Clinical Cases

Question 1

____ % of secondary intracranial neoplasia in dogs is attributed to pituitary tumors or other sellar masses

List nonpituitary sellar masses (6)

Answer 1

35% of secondary intracranial neoplasia in dogs is attributed to pituitary tumors or other sellar masses

• Pituitary tumors most common, followed by meningiomas
• “Although larger masses can lead to more neurologic deficits, the size of the sellar mas does not always corelate with the degree of neurologic disease”

Nonpituitary sellar masses

1. Meningioma
2. Craniopharyngioma
3. Ependymoma
4. Oligodendroglioma
5. Lymphoma
6. Metastatic disease

Vet Clin N America SAP

Question 2

RT for canine pituitary mass:

• Generally shrinks the tumor how much?
• What was the 1-year survival? mean survival?

Answer 2

• RT generally shrinks the tumor by 25 - 50%
• Dogs with a pituitary mass treated with radiation had a 93% survival at 1 year
  
  • Mean survival of 1405 days

Vet Clin N America SAP

Question 3

What are the dimensions for a normal canine pituitary gland on MRI?

Pituitary height to brain area ratio cut off for enlarged pituitary gland in the dog?

Why is the posterior lobe of the pituitary gland hyperintense on noncontrast T1W imaging?

Answer 3

Normal canine pituitary gland: 6-10mm in length, 5-9mm width, 4-6mm height

P/B ratio < 0.31 = normal

Arginine vasopressin secretory granules –> T1W hyperitnense posterior pituitary gland (neurohypophysis)

Vet Clin N America SAP

Question 4

What is the “pituitary flush” and how can it be used to diagnose a pituitary microadenoma?

Answer 4

Dynamic contrast-enhanced CT can identify a “pituitary flush”

Normal: Arterial blood supply of the neurohypophysis is seen slightly earlier than enhancement of the adenohypophysis through the portal blood supply

Displacement, distortion, reduction or disappearance of the pituitary flush sign in the early phase of dynamic CT can be used to identify microadenomas

Vet Clin N America SAP

Question 5

Extracranial abnormalities identified on imaging of the head in agromegalic cats?

Answer 5

Thick frontal bone

Soft tissue accumulation in the nasal cavity, sinuses, and pharynx

Vet Clin N America SAP

Question 6

T/F: pituitary adenomas can show evidence of hemorrhage

T/F: Functional tumors are more likely to be adenomas than adenocarcinomas

Answer 6

Pituitary adenomas can show evidence of hemorrhage: True

Functional tumors are more likely to be adenomas than adenocarcinomas: FALSE - TUMOR FUNCTIONALITY DOES NOT PREDICT TUMOR TYPE

Vet Clin N America SAP

Question 7

What imaging characteristics are associated with worse surgical outcome for canine hypophysectomy

Answer 7

(dogs with hyperadrenocorticism)

Occupation of the third ventricle

Touching the interthalamic adhesion

Involvement of the arterial circle or cavernous sinus

Vet Clin N America SAP

Question 8

What is the remission rate for dogs with PDH treated with TSH? Survival at 1-4 years?

Answer 8

Remission rates for dogs with PDH treated with TSH are 86 - 95% with a recurrence of 25% and mortality of 12 - 20%

Survival at 1y = 86%, 2y = 79%, 3y = 74%, 4y = 72%

P/B ratio > 0.31 –> significantly shorter survival and disease free interval than dogs with small tumors

“Surgery is more effective than medical management or RT at controlling endocrine related signs associated with a functional pituitary adenoma, and can address neurologic signs associated with mass effect”

Vet Clin N America SAP

Question 9

Meij et al: what 4 factors were associated with disease recurrence following TSH for PDH?

Answer 9

Lg pituitary size

Thick sphenoid bone

High UCCR

High concentration of alpha melanocyte-stimulating hormone

Vet Clin N America SAP

Question 10

Dysfunction of the _______ receptor due to mutation of the _______ gene has been identified as the cause of genetic cataplexy in dogs?

What breeds?

Answer 10

Orexin receptor (hypocretin receptor) due to mutation of the type II orexin receptor gene (OxR2) has been identified as the cause

Breeds: dachshund, labrador retrievers, Dobermans

Acquired narcolepsy - depletion of CSF hypocretin has been recognized - suggests dysfunction of the neurons in the ventral lateral nucleus of the hypothalamus

Question 11

What is the difference between a tremor and myoclonic movement (twitch)

Answer 11

Tremor - involuntary, rhythmic, oscillatory or sometimes sinusoidal movement of a body part

Myoclonic movement = twitch - brief, shock-like contraction

ACVIM Proceedings

Question 12

MRI characteristics associated AA luxation when compared to control? Association to neurologic grade?

Answer 12

1. Affected vs. nonaffected with AA luxation
   
   • No increased incidence with respect to the presence of syringohydromyelia, hydrocephalus, and Chiari-like malformation in affected vs. nonaffected
   • Affected dogs less likely to have a dens, apical ligament and transverse ligament
   • Presence of spinal cord intensity, increased AA joint cavity size, % cross-sectional spinal cord compression (at the dens and C2) - associated with affected status
2. Lack of dens and/or odontoid ligaments - associated with larger luxations
3. Neurologic grade not associated with MRI findings

ACVIM Proceedings

Question 13

RE Degenerative myelopathy: ambulatory paresis/ataxia to nonambulatory status occurs within a median time of ____________ months

Answer 13

10 months

Median disease duration in Pembroke Welsh Corgi was 19 months

ACVIM Proceedings

Question 14

What are the 4 stages of DM?

Answer 14

1 - UMN paraparesis

2 - Nonambulatory paraparesis to paraplegia

• mild/mod muscle loss, reduced/absent spinal reflexes, +/- urinary and fecal incontinence

3 - LMN paraplegia to thoracic limb paresis

• Flaccid paraplegia, severe loss of muscle mass in PL, urinary and fecal incontinence

4 - LMN tetraplegia and brainstem signs

• Flaccid tetraplegia, difficulty swallowing and tongue movements, reduced to absent cutaneous trunci, generalized and severe loss of muscle mass, urinary and fecal incontinence

ACVIM Proceedings

Question 15

Electrodiagnostic findings in patients with DM?

Answer 15

Later in the disease with the emergence of LMN signs

• EMG - multifocal spontaneous activity, fibrillation potentials, positive sharp waves in the appendicular muscles
• Nerve stimulation - decreased CMAP consistent with axonopathy
  
  • decreased motor nerve conduction velocity consistent with demyelination

ACVIM Proceedings

Question 16

Most common clinical signs of feline hyperesthesia syndrome?

Answer 16

Attacking/overgrooming tail or flank

Tail mutilation

Rippling of the thoracolumbar skin

ACVIM Proceedings

Question 17

Mechanisms thought to cause diabetic neuropathy?

Answer 17

Physiologic mechanism is thought to be abnormal Schwann cell and myelin function caused by

1. microvascular compromise
2. accumulation of sorbitol with subsequent free-radical formation and membrane damage
3. immune mediated axonal/myelin damage

ACVIM Proceedings

Question 18

MRI variables suggested to be associated with IVD protrusion vs. extrusion?

Answer 18

Protrusion:

1. Midline instead of lateralized intervertebral disc herniation
2. partial instead of complete intervertebral disc degeneration

Extrusion

1. single instead of multiple intervertebral disc herniations
2. dispersed intervertebral disc material beyond the borders of the intervertebral disc space

ACVIM Proceedings

Question 19

What respiratory patterns are described:

1. Rapid and regular respiration at a rate of about 25/minute
2. Cyclic pattern of prolonged inspiration followed by expiration and an apneic phase
3. Shallow, slow but regular ventilation
4. Waxing and waning of the depth of respiration, with regularly recurring periods of apnea

Answer 19

1. Rapid and regular respiration at a rate of about 25/minute = Central neurogenic hyperventilation
   
   • Injury to the pons/caudal midbrain, also occurs with cerebral hypoxia/acidosis
2. Cyclic pattern of prolonged inspiration followed by expiration and an apneic phase = Apneustic respiration
   
   • Caudal brainstem (medulla oblongata) injury - carriers a poor prognosis
3. Shallow, slow but regular ventilation = Central alveolar hypoventilation
   
   • Lesions in the medulla oblongata
4. Waxing and waning of the depth of respiration, with regularly recurring periods of apnea = Cheyne-Stokes respiration
   
   • Cerebral lesion

(Braund IVIS)

Question 20

Multiple cranial nerves (trigeminal, hypoglossal, glossopharyngeal) are thickened in animals with ___________

Answer 20

Fucosidosis

(Braund IVIS)

Question 21

Clinical signs of midbrain syndrome (7)

Answer 21

1. Spastic weakness/paralysis in all 4 limbs or contralateral limbs
2. Increased reflexes and muscle tone in all limbs, or contralateral limbs
3. Opisthotonus
4. Postural reaction deficits in all limbs or contralateral limbs
5. Mental depression or coma
6. Ipsilateral deficits of CN 3 (ventrolateral strabismus, dilated unresponsive pupil w/ normal vision, ptosis
7. Hyperventilation

(Braund IVIS)

Question 22

Site of predilection for intracranial intra-arachnoid cysts?

Answer 22

Quadrigeminal cistern (above the midbrain, between the rostral and caudal colliculi)

(Braund IVIS)

Question 23

Clinical signs of motor neuropathy vs. sensory neuropathy vs. autonomic neuropathy

Answer 23

Motor neuropathy:

• Flaccid paresis/paralysis
• Neurogenic muscle atrophy
• Reduced/absent reflexes and muscle tone
• Muscle fasiculations

Sensory Neuropathy

• Hypalgesia, hypesthesia
• Proprioceptive deficits
• Abnormal sensation/sensitivity (paresthesia) of face, trunk or limbs
• Self mutilation
• Reduced/absent reflexes without muscle atrophy

Autonomic neuropathy

• Anisocoria or dilated pupils
• Decreased tear secretion
• Decreased salivation
• Bradycardia

(IVIS Braund)

Question 24

What is the most common presentation of CNS cryptococcus?

MRI characteristics?

How useful is CSF?

Answer 24

Lesions of the nasal cavity, fronto-olfactory region, retrobulbar extension

• Dogs - neurologic cryptococcus predominates
• Cats - nasal, ocular, cutaneous predominate over neurologic

MRI - Multifocal parenchymal T2 hyperintense lesions most common, Ill-defined enhancement of parenchymal lesions, Diffuse meningeal enhancement

Cryptococcal organisms identified in CSF of 20/26 dogs and cats

Vet Clin N. America

Question 25

Most common form of CNS blastomycosis?

What are the most common systemic manifestations of blastomycosis?

Answer 25

Sinonasal and intracranial; ventriculitis w/ systemic disease

NonCNS - Respiratory, lymphatic, ocular

Vet Clin N. America

Question 26

Most common CNS manifestation of Aspergillus ?

Most common CNS manifestation of Histoplasmosis?

Answer 26

Aspergillus - Multifocal brain lesions +/- sinonasal lesions on MRI, also discospondylitis

Histoplasmosis - Multisystemic disease + meningoencephalitis

Vet Clin N. America

Question 27

Which two fungal organisms most commonly present as CNS granulomas without extraneural lesions?

Answer 27

Cladophialophora bantiana and Coccidiomycosis

Vet Clin N. America

Question 28

4 antifungals that cross the BBB

Negative prognostic indicator for CNS mycosis

Answer 28

1. fluconazole
2. voriconazole (neurotoxic in cats!)
3. posconazole
4. liposomal or lipid complex amphotericin B

altered mental status - neg prognostic indicator

Vet Clin N. America

Question 29

Formula for cerebral perfusion pressure?

What determines cerebral blood flow?

What determines cerebral vascular resistance?

Answer 29

CPP = MAP - ICP

Cerebral blood flow = CPP / cerebral vascular resistance

Cerebral vascular resistance: Ln/πr⁴

L = vessel length, n = viscosity, r = vessel radius

• cerebral vascular resistance is controlled via pressure autoregulation (ability to maintain constant CBF and ICP from MAP 50 - 150mmHg)
  
  • influenced by PaCO2
  • influences vessel diameter

Vet Clin N. America

Question 30

In a study of dogs with mild head injury, what % had skull fractures, what percent had intracranial hemorrhage

In dogs and cats with severe head injury, what % had intracranial hemorrhage?

