Neurology

Question 1

define “resting membrane potential”

Answer 1

at rest, an excitable cell like a neuron has san electrical change across the membrane with the inside of the cell negative relative to the outside. this is the RMP.

Question 2

what pump is most responsible for formation of the resting membrane potential?

Answer 2

Na/K ATPase

Question 3

what is equilibrium potential?

Answer 3

the voltage difference across a cell membrane at which the force of negative/positive and concentration gradient are in balance and no diffusion occurs (i.e. for potassium, if a K+ channel opens, it wants to move down its concentration gradient and out of the cell; but there are more negatively charged anions inside the cell that attract the positively-charged K+)

Question 4

what is the resting membrane potential for neurons?

Answer 4

-65 mV

Question 5

what is a channelopathy? give an example in cats and an example in dogs

Answer 5

diseases that affect ion channel function and alter excitability of the neuronal membrane. cats with complex partial seizures have antibodies against voltage-gated potassium channels. dogs with a mutation in the gene that codes for a portion of the potassium channel complex have benign familial juvenile epilepsy. these diseases alter Pk and thus the excitability of the cell membrane = excessive neuronal activity and seizures

Question 6

what is the threshold for voltage-gated Na channels to open, beginning the action potential?

Answer 6

-55 mV

Question 7

how does phenytoin prevent seizures?

Answer 7

enhance inactivation of sodium channels, making it less likely that an action potential will be propagated

Question 8

how do pyrethrins increase tremors and seizures?

Answer 8

block sodium channel inactivation, increasing action potential generation

Question 9

what two factors influence the speed at which the action potential travels down an axon?

Answer 9

axonal diameter and myelin

Question 10

what is the name for an unmyelinated area on a nerve? how do ions flow in these areas?

Answer 10

node of ranvier. ions flow in a saltatory fashion.

Question 11

how does polyradiculoneuritis cause weakness?

Answer 11

demyelination increases capacitance of axonal membrane, slowing the conduction velocity and potentially blocking propagation of action potential

Question 12

describe the basic process of neurotransmitter release

Answer 12

neurotransmitters are packaged into vesicles in the nerve terminal. when the AP depolarizes the nerve terminal, voltage-gated Ca channels open, allowing Ca to flow into cell. the Ca activates a series of synaptic vesicle proteins that dock the vesicle to the presynaptic membrane where it fuses with the cell membrane, releasing the neurotransmitter into the synaptic cleft

Question 13

how does botulism toxin cause weakness?

Answer 13

binds to one of the vesicle docking proteins, preventing release of acetylcholine at the neuromuscular junction

Question 14

what are the two receptor types at the post-synaptic cell?

Answer 14

ionotropic: regulate ion channels. Metabotropic: act through second messengers.

Question 15

what are the three families of ionotropic receptors?

Answer 15

1) nicotinic ACh, GABA, and glycine; 2) glutamate; 3) ATP or purine P2X receptors

Question 16

is ACh excitatory or inhibitory? explain.

Answer 16

excitatory: when ACh binds to the nicotinic receptor, the pore becomes permeable to cations (primarily Na). Na diffuses in, depolarizing the cell and leading to excitatory post-synaptic potential.

Question 17

What is the function of acetylcholinesterase?

Answer 17

breaks down ACh in the synaptic cleft into choline and acetic acid, which are taken up into the presynaptic terminal and used to resynthesize ACh

Question 18

How does myasthenia gravis cause weakness?

Answer 18

autoantibodies directed against the alpha1 subunit partially block the ACh receptor in the NMJ. this makes it more difficult for ACh to open the channel and produces fatigue.

Question 19

what is the mechanism behind the treatment for myasthenia gravis?

Answer 19

acetylcholinesterase inhibitors prolong the interaction of ACh with the receptor and reverse c/s

Question 20

Is GABA excitatory or inhibitory? explain.

Answer 20

inhibitory. the GABA-A receptor and closely-related glycine receptor have a similar structure to the ACh receptor, but the ion channel is only permeable to Cl. when the channel opens, Cl can diffuse into the cell, creating an inhibitory post-synaptic potential that hyper polarizes the cell.

Question 21

how does phenobarbital stop seizures?

Answer 21

it binds to extracellular sites on the GABA-A receptor (GABA is inhibitory). it doesn’t open the ion channel, but it alters the kinetics of the Cl channel, increasing the time the pore is open when GABA binds to its receptor

Question 22

how does diazepam stop seizures?

Answer 22

it binds to extracellular sites on the GABA-A receptor (GABA is inhibitory). it doesn’t open the ion channel, but it alters the kinetics of the Cl channel, increasing the time the pore is open when GABA binds to its receptor

Question 23

what is the major excitatory neurotransmitter in the CNS?

Answer 23

glutamate

Question 24

discuss the mechanism of glutamate function

Answer 24

there are two subtypes of ionotropic glutamate receptors: AMPA and NMDA. glutamate must bind both receptors to produce an effect. binding to AMPA receptor partially depolarizes the membrane, releasing a Mg ion that blocks the NMDA channel. Binding to the NMDA receptor can then allow additional Na conductance, which enhances the EPSP produced by activation the AMPA receptor. the NMDA channel is permeable to Ca as well. the increase in intracellular Ca that results can trigger second messenger systems that have more prolonged effects on the synapse. with excessive NMDA receptor activation, the accumulation of intracellular Ca can trigger cell death (AKA excitotoxicity)

Question 25

List the metabotropic receptors

Answer 25

muscarinic acethylcholine receptors, metabotropic glutamate receptors, GABA-B receptors, serotonin receptors, receptors for norepinephrine, epinephrine, histamine, dopamine, neuropeptides, and endocannabinoids

Question 26

how do metabotropic receptors work?

Answer 26

through second messenger systems such as G-proteins; because of this, they produce a longer influence on function

Question 27

contrast what happens when ACh binds to an M2 versus M1 muscarinic ACh receptor

Answer 27

when ACh binds to the M2 muscarinic ACh receptor, a G-protein binds GTP and dissociates a subunit that then binds to G-protein-coupled inward-rectifying potassium channel (GIRK). this opens the ion channel and allows K to diffuse from cell, hyper polarizing the membrane. In contrast, M1 receptor activation closes the M-type K channel, producing a prolonged EPSP.

Question 28

describe long-term depression

Answer 28

the metabotropic glutamate receptor mGluR1 is found in high concentration on purkinje cells in the cerebellum. when glutamate binds to the receptor, it activates a G-protein, which works through a series of other second messengers to activate a protein kinase C. this reeves a phosphate from the AMPA receptor, causing internalization and degradation of the receptor. this makes that synapse less responsive to excitatory glutamatergic stimulation, a process termed long-term depression, which is a part of learning and memory.

Question 29

What dog breed has a mutation in the mGluR1 gene? what does this cause?

Answer 29

Coton de Tulear. they have impaired motor learning and severe cerebellar ataxia.

Question 30

discuss dopamine and adenosine’s actions on cAMP

Answer 30

stimulating D2 dopamine receptor decreases cAMP and increases arousal. stimulating adenosine receptor increases cAMP and decreases arousal.

Question 31

how does fluoxetine work/

Answer 31

selectively blocks serotonin transporters. the activity of serotonin on its post-synaptic receptor is terminated by reuptake of serotonin into the presynaptic terminal by the serotonin transporter.

Question 32

describe the role of kinesins and dyneins

Answer 32

kinesins transport things along the cell’s microtubules from the cell body to the nerve terminals (anterograde); dyneins transport from the nerve terminal back to the cell body (retrograde)

Question 33

explain the difference between temporal and spacial summation

Answer 33

temporal: EPSPs from a run of several Laps can summate to depolarize the post-synaptic membrane above thrshehold. Spatial: axons from multiple presynaptic neurons converge on a single neuron and more than one AP converges on the neuron simultaneously

Question 34

what is an interneuron?

Answer 34

inhibitory neuron that controls excitation. they often synapse closer to the cell body, where they can block propagation of an EPSP to the axon hillock

Question 35

what is a renshaw cell and what does it do?

Answer 35

inhibitory interneuron. an excitatory impulse to a motor neuron will activate the Renshaw cell, which inhibits surrounding motor neurons in a process of collateral inhibition

Question 36

how does tetanus toxin cause tetany?

Answer 36

it blocks glycine release (from renshaw cells), resulting in excessive excitation of the motor neurons

Question 37

what is lateral inhibition?

Answer 37

when a second order neuron generates an AP, branches of the second order neuron’s axon synapse on inhibitory interneurons that project to surrounding second order neurons

Question 38

what is the reticular activating system?

Answer 38

projections to the forebrain from monoaminergic (epinephrine, norepinephrine, dopamine, serotonin, histamine) and cholinergic neurons in the brainstem and basal forebrain; mediates arousal of the brain needed for consciousness and attention. lesions here produce stupor and coma.

Question 39

crossed extensor reflex: what is it, and when do you see it?

Answer 39

in a patient in lateral recumbency, if you pinch a toe and they withdraw the leg, the contralateral leg should not extend. if there is an upper motor neuron lesion, you will see the crossed-extension reflex

Question 40

recumbency can be associated with disease in which three areas? what sets each apart?

Answer 40

brainstem, cervical spinal cord, diffuse neuromuscular disease. brainstem is the only that affects sensorium.

Question 41

alteration in sensorium is due to disease where?

Answer 41

ascending reticular activating system (ARAS) and/or limbic system components of the cerebrum or rostral brainstem (diencephalon)

Question 42

describe decerebrate rigidity

Answer 42

opisthotonus with rigid extension of the neck and all four limbs; associated with midbrain or rostral cerebellar lesions

Question 43

describe decerebellate rigidity

Answer 43

from severe cerebellar lesions; characterized by opisthotonus with extensor rigidity of the limbs, but hips flexed

Question 44

describe pleurothotonus

Answer 44

deviation fo the head and neck to one side; may be present with mid to rostral brainstem or cerebral lesions

Question 45

what are the two key UMN pathways that function in gait generation?

Answer 45

reticulospinal and rubrospinal

Question 46

what are the two main general propioceptive pathways?

Answer 46

spinocerebellar and conscious proprioceptive

Question 47

what is the modified frankel score?

Answer 47

spinal cord lesions: 0 = tetraplegia or paraplegia with no deep nociception. 1 = tetra/paraplegia with no superficial nociception. 2 = tetra/paraplegia with nociception. 3 = nonabmulatory tetra/paraparesis. 4 = ambulatory tetra/paraparesis and GP ataxia. 5 = spinal hyperesthesia only or no dysfunction

Question 48

unilateral pros encephalic lesions result in ipsi or contralateral postural reaction deficits? menace? sensory deficits?

Answer 48

contralateral for all

Question 49

unilateral brainstem lesions cause ipsi or contralateral postural reaction deficits?

Answer 49

ipsi

Question 50

unilateral spinal cord lesions cause ipsi or contralateral postural reaction deficits?

Answer 50

ipsi

Question 51

what are the parts of the LMN unit?

Answer 51

cell body, nerve root, peripheral nerve, NMJ, muscle

Question 52

the patellar reflex test is mediated by what nerve? what spinal cord segments?

Answer 52

femoral nerve, L4-L7

Question 53

the biceps reflex is mediated by what nerve? what spinal cord segments?

Answer 53

musculocutaneous nerve; C6-C8

Question 54

the triceps reflex is mediated by what nerve? what spinal cord segments?

Answer 54

radial nerve; C7-T2

Question 55

the forelimb withdrawal involves which nerves? which spinal cord segments?

Answer 55

thoracodorsal, axillary, musculocutaneous, median, ulnar, radial nerves - median and ulnar on palmar surface of paw, radial on dorsal paw and craniolateral antebrachium, ulnar caudally and musculocutaneous medially; C6-T2

Question 56

the pelvic withdrawal involves which nerves? which spinal cord segments?

Answer 56

sciatic nerve; L6-S1

Question 57

dogs with sciatic nerve paralysis can still support weight if which nerve is intact?

Answer 57

femoral

Question 58

discuss the sensory innervation of the pelvic paw

Answer 58

peroneal nerve - dorsal surface; tibial nerve - plantar surface; saphenous (branch of femoral, L4-6) - medial

Question 59

what happens if the medial surface of the paw is stimulated in a pet with a pure sciatic injury?

Answer 59

animal will flex the hip because of intact innervation of the iliopsoas muscle, but stifle, tarsus, and digits will not flex

Question 60

the perineal reflex is mediated by what nerve?

Answer 60

branches of the sacral and caudal segments of the spinal cord through the pudendal nerve

Question 61

discuss the pathway for noxious stimuli

Answer 61

stimulus -> peripheral nerves + dorsal nerve root -> bilateral tracts in lateral funiculus of spinal cord -> through medulla, pons, midbrain to specific nuclei in thalamus -> relay to somatic sensory areas of cerebral cortex

Question 62

cranial nerve I: name and function

Answer 62

olfactory. smell

Question 63

cranial nerve II: name and function

Answer 63

optic. vision and response to light

Question 64

cranial nerve III: name and function

Answer 64

oculomotor. motor to extra ocular muscles; parasympathetic to pupil

Question 65

cranial nerve IV: name and function

Answer 65

trochlear. motor to dorsal oblique muscle

Question 66

cranial nerve V: name and function

Answer 66

trigeminal. motor to muscles of mastication (mandibular), sensory to face (ophthalmic and maxillary)

Question 67

cranial nerve VI: name and function

Answer 67

abducent. motor to lateral rectus and retractor bulbi

Question 68

cranial nerve VII: name and function

Answer 68

facial. motor to muscles of facial expression; parasympathetic to lacrimal glands; sensory (taste) to rostral tongue

Question 69

cranial nerve VIII: name and function

Answer 69

vestibulocochlear. balance, hearing

Question 70

cranial nerve IX: name and function

Answer 70

glossopharyngeal. sensory and motor to pharynx

Question 71

cranial nerve X: name and function

Answer 71

vagus. sensory and motor to pharynx, larynx, and viscera

Question 72

cranial nerve XI: name and function

Answer 72

accessory. motor to trapezius

Question 73

cranial nerve XII: name and function

Answer 73

hypoglossal. motor to tongue muscles

Question 74

menace response: pathway? anything notable? Tests ipsi or contralateral?

Answer 74

learned - may not be present in those <10-12 wks. need functional optic nerve, optic tract (diencephalon), optic radiation up to occipital cortex, efferent pathway includes facial neurons and orbiculares oculists muscle, and cerebellum is somewhere in there. Contralateral.(caudal to the optic chiasm)

Question 75

indirect PLR occurs because optic nerve fibers cross where?

Answer 75

optic chasm and pretectal nucleus

Question 76

PLR tests what cranial nerves?

Answer 76

optic nerve and oculomotor nerve

Question 77

what are the potential causes of ptosis?

Answer 77

1) dysfunction of CN III with secondary paresis of the elevator palpebral superiors muscle. 2) dysfunction of CN V (mandibular branch) with secondary atrophy of masticatory muscles. 3) sympathetic dysfunction with loss of orbital smooth muscle tone. Atrophy of masticatory muscles or sympathetic dysfunction can both lead to elevated 3rd eyelid.

Question 78

ventrolateral strabismus is associated with dysfunction of what?

Answer 78

oculomotor nerve

Question 79

medial strabismus is associated with dysfunction of what?

Answer 79

abducent nerve

Question 80

eyeball extorsion (outward rotation) is seen with dysfunction of what?

Answer 80

trochlear nerve

Question 81

describe the pathway for physiologic nystagmus

Answer 81

cranial nerve VIII -> brainstem -> vestibular nuclei -> medial longitudinal fascicles -> abducent and oculomotor neurons (for abduction and adduction of the eyeball, respectively)

Question 82

a positional, ventrolateral strabismus is associated with what?

Answer 82

vestibular disease

Question 83

palpebral reflex tests what nerves?

Answer 83

sensory branches (ophthalmic - medial, maxillary - lateral) of trigeminal nerve; facial nerve

Question 84

what would you see on a physical exam with unilateral versus bilateral mandibular nerve dysfunction?

Answer 84

uni/bi: muscle atrophy of temporals and masseter muscles. bi: dropped jaw, excessive drool

Question 85

nasal hypalgesia indicates a problem where?

Answer 85

ipsilateral trigeminal nerve (ophthalmic branch) OR contralateral prosencephalic lesion (via nociceptive pathways that project to contralateral thalamus and somesthetic cerebral cortex)

Question 86

the gag reflex tests which CN?

Answer 86

glossopharyngeal, vagus, hypoglossal

Question 87

dysphagia can be seen with dysfunction of what CN?

Answer 87

IX and X

Question 88

what are the two parts of the prosencephalon?

Answer 88

cerebrum, thalamus

Question 89

what are the three parts of the brainstem?

Answer 89

midbrain, medulla oblongata, pons

Question 90

the thalamus belongs to which neuroanatomic region?

Answer 90

prosencephalon

Question 91

midbrain belongs to which neuroanatomic region?

Answer 91

brainstem

Question 92

medulla belongs to which neuroanatomic region?

Answer 92

brainstem

Question 93

pons belongs to which neuroanatomic region?

Answer 93

brainstem

Question 94

what type of circling do you see with disease in the prosencephalon?

Answer 94

wide, ipsilateral

Question 95

prosencephalic disease: postural reaction deficits or ipsi or contralateral?

Answer 95

contralateral

Question 96

prosencephalic disease: describe spinal reflex deficits

Answer 96

normal (no deficit)

Question 97

prosencephalic disease: cutaneous sensation deficit

Answer 97

contralateral (often facial/nasal) hypalgesia

Question 98

prosencephalic disease: menace deficits are contra or ipsi?

Answer 98

contralateral

Question 99

prosencephalic disease: PLRs or normal or abnormal? ipsi or contra?

Answer 99

normal if optic radiation or occipital cortex; abnormal if optic chasm, optic tracts; if abnormal, contralateral

Question 100

prosencephalic disease: what changes might you see/hear about that aren’t part of the typical neuro exam?

Answer 100

abnormalities in thirst, appetite, thermoregulation, electrolyte and water balance, sleep patterns

Question 101

brainstem disease: discuss posture/gait

Answer 101

UMN tetra paresis/plegia and proprioceptive deficits; vestibular ataxia with pontine or medullary lesions; opisthotonus with midbrain lesions

Question 102

brainstem disease: postural reaction deficits are ipsi or contralateral?

Answer 102

ipsi if pons and medulla (caudal brainstem); contralateral of rostral midbrain (i think this is very rare - check with AT’s notes)

Question 103

brainstem disease: what cranial nerves could be affected?

Answer 103

3-12

Question 104

what are the two parts of the prosencephalon? what is included in each of these?

Answer 104

telencephalon (cerebral hemispheres), diencephalon (epithalamus, thalamus, hypothalamus)

Question 105

the gait is normal or abnormal with procencephalon disease? why?

Answer 105

normal - the UMNs responsible for gait generation are located in midbrain, pons, and medulla

Question 106

describe adverse syndrome

Answer 106

AKA semi-neglect; pet ignores all sensory input perceived from its environment that is CONTRAlateral to prosencephalic lesion

Question 107

central vestibular disease: postural reactions are contra or ipsilateral?

Answer 107

ipsilateral

Question 108

vestibular disease: head tilt is contra or ipsilateral?

Answer 108

ipsilateral (toward lesion)

Question 109

where do lesions have to be to get a paradoxical head tilt? is it ipsi or contralateral?

Answer 109

caudal cerebellar peduncle or flocculonodular lobules of cerebellum; contralateral

Question 110

with vestibular disease, is nystagmus towards or away from lesion?

Answer 110

peripheral vestibular disease - FAST phase is AWAY from lesion. central disease - unreliable (either way or changing)

Question 111

facial nerve disorder is seen with peripheral or central vestibular disease?

Answer 111

both

Question 112

describe Horner’s syndrome as seen with a brainstem lesion

Answer 112

occurs because of involvement of the UMN (hypothalamo-tecto-tegmental) sympathetic pathway; requires a severe brainstem lesion and patient will usually be tetraplegic with marked mentation changes

Question 113

describe sensorium with peripheral and central vestibular lesions

Answer 113

unaffected with peripheral; dull to comatose with central if ARAS is affected

Question 114

discuss the rebound phenomenon

Answer 114

when the head of a pet with cerebellar disease is extended and then support is withdrawn suddenly, the head drops excessively in a ventral direction

Question 115

cerebellar disease: head tilt is ipsi or contra?

Answer 115

head tilt away from lesion (paradoxical)

Question 116

cerebellar disease: menace deficit is ipsilateral or contralateral?

Answer 116

ipsilateral (bilateral if diffuse disease)

Question 117

cerebellar disease: postural reaction deficits are ipsi or contralateral?

Answer 117

ipsilateral

Question 118

what pupillary change can you see with cerebellar disease?

Answer 118

anisocoria

Question 119

Horner’s disease is seen with lesions in what spinal cord segments?

Answer 119

C1-C5 (UMN) (ipsilateral), T1-T3 (ipsilateral)

Question 120

LMN cell bodies for the limbs are located where?

Answer 120

ventral grey matter of the cervicothoracic (C6-T2) and lumbosacral (L4-S3) intumescences

Question 121

ascending and descending pathways compose which area of the spinal cord?

Answer 121

white matter (more superficial than the LMN cell bodies in the grey matter)

Question 122

the classic 2-engine gait is seen with lesions where?

Answer 122

C6-T2 (short and choppy FL, long strided HL)

Question 123

discuss schiff-sherrington syndrom

Answer 123

peracute T3-L3 lesions that produce a marked spasticity in the thoracic limbs; results from disruption of ascending inhibitory axons arising from interneurons located in the dorsolateral border of the ventral gray column of spinal cord segments L1-L7 - these ascending interneurons exert an inhibitory influence on the LMNs of the cervical intumescence. Postural reactions are delayed in C1-C5 but normal in S-S.

Question 124

discuss spinal shock

Answer 124

T3-L3 lesion with LMN signs in pelvic limbs; commonly accompanied by schiff-sherrington. thought to be secondary to a transient disconnection between the descending UMNs and LMNs of the LS intumescence. transient (hours to days).

Question 125

T3-L3 lesions that produce LMN signs in pelvic limbs WITHOUT schiff-sherrington syndrome is most commonly seen with which disease?

Answer 125

fibrocartilaginous embolic myelopathy (FCEM)

Question 126

what are the differentials for a diffuse CNS localization?

Answer 126

dysmyelinogenesis, diffuse meningitis (idiopathic tremor syndrome, disseminated granulomatous meningoencephalomyelitis, infectious meningitis) and toxicoses (molds, algae, ethylene glycol)

Question 127

describe cushing’s reflex

Answer 127

with increasing intracranial pressure, systemic blood pressure increases to maintain cerebral perfusion, which can cause reflex increases in vagal tone and decrease in HR/RR

Question 128

what are the three places the brain tissue can herniate?

Answer 128

falx cerebri (lateral) or tentorium (caudal) or through the foramen magnum

Question 129

what are the three types of brain edema?

Answer 129

cytotoxic, vasogenic, interstitial

Question 130

discuss cytotoxic brain edema

Answer 130

results from fluid accumulation in neurons. energy depletion d/t failure of ATP-dependent Na/K ATPase pump and other ion channels results in intracellular translocation of extracellular water. Usually occurs as a result of ischemia or processes that alter the cellular membrane

Question 131

discuss vasogenic brain edema

Answer 131

results from physical or functional disruption of the vascular endothelium, often in associated with the BBB. fluid accumulation is extracellular and preferentially distributed within the white matter because its myelinated neuronal fibers are diffusely distributed within a matrix of glia and capillaries.

Question 132

describe interstitial edema

Answer 132

accompanies obstructive hydrocephalus, causing compartmentalized CSF to cross ependymal linings and creating extracellular periventricular interstitial brain edema

Question 133

how do you treat cytotoxic, interstitial, and vasogenic edema?

Answer 133

cytotoxic and interstitial edemas - treat underlying cause; vasogenic - osmotic and corticosteroid therapy

Question 134

what makes up the BBB?

Answer 134

endothelial cells, basement membranes, neighboring perivascular pericytes, glial cells (astrocytes, microglia) and neurons

Question 135

in T1 weighted MRI, fat is bright or dark? water is bright or dark?

Answer 135

bright fat. dark water

Question 136

in T2 weighted MRI, fat is bright or dark? water is bright or dark?

Answer 136

bright water. dark fat. edema is apparent as increased signal.

Question 137

what is the purpose of the FLAIR MRI sequence?

Answer 137

fluid attenuated inversion recovery: suppresses signal from fluid with low or no protein (ie CSF) so that it is hypo intense and allows improved ID of pathologies (tissue edema) and lesions near ventricles

Question 138

what is the purpose of the STIR MRI sequence?

Answer 138

short-tau inversion recovery: allow for fat suppression

Question 139

what is the purpose of the T2* MRI sequence?

Answer 139

gradient echo (GRE) T2W: detect artifact from blood products that are formed in hemorrhage

Question 140

what is the purpose of the DWI MRI sequence?

Answer 140

diffusion weighted imaging: can aid in ID’ing issues like cytotoxic edema associated with ischemic infarction

Question 141

discuss hypo- and dysmyelinogenesis

Answer 141

the numbers of oligodendrocytes are decreased or are unable or retarded in producing functional myelin. typically myelin throughout the CNS is affected but peripheral nerves are spared. reflexes are normal or exaggerated. Dz manifest with whole body tremors, dysmetria noticeable from first attempts at walking and nystagmus

Question 142

what clinical signs do you see with leukodystrophy?

Answer 142

general proprioceptive ataxia and upper motor neuron paraparesis, which progress to tetra paresis +/- signs of cerebellar involvement and seizures

Question 143

what are the histopathologic changes seen in leukodystrophy?

Answer 143

myelin degeneration w/o producing vacuolation, that is replaced by severe astrogliosis or Rosenthal fibers (astrocytic processes); widespread throughout brain and spinal cord

Question 144

describe myelinolysis

Answer 144

characterized by disintegration of initially normally formed myelin; presumed d/t autosomal recessive inheritance; age at onset ranges from weeks to a few years; acute paraparesis. bilateral and symmetrical loss of myelin with cavitations that are most severe in alls spinal cord funiculi with tapering extension into the brainstem.

Question 145

compare and contrast myelinolysis in the afghan hound and dutch kooiker

Answer 145

myelin is predominantly affected but axons are usually spared in Afghan Hound myelopathy, indicating primary myelinopathy, whereas prominent wallerian degeneration in the Dutch Kooiker is more indicative of an axonopathy

Question 146

what is spongy degeneration?

Answer 146

denotes affected tissue vacuolation, seen in disorders that involve separation of the myelin sheath or that involve the neuronal cell body (ie transmissible spongiform enceophalopathy, the prion diseases)

Question 147

what symptoms may you see in spongiform leukoencephalomyelopathy?

Answer 147

cerebellar ataxia, seizures, opisthotonus; c/s occurs w/in 1-9 mo’s of age, progressive

Question 148

describe central axonopathy

Answer 148

bilateral and symmetrical degeneration of axon AND myelin, affecting spinal cord sensory and motor tracts with the longest fibers being the most vulnerable. lesions are diffuse myelinated fiber loss of varying severity in the cerebellar white matter and/or dorsal funiculi and pyramidal tracts in spinal cord that extend into the brainstem

Question 149

what are the c/s of central axonopathy?

Answer 149

general proprioceptive or cerebellar ataxia and UMN paresis

Question 150

what is the treatment for neurodegenerative disease?

Answer 150

currently there is none

Question 151

describe neonatal encephalopathy with seizures (NEWS)

Answer 151

hereditary disorder of St poodles - developmental delay with seizures and death before weaning; few biochemical or histological changes. suspected d/t mutation in ATF2 (major transcription factor that affects normal programming of neuronal development)

Question 152

what is subacute necrotizing encephalopathy? what c/s does it cause?

Answer 152

defects of mitochondrial respiratory chain or pyruvate metabolism. lesions are attributed to vascular congestion, caused by lactic acidosis resulting in hypoxemia and necrosis. c/s: ataxia, paresis, movement disorders, cognitive deficits, nystagmus, siezures

Question 153

what c/s do you see in mitochondria encephalopathy in alaskan husky puppies?

Answer 153

acute proprioceptive ataxia, seizures, behavior changes, central blindness, tetra paresis, facial sensation deficits

Question 154

what is the purpose of cellular malonic acid?

Answer 154

regulate use of carbohydrates or fatty acids as energy in fed versus fasted states, respectively

Question 155

cobalamin is a necessary cofactor in the conversion of what to what?

Answer 155

methylmalonyl CoA to succinyl CoA (part of the kreb’s cycle)

Question 156

what is imerslund-grasbeck syndrome?

Answer 156

selective cobalamin malabsorption

Question 157

what symptoms might you see with cobalamin malabsorption syndrome?

Answer 157

altered mentation, inappetence, seizures associated with hyperammonemia and blood dyscrasias; these resolve with cyanocobalamin supplementation

Question 158

how do you diagnose cobalamin malabsorption syndrome?

Answer 158

high urinary methylmalonic acid and low serum cobalamin

Question 159

cobalamin deficiency with elevated urine MMA and neurologic signs in cats is due to what?

Answer 159

deficiency of intrinsic factor (which is necessary for absorption of cyanocobalamin), GI disease

Question 160

why do cats with GI disease develop D-lactic acidosis?

Answer 160

excessive bacterial production of the D isoform in intestines

Question 161

what is the difference between the D and L isoforms of lactate?

Answer 161

D isn’t detected by most routine lactate assays, but is more likely to produce encephalopathy

Question 162

what is lysosomal storage disease?

Answer 162

characterized by accumulation of metabolic byproducts within lysosomes, the cellular organelle responsible for breakdown of complex macromolecules. storage diseases are caused by key enzyme deficiencies, resulting in a failure to break down molecules and substrate accumulation.

Question 163

what substrates are found within lysosomes that help in catabolism?

Answer 163

sphingolipids (a component of myelin), oligosaccharides, mucopolysaccharides, glycoproteins, proteins

Question 164

what c/s do you commonly see with lysosomal storage diseases?

Answer 164

cerebellar signs of dysmetria, truncal ataxia, nystagmus at first, progressing to UMN weakness, behavioral abnormalities, seizures

Question 165

if you suspect a lysosomal storage disease, what are some diagnostic options?

Answer 165

blood smear - storage vacuoles in WBC. CSF. LNN, liver, spleen, muscle - bx or FNA to see vacuoles. MRI, necropsy. electron microscopy looking at lysosomes. metabolites in urine. DNA testing for mutations / finding deficient enzyme activity in affected tissues, leukocytes, or fibroblasts

Question 166

what is a neuronal ceroid lipofuscinosis? what is another name for it?

Answer 166

AKA batten disease. subset of lysosomal storage diseases in which the storage products are proteins with characteristic autofluorescence, similar to ceroid and lipofuscin pigments which accumulate normally with aging. the storage products in NCLs are subunit C of mitochondrial ATP or sphingolipid activator proteins (saponins A and D), due to deficient soluble enzymes. membrane proteins are located in the lysosome, endoplasmic reticulum, or in synaptic vesicle-associated proteins.

Question 167

what c/s might you see with a neuronal ceroid lipofuscinosis?

Answer 167

progressive visual impairments (usually the first sign), decline in cognition and motor functions, seizures, generalized brain atrophy, and death in young to middle age. behavior changes become prominent with disease progression and include timidness, hyperesthesia, confusion, unprovoked aggression, seizures, jaw chopping, bruxism, myoclonus. general proprioceptive and cerebellar ataxia are later manifestations (although they are the most prominent sign on american bulldogs with cathepsin D deficiency)

Question 168

what options do you have for diagnosis of neuronal ceroid lipofuscinosis?

Answer 168

cross-sectional imaging shows generalized brain atrophy, but definitive diagnosis requires recognition of auto fluorescent material in the brain or other tissues. DNA testing.

Question 169

treatment for neuronal ceroid lipofuscinosis?

Answer 169

none. symptomatic therapy for seizures and behavior changes.

Question 170

intra-axial tumors come from what types of cells? give tumor examples.

Answer 170

neuroepithelial cells. astrocytoma, oligodendroglioma, gliomatosis cerebri, medulloblastoma/primitive neuroectodermal tumor (PNET), ependymoma, choroid plexus tumor

Question 171

astrocytoma comes from what type of cell? intra- or extra- axial?

Answer 171

neuroepithelial, intra-axial

Question 172

oligodendroglioma comes from what type of cell? intra- or extra- axial?

Answer 172

neuroepithelial, intra-axial

Question 173

gliomatosis cerebri comes from what type of cell? intra- or extra- axial?

Answer 173

neuroepithelial, intra-axial

Question 174

medulloblastoma / primitive neuroectodermal tumors come from what type of cell? intra- or extra- axial?

Answer 174

neuroepithelial, intra-axial

Question 175

ependymoma comes from what type of cell? intra- or extra- axial?

Answer 175

neuroepithelial, intra-axial

Question 176

choroid plexus tumor comes from what type of cell? intra- or extra- axial?

Answer 176

neuroepithelial, intra-axial

Question 177

extra-axial tumors come from what cells? list tumor examples

Answer 177

meninges: meningioma, granuloma cell tumor

Question 178

meningioma is intra- or extra-axial?

Answer 178

extra-axial

Question 179

what is the most common primary brain tumor in dogs?

Answer 179

meningiomas (50% of primary brain tumors)

Question 180

what is the second most common primary brain tumor in dogs?

Answer 180

gliomas (30-40% of primary brain tumors)

Question 181

what is the most common primary brain tumor in cats?

Answer 181

meningiomas (60%)

Question 182

what is the second most common primary brain tumor in cats?

Answer 182

gliomas

Question 183

what primary brain tumors have a potential for extraneural spread?

Answer 183

meningioma, PNET, malignant glioma, histolytic tumor, choroid plexus tumor

Question 184

where do meningiomas metastasize to? how common is this?

Answer 184

lung, pancreas - rare

Question 185

rank in order of median age for development in dogs: glioma (astrocytoma, oligodendroglioma), meningioma, choroid plexus tumor

Answer 185

choroid plexus tumor (5-6y), glioma (8y), meningioma (10-14y)

Question 186

what breeds have increased risk of primary intracranial neoplasia?

Answer 186

boxer, boston terrier, golden retriever, french bulldog, rat terrier

Question 187

over expression of this growth factor is common in primary brain tumors in dogs

Answer 187

VEGF

Question 188

young cats with this storage disease have a high incidence of meningioma

Answer 188

mucopolysaccharidosis type I

Question 189

in terms of signalment of those developing primary brain tumors, how are dogs and cats different

Answer 189

cats are older, whereas dogs can be younger

Question 190

in cats with meningiomas, are males or females more commonly affected?

Answer 190

males

Question 191

what tumor location is most likely to press to the brain by direct extension?

Answer 191

nasal tumors (through cribriform plate)

Question 192

what tumor types can invade the brain by direct extension?

Answer 192

otic SCC, pituitary tumor, calvarial tumor (osteochondrosacoma, chondrosarcoma, multilobular osteochondrosarcoma), nerve sheath tumor (CN V tumor)

Question 193

secondary neoplasia accounts for X% of all canine intracranial tumors

Answer 193

50%

Question 194

what is the most common tumor to metastasize to the brain in dogs?

Answer 194

hemangiosarcoma

Question 195

metastases most commonly affect what part of the brain?

Answer 195

cerebrum

Question 196

secondary neoplasia accounts for X% of all feline intracranial tumors

Answer 196

22%

Question 197

what is the most common tumor to metastasize to the brain in cats?

Answer 197

lymphoma (renal, in particular) and pituitary tumors

Question 198

what is the most common c/s associated with a brain tumor in dogs? cats?

Answer 198

seizures in dogs; altered mentation in cats

Question 199

what is the difference between intra- and extra-axial brain tumors?

Answer 199

extra-axial arise from outside the brain (meninges, calvaria, ventricles). intra-axial arise from within the brain parenchyma

Question 200

a tumor that has come to the brain via hematogenous spread is usually located where?

Answer 200

at the gray-white matter interface

Question 201

what CSF finding is typical for an intracranial neoplasm?

Answer 201

albuminocytologic disassociation: increased protein concentrations and a normal to mild increase in total nucleated cell count

Question 202

what tumor type is associated with the most marked elevation in CSF total protein?

Answer 202

choroid plexus tumors

Question 203

discuss prognosis with surgical removal of meningiomas in cats versus dogs

Answer 203

MST dogs 7mo, MST cats 36mo

Question 204

what tumor is most amenable to surgical removal?

Answer 204

meningioma near the brain surface and noninvasive (which is why cats have a better prognosis - less likely to be invasive)

Question 205

what acute adverse effects of radiation can you see with RT of brain tumors?

Answer 205

cerebral edema linked to BBB disturbance, which may result in demyelination and responds to corticosteroids

Question 206

what delayed adverse effects of radiation can you see with RT of brain tumors?

Answer 206

focal CNS radiation necrosis, severe vascular lesions

Question 207

what is the survival time for gliomas after imaging diagnosis?

Answer 207

<80 days

Question 208

supratentorial versus infratendorial tumors: which has a longer MST?

Answer 208

supratentorial has a longer MST

Question 209

IVETF and ACVIM consensus statements recommend initiating long-term anti-epileptic therapy in animal with epilepsy when any of these 5 criteria are met?

Answer 209

1) identifiable structural lesion or prior history of brain disease/injury; 2) acute repetitive seizures (status epilepticus); 3) interictal period < 6 mo’s (2+ seizures within 6 months); 4) prolonged, severe, or unusual post-octal periods; 5) epileptic seizure frequency and/or duration is increasing and/or seizure severity is worse over three interictal periods

Question 210

measurement of anti-epileptic drug concentrations takes place after establishment of a steady-state concentration based on X elimination half-lifes

Answer 210

5

Question 211

a drop of X% or more in the trough serum concentration of anti-epileptic drugs is an indicator of poor administration compliance

Answer 211

20%

Question 212

describe the target and transporter hypotheses for drug-related mechanisms of epilepsy refractory to medicaitons

Answer 212

Target: genetic or disease-related alterations in cellular targets of AEDs. Transporter: postulates altered transport of drugs across the BBB

Question 213

describe metabolic tolerance in terms of refractory epilepsy

Answer 213

increasing the drug dosage does not result in a parallel increase in serum drug concentration

Question 214

what factors are associated with reduction in seizures in epileptic dogs taking AEDs?

Answer 214

female gender, neutering, no history of cluster seizures, older age at onset

Question 215

of epileptic dogs taking AEDDs, what dog breeds are least likely to go into remission or have a >50% in seizure reduction?

Answer 215

border collie, GSD, staffordshire terrier

Question 216

what are the risk factors for euthanasia amongst epileptic dogs?

Answer 216

younger age of onset, high initial seizure frequency, poor seizure control, episodes of status epilepticus

Question 217

define a transient ischemic attack

Answer 217

cerebrovascular accident where c/s resolve within 24 hours

Question 218

what is the most common CVA recognized in dogs?

Answer 218

nonhemorrhagic ischemic infarcts

Question 219

what are the most common sites for ischemic stroke in dogs?

Answer 219

cerebellum, striatocapsular region, thalamus

Question 220

lacunar thalamic/midbrain infarcts are more common in large or small breed dogs?

Answer 220

large

Question 221

why are miniature schnauzers at increased risk of CVAs?

Answer 221

hyperlipidemia

Question 222

what diseases predispose dogs to nonhemorrhagic ischemic stroke/

Answer 222

metabolic disorders (hypothyroidism, pheochromocytoma, hypertension) or hypercoagulopathy (DM, HAC, renal disease, PLN)

Question 223

what diseases predispose dogs to hemorrhagic ischemic stroke?

Answer 223

coagulopathy, hypertension, sepsis, inflammation, metastasis (hemangiosarcoma)

Question 224

what parasite has been reported in dogs with hemorrhagic strokes?

Answer 224

angiostrongylus vasorum

Question 225

discuss feline ischemic encephalopathy

Answer 225

cerebral infarction syndrome; usually involves the middle cerebral artery. some cases have been associated with aberrant migration of Cuterebra larvae.

Question 226

use of what drug in brachycephalic breeds predisposes them to global ischemia?

Answer 226

ketamine

Question 227

use of mouth gags in cats has been associated as a risk factor of developing what?

Answer 227

cerebral ischemia, hearing loss, and blindness. blood flow through maxillary arteries is occluded, which can lead to further vision and hearing loss

Question 228

when does watershed infarction develop?

Answer 228

when cerebral blood flow is lowered below the point of compensation by cerebral auto regulatory mechanisms, causing widespread bilateral brain dysfunction

Question 229

what are the most common c/s seen in CVAs?

Answer 229

altered mentation, hemiparesis, seizures, vestibular dysfunction; motor dysfunction and general proprioceptive ataxia reported in 78%, including signs of sensory hemi-neglect and contralateral motor deficits

Question 230

ischemic stroke in dogs most commonly involves what blood vessel? what c/s may this cause?

Answer 230

middle cerebral artery (70%) - signs of sensory hemi-neglect and contralateral motor deficits

Question 231

onset of ischemic stroke is usually acute to parachute; deterioration typically occurs after the insult, but then becomes static or improves after the first X hours

Answer 231

24 hours

Question 232

how long is the window of opportunity for instituting supportive care therapy after a CVA?

Answer 232

6 hours

Question 233

what is a penumbra?

Answer 233

The area of infarcted brain consists of an ischemic core with permanent loss of blood flow and irreversible neuronal injury surrounded by a PENUMBRA, where blood flow is decreased but still-viable neurons are at risk for irreversible injury.

Question 234

identification of this condition in dogs with non-traumatic intracranial hemorrhage is a poor prognostic indicator

Answer 234

hypertension

Question 235

in dogs with intracranial hemorrhage and multiple lesions >5 mm, this infection was the only concurrent conditional with a good outcome

Answer 235

angiostrongylus vasorum

Question 236

for animals with multifocal/diffuse encephalopathy, what types of diseases should be highest on the differential list?

Answer 236

inflammatory, metabolic, multifocal/metastatic neoplasia, toxins

Question 237

list 4 differentials for degenerative disorders that can cause multifocal/diffuse brain dysfunction

Answer 237

lysosomal storage dz, cognitive dysfunction syndrome, leukodystrophy/spongy degeneration, neuronal vacuolation and spinocerebellar degeneration in Rottweilers and boxers

Question 238

list 6 differentials for anomalous disorders that can cause multifocal/diffuse brain dysfunction

Answer 238

COMS, intracranial arachnoid cyst, congenital hydrocephalus, neuronal migration disorder, atlanto-occipital overlap, dandy-walker syndrome

Question 239

what is dandy-walker syndrome? it has been associated with a mutation in what receptor?

Answer 239

agenesis of the cerebellar vermis and hydrocephalus; mutation in VLDR, encoding the very low density lipoprotein receptor (seen in a eurasier dog)

Question 240

list 8 differentials for metabolic disorders that can cause multifocal/diffuse brain dysfunction

Answer 240

hepatic encephalopathy, hypoglycemia, electrolyte-associated encephalopathy, endocrine (hypothyroidism, hyperthyroidism), renal encephalopathy, kernicterus, mitochondrial encephalopathy, organic acidurias

Question 241

what two vitamin deficiencies can cause multifocal/diffuse brain dysfunction

Answer 241

thiamine; cobalamin (border collies)

Question 242

what three inflammatory/noninfectious diseases can cause multifocal/diffuse brain dysfunction

Answer 242

GME, NME, EME

Question 243

list 9 toxins that can cause multifocal/diffuse brain dysfunction

Answer 243

bromethalin, marijuana, metaldehyde, TCA, brunfelsia, lead, methylxanthine overdose, nicotine, salt intoxication (including paintballs)

Question 244

what types of cells are found in increased numbers in the brain and/or spinal cord in GME?

Answer 244

mononuclear cells: lymphocytes, macrophages, plasma cells

Question 245

what type of immune reaction is GME suspected to be?

Answer 245

delayed-type (T-cell mediated) hypersensitivity

Question 246

In GME, are lesions in the grey or white matter?

Answer 246

white

Question 247

what are the 3 clinical forms of GME?

Answer 247

focal, multifocal/disseminated, ocular

Question 248

what is the typical signalment of a GME patient?

Answer 248

young to middle-aged (median of 5yo) female dogs of small breeds (poodle, terrier)

Question 249

what c/s are most common in GME patients?

Answer 249

seizures, cerebellovestibular dysfunction, cervical hyperesthesia

Question 250

describe the CSF of a GME patient

Answer 250

mononuclear pleocytosis, variable % of neutrophils and elevated protein level

Question 251

list 4 drugs used for treatment of GME

Answer 251

prednisone, procarbazine, cytosine arabinoside, cyclosporine

Question 252

necrotizing encephalitis involves grey or white matter?

Answer 252

both

Question 253

NME lesions are found where?

Answer 253

cerebrum, with consistent meningeal involvement

Question 254

NLE lesions are found where?

Answer 254

brainstem, cerebrum; less consistent involvement of meninges and cerebral cortex than NME (ie mainly white matter)

Question 255

what types of cells are commonly found in necrotizing encephalitis?

Answer 255

necrotic nonsuppurative inflammatory lesions.

Question 256

clinical signs of dysfunction in what neuro localization predominate in dogs with necrotizing encephalitis?

Answer 256

forebrain: seizures, circling, obtunded, head pressing, visual deficits with normal PLR; can also see neck pain

Question 257

in addition to c/s of XX dysfunction and XX, yorkies with NLE often show c/s of XX dysfunction

Answer 257

forebrain, neck pain; brainstem (i.e. central vestibular disease)

Question 258

describe the typical CSF associated with NME and NLE

Answer 258

mononuclear pleocytosis. mononuclear cells in NME are mostly lymphocytes; in NLE are a mixture of lymphocytes and monocytes

Question 259

eosinophilic meningoencephalitis typically has inflammation where?

Answer 259

meninges

Question 260

what does the CSF typically look like in an EME case?

Answer 260

eosinophilic pleocytosis with >10% eosinophils

Question 261

what infectious agents have been reported to cause EME?

Answer 261

cryptococcus neoformans, neospora caninum, baylisascