cerebrum and thalamus
37
Unilateral prosencephalic lesions (cerebrum and/or thalamus) will result in postural reaction deficits on what side? They are usually accompanied by what other changes?
- 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
38
Describe the characteristic physical exam findings with a T3-L3 lesion
- 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
39
Describe the characteristic physical exam findings with a C1-C5 lesion
- 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
40
Describe the characteristic physical exam findings with a C6-T2 lesion
- 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
41
What mediates the patellar reflex?
Femoral nerve through the spinal cord segments L4-L7
42
In the thoracic limbs, the nerves responsible for the withdrawal reflex arise from what spinal cord segments?
C6-T2
43
In the pelvic limbs, the nerves responsible for the withdrawal reflex arise from what spinal cord segments?
Mediated by the sciatic nerve through L6-S1
44
With spinal cord lesions, where will the cutaneous trunk reflex stop?
Typically it is preserved for 1-2 vertebral bodies caudal to the level of the lesion
45
Deficits in cranial nerve III will lead to what clinical signs?
Oculomotor nerve = motor to the extraocular muscles and parasympathetic to the pupil
- Ventrolateral strabismus
- Diminished to absent PLRs with dilated pupils
46
Deficits in cranial nerve IV will lead to what clinical signs?
Trochlear nerve = motor to the dorsal oblique muscle
- Dorsomedial strabismus
47
Deficits in cranial nerve V will lead to what clinical signs?
Trigeminal = motor to the muscles of mastication, sensory to the face
- Masticatory muscle atrophy, dropped jaw if bilateral
- Decreased or absent facial sensation
48
Deficits in cranial nerve VII will lead to what clinical signs?
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
49
Deficits in cranial nerve VIII will lead to what clinical signs?
Vestibulocochlear = balance, hearing
- Head tilt, vestibular ataxia, nystagmus
- Deafness
50
Deficits in cranial nerve IX will lead to what clinical signs?
Glossopharyngeal = sensory and motor to the pharynx
- Diminished gag reflex, dysphagia
51
Deficits in cranial nerve X will lead to what clinical signs?
Vagus = sensory and motor to the pharynx, larynx, and viscera
- Diminished gag reflex, dysphagia
- Laryngeal paralysis
- Megaesophagus
52
The menace response may be absent until what age in puppies and kittens?
10-12 weeks
53
What must be intact for the menace response to occur?
- 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)
54
Deficits caudal to the optic chiasm will result in an absent menace on what side?
Contralateral side
55
What must be intact for a pupillary right reflex to occur?
- Functional optic nerve (CN II)
- Intact optic tract (thalamus)
- Optic radiation up to the occipital cortex
- Functional oculomotor nerve (CN III)
56
If a patient has an absent direct PLR but a positive indirect PLR in one eye, where is the lesion?
In the eye itself or the optic nerve on that side
57
What must be intact for palpebral reflex to occur?
CN V and VII
58
What must be intact for physiologic nystagmus to occur?
- Vestibulocochlear (CN VIII) relays impulses to the brainstem
- Abducent (VI) and oculomotor (III) neurons => abduction and adduction of the eyeball
59
What is Schiff-Sherrington sign? It occurs with lesions in what portion of the spinal cord?
- Spastic paraplegia in the thoracic limbs with either UMN signs or paradoxical LMN signs in the pelvic limbs
- Occurs with T3-L3 lesions
60
What gene leads to dramatically accelerated intervertebral disc degeneration in chondrodystrophic breeds?
Expression of fibroblast growth factor 4 (FGF4) on chromosome 12
61
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?
Early chondroid metaplasia, degeneration, and mineralization
62
What is the nucleus pulposus?
The highly hydrated central portion of the disc
63
What is the annulus fibrosis?
The ligament that makes up the periphery of the disc and attaches to the vertebral endplates
64
What characterizes Hansen type II IVDE?
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)
65
Compare the signalment and presentation of dogs with type I vs type II IVDE
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
Which imaging modality can provide prognostic information about locomotor outcome and risk of progressive myelomalacia in dogs with IVDE?
MRI- consider in paraplegic, deep pain negative dogs rather than a CT
67
When performing MRI for IVDE, what images should be acquired at minimum?
- T2 weighted sagittal and transverse images at minimum
- HASTE may be helpful for prognostic info
68
In young to middle aged, chondrodystrophic dogs with suspected acute TL-IVDE, what imaging modality can be recommended first-line?
CT scan - mineralized discs show up well, low likelihood of missing a compressive lesion, shorter scan time and lower cost compared to MRI
69
Ambulatory dogs can be managed medically for IVDE. However, they have a higher risk of what compared to dogs managed surgically?
Recurrence 80% positive outcome with medical management vs 93-98% with surgery
70
What percent of paraplegic deep pain positive dogs recover with medical vs surgical management?
60% medical, 93% surgical
71
What percent of paraplegic deep pain negative dogs recover with medical vs surgical management?
21% medical, 60% surgical
72
Surgery should be considered for what cases of ambulatory IVDE?
- Young, active dog with multiple mineralized disc, particularly with recurrence
- Progressive, unimproved neurologic signs
- Persistent pain despite medical management
73
Surgery is always recommended for dogs with what clinical signs of IVDE?
Non-ambulatory paraparetic or paraplegic, deep pain positive OR negative dogs
74
What are the core components of medical management for IVDE?
1. Activity restriction
2. Pain management
3. Treatment of retention incontinence
4. Prevention and treatment of skin damage and decubital ulcers
75
How long should activity be restricted in dogs medically managed for IVDE?
At least 4 weeks - crate or small room, no off leash walking, jumping, or stairs
76
What class of anti-inflammatory medication is recommended for IVDE? What is not recommended?
- NSAIDs
- Glucocorticoids not recommended for acute TL-IVDE - associated with poor outcome and decreased QOL, higher rate of recurrence
77
How long should NSAIDs be used for acute IVDE cases?
5-7 days - if the dog remains painful despite activity restriction beyond this point, consider surgery
78
What adjunctive treatment has a low level of evidence for improving outcome in TL-IVDE dogs compared to medical management alone?
Electroacupunture
79
What surgical procedure may improve outcome and lessen the risk of PMM in dogs with severe neurologic signs?
Durotomy
80
What is prophylactic fenestration?
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
Is fenestration recommended?
- 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
When is fenestration NOT recommended?
L4-L5 and more caudal sites
T10-11 and cranial
83
How long can pain persist after hemilaminectomy?
Up to 6 weeks, smaller percent (15%) develop chronic neuropathic pain
84
What pain management protocol should be used following surgical correction of IVDE?
- 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
Normal bladder function lags behind the initial appearance of voiding and can be suboptimal for how long after motor recovery?
6 weeks
86
In dogs in which the bladder cannot be manually expressed, what medications should be administered?
Alpha adrenergic antagonist +/- diazepam
87
Is intensive rehabilitation useful post-operatively in dogs with IVDE?
Safe, but failed to improve the rate or extent of recovery of walking compared to dogs only receiving basic PROM and assisted walking
88
How soon can rehabilitation be started in dogs post-operatively?
24 hours post-op - earlier initiation of rehab may improve likelihood of deep pain negative dogs recovering ambulation
89
What rehabilitation exercise are recommended in dogs post-operatively?
Cryotherapy, PROM, massage, assisted standing and walking
90
What is progressive myelomalacia (PMM)?
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
When does PMM develop after an acute IVDE injury?
24 hours to 14 days
92
What are the risk factors for PMM?
- 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
When should anti-epileptic drugs be started?
- 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
Where is the majority of phenobarbital metabolized and what enzymes does it induce?
- 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
What two anti-epileptic drugs have been shown to reduce seizures by >50% for more than 6 months and are highly recommended as monotherapy?
Phenobarbital
Imepitoin
96
What is primidone?
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
When should serum phenobarbital concentrations be measured?
- 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
When should phenobarbital levels be obtained?
In the morning, before dosing, in a fasted dog (trough levels)
99
What is the safe and effective therapeutic serum concentration range for dogs treated with phenobarbital?
15-35 ug/mL
100
When should potassium bromide serum concentrations be measured?
- 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
When should potassium bromide serum concentrations be measured?
At any time point >2h after dosing
102
Should levetiracetam serum levels be measured?
- 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
When should serum zonisamide levels be measured?
- 1-2 weeks after starting the drug, then with dosage adjustment or if seizure frequency increases
104
What are the dose dependent CNS effects of anti-epileptic drugs?
Sedation, ataxia, imbalance, cognitive impairment
105
What idiosyncratic reactions can occur with phenobarbital use? When and how often do they occur?
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
How does phenobarbital affect testing for hypothyroidism?
Causes low serum total and free T4
107
What idiosyncratic reactions can occur with zonisamide use?
- KCS and polyarthropathy (reported in 1 dog)
- Acute toxic hepatopathy
- Renal tubular acidosis (reported in 1 dog)
108
When should a second anti-epileptic drug be started?
Based on seizure frequency and severity (duration, cluster activity, postictal effects)
109
When selecting a second anti-epileptic drug, what factors should be considered?
Select a drug with:
- Different mechanism of action
- Minimal drug-drug interactions
- Avoid additive toxicity
110
What are movement disorders?
Involuntary movements without changes in consciousness
- Includes tremors, myoclonus, paroxysmal dyskinesia, etc
111
What is canine paroxysmal dyskinesia?
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
What portion of the telencephalon is vital to the control of movement?
The basal nuclei
113
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?
D1 = increased glutamatergic activity
D2 = decreased glutamatergic activity
114
What is dystonia?
Sustained, involuntary muscle contraction that produces an abnormal posture or twisting movement - can be generalized, segmental, or focal
115
What causes dystonia?
Cocontraction of agonist and antagonist muscles with spread from the origin to extraneous muscles
116
Define tremors
- 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
What is the difference between a "rest tremor" and an "active tremor"?
- 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
A kinetic, active tremor is typically indicative of disease where?
Cerebellar disease
119
Idiopathic head tremors would be classified as what type of tremor?
Postural (orthostatic), active tremor
120
What is myokymia?
- 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
What is neuromyotonia?
- Higher frequency (150-300 Hz) bursts of motor unit potentials that originate in motor axons
- Abrupt onset and offset
122
What makes myokymia and neuromyotonia unique among movement disorders?
Persist during sleep and general anesthesia, unless given a neuromuscular blocking agent
123
What are tetanus and tetany? Name 2 causes
- Sustained muscle contractions without relaxation
- Results from disinhibition of extensor motor neurons
- Can results from the disease tetanus (clostridial neurotoxin tetanospasm) or hypocalcemia
124
What is "spinal walking"?
- Acquisition of involuntary motor function in paraplegic animals without pain sensation (complete TL spinal cord lesion)
- Reflex gait
125
In paraplegic, deep pain negative dogs that underwent intensive rehabilitation, what percent achieved spinal walking? How long did it take?
- 59%
- 75 days
126
In paraplegic, deep pain negative dogs that underwent intensive rehabilitation, what factors were associated with achieving spinal walking?
Younger age, earlier start of physiotherapy, light weight
127
What is syringomyelia?
- Fluid filled cavities within the central spinal cord
- Develops as a consequence of obstruction of CSF, most commonly from Chiari-like malformations
128
What are the clinical signs of syringomyelia?
- 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
In a retrospective study, what clinical sign was inversely associated with syrinx size?
Head scratching/rubbing
130
What is the underlying cause of acquired myasthenia gravis?
- Complement fixing autoantibodies against the nicotinic acetylcholine receptors at the post-synaptic membrane (against the main immunogenic region of the alpha chain)
131
Seronegative myasthenia gravis occurs in what percent of dogs with the generalized form?
2%
132
How is myasthenia gravis treated?
- Anticholinesterase drugs - increase the half life of acetylcholine in the synaptic cleft to increase binding
+/- Immunosuppressives
133
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?
31%
134
What percent of dogs with myasthenia gravis did not improve with treatment?
30%
135
What factors were associated with clinical remission in dogs with myasthenia gravis? With lack of remission?
Remission: younger age, comorbid endocrine disease
Lack of remission: higher initial AChR antibodies, regurgitation
136
What is the most common cause of unilateral masticatory muscle atrophy?
Neoplasia of the mandibular branch of the trigeminal nerve - nerve sheath tumor >> lymphoma, etc
137
Primary CNS histiocytic sarcoma causes what changes on CSF tap?
- Marked inflammation
- Neoplastic cells detected in 52%
138
What was the MST for CNS histiocytic sarcoma?
No treatment <1 day
Palliative intent radiation: 5 days
Definitive intent: 44 days
139
In dogs with lesions that neurolocalize to the brain or cervical spinal cord, where should CSF be collected from? Thoracolumbar lesions?
- 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
In a study comparing intranasal and IV midazolam for status epilepticus, which route was superior for cessation of seizure activity?
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
How long did intranasal and IV midazolam take to stop seizures in dogs with status epilepticus?
IN 33 sec, IV 64 sec after administration
142
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?
Neoplasia (12 times more likely than little dogs) and fibrocartilaginous embolic myelopathy (7 times more likely than little dogs)
143
What is congenital myasthenic syndrome?
Heterogenous group of inherited disorders of neuromuscular transmission. Can be presynaptic, synaptic, or post-synaptic
144
What are the clinical signs of congenital myasthenic syndrome?
- Progressive muscle weakness, worsened by exercise that starts after weaning
- Megaesophagus is NOT a common feature
145
Congenital myasthenic syndrome has been observed in what breeds? What are the mutations associated?
- COLQ mutations in Labs and Goldens
- CHRNE mutations in Jack Russel Terriers and Heideterriers
146
What anti-epileptic drug has been shown to be an excellent treatment for noise phobia in dogs?
Imepitoin - GABA agonist
147
What breeds are most commonly affected by idiopathic head tremor syndrome?
Dobermans, Bulldogs, Boxers, Labs
148
What is the clinical appearance of idiopathic head tremor syndrome?
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
What anti epileptic drug was NOT effective for the treatment of idiopathic head tremors?
Imepitoin
150
What is acute or idiopathic polyradiculoneuritis?
- 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
What causes idiopathic polyradiculoneuritis?
- Immune mediated disorder affecting the ventral spinal nerve roots more severely with minimal dorsal nerve root involvement
152
What percent of patients with idiopathic polyradiculoneuritis have cranial nerve involvement? What nerve is most commonly involved?
80% - most commonly affects the vagal nerve => dysphonia
153
What antibodies have been identified in dogs with idiopathic polyradiculoneuritis?
anti-GM2 ganglioside antibodies - very similar to human Guillain-Barré syndrome
154
What are the risk factors for developing idiopathic polyradiculoneuritis?
- 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
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?
100% - 4 did not receive any treatment and resolved. Wild.
156
What is myotonia?
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
Paradoxical pseudomyotonia has been described in what two breeds?
English Springer Spaniel and Cocker Spaniel
158
Border terriers have an inherited form of what movement disorder? What is it characterized by?
Paroxysmal dyskinesia - dystonia, muscle fasciculations, falling over while retaining consciousness
159
Antibodies against what antigens have been identified in the CSF of dogs with MUE?
Neuronal cell surface antigens - NMDAR1, GFAP
160
What factors can precipitate seizures in dogs with idiopathic epilepsy?
Stressful situations, sleep deprivation, weather, hormonal factors (estrus) - more likely to trigger focal seizures vs generalized
ACVIM: SAIM Specialty boards study 2023
flashcards
Decks in class (38)
# Cards
-
Genetics32
-
Dermatology36
-
Ophthalmology24
-
Neurology65
-
Effusions and edema13
-
Metabolism and metabolic diseases19
-
Respiratory316
-
Cardiology20
-
GI disease: oral, pharyngeal, esophagus106
-
GI: microbiome and enteral nutrition54
-
GI: gastric disease68
-
GI: Physiology56
-
GI: Small Intestine197
-
Random facts (epidemiology, etc)5
-
GI: Large intestine and ulcers107
-
Hepatic disease301
-
Gallbladder disease44
-
Pancreas64
-
General renal and AKI114
-
Renal transplant and renal replacement therapy38
-
CKD103
-
Calcium physiology, hypercalemia, renal secondary hyperparathyroidism139
-
Renal biomarkers36
-
Renal tubular and glomerular diseases136
-
Hypertension and RAAS74
-
Lower urinary tract disease162
-
Lower urinary tract part 238
-
Endocrine: GH disorders and hypothyroidism68
-
Endocrine: Hyperthyroidism and some acromegaly40
-
Insulinoma and Diabetes Mellitus87
-
Endocrine: Hyper and hypoadrenocorticism, adrenal tumors83
-
Immune mediated disease149
-
General hematology217
-
Vector borne disease80
-
General infectious disease123
-
Cardiology134
-
Neurology160
-
Oncology59