Answer 30

Mild head injury - 89% had skull fractures 11% had intracranial hemorrhage

Severe head injury - 96% had hemorrhage

Vet Clin N. America

Question 31

Components of secondary traumatic brain injury (5)

Answer 31

1. Excitotoxicity
2. Depletion of ATP
3. Production of ROS
4. NO accumulation
5. Lactic acidosis

Vet Clin N. America

Question 32

Pathophysiology of Cushing reflex of elevated ICP:

Answer 32

Severely increased ICP –> CBF decreases –> CO2 accumulates locally

Vasomotor center of the brain detects increase in CO2 –> Increase sympathetic tone –> peripheral vasoconstriction –> increases MAP

Baroreceptors sense hypertension –> reflex bradycardia

Vet Clin N. America

Question 33

What are the 3 components of the MGCS?

Studies have shown that an MGCS of _______ within the first 48 hours of hospitalization approximates a 50% probability of survival

Animal trauma triage: In dogs with head trauma, a score of _____ approximated 50% survival

Which is more predictive?

Answer 33

1. Motor activity
2. Brainstem reflexes
3. Level of consciousness

Studies have shown that an MGCS of 8 within the first 48 hours of hospitalization approximates a 50% probability of survival

Animal trauma triage: In dogs with head trauma, a score of 9 approximated 50% survival

A recent retrospective study determined the strongest predictor for nonsurvival was a decreased MGCS

Vet Clin N. America

Question 34

Duration of action of fluid redistribution after administration of HTS?

Should colloids be used for head trauma?

Answer 34

75 minutes

Colloids should not be used - leakage of albumin through a disrupted BBB may create oncotic shifts, promote edema formation leading to increased ICP and mortality

• synthetic colloids have not been evaluated, only albumin

Vet Clin N America

Question 35

Mannitol:

• What are immediate effects?
• What happens in 15 - 30 minutes
• Other MOA?

Answer 35

Immediately - osmotic effect expands the plasma volume, reduces viscosity, improves microcirculatory flow

• Reduction in viscosity –> reflex vasoconstriction of pial arterioles

15-30 minutes - osmotic gradient across BBB forms, persists for 2-5h, and shifts fluid from the brain into the intravascular space

Also acts as a free radical scavenger

** in people, no difference in outcome has been found between patients with intracerebral hemorrhage that did or did not receive mannitol

** Concurrent use of furosemide is unproven

Vet Clin N America

Question 36

How do inhalant anesthetics affect ICP?

Answer 36

As concentrations increase > 1 - 1.5x minimum effective alveolar concetration, ICP increases

• At lower concentrations, vasodilatory effects of inhalants may improve CPP
• If the ICP is increased, inhalants are contraindicated and total IV anesthesia is recommended
  
  • Propofol improves cerebral perfusion and maintains pressure autoregulation better than inhalant anesthetics
    
    • May be neuroprotective via modulation of GABA receptors, antioxidant effects
    • May cause hypotension and hypoventilation

Vet Clin N America

Question 37

What is the rate of posttraumatic epilepsy compared to standard population epilepsy rate?

Answer 37

Posttraumatic epilepsy: 3.5 - 6.8%

Standard population epilepsy: 1.4%

Vet Clin N America

Question 38

Under normal conditions, _____ is the most powerful determinant of CBF

Answer 38

PaCO2

Vet Clin N America

Question 39

Components of Dandy Walker Syndrome

Answer 39

1. Aplasia or hypoplasia of the cerebellar vermis
   
   • Pyramis, uvula, and nodulus lobules involved in several dogs (hemispheres and flocculus also affected in some)
   • Retrograde degeneration of brainstem nuclei
2. Cyst-like dilation of the 4th ventricle
   
   • Fluid-filled cyst-like structure continuous with a dilated 4th ventricle that fills the posterior fossa
3. Hydrocephalus
   
   • Lat aperatures appear normal
   • Hydromyelia not usually a feature

• believed to be a disorder of fusion of dorsal midline structures of the primitive neural tube
• +/- syringomyelia and agenesis of the corpus callosum

(Braund)

Question 40

What are the 4 major disease conditions that cause acute flaccid tetraparesis in dogs and cats?

How can they be differentiated? (Weakness, CN, other, lumbar CSF, electrodiagnostics)

Less common causes (5)

Answer 40

1. Idiopathic polyradiculoneuritis/coonhound paralysis
2. Botulusm
3. Tick paralysis
4. Acute fulminating myasthenia gravis

Weakness: all acute tetraparesis/tetraplegia with areflexia except TP - normoreflexia in mild cases; MG - normoreflexia

CN: Dysphonia/aphonia for all
Facial weakness - APN, MG
Megaesophagus/dysphagia - botulism, MG
Mydriasis/decreased PLR - botulism

CSF - elevated protein in APN, rest normal

Other - APN - hyperesthesia; Botulism - decreased mentation, urinary retention/incontinence; MG - urinary retention

EMG - increased spontaneous activity in APN, rest normal

CMAP - decreased amplitude in all except MG

MNCV - normal in all excent APN - normal or mildly slow

F-wave: normal ratio/latency in all except APN - slow F wave latency and prolonged ratio

Supramax RNS - normal or incremental response for botulism; decremental response MG

Less common:

1. Coral snake evenomation
2. Blue and green algae intoxication
3. Black widow spider evenomation (later stages)
4. Other rare toxicities (lasalocid in cattle feed)
5. Polymyositis

(Vet Clin N America)

Question 41

5 etiologic factors for APN/CHP?

4 Pathologic findings for APN biopsy?

Answer 41

1. Contact with racoon saliva
2. Recent vaccination (especially Rabies)
3. Recent upper respiratory viral infection
4. Recent bacterial/viral GI infection
5. Toxoplasma gondii infection

Biopsy:

1. Axonal degeneration
2. Paranodal/segmental demyelination
3. Infiltration of inflammatory cells (cells vary acute vs. chronic)
   
   • Lumbar/sacral ventral roots more severely affected
   • MILD involvement of the dorsal roots
4. Denervation in muscle

(Vet Clin N America)

(Vet Clin N America)

Question 42

What type of antibodies are found in APN?

What type of immune-response and what type of immune-cells involved? Important cytokine?

Answer 42

A recent study in dogs has demonstrated the presence of anti-GM2 ganglioside ABs in the sera from a high percentage of dogs with APN

• In general IgG or IgM most common
• Demonstration of anti-GM2 circulating ABs in serum has shown diagnostic sensitivity of 60% and specificity of 97%

Strong evidence for a role of cell-mediated immunity

• initial breakdown of blood-nerve-barrier is induced by the release of IFN-gamma from circulating activated T cells
• Autoreactive CD4+ T cell interaction with APCs –> clonal proliferation of B cells –> production of antiganglioside, antiglycolipis, and antimyelin protein antibodies

Fun fact - APN usually has INTACT pernieal reflex

(Vet Clin N America)

Question 43

APN:

• EMG
• CMAP
• MNCV
• F wave latency, ratio
• Sensory nerve conduction

Answer 43

• EMG - spontaneous activity (after day 4)
• CMAP - decreased amplitude/increased temporal dispersion
• MNCV - normal or mildly decreased
• F wave latency, ratio - prolonged latency, decreased amplitude, increased ratio
• Sensory nerve conduction - normal or mild decrease

“All these findings indicate a motor neuron axonopathy affecting the entire length of peripheral nerves, more severe in the proximal portions of motor nerves, ventral nerve roots, or both. In addition, prolonged F-wave latencies and ratios indicate there is also demyelination in the ventral nerve roots and proximal portions of motor nerves.”

(Vet Clin N America)

Question 44

Botulism neurotoxin that affects dogs and cats? horses and cattle?

What type of bacteria is C. botulinum?

Answer 44

Dogs and cats - type C

Horses - B and C

Cattle - C and D

Clostridium botulinum = G+ spore forming, anaerobic

(DeLahunta)

Question 45

Modes of infection with C. botulinum?

Answer 45

1. Ingestion of preformed toxin in a feed source (most common)
2. Ingestion of spores in the soil
3. Wound infection with organisms

(Vet Clin N America)

Question 46

Process of botulism absorption/toxicity?

How does the amount of toxin influence severity and rate of development of clinical signs?

Autonomic signs of Botulism?

Answer 46

• Ingestion of spores/bacteria –> lysis of cells/spores –> release of progenitor BoNT
• BoNT stable at low pH, once reach small intestine the alkaline pH causes dissociation of progenitor toxin and release of BoNT
• Small intestinal endocytosis of BoNT –> lymphatic –> blood
• BoNT reaches cholinergic nerve junctions
• Rapid and specific binding of BoNT to neuronal surface receptors (irreversible, susceptible to antitoxin, differences in affinity explain species susceptibility)n
• Internalization of BoNT into endosome (no longer susceptible to inactivation)
• Membrane translocation
• Enzymatic cleavage of SNARE –> inhibit docking and fusion of synaptic vesicles –> LMN paralysis and autonomic dysfunction
• Clinical signs develop in 6h - 6 days. More toxin –> more rapid/severe clinical signs
• Autonomic clinical signs: tachycardia/bradycardia, mydriasis, slow PLR, constipation, urinary retention, KCS

(Vet Clin N America)

Question 47

What clinical features can help distinguish botulism from APN?

Diagnosis of botulism?

How long until dog recovers from botulism?

Answer 47

Loss of exernal anal sphincter tone and megaesophagus

Botulism diagnosis

• Mouse innoculation test - demonstrate BoNT in blood, feces, vomit, stomach contents or spoiled food
• ELISA, mass spectrophotometry, PCR - measure activity of BoNT by cleavage of artificial substrates
  
  • Less sensitive than mouse inoculation test
• Demonstration of 4x increase in BoNT-antibody titer

All affected dogs recover spontaneously in 14-24 days unless secondary complications develop

The Veterinary clinics of North America. Small animal practice

Question 48

What 2 species of ticks can cause tick paralysis in the US?

Male or female tick causes the disease?

Answer 48

Dermacentor variabilis (American dog tick)

Dermacentor andersoni (Rocky mountain wood tick)

Female tick ! (those bitches)

(Vet Clin N America)

Question 49

Pathophysiology of tick paralysis?

Unique clinical signs of paralysis. When do they develop after exposure?

Answer 49

Neurotoxin is created in the salivary glands of the female tick

Tick bites –> neurotoxin enters the bloodstream –> interferes with the function of CALCIUM in the release of ACh from axon terminal

Clinical signs:

• Develop 5-9d after exposure, P is recumbent in 24 - 72 hrs
• Spinal reflexes depressed/absent (stretch reflexes lost before withdrawal)
• Urethral and sphinchter functions unaffected
• Nociception normal, hyperesthesia absent
• CN LMN signs uncommon (occasionally ME)

(Vet Clin N America)

Question 50

Pathophysiology of MG?

Answer 50

Antibodies bind NICOTINIC AChR –> prevent attachment of ACh

Once the antibody is bound, the entire unit is internalized into the muscle/no longer available

Lg abundance of receptors provides a safety factor - many are spared from this antibody binding

Fuminating form - antibodies are able to bind to nearly all of the receptors

(Vet Clin N America)

Question 51

What muscles tend to be affected by focal MG?

What ages are affected by acquired MG?

Breeds affected by acquired MG?

Answer 51

Focal MG: esophagus, laryngeal muscles, facial muscles

Acquired MG - bimodal distribution of age (3y ad 10y) in both dogs and cats

Breeds:

• Akitas
• Scottish terriers (and other terriers)
• German shorthair pointers
• Chihuahua
• German shepherd
• Golden retrievers
• Labs
• Dachshunds
• Observed in Newfoundlands and litter of great dane puppies
• Cats - Abyssinian and Somali

(Vet Clin N America)

Question 52

Pathophysiology of congenital MG?

Diagnosis and treatment?

Breeds? Inheritance?

Answer 52

Abnormal structure of AChR, insufficient # of AChR have developed, defect in ACh resynthesis/repackaging

Treatment: some respond to acetylcholinesterase therapy, occasionally grow out of it (usually fatal)

Diagnosis: biopsy external intercostal muscle –> Localization of AChE, AChR, AChR subunits, EgG and complement components at the NMJ,
Total volume of AChR determined (only helpful when deficiency of AChR is the cause)
Positive tensilon test can be consistent with diagnosis of acquired MG but does not differentiate it from autoimmune acquired MG.

Autosomal recessive gene in: Smooth fox terrier, Parson russel terrier, Honsehund (also Brahman calves - PCR DNA test is available)

Reported in: Springer spaniel, miniature smooth dachshund, samoyed

RARE IN CATS

(Vet Clin N America)

Question 53

What % of dogs with acquired MG have a thymic mass? cats?

What endocrine dz is associated with acquired MG?

What drug can cause acquired MG in the cat?

Electrodiagnostic diagnosis of MG?

Answer 53

<5% of dogs, 25% of cats have a thymic mass

Hypothyroidism in dogs with acquired myasthenia gravis has a significant incidence (causation unclear)

Methimazole –> acquired MG in cats

Electrodiagnostics (not recommended) - RNS –> immediate decrement in the response of the muscle (improves after tensilon)

(Vet Clin N America)

Question 54

Clinical signs and age of onset of Rottweilers with neuronal vacuolation and spinocerebellar degeneration?

Course of progression?

Answer 54

Onset between 6 and 16 weeks of age, most within 2 mos of age

• Generalized weakness and ataxia (worse in the PL)
• Hypermetric gait
• Abnormal proprioceptive placing
• Normal reflexes (exception of 1 dog)
• INSPIRATORY STRIDOR - consistent clinical feature due to laryngeal dysfunction
• Other: positional strabismus, intention tremor, nystagmus
• Some dogs with this disorder had concurrent ocular abnormalities

Progression over several weeks. There is no treatment and the prognosis is grave

Boxer dogs presented at 2 mos of age

Question 55

Cocker spaniels with multisystem neuronal degeneration/abiotrophy

• Age of onset of signs?
• Progrssion?
• Clinical signs?

Answer 55

• Forebrain and cerebellar dysfunction
• Onset approximately 1 year of age
• Progresses over several months
• No treatment, prognosis grave

(Dewey)

Question 56

What brain changes occur with canine cognitive dysfunction syndrome?

Answer 56

1. Cerebral vascular changes (blood vessel wall fibrosis), microhemorrhages
2. Meningeal thickening
3. Gliosis
4. Cerebral atrophy/ventricular dilation
5. Progressive accumulation of beta-amyloid in and around neurons
   
   • Form neuritic plaques most prominent in the frontal cerebral cortex and hippocampus
   • The degree of beta-amyloid accumulation correlates with degree of cognitive impairment
6. Intraneuronal accumulation of tau protein
   
   • The tau protein does not form neurofibrillary tanlges
7. Amyloid deposition (meningeal and parenchymal
8. Axonal degeneration with myelin loss
9. Astroglial hypertrophy and hyperplasia
10. Intraneuronal accumulation of lipofuscin, polyglucosan bodies, ubiquitin)

(Dewey)

Question 57

Clinical signs of cognitive impairment in dogs:

Answer 57

DISHAAL

• Disorientation/confusion
• Interactions/social relationships abnormal
• Sleep-wake cycles abnormal
• House soiling
• Activity (increased/repetitive or apathetic/depressed)
• Anxiety
• Learning and memory abnormal

(Dewey)

Question 58

What is the MOA of selegiline?

Answer 58

• irreversible inhibitor of monoamine oxidase B
• Reported to restore dopaminergic balance
• Enhance catecholamine levels
• Decrease free radicals
• Questionable if it works

(Dewey)

Question 59

How do basilar artery resistive index via doppler ultrasonography, and ventricle to brain ratio in dogs with ventriculomegaly correlate to clinical signs of hydrocephalus?

EEG abnormalities in patients with hydrocephalus?

Answer 59

RI and VB ratio were both significantly higher in clinically hydrocephalic dogs compared with dogs having ventriculomegaly with no signs of dysfunction

• RI changed with changes in neurologic status

EEG - slow-frequency, high voltage activity

(Dewey)

Question 60

What is believed to be the MOA of gabapentin and pregablin? What is the elimination half life of gabapentin vs. pregablin?

Answer 60

Bind to alpha-2-delta-1 subunit of GABA receptor –> inhibit calcium influx

Pregablin has higher affinity for the alpha2-delta-1 subunit

Gabapentin half life 3-4 hrs
Pregablin half life 7 hrs

(Dewey)

Question 61

Clinical signs associated with supracollicular fluid accumulation?

______ are congenital diseases thought to be related to abnormal cerebral cortical neuronal migration during fetal development

Answer 61

Forebrain signs/seizure
Cerebellovestibular dysfunction
Neck pain

Lissencephaly/pachygyria and polymicrogyria

• Lissencephaly/pachygyria - reduced numbers, or the absence of gyri on the surface of the cerebral hemispheres and an abnormally thickened, histologically disorganized cerebral cortex
  
  • Clinical signs - prosencephalic dysfunction, seizures @ 10-12mos
  • Most common in the lhasa apso
  • Also described in the wirehaired fox terrier, Irish setter, Korat cat
• Polymicrogyria - excessive small gyri on the cerebral cortex
  
  • Described in 4 related standard poodles that also displayed asymmetric dilation of the lateral ventricles
  • Disorganization of the cerebral cortex was also evident histologically in these standard poodles

Question 62

Neurotransmitter imbalances seen with hepatic encephalopathy

Answer 62

1. Increased circulating levels of aromatic amino acids
2. Increased circulating benzodiazepine-like substances
3. Increased glutamine, decreased glutamate –> oxidative damage and astrocyte mitochondria dysfunction
4. Increased GABAergic tone
5. Changes in serotonin metabolism
6. Astrocyte accumulation of manganese –> oxidative damage

Acute HE - major pathologic consequence is cerebral edema and raised intracranial pressure

Chronic HE - major consequence is neurotransmitter dysregulation

Question 63

How does hypernatremia (acute/chronic) lead to encephalopathy

Answer 63

Hyperosmolality/hypernatremia –> shrinkage of brain parenchymal cells –> stretching and tearing of small intracranial blood vessels - hemorrhage

• Intracellular dehydration and hemorrhage may contribute to encephalopathy
• Chronic hypernatremia: brain produces idiogenic osmoles to compensate for increased extracellular osmolality. Correction of hypernatremic state –> cerebral edema
• Chronic uremia also causes hyperosmolality and rapid dialysis can cause dialysis disequilibrium syndrome via same mechanism
• Ketotic and nonketotic diabetes mellitus can both contribute to hyperosmolality

(Dewey)

Question 64

How does hyponatremia cause encephalopathy

Answer 64

Hyponatremia can result in swelling of brain parenchymal cells with subsequent brain edema - compensates by EXTRUDING cosmetically active particles (potassium, amino acids)

• Hyponatremia is corrected –> axonal shrinkage due to relative lack of intracellular osmolality and subsequent demyelination in the brainstem (particularly thalamus) similar to central pontine myelinolysis in people

Question 65

Hypercalcemia causes (increased/decreased) excitability of neuronal cell membranes

Answer 65

Decreased excitability of neuronal cell membranes

(Dewey)

Question 66

How does CRP correspond to outcome for patients with discospondylitis?

Answer 66

All dogs with a poor outcome (3/18) had an elevated CRP, there was a trend for the median CRP to be higher in the dogs with a poor outcome

ROC analysis - CRP concentration of > 8.6 was 100% specific for predicting a poor outcome

Retrospectice study

(ACVIM 2017)

Question 67

What enzyme is responsible for degrading the CNS/PNS myelin lipids galactosylceramide and galactosylsphingosine?

Survival time for dogs with brachial plexus NST treated with surgery vs. radiotherapy

Answer 67

Galactosylceramidase (GALC)

Similar MST

• Survival time for stereotactic radiation therapy was approximately 371 in one study, (240 days progression-free interval)

(ACVIM 2017)

Question 68

Median survival time for meningioma treated with surgery followed by fractionated radiation therapy?

Answer 68

540 - 900 days

(ACVIM 2017)

Question 69

T/F: The degree of kyphosis associated with the vertebral malformations determines the likelihood of developing neurologic dysfunction

What large breed dog is predisposed to vertebral malformations?

Answer 69

True

• Although some of these abnormalities often also produce some degree of scoliosis, this does not seem to have a substantial additional impact on the development of neurologic impairment

Doberman Pinscher and German Shorthaired Pointer

(Dewey et al)

Question 70

Answer 70

Block Vertebrae

(Vet Clin N America)

Question 71

Answer 71

Right: Ventral aplasia

Left: ventral wedge-shaped

(Vet Clin N America)

Question 72

Answer 72

Left: lateral hemivertebra

Right: lateral wedge shape

(Vet Clin N America)

Question 73

Answer 73

Left: Doso-lateral hemivertebra

Right: Butterfly vertebra

(Vet Clin N America)

Question 74

Vertebral body malformations:

• Age at presentation
• Sex predilection
• Most common location

Answer 74

• Age at presentation - 60% under 1 year, 40% over 1 year
• Sex predilection: none
• Most common location: usually between T6 and T9, in one report, T7 was the most commonly affected vertebra, followed by T8 and T12

(Vet Clin N America)

Question 75

What is the albumin quotient?
What is IgG index?

Answer 75

Q alb = CSF albumin / serum albumin x 100
Elevation suggests disrupted BBB

Q IgG = CSF IgG / serum IgG x 100
Serum IgG concentrations are at least 1000x higher than those in the CSF - there is a strong association between the 2 values
Elevations suggest intrathecal IgG production

IgG index = Q IgG x Q alb
Elevation suggests intrathecal IgG synthesis and BBB dysfunction

Can also use antibody index and the goldman-witmer coefficient - techniques that are believed to be more accurate than the IgG index as they use antigen-specific antibody titers rather than total IgG
IgM is not normally found in CSF - presence of IgM in serum and/or CSF is considered more specific than IgG or total immunoglobulin levels for detection of active infectious diseases

(De Terlizzi)

(De Terlizzi)

Question 76

What CSF biomarker can be used to differentiate between CSF bacterial vs. viral meningoencephalitis?

What CSF biomarker is higher in lumbar CSF of dogs with degenerative myelopathy?

Answer 76

CRP - bacterial vs. viral meningoencephalitis

Myelin basic protein - suggests active demyelinating process in DM (study also confirmed relationship between MBP level and severity of demyelination)

(De Terlizzi)

Question 77

Technique for counting cells in CSF?

Answer 77

Hemocytometer is used

Chamber is placed in a humidified environment for 10-15 minutes to allow the cells to settle to the surface of the glass

Neubauer chamber - total cells in all 9 squares are counted, average of 2 counts x 10⁹ = cells / uL

Fuchs-Rosenthal chamber, total cells present in 16 x 1mm2 areas are counted x 10⁹ = cells / uL

(De Terlizzi)

Question 78

What process can differentiate erythrocytes from WBCs in the hemocytometer?

Answer 78

Phase microscopy - used to differentiate RBCs from WBCs in the haemocytometer chamber

When an unstained specimen is examined, it is necessary to lower the microscope condenser to reduce the light intensity

Alternatively, the cells may be stained with a small amount of new methylene blue stain

(De Terlizzi)

Question 79

Disease processes known to cause albuminocytologic dissociation?

Answer 79

Viral nonsuppurative encephalomyelitis, neoplastic disease, traumatic, vascular, degenerative, and compressive spinal cord lesions

Essentially, nonspecific finding

(De Terlizzi)

Question 80

CSF levels of ________ were higher in dogs with IVDD and more severe clinical signs than dogs with less severe clinical signs

Answer 80

MMP9

(De Terlizzi)

Question 81

What is the mechanism of cytocentrifugation for CSF analysis?

What artifactual changes can be seen?

What kind of stain is used?

Answer 81

Slow-speed centrifugation and acceleration to concentrate cells from 100 - 400uL into a small circular area on a glass slide

• Cellular detail is excellent because the elements are gently spread out on the slide
• Alternative method is sedimentation. Cell morphology considered better with cytocentrifugation, BUT the greater number of cells on sedimentation preparations were thought to be more accurate in calculating leukocyte differential. Cell yield and LDIF on cytocentrifugation preparations is imprecise

Artifactual changes in the cells:

1. Increased vacuolation
2. Alteration in structure particularly of monocytoid cells and macrophages

Cytospin is air dried and stained with Romanowsky stains

(De Terlizzi)

Question 82

_____% of nondegenerate neutrophils are normal in healthy animal

From most common to least common cell types in CSF:

Answer 82

10% or less in dogs (8% or less in cats)

(some authors have suggested that the presence of neutrophils or eosinophils in the CSF is indicative of an abnormality)

Monocytes > lymphocytes > neutrophils > macrophages > eosinophils
**small lymphocytes and mononuclear cells predominate in dogs; monocytes predominate in cats

(De Terlizzi)

Question 83

CSF neutrophilic pleocytosis seen in which conditions?

Answer 83

1. Trauma
2. Hemorrhage
3. Post myelographic meningitis
4. Bacterial, fungal infections, FIP
5. Immune-mediated disease (SRMA)
6. Neoplasia
7. Severe seizures

SRMA and necrotizing vasculitis - neturophilic response
Neutrophils well preserved, non-degenerate or hypersegmented
CSF culture neg for bacteria
Neutrophilic pleocytosis > 500 cells/uL with neutrophil % between 75 - 100%

Of patients that had abnormal CSF w/ meningioma, most had neutrophilic pleocytosis (suspected from tumor necrosis)

(De Terlizzi)

Question 84

CSF: Small/mature lymphocytes > ________% = mononuclear pleocytosis

Answer 84

> 70% = mononuclear pleocytosis

• Also increase in number of monocytoid/macrophages
• Reactive lymphocytes w/ normal TNCC = CNS disease
  
  • Ex/ CNS viral dz
• Canine distemper - mild to moderate lymphocytic pleocytosis
  
  • CSF in CDV may show an increase in macrophages

(De Terlizzi)

Question 85

A moderate to marked lymphocytic pleocytosis with > ______% lymphocytes is consistent with a necrotizing meningo/leukoencephalitis

Answer 85

80% lymphocytes

Lymphocytic pleocytosis seen in:

• CDV
• GME
• NLE/NME
• CNS lymphoma
• Ehrlichiosis
• Toxoplasma/Neospora
• Bacterial meningitis following treatment

(De Terlizzi)

Question 86

Causes of mixed-cell pleocytosis

Answer 86

1. GME (most common cause)
2. Chronic SRMA
3. Infections (fungal, ehrlichia, Toxoplasma/Neospora, Protothecosis)
4. Trauma/vascular (Disc, myelomalacia, ischemia/infarction)

(De Terlizzi)

Question 87

Causes of CSF eosinophilic pleocytosis

Answer 87

1. Steroid-responsive eosinophilic meningitis
2. Infection (Toxo/Neospora, fungal, aberrant parsitic migration, CDV, Rabies)

(De Terlizzi)

Question 88

Normal nucleated cell count for CSF including units!!

Normal protein concentrations (including units)

Answer 88

<5 cells/uL in the dog
<8 cells/uL in the cat

< 25-30mg/dL for cisternal

< 45mg/dL for lumbar

(Sharkey)

Question 89

Viral causes of hypomyelination in lg animals:

Answer 89

• Pigs - hog cholera, swine fever, circovirus
• Sheep - BVD and border disease
• Cattle - BVD

(de Lahunta)

Question 90

What breed of cats gets an inherited hypokalemic myopathy?

Answer 90

Burmese cats

• Observed most often with onset at 2-6 mos old in Burmese kittens
• Hypokalemia is from excessive loss through the kidneys
• Genetic studies - mutation of WNK4 gene

(de Lahunta)

Question 91

What neuromuscular disease of young labrador retrievers presents with decreased/absent patellar reflexes?

Answer 91

Centronuclear (Type II deficiency) Autosomal Recessive Polymyopathy in labrador retrievers

• Muscle biopsy:
  
  • Variation in muscle fiber size
  • Depletion of type II muscle fibers
  • Few cells with centrally positioned nuclei but no necrosis of cells
  • Light and EM show progressive changes in:
    
    • Internal tubuloreticular and sarcolemmal membranes
    • Triads
    • Mitochondria
• Mutation in PTPLA gene
• ABSENT PATELLAR REFLEX
• Serum CK is normal/slightly elevated
• EMG - few denervation potentials or bursts of CRD

Question 92

What 2 snake envenomations can cause diffuse neuromuscular signs?

Answer 92

1. Coral snake
2. N American rattlesnake

• Both cause postsynaptic blockade of neuromuscular junction
• Rapid onset of clinical signs

(de Lahunta)

Question 93

How does organophosphage toxicity cause neuromuscular signs? How is it treated?

Answer 93

Chlorpyrifos and fenthion - acetylcholinesterase inhibitors

• Accumulation of ACh –> blockade at the receptor –> LMN paralysis
• Clinical signs within minutes to hrs of exposure
• Diagnosis via history and decreased levels of cholinesterase in the blood
• Tx: atropine for muscarinic signs, pralidoxime chloride for nicotinic signs
  
  • In some toxicities, diphenhydramine may help block action of the toxin

(de Lahunta)

Question 94

Clinical signs of:

• Constant drooling
• Decreased ROM of the mouth
• Diffuse muscle atrophy
• Short-strided gait, arched back, low head
• Normal patellar reflex

In a young labrador puppy should raise concern for?

Answer 94

Sex-linked muscular dystrophy

• Deficiency of dystrophin
  
  • • Hypertrophy of:
  • Pharyngeal and laryngeal muscles
  • Caudal thigh
  • diaphragm
• Atophy of:
  
  • Most axial and appendicular muscles
  • Diagnosis:
  • ​Dystrophinopathy - muscle fiber necrosis is severe - elev CK (severe), AST, ALT
• • Muscle biopsy:
• • Extensive muscle cell necrosis
• • Lg accumulation of macrophages
• • Fibrosis
• • Satellite cells = regeneration
• • Immunohistochemistry - lack of dystrophin in the muscle cell membrane
• • Sex-linked recessive gene
• • Only male dogs clinically affected
• • Carrier female - may have elev. CK but rarely clinical signs
• • Young male dogs presented for fatigue while exercising, inactivity, slow growth
• • • • (de Lahunta)

Question 95

Clinical signs of exercise induced collapse in labrador retrievers?

Mutation in what protein causes the signs?

Answer 95

Collapse after vigorous exercise

Juvenile or young adult dogs when they are engaging in strenuous activity with a high level of excitement

Mutation in dynamin 1 gene

(deLahunta)

Question 96

Common cause of extradural progressive spinal cord compression in cattle and cats?

Answer 96

Lymphoma

(de Lahunta)

Question 97

Cats undergoing declawing procedure may sustain and injury to the ___________ nerve from the tourniquet placed proximal to the elbow

Answer 97

Radial nerve

(de Lahunta)

Question 98

Horses that run into a doorway or fencepost with the cranial aspect of the scapula may injure the _____________ nerve where it crosses the scapular notch on the cranial surface of the neck of the scapula

Answer 98

Suprascapular nerve

• May cause a slight lateral deviation, abduction or lateral buckling of the shoulder when weight is borne on that limb
• Denervation atrophy of the supraspinatus and infraspinatus

(de Lahunta)

Question 99

What is the inheritance of Leonberger Inherited Neuropathy?

Answer 99

Autosomal recessive, more common in males

Onset of clinical signs from 1-3 years

Dying back neuropathy - sciatic and recurrent laryngeal

(de Lahunta)

Question 100

What breed developed an inherited hypertrophic neuropathy?

Answer 100

Autosomal recessive in Tibetan Mastiffs

Clinical signs start between 7-12 weeks and progress rapidly

Nerve biopsy - Widespread demyelination and Schwann cell hyperplasia, onion bulb formation with minimal axonal degeneration

(deLahunta)

Question 101

What are the three muscles that are affected by fibrotic myopathy?

Answer 101

Gracilis, semitendinosus, semimembranosus

(de Lahunta)

Question 102

What are the 4 causes of plantigrade posture?

Answer 102

Tibial nerve dysfunction (innervates extensors of the tarsus)

Rupture of part or all of the common calcanean tendon

Fracture of the calcaneus

Disrution of the long plantar ligament

Rupture of the gastroc tendon with the SDF spared –> tarsus overflexes and the digits flex because of stress put on intact superficial digital flexor that attaches to the calcaneus
DDx w/ ultrasound

Question 103

What is seen in muscle biopsy in goat kids with vitamin E deficiency myopathy?

Answer 103

Rhabdomyolysis

On BW - severe elev. CK/muscle enzymes

(de Lahunta)

Question 104

DDx for cervical flexion in the cat? (8)
Workup?

Answer 104

1. Hypokalemia
2. Thiamine deficiency
3. Hyperthyroidism
4. MG
5. Diabetes mellitus
6. Polymyositis
7. Organophosphate toxicity
8. Cervical myelopathy

CBC/Chem including CK, thyroxine, AXR, TXR, cervical rads, AChR titer, serology for FeLV/FIV, cryptococcus, T. gondii

(de Lahunta)

Question 105

What abnormalities can be seen in lg animals with CN 7 dysfunction that are not typically seen in small animals?

Answer 105

Deviation of the nose

Narrowed palpebral fissure - suggests the levator anguli oculi medialis muscle plays a significant role in the eyelid elevation in horses and farm animals

Occasionally, this fissure is slightly smaller on the affected side

(de Lahunta)

Question 106

Touch med/lat canthus –> p blinks both eyes, where does the pathway cross?

Answer 106

Ipsilateral spinal nucleus of the trigeminal nerve –> GSE neurons of BOTH facial nuclei

(de Lahunta)

Question 107

In horses, what condition is associated with secondary proliferation of the stylohyoid, tympanohyoid, and temporal bones?

Answer 107

Otitis media

Question 108

What are the 2 most common clinical signs of guttural pouch mycois?

Answer 108

Dysphagia - involvemet of pharyngeal branches of CN 9 and 10

Epistaxis - erosion of the internal carotid or maxillary artery

Other neurologic signs:

• Laryngeal hemiparesis (vagus involvement)
• Horner (cranial cervical ganglion or its postganglionic axons on the internal carotid nerve)
• Facial nerve paresis
• Hypoglossal paresis
• Vestibular (rare)

(de Lahunta)

Question 109

The guttural pouch is a diverticulum of what structure?

What region of the GP is the most common site of involvement in guttural pouch mycosis?

Answer 109

Auditory tube

Dorsocaudal aspect of the medial compartment

• Pharyngeal branches of 9 and 10 course ventrally adjacent to this medial compartment –> pharyngeal muscles

(de Lahunta)

Question 110

What type of neuropathy causes equine laryngeal hemiparesis?

Answer 110

Microscopic study of the recurrent laryngeal nerves shows an axonal degeneration and demyelination that is most pronounced at the larynx and decreases in the retrograde direction

• Current hypothesis is that this is a dying back neuropathy, unable to maintain such long axons
• Both nerves are affected
• Denervation atrophy occurs on both sides but is worse on the left side
• Similar lesions may be seen in the distal branches of the sciatic nerve where they innervate the crural muscles

Left recurrent laryngeal nerve has a longer course, passes around the ligamentum arteriosum and aortic arch before continuing cranially along the trachea to the larynx

Right only has to pass around the right subclavian artery

(de Lahunta)

Question 111

Clinical signs of hypoglossal dysfunction

Answer 111

Innervates: extrinsic tongue muscles, intrinsic tongue muscles, geniohyoideus

Clinical signs: impaired function of the tongue in prehension, deglutittion, mastication and phonation

Most reliable clinical sign in unilateral dysfunction is unilateral tongue atrophy, may have muscle fasiculations

(de Lahunta)

Question 112

What is a toxic cause of leukoencephalomalacia in horses?

Answer 112

Moldy corn poisoning - ingestion of fumonisin B1 (mycotoxin produced by Fusarium moniliforme)

Sudden destruction of cerebral white matter sometimes results in dysphagia

(de Lahunta)

Question 113

What is a common cause of cranial nerve dysfunction and caudal brainstem dysfunction in cattle?

Answer 113

Listeriosis

• L. monocytogenes
• Predominance of lesions are in the pons
• Various combinations of facial paralysis and vestibular ataxia are the most common clinical signs (ddx otitis media internal)
• Treated with high doses of penicillin, fair prognosis if the cow is still standing

(de Lahunta)

Question 114

Clinical signs of a complete oculomotor nerve lesion:

Answer 114

GVE dysfunction - dilated pupil that is unresponsive to light

GSE dysfunction - ptosis and ventrolateral strabismus. Does not adduct well on testing normal nystagmus

(de Lahunta)

Question 115

Clinical signs of loss of sympathetic innervation to the head (aside from miosis, ptosis, enophthalmos, elevated third eyelid)

What is the result of loss of parasympathetic innervation to the nasal mucosa?

Answer 115

• Congestion of the bulbar conjunctiva
  
  • Fundic exam - congested retinal blood vessels
• Warmer, pinker skin on the side affected
  
  • Due to peripheral vasodilation of the head
• Nasal mucosa -
  
  • Vasodilation –> decreased airflow –> increased tissue rigidity
  • Disinhibition –> increased nasal gland secretion
  • Results in accumulation of dried secretion (crusts) within the naris
  • Sympathetic innervation to the nose:
    
    • Cr. cervical ganglion –> internal carotid artery –> sympathetic fibers leave as the deep petrosal nerve –> join the major petrosal nerve (parasympathetic fibers from the facial nerve) –> nerve of the pterygoid canal (sympathetic and parasympathetic fibers) –> pterygopalatine ganglion (only parasympathetic fibers synapse here) –> caudal nasal nerve –> nasal cavity

Loss of parasympathetic innervation to the nasal mucosa –> loss of moisture from the lateral nasal gland –> hyperkeratosis

(de Lahunta)

Question 116

How does sympathetic denervation affect sweating in animals EXCEPT the horse?

Answer 116

All domestic animals except the horse, sweating is decreased on the surface of the body that is deprived of its sympathetic innervation

• Called hypohydrosis or anhidrosis
• Difficult to appreciate except on the nasal planum of the ox

(de Lahunta)

Question 117

How does sympathetic dysfunction affect sweating in the horse?

Answer 117

Sympathetic paralysis –> excessive sweating (hyperhidrosis) in the area of the skin that is denervated

• Often the initial clinical sign that is observed (especially if the disorder is acute)
• If the paralysis persists, sweating may decrease with time (may remain present at the base of the ear)
• ( loss of sympathetic innervation to the head may be an early sign of equine grass sickness )

(de Lahunta)

Question 118

What are the most reliable clinical signs of loss of GVE LMN sympathetic innervation to the head in cattle, sheep and goats?

Answer 118

Smaller palpebral fissure

Palpable hyperthermia of the ear

Miosis and protrusion of the third eyelid are subtle

Cattle - less sweating occurs on the planum nasolabiale on the affected side

Vasodilation in the nasal mucosa –> narrow airway –> difference felt on expiration

(de Lahunta)

Question 119

Where is the vertebral nerve found

Answer 119

Starts at the cervicothoracic ganglion –> follows vertebral artery into the transverse foramen of C6 and continues cranially through these foramina to C1

All axons are ganglionic axons

As it passes between each cervical vertebra, it supplies a ramus to the cervical spinal nerve at each of the intervertebral foramina

(de Lahunta)

Question 120

What are the 2 parasympatholytic drugs that can be used to dilate the pupil?

Answer 120

Tropicamide

Atropine

(Slatter)

Question 121

What are the direct and indirect-acting sympathomimetic drugs that can be used to dilate the pupils?

Answer 121

Direct acting (stimuate adrenoreceptors same way norepinephrine would)

• Epinepherine (penetrates eye poorly, causes systemic effects)
• Phenylephrine
• Dipivefrin (epinephrine prodrug)

Indirect acting

• Hydroxyamphetamine - facilitates neuronal release of norepinephrine
• Cocaine - prevents reuptake of norepinephrine

(Slatter)

Question 122

What are the parasympathomimetic drugs that can be used to constrict the pupil? (direct (1) ad indirect-acting (3))

Answer 122

Direct-acting

• Pilocarpine - directly stimulates the muscarinic receptors on smooth muscle cells of the pupillary sphincter and ciliary body
  
  • Effective even in the denervated eye
  • Increased lacrimal production
  • Side effects - salivation, vomiting, diarrhea

Indirect acting

• Physostigmine - cholinesterase inhibitor
• Organophosphate - inhibit cholinesterase (rarely used due to potential for toxicity, especially if OP flea/tick preventative)
  
  • ex/ Demecarium, carbachol

(Slatter)

Question 123

Pharmacologic testing for horner syndrome?

Answer 123

Instill 0.2 - 1% pilocarpine into the conjunctival sac of both eyes

• If the eye w/ horner responds (pupil dilation) BEFORE the contralateral (normal) eye –> denervation hypersensitivity –> suggests ganglionic neuron (after cr. cervical ganglion) is abnormal
• If the eye w/ horner responds slowly - suggests preganglionic lesion

Denervation hypersensitivity - following sympathetic denervation of the ocular muscles, there is increased sensitivity of the iris muscle to neurotransmitters

(Slatter)

Question 124

Experimental studies in dogs show that

Mild compression of the rostral midbrain –> ___________(mydriasis/miosis)

Continued compression –> ___________ (mydriasis/miosis)

Answer 124

Mild compression of the rostral brainstem –> miosis (increased activity of oculomotor GVE)

Continued compression –> mydriasis (loss of oculomotor GVE)

(de Lahunta)

Question 125

What anatomic difference exists related to the muscles of the third eyelid in the cat?

How can a cerebellar medullary lesion affect the third eyelid?

Answer 125

Cat - slips of striated muscle from the lateral rectus and levator palpebrae superiors attach to the 2 extremities of the eyelid and may actively contribute to its protrusion

Experimental medullary lesion that affect the cerebellar nuclei –> protruded third eyelid but the clinical signs of cerebellar ataxia predominate

(de Lahunta)

Question 126

What is complex regional pain syndrome?

Answer 126

Clinical syndrome that involves dysfunction of the cutaneous distribution of sympathetic nerves

• Chronic pain with localized hyperalgesia
• Clinical signs of dysregulation of the cutaneous sympathetic innervation include
  
  • Hyperthermia, hypothermia
  • Hyperhidrosis, hypohidrosis
  • Edema
• Trauma of some sort is usually a precipitating event at some time in the history of the patient
• Reported in horse and dog

(de Lahunta)

Question 127

What is the estimated prevalence of epilepsy in the general population of dogs?

Answer 127

0.6 - 0.75%

(Task Force)

Question 128

_______ is the term for any sudden, short lasting and transient event. It does not imply the event is epileptic

Answer 128

Seizure

(Task Force)

Question 129

_________ is defined as manifestation of excessive synchronous, usually self-limiting epileptic activity in neurons in the brain. This results in a transient occurrence of signs which may be characterized by short episodes with convulsions or focal motor, autonomic, or behavioral features and due to abnormal excessive and/or synchronous epileptic neuronal activity in the brain

Answer 129

Epileptic seizure

(Task Force)

Question 130

_____________ is defined as a seizure occurring as a natural response from the normal brain to a transient disturbance in function (metabolic or toxic in nature) - which is reversible when the cause or disturbance is rectified.

Answer 130

Reactive seizure

A provoked seizure is considered synonymous with reactive seizure

(Task Force)

Question 131

_________ is defined as a disease of the brain characterized by an enduring predisposition to generate epileptic seizures.

Answer 131

Epilepsy

This definition is usually practically applied as having at least 2 unprovoked epileptic seizures > 24h apart

(Task Force)

Question 132

What is the difference between the following types of idiopathic epilepsy:

• Genetic epilepsy
• Suspected genetic epilepty
• Epilepsy of unknown cause

Answer 132

Idiopathic epilepsy:

• Genetic epilepsy - causative gene for epilepsy has been identified/confirmed genetic background
• Suspected genetic epilepsy - a genetic influence is supported by:
  
  • A high breed prevalence > 2%
  • Genealogical analysis
  • And/or familial accumulation of epileptic individuals
  • “It seems very likely that the genetic influences in idiopathic epilepsies probably are complex involving multiple genes and interactions between genes (epistatic) and between genes and the environment (epigenetic)”
• ​Epilepsy of unknown cause - epilepsy in which the nature of the underlying cause is as yet unknown, and with no identification of structural epilepsy

(Task Force)

Question 133

______________ is characterized by epileptic seizures which are provoked by intracranial/cerebral pathology including: vascular, inflammatory/infectious, traumatic, anomalous/developmental, neoplastic and degenerative diseases confirmed by diagnostic imaging, CSF, DNA testing, or post mortem findings

Answer 133

Structural epilepsy

(Task Force)

Question 134

_________ epileptic seizures are characterized by lateralized and/or regional signs. Tie ictal onset is consistent from one epileptic seizure to another. They may be discretely localized or more widely distributed.

Answer 134

Focal epileptic seizures.

Focal epileptic seizures are characterized by lateralized and/or regional signs (motor, autonomic or behavioural signs, alone or in combination). The ictal onset is consistent from one epileptic seizure to another. They may be discretely localised or more widely distributed. Focal epileptic seizures may originate in subcortical structures, with preferential propagation patterns that can involve the contralateral hemisphere. With focal epileptic seizures, the abnormal electrical activity arises in a localized group of neurons or network within one hemisphere. The clinical signs reflect the functions of the area or areas involved.

(Task Force)

Question 135

What are the 3 types of focal seizures?

Answer 135

Motor: episodic focal motor phenomena

Autonomic: parasympathetic and epigastric components

Behavioral: Focal epileptic seizure which in humans can represent psychic and/or sensory seizure phenomena, may in animals represent a short-lasting episodic change in behavior such as anxiousness, restlessness, unexplainable fear reactions, abnormal attention seeking/clinging to the owner

(Task Force)

Question 136

__________ epileptic seizures are characterized by bilateral involvement (both sides of the body, and therefore both cerebral hemispheres involved) with the loss of consciousness.

Answer 136

Generalized epileptic seizures

• May occur alone, or evolve from a focal epileptic seizure start
• Dogs and cats - generalized epileptic seizure predominantly present as tonic, clonic, or tonic-clonic epileptic seizures.
• As a rule the animal will loose consciousness during convulsive epileptic seizures (myoclonic seizures excluded)
• Salivation, urination and/or defecation furthermore also occur (myoclonic seizures excluded)

Question 137

What are the 2 types of generalized seizures?

Answer 137

Generalized convulsive

• Tonic-clonic
• Tonic
• Clonic
• Myoclonic (jerking movements usually affecting both sides of the body)

Generalized non-convulsive

• Atonic (also called drop attacks)
  
  • Sudden loss or diminution of muscle tone without an apparent preceding myoclonic or tonic event lasting 1-2 seconds or more, involving head, trunk, jaw or limb musculature

(Task Force)

Question 138

How should focal epileptic seizures be classified with regard to consciousness?

Answer 138

Trick question - they should not.

Consciousness should always be a subjective interpretation in animals, therefore it is not meaningful to subclassify focal epileptic seizures using consciousness.

(Task Force)

Question 139

___________ is a sudden neurological occurrence such as a stroke or an epileptic seizure

Answer 139

Ictus

(Task Force)

Question 140

What are the two types of tonic movements used to describe seizures?

Answer 140

Tonic: a sustained increase in muscle contraction lasting a few seconds to minutes

Versive: A sustained, forced conjugate ocular, cephalic, and/or truncal turning/rotation or lateral deviation from the midline

Dystonic: Sustained contractions of both agonist and antagonist muscles producing athetoid or twisting movements, which when prolonged may produce abnormal postures

(Task Force)

Question 141

___________ is a sudden, brief < 100msec involuntary single or mulitple contraction(s) of muscle(s) or muscle groups of variable topography (axial, proximal limb, distal)

Answer 141

Myoclonic/myoclonus

Clonic: myoclonus which is regularly repetitive, involves the same muscle groups, at a frequency of about 2-3 seconds and is prolonged (synonym - rhythmic myoclonus)

(Task Force)

Question 142

______________ is a coordinated, repetitive, motor activity usually occurring when cognition is impaired and for which the subject is usually amnesic afterwards. This often resembles a voluntary movement and may consist of inappropriate continuation of ongoing preictal motor activity

Answer 142

Automatism

• Oroalimentary - lip smacking, lip pursing, chewing, licking, teeth grinding or swallowing
• Pedal - principally distal component involvement, bilateral or unilateral. Usually running movement

(Task Force)

Question 143

What is aura and why should it not be used in veterinary medicine?

Answer 143

Aura: a subjective ictal phenomenon that, in a given patient, may precede an observable seizure; If alone, constitutes a sensory seizure. This can result in behavioral changes such as fear, aggression, searching behavior, attention, body sensation

What is an aura - Commonly owners report that they can forsee a motor seizure when specific and well-known signs repeatedly appear within seconds or minutes prior to convulsions. The term has been used to describe a forewarning of convulsions.

The group recommends the term aura is not used in veterinary medicine. The signs occurring as the first indication of seizure activity (marking beginning of ictus) and interpreted by the dog owner as a warning sign is indeed a focal seizure onset, and should be referred to as such.

(Task Force)

Question 144

What terms can be used to describe the incidence of seizures?

Answer 144

Incidence: refers to the number of epileptic seizures within a time period, or the number of seizures days per unit of time

• Regular - consistent or predictable intervals between such events
• Irregular - inconsistent interval
• Cluster - Incidence of epileptic seizures within a given period (one or a few days) which exceeds the average incidence over a longer period for the patient. Cluster seizures can be divided clinically as 2 or more seizures within a 24 hour period
• Provocative factor - transient and sporadic endogenous or exogenous element capable of augmenting seizure incidence in the patient with chronic epilepsy and evoking seizures in susceptible non-epileitic individuals

(Task Force)

Question 145

________ is an epileptic seizure lasting greater than 5 minutes of continuous epileptic seizures, or 2+ discrete epileptic seizures between which there is incomplete recovery of consciousness (for generalized convulsive seizures)

Answer 145

Status epilepticus

“An epileptic seizure which shows no clinical signs of arresting after a duration encompassing the great majority of seizures of that type in most patients or recurrent epileptic seizures without resumption of baseline central nervous system function interictally”

(Task Force)

Question 146

______________ is any unilateral postictal dysfunction relating to motor, somatosensory and/or integrative functions including visual, auditory or somatosensory

Answer 146

Lateralizing phenomenon = TODD’s phenomenon = bravais’ phenomenon

(Task Force)

Question 147

What are post-ictal MRI changes and what are the diagnostic recommendations when these findings are observed?

Answer 147

1. T2W hyperintensities predominantly in the piriform and temporal lobes, cingulate gyrus and hippocampus
2. Mild contrast uptake +/-

CSF analysis (can be unhelpful because post-ictal pleocytosis can occur) - if abnormal, repeat in 6 weeks
\*\* a study in idiopathic epileptic dogs identified an association between CSF WBC count and time interval between the last seizure and the collection of CSF

Repeat imaging in the postictal period and assess changes in brain volume/atrophy

Post-ictal MRI changes usually resolve within 16 weeks

(Task Force)

Question 148

What is the pathology?

Answer 148

Post-ictal changes in the temporal and parietal lobe. Images obtained in a 1.5 T Siemens Symphony, Erlangen, Germany. Post-ictal oedema in the temporal lobe (short white arrow), hippocampus (long white arrow) and cingulate gyrus (yellow arrow) in a 2 year male English Bulldog that presented in status epilepticus

Question 149

What features of the hippocampus should be evaluated on MRI in patients with suspected idiopathic epilepsy?

Answer 149

• Atrophy
• Asymmetry in size
• Loss of defined morphologic structure
• Increased T2W/FLAIR signal
• Decreased T1W signal

Reduced volume of the hippocampus/hippocampal atrophy has been demonstrated in epileptic dogs

Hippocampal T2W hyperintensity is well correlated with pathology and hippocampal sclerosis

Volumetric studies would be beneficial however it is labor intensive and not routinely done

(Task Force)

Question 150

Tier I, II and III confidence level for the diagnosis of IE:

Answer 150

Tier I:

• History of 2 or more unprovoked epilepic seizures occurring at least 24h apart
• Age at epileptic seizure onset of between 6m and 6y
• Unremarkable inter-ictal physical and neurological examination
• No significant abnormalities on minimum data base blood tests and urinalysis

Tier II

• Factors listed in tier I and
• Normal fasting and post-prandial bile acids
• MRI of the brain (based on epilepsy specific brain protocol)
• CSF analysis

Tier III

• Factors listed in tiers I and II
• Identification of electroencephalography abnormalities characteristic for seizure disorders

(Task Force)

Question 151

3 excitatory neurotransmitters

4 inhibitory neurotransmitters

Answer 151

Excitatory: glutamate, aspartate, acetylcholine

Inhibitory: GABA, glycine, norepi, taurine

(de Lahunta)

Question 152

What medications can be used to treat narcolepsy/cataplexy and what are their MOA? (4)

Answer 152

1. Imipramine - inhibits reuptake of norepi, anticholinergic
2. Selegiline - MAOI that results in an increase in concentration of norepi in the CNS
3. Methylphenidate for excessive sleepiness
4. Yohimbine - alpha 2 adrenergic antagonist - increases release of norepi

(de Lahunta)

Question 153

What is the end result of Ca channel disorders, Cl channel disorders, and Na channel disorders?

Answer 153

Ca channel disorders - paralysis

Cl channel disorders - myotonia

Na channel disorders - both

(Vet Clin N America)

Question 154

How common is megaesophagus and aspiration pneumonia in patients with congenital myasthenia gravis?

Answer 154

It has been reported but not as common in acquired MG (approximately 90% of acquired MG dogs have megaesophagus)
Tendon reflexes usually normal (may be fatigable)

(VCNASAP Shelton)

Question 155

What type of test for AChR is the gold standard for diagnosis of myasthenia gravis?

Why is ELISA less sensitive/specific?

Answer 155

Demonstration of serum autoantibodies against muscle AChR by immunoprecipitation of serum autoantibodies against muscle AChR by immunoprecipitation radioimmunoassay

• Seronegative myasthenia occurs in approximately 2% of the dogs with generalized MG
• False positive results are rare
• A species specific assay should be used

ELISA - uses oligopeptide from the canine AChR-alpha subunit protein fraction

• Potential for false negative (if autoantibodies do not recognize denatured antigen)
• Potential for false positive - The peptides are produced in an E. coli expression system, may be contaminated with E. coli proteins

(VCNASAP Shelton)

Question 156

What is the approximate remission rate of acquired MG?

Answer 156

Shelton - focal, generalized and acute fulminating MG treated with anticholinesterase (or no meds at all) - 47/53 (88.7%) went into spontaneous remission

The 6 dogs that did not go into remission developed neoplasia (thymoma, melanosarcoma, thyroglossal duct papillary cysadenocarcinoma) 1-3y after diagnosis

(VCNASAP Shelton)

Question 157

What antibiotics should be avoided in patients with myasthenia gravis?

Answer 157

Ampicillin + aminoglycoside

Ampicillin - exacerbated MG in humans

Aminoglycoside - reported to antagonize neostigmine

Question 158

What are the criteria for diagnosis of seronegative myasthenia gravis?

Answer 158

1. Clinical signs consistent with MG
2. Consistent pharmacologic (positive derophonium response) and electrophysiologic (decrement) findings
3. Normalization of limb muscle weakness after anticholinesterase therapy
4. At least 2 negative serum AChR antibody titers by radioimmunoassay
   
   • Seroconversiom may occur, thus antibody titers should be repeated 1-2 months after a negative AChR antibody titer

Shelton (VCNASAP)

Question 159

What are explanations for seronegative MG?

Answer 159

1. Antibodies directed against non-AChR end-plate determinants
2. Antibodies directed against the toxin binding site, such that patients with antibodies to this site would seem to be seronegative
3. Antibodies are bound to the endplates without detectable circulating serum antibodies (antigen excess)
4. Antibodies are directed against antigenic determinants that may be lost during the AChR extraction procedure

Question 160

What are clinical signs of chronic organophosphate toxicity in cats?

What are clinical signs of fenthion toxicity?

Answer 160

Stiff rigid gait, muscle tremors, fasiculation
Peripheral neuropathy may occur some time after exposure

Fenthion toxicity - differs from classic OP poisoning with weakness predominating and little evidence of autonomic dysfunction
Chronic exposure may occur before clinical signs appear, and the onset of signs may be delayed

(VCNASAP Shelton)

Question 161

what medication can be used to treat organophosphate toxicity (besides atropine)

Answer 161

Pralidoxime chloride (2-PAM), or protopam chloride - work by breaking up the OP-ChE complex and increasing OP excretion via the urine 
Work best when combined with atropine

Should NOT be used in carbamate toxicity

Pralidoxime chloride has also been useful in cases of chlorpyrifos toxicity in cats

Diphenhydramine has been recommended to relieve muscle weakness and tremors in fenthion toxicity

(VCNASAP Shelton)

Question 162

What medications should be avoided in patients with myasthenia gravis

Answer 162

Several drugs have been shown to reduce the safety margin of neuromuscular transmission, including aminoglycoside antibiotics, antiarrhythmic agents, phenothiazines, and magnesium, given parenterally or in cathartics

Methimazole

these agents can potentiate neuromuscular blocking agents used during surgical procedures, and may worsen or unmask preexisting disorders of neuromuscular transmission

(VCNASAP Shelton)

Question 163

What are the most common clinical signs of dysautonomia? (6)

Answer 163

1. Dysuria
2. Regurgitation
3. Purulent nasal discharge
4. Photophobia
5. Anorexia
6. Weight loss

Average duration of clinical signs - 2 weeks
Clinical signs predominantly reflect loss of parasympathetic dysfunction (sympathetic dysfunction also present)

(VCNASAP O’Brien)

Question 164

How is dysautonomia confirmed?

Pharmacologic testing of the pupils with pilocarpine?

Answer 164

Documenting sympathetic and parasympathetic dysfunction without significant somatic motor system involvement (except for anal sphincter involvement) or sensory loss

Necropsy - autonomic ganglia degeneration with minimal inflammation

Pilocarpine - diluted to from 1% to 0.05% with normal saline. 1-2 drops placed in 1 eye. Dogs with dysautonomia should have denervation hypersensitivity and respond rapidly. (normal dog may respond but it will take longer).
If no response, can try full strength pilocarpine

Question 165

Dog w dysautonomia - how can sympathetic involvement be confirmed?

Answer 165

Orthostatic hypotension: measure BP with dog in lateral recumbency, then tilted at an angle of 30-45 degrees.

Normal dog - this has little effect on BP

Dogs with dysautonomia - BP drops in the elevated limbs and increases in the limbs placed downward

Other: HR usually within normal limits, but does not increase as expected when BP drops or when the animal becomes excited

Question 166

Pathologic changes in autonomic ganglia in dogs with dysautonomia?

Answer 166

• Reduced neuronal density
• Degenerate neurons that lack Nissl substance
• Longer duration cases - inflammation can be locally pronounced, interstitial clusters of lymphocytes
• Neuronal loss may occasionally dominate the histopathologic features
• Lesions in parasympathetic postganglionic neurons is less consistent
• Involvement among ganglia is not uniform - several ganglia need to be examined

(VCNASAP O’Brien)

Question 167

What are the exam findings associated with supraspinatus muscle contraction

Answer 167

decreased elbow flexion with the shoulder placed in adduction

internal (medial) rotation

Question 168

Treatment for thiamine deficiency in cattle

Answer 168

Mannitol

All cattle treated with thiamine

grain slowly replaced with hay fiber

As patients respond to treatment, blindness is usually the last deficit to resolve and the one that occasionally persists

(de Lahunta)

Question 169

Parasympathetic preganglionic neurons provide (facilitatory/inhibitory) GVE LMN innervation to the descending colon and rectum

Sympathetic preganglionic neurons provide (facilitatory/inhibitory) GVE LMN innervation to the descending colon and rectum

Answer 169

Parasympathetic - facilitatory GVE LMN input (via pelvic nerves, postganglionic neuron in the wall of digestive tract)

Sympathetic - inhibitory (except to the internal anal sphincter)
Ganglionic neurons in the caudal mesenteric ganglion

Same as urinary bladder/urethra

(de Lahunta)

Question 170

Why does a lesion at the level of the rostral and caudal colliculi result in opisthotonus?

Answer 170

The facilitatory centers in the pontomedullary reticular formation and vestibular system can function autonomously

The inhibitory centers in the pontomedullary reticular formation require continual input from the cerebral cortex, basal nuclei, and cerebellum

Question 171

A lesion in what prosencephalic structures will cause an abnormality in head, neck, or eye position?

Answer 171

This abnormality has been observed in dogs with a focal ischemic stroke or ischemic infarction of:

• Cerebral extrapyramidal nuclei
• Thalamic nuclei
• Subthalamus

Usually contralateral to the side of the lesion

Consist of abnormal head posture (head tilt or turn), neck posture (cervical dystonia/torticollis or pleurothotonus) or both

Abnormal nystagmus, strabismus or both

(de Lahunta)

Question 172

If a patient is immobilized on a surgical table by placing ties _______ the compression of sensory branches of the fibular nerves may result in the dog walking on the dorsal aspect of its digits?

Answer 172

just proximal to the tarsus

compression of sensory branches of the fibular nerves

at this level the GSE LMN axons that innervate the cranial crural muscles have left the fibular nerves, leaving only GP and GSA axons to be compressed

Hypalgesia or analgesia of the dorsal surface of the paw may accompany this abnormal paw position

(de lahunta)

Question 173

Adult dog with sudden onset:

• cerebellar-like gait disorder, balance well preserved
• Delayed postural reactions
• Normal withdrawal, patellar reflex depressed or absent
• Facial hypalgesia
• Difficulty prehending food, gagging
• Megaesophagus
• Masticatory muscle atrophy

Answer 173

Consider sensory ganglioneuritis

Autopsy - diffuse, nonsuppurative lymphoplasmacytic inflammation of multiple cranial and spinal nerves, and spinal nerve ganglia and dorsal roots

• Loss of neuronal cell bodies is recognizable in these ganglia –> wallerian degeneration of the associated dorsal roots and distal nerves
• Inflammation of the trigeminal ganglia –> inflammation of GSE LMN neurons that pass through this ganglia

Diagnosis - biopsy of a spinal ganglion

(de Lahunta)

Question 174

Wallerian-type degeneration limited to the dorsal funiculi at ALL levels of the spinal cord + absence of other spinal cord lesions - where is the lesion?

Answer 174

Dorsal root

What is seen is Wallerian degeneration of the general proprioceptive axons which directly enter the dorsal funiculi without synapse until they reach the caudal medulla

(de Lahunta)

Question 175

Facial paralysis + vestibular dysfunction + facial hypalgesia - where is the anatomic diagnosis?

Answer 175

Petrous temporal bone or intracranial/brainstem lesion at that level

(de Lahunta)

Question 176

What is thalamic pain syndrome?

Answer 176

Spontaneous discomfort related to a thalamic lesion (often neoplasm)

Loss of GSA thalamic relay nucleus that modulates pain –> results in hyperalgesia

Report of unilateral thalamic glioma in a dog described spontaneous discomfort on the contralateral side of the body

(de Lahunta)

Question 177

Locations of CNS lesions that cause pain by affecting the GSA pathway

Answer 177

1. Lesions within the dorsal gray column
2. Loss of inhibition of the neurons involved in nociception
3. Pontomedullary lesions that interfere with nuclei of the caudally projecting pathways that are the source of inhibition of neurons involved in nociception
4. Thalamus (thalamic relay nucleus responsible for inhibiting pain signals)

(de Lahunta)

Question 178

Where are the border cells of the spinal cord found?

How quickly do Schiff Sherrington signs resolve

Answer 178

L1-5 dorsolateral border of the ventral gray column

The axons course cranially in the fasiculus proprius and terminate by synapsing on thoracic limb extensor LMNs in the cervical intumescence

Their purpose is to synchronize extension of the pelvic limbs with flexion of the thoracic limbs

Schiff-Sherrington - spontaneously resolves in about 10-14 days

(de Lahunta)

Question 180

8 causes of feline cervical flexion?

Answer 180

1. Subacute/chronic OP toxicity
2. MG
3. Hyperthyroidism
4. Thiamine deficiency
5. Hereditary myopathy (Devon rex, sphynx)
6. Polymyositis
7. Hypokalemia (also hypernatremia, hypocalcemia)
8. PSS + HE (also NH3 chloride toxicity)

(VCNASAP Dickinson)

Question 181

What is the recovery rate for feline tail pull injury with signs of injury of caudal nerves of the tail only?

What is the recovery rate for feline tail pull injury with signs of caudal nerve deficits plus urinary retention + decreased/absent anal tone/perineal sensation + decreased urethral sphincter tone?

Answer 181

Caudal nerve/tail deficits only 100%

Caudal nerve deficits + urinary retention + decreased/absent anal tone/perineal sensation + decreased urethral sphincter tone - 50% recovery

“Recoveryrates decreased from 100% to 50% for cats in the following order:

1. Caudal nerve (tail) deficits only
2. Caudal nerve deficits plus urinary retention
3. Caudal nerve deficits plus urinary retention plus decreased anal tone/perineal sensation
4. Caudal nerve deficits plus urinary retention plus decreased/absent analtone/perineal sensation plus decreased urethral sphincter tone”

** cats that did not recovery normal urinary function within 1 month were likely to have permanent micturition abnormalities of varying severity

(VCNASAP Dickinson)

Question 182

What are common findings of feline leukemia virus neuropathy? (2)

Answer 182

• Anisocoria with persistent mydriasis and decreased/absent PLR
  
  • EM or IFA has revealed a C-type RNA virus localization in the short ciliary nerves or ciliary ganglion of affected cats
• Generalized peripheral neuropathy with progressive tetraparesis
  
  • Experimental FeLV infection - abnormalities in peripheral nerve conduction velocities
• Urinary incontinence - suggested to be a potential manifestation of FeLV infection

(VCNASAP Dickinson)

Question 183

What are the most common neurologic abnormalities associated with FIV in cats?

Are any neuromuscular manifestations identified?

Answer 183

Primarily behavioral and mood changes

Neuromuscular - subclinical myopathy reported, decreased MNCV and SNCV reported in experimentally infected cats

(VCNASAP Dickinson)

Question 184

6 causes of toxic polyneuropathy in the cat?

Answer 184

1. Organophosphates
2. Heavy metals
3. Vincristine
4. Salinomycin
5. Acrylamide
6. Pyrethrins (?)

(VCNASAP Dickinson)

Question 185

Clinical signs of mercury intoxication in cats?

Answer 185

• Necrosis of CNS neurons –> ataxia, seizures, tremors
• Degeneration of sensory neurons also described

Other heavy metal toxicities associated with neuromuscular dz:

• Thallium (in rodenticides) - hypotonia and ataxia
• Lead poisoning - typically GI and CNS dz, megaesophagus reported

(VCNASAP Dickinson)

Question 186

Vincristine has been associated with ________ neuropathy in experimental cats

Answer 186

Sensory-motor neuropathy

Pathologic changes predominantly in proximal portions of peripheral nerves

(VCNASAP Dickinson)

Question 187

What is the MOA of pyrethrin toxicity?

Answer 187

Persistent influx of Na ions into excitable cells of the nervous system and muscle

Clinical signs

• Hyperexcitability
• Tremors
• Convulsions
• Neuromuscular weakness (28%)

(VCNASAP Dickinson)

Question 188

Feline ischemic neuromyopathy - What pathologic changes are seen in the nerves?

What pathologic changes are seen in muscle, and which muscle seems most affected by “saddle thrombus”

Answer 188

Ischemia –> demyelination and Wallerian-like degeneration
Central fibers in a nerve fasicle seem most susceptible than peripheral fibers

Muscle:
Ischemic myopathy with myofiber necrosis
Affects cranial tibial muscles most severely

(VCNASAP Dickinson)

Question 189

What are the 2 proposed MOA of diabetic neuropathy?

Answer 189

1. Hyperglycemia –> polyol pathway flux –> depletion of myoinositol and modification of proteins by glycation –> metabolic nerve changes
   
   • One study found an association between functional and structural deficits and increased polyol pathway flux with a decrease in nerve myoinositol levels
2. Vascular changes –> peripheral nerve oxidative stress

(VCNASAP Dickinson)

Question 190

Reported causes of acquired laryngeal paralysis in the cat? (5)

Answer 190

1. Neoplastic infiltration
2. Generalized neuromuscular disease
3. Lead toxicosis
4. Surgical or ablational procedures involving the thyroid gland
5. Trauma

(VCNASAP Dickinson)

Question 191

Nutritional cause of polyneuropathy in the cat?

Answer 191

Described in experimental cats with dietary restriction of phenylalanine and tyrosine

(VCNASAP Dickinson)

Question 192

What is the MOA of elapid neurotoxin

Answer 192

Elapid = snake family (coral snakes)

• Act @ NMJ
• Postsynaptic toxins: curare-like activity - block AChR (can be reversed w/ antiserum)
• Presynaptic toxins: irreversible depletion of ACh vesicles in axonal terminal
• Presenting clinical signs - PL weakness/ataxia to flaccid tetraplegia and respiratory paralysis
  
  • Onset may be delayed for several hours; progression is usually rapid
• Pupillary dilation with decreased PLR and glycosuria are common findings in Tiger snake evenomation
• EMG usually normal, but reduced/absent CMAP on NCV

(VCNASAP Dickinson)

Question 193

What is the MOA of black-widow spider envenomation toxicity?

Answer 193

Neurotoxin = alpha-latrotoxin

Toxin binds to sympathetic, parasympathetic, and motor nerve terminals –> influx of Ca –> nonspecific exocytosis of synaptic vesicles

Release of ACh –> muscle spasm, pain, SLUDD, hypertension, restlessness

Spasticity followed within 12-24 hours by flaccid paralysis as a result of the destruction of motor end plates, and prolonged depolarization

No specific diagnostic tests are available, bites are not usually apparent
Cats reported to be particularly sensitive - 20/22 envenomated cats dying in one report

(VCNASAP Dickinson)

Question 194

What is the difference between organophosphate and carbamate MOA?

2 examples of organophosphates?

Answer 194

OP: irreversible inhibitors of acetylcholinesterase via time-dependent aging process

Carbamates are slowly reversible inhibitors

Cats are reported to be particularly sensitive to the acute and delayed toxic effects of OPs - a delayed neuropathy has been reported in cats with OP toxicity (not carbamate toxicity) typically 1-4 weeks after exposure
Symmetric distal axonal degeneration of peripheral and central nerve fibers –> LMN paraparesis
MOA of delayed toxicity unknown - may involve inhibition of neuronal esterase

OP: chlorpyrifos, fenthion

(VCNASAP Dickinson)

Question 195

How can OP/Carbamate toxicity be tested for?

Answer 195

Determination of acetylcholinesterase levels in plasma, erythrocytes, or whole blood may indicate exposure to acetylcholinesterase-inhibiting toxins
There is disagreement as to whether feline RBC ChE activity is measurable

ChE activity in whole blood may be the most reliable diagnostic tool - value < 25% normal - suggested as indicative of toxicity

Postmortem - specific identification of compounds can be done using frozen samples of vomitus, skin, hair, fat, brain, or liver

(VCNASAP Dickinson)

Question 196

T/F: Feline muscular dystrophy is associated with x-linked dystrophin deficiency and sarcoglycan deficiency?

Answer 196

False - dystrophin deficiency and laminin alpha 2 = merosin deficiency

(VCNASAP Dickinson)

Question 197

What 2 breeds of cats develop a hereditary muscular disease?

Answer 197

Hereditary myopathy of Devon Rex cats - autosomal pattern of inheritance

• Onset 3-23 weeks
• CK normal
• Histopathologic examination of muscle demonstrated alterations consistent with muscular dystrophy
• Immunohistochemical staining of muscle biopsy specimens for dystrophin was normal

Sphynx cats - Muscular dystrophy

• Noninflammatory myopathy

(VCNASAP Dickinson)

Question 198

T/F: Nemaline rod myopathy has not been described in the cat?

Answer 198

False - reported in 5 related cats

• Onset from 6 mos to 1.5 years of age - reluctance to move, hypermetria, muscle twitching, hyporeflexia, muscle wasting
• Most prominent in thee proximal muscles of the forelimbs
• Lg but variable numbers of nemaline rods
• FIber-size variation with atrophy fo type I and 2A fibers

(VCNASAP Dickinson)

Question 199

Condition of cats that results in:

• Progressive stiffness of gait affecting young to middle-aged cats of both sexes
• Enlargement of proximal limb musculature
• Radiography - multiple mineralized densities within the affected musculature

Answer 199

Myositis ossificans

(VCNASAP Dickinson)

Question 200

__________ are forceful, involuntary, painful contractions with an acute onset, short duration, and lasting seconds to minutes

Answer 200

Muscle cramps

• Arise from abnormal discharges of nerve terminals in a muscle, can occur with activity or rest
  
  • Most are caused by hyperactivity of the peripheral nerve terminals or CNS rather than a primary muscle disease
• Can result in myoglobinuria if severe
• EMG - high-frequency, high-amplitude discharge of potentials resembling motor unit action potentials
• Electrically silent muscle cramps occur with strenuous or ischemic exercise in metabolic myopathies associated with defects of glycolysis of glycogenolysis

(VCNASAP Shelton)

Question 201

______________ are brief, fine twitches of resting muscles caused by spontaneous activation of motor units

Answer 201

Fasiculations

• May be seen as transient, longitudinal depressions of the skin surface
• Fasiculations potentials are spontaneous discharges of single motor neurons
• Most commonly associated with motor neuron diseases
  
  • May be found in normal individuals treated with anticholinesterase drugs

(VCNASAP Shelton)

Question 202

________________ is caused by successive spontaneous contractions of motor units or groups of muscle fibers, resulting in a continuous undulation of the overlying body surface

Answer 202

Myokymia

• Movements are slower and more prolonged than fasciculations
• EMG - myokymic discharges are groups of 2-10 potentials, probably arising from motor units and firing at 5-60Hz
• They arise in the peripheral axon of chronically damaged nerves and are associated with clinical myokymia or with syndromes of continuous muscle fiber contraction

(VCNASAP Shelton)

Question 203

What are “rippling muscles?”

Answer 203

Characterized by self-propagating rippling of muscles induced by stretch or percussion in which the ripple propagates at approximately 0.6m/s, 10x slower than muscle fiber conduction velocities

Muscles are electrically silent - which differentiates them from myokymia and neuromyotonia

(VCNASAP Shelton)

Question 204

____________ is a painless, sustained muscle contraction associated with abnormal repetitive depolarization of the muscle fibers –> tetanic contraction

Answer 204

Myotonia

• important form of spontaneous activity in muscle disease resulting from alterations in the ion channels in the muscle fiber membrane
• diagnosis via EMG

(VCNASAP Shelton)

Question 205

_______________________ is a syndrome characterized by stiffness at rest, myokymia and delayed muscle relaxation

Answer 205

Neuromyotonia

• Caused by hyperexcitability of peripheral nerves
• Muscle stiffness at rest, myokymia and delayed muscle relaxation resembling myotonia
• EMG recordings - bursts of MUAP firing at high rates WITHOUT typical waxing and waning of myotonia
• Abnormal spontaneous activity persists during sleep but is lessened
• Blockade of neuromuscular transmission abolishes the abnormal activity (presumably arises in the distal motor nerves or nerve terminals)

(VCNASAP Shelton)

Question 206

What kind of disorder is Scottie cramp?

Answer 206

Hypertonicity syndrome

• Inherited as a recessive trait
• Clinical signs most commonly found in Scottish Terriers from 6 weeks to 18 most of age, may be elicited by stress, excitement or exercise
• Limbs gradually stiffen until the animal is unable to move
• Arching of the lumbar spine and PL stiffness may progress to somersaults and falling (do not lose consciousness)
• Clinical signs resolve within 10 minutes
• Thought to be associated with serotonin deficiency
  
  • Methylsergide - serotonin antagonist –> exercise 2h later will induce clinical signs

(VCNASAP Shelton)

Question 207

What drug can be used to treat hypertonicity syndrome in CKCS?

Answer 207

Clonazepam TID
Tolerance may develop

By 2 years of age, resolution of clinical signs can occur and dog may no longer need medication

(VCNASAP Shelton)

Question 208

What breed is “canine epileptoid cramping syndrome” recognized in and how is it treated?

Answer 208

Border Terrier

• Hypothesized to represent a form of paroxysmal non-kinesigenic dyskinesia
• First episodes usually occur before 3 years of age
• Occur spontaneously, excitement, or when waking up from sleep
• Attacks last 2-30 min, up to 3x daily, often associated with mild tremor and borborgymi
• GI upset before or after in 50% of dogs
• Antiepileptic drugs ineffective
• Response to gluten-free diet
  
  • Affected border terriers had increased serum titers of antitransglutaminase 2 and angigliadin antibodies, normalized when fed gluten free diet

Question 209

What movement disorder is seen in the Wheaton terrier

Answer 209

Hereditary paroxysmal dyskinesia

• Heterogeneous group of movement disorders
• Young adult onset
• Autosomal recessive
• Episodes of hyperkinesia and dystonia lasting from several minutes to several hours could occur up to 10 times daily
• Not associated with strenuous exercise or fasting, sometimes triggered by excitement
• A mutation in PIGN gene identified

Kolicheski et al

Question 210

_____________ is a clinical syndrome classically characterized by skeletal muscle rigidity, tachypnea, rapid elevation of core body temperature, severe metabolic acidosis, hypercarbia, cardiac arrhythmias

Answer 210

Malignant hyperthermia syndrome

All clinical and laboratory manifestations of MHS derive from a breakdown of calcium sequestration in the sarcoplasmic reticulum of skeletal muscle –> unopposed muscle contracture, release of cations and enzymes (CK) into circulation, and production of heat and acid

VCNASAP

Question 211

Mutation in what channel is associated with malignant hyperthermia in dogs?

Answer 211

RYR1 ryanodine calcium channel

(VCNASAP)

Question 212

What is the most prominent clinical sign of malignant hyperthermia in dogs?

Answer 212

Increased production of CO2

MH in dogs not typically characterized by early onset of lactic acidosis or muscle rigidity

Use of dantrolene - shown to be efficacious in reversing signs of the canine sydnrome

(VCNASAP)

Question 213

Safe anesthesia for possible malignant hyperthermia patient?

Answer 213

Avoid volatile anesthetics - halothane, isoflurane, sevoflurane and depolarizing neuromuscular blocking agents (succinylcholine)

Safe anesthetic drugs include: benzodiazepines, phenothiazine, barbituates, etomidate, propofol, dissociative agents, opioids, NO, nondepolarizing neuromuscular blockers, local anesthetics

Total IV anesthesia or regional/local anesthetic techniques can be safely used

(VCNASAP)

Question 214

Clindamycin

• MOA
• CNS/CSF penetration?

Answer 214

MOA - inhibition of 50s ribosomal subunit

Dosage for protozoal infections are often higher than those used for susceptible aerobic bacterial disease

Completely absorbed after oral admin, widely distributed due to high lipophilicity

Low concentrations in CSF, high concentration in parenchyma (high lipid solubility)

(VCNASAP Kent)

Question 215

Possible adverse effects of clindamycin

Answer 215

V/d

Decreased vitamin K absorption –> clotting factors

Neuromuscular blocking agents - potentiate nondepolarizing neuromuscular agents during anesthesia

(VCNASAP Kent)

Question 216

TMS:

• MOA
• Adverse effects

Answer 216

MOA: TMP inhibits tetrahydrofolate reductase
Sulfonamide acts as an analog for PABA

The combination has a greater affinity for bacterial enzymes than for mammalian enzymes

Adverse: Hypothyroidism, Hypersensitivity reactions (hepatotoxicity), KCS, blood dyscrasias

Used for treatment of protozoal disease - Neospora, Toxoplasma, and Hepatozoon

(VCNASAP Kent)

Question 217

Multidrug regimen for Hepatozoon?

Answer 217

14-day course of TMP SDZ + Clindamycin + Pyrimethamine

Followed by decoquinate - stops formation of sporozoites in the intestinal tract

(VCNASAP Kent)

Question 218

Definitions of:

• Increased resistance to change in position or angle of joints
• Brief, automatic jerking movement
• Abnormal repetitive shaking movement of the body
• Sustained muscular contraction without relaxation
• Intermittent tonic muscular contractions
• State of increased tone of a muscle

Answer 218

• Rigidity - Increased resistance to change in position or angle of joints
• Spasm - Brief, automatic jerking movement
• Tremor - Abnormal repetitive shaking movement of the body
• Tetany - Sustained muscular contraction without relaxation
• Tetanus - Intermittent tonic muscular contractions
• Spasticity State of increased tone of a muscle

(Dewey)

Question 219

Neuromyotonia associated with a mutation in KCNJ10 is seen in what breed?

Answer 219

Jack Russel Terrier

• Neuromyotonia is clinically characterized by muscle twitching or myokymia, persistent muscle contraction, muscle stiffness or cramps, and impaired muscle relaxation
  
  • Episodes of severe myokymia + collapse
• Homozygosity of this gene –> spinocerebellar ataxia (hereditary ataxia)
• KCNJ10 –> Kir4.1 K+ channel

(Dewey)

Question 220

Great Dane with orthostatic tremor - what is the frequency of the discharges on EMG?

Answer 220

13 - 16Hz

Seen only when dog is weight bearing

(Dewey)

Question 221

Breeds with recognized paroxysmal dyskinesias? (8)

Answer 221

1. Bichon frise
2. Scotty cramp
3. CKCS - episodic hypertonicity
4. Irish Wolfhound - startle disease
5. Labrador retriever - generalized muscle stiffness
6. Chinooks - paroxysmal dyskinesia
7. Miniature wirehaired dachshund - Lafora disease

(Dewey)

Question 222

What is the physiologic basis for each of the following biomarkers?

• Neuron-specific enolase
• Myelin basic protein
• GFAP
• Cleaved tau protein
• Phosphorylated neurofilament heavy chain
• MMPs
• VEGF

Answer 222

• Neuron specific enolase - found in the cytoplasm of neurons (also localized in neuroendocrine cells, oligodendrocytes, thrombocytes, and erythrocytes)
  
  • An increase of the CSF NSE might be useful for detecting evidence of neuronal damage in the CSF
• Myelin basic protein - produced by oligodendrocytes, major constituent of the axonal myelin sheath
  
  • Predicted to be a marker of white matter injury
  • Higher CSF MBP in dogs with thoracolumbar IVD that had unsucessful outcome
  • Increased in CSF of DM patients
• GFAP - intermediate filament in astrocytes
  
  • Serum GFAP - high specificity for predicting myelomalacia (75% sensitivity)
  • Serum GFAP - Sn 67%, Sp 100% for diagnosing NME
• Cleaved tau protein - binds to axonal microtubules, part of the axonal cytoskeleton
  
  • Dogs with IVDH, ROC analysis showed a moderate correlation between CSF c-tau concentration and prognosis
  • Did not correlate with T2W spinal cord hyperintensity on MRI (which is known to be associated with functional outcome)
• Phosphorylated neurofilament heavy chain - cytoskeletal component in axons
  
  • Paraplegic dogs with absence of DPP - ROC analysis revealed a weak correlation between the serum pNF-H concentration and prognosis
• MMPs
  
  • MMPs are Zn-dependent endopeptidases that degrade various components of the extracellular matrix
  • Dogs with thoracolumbar IVDH - paraplegic at admission, significantly higher elevated MMP than those with voluntary motor activity
• VEGF
  
  • Strongly expressed in canine meningiomas, the degree of VEGF associated with survival times
  • Intratumoral VEGF expression may be a useful marker for predicting prognosis of meningiomas

(VCNASAP)

Question 223

What 4 muscles attach to the dorsal median raphe of the cranial cervical region?

What muscle is exposed after cutting through the dorsal median raphe, attached to the spinous process of C2?

Answer 223

1. Superficial cervical muscles
2. Brachiocephalicus (cervical cleidocephalicus)
3. Trapezius - cervical part
4. Splenius

Cut through - rectus capitus exposed

(Slatter)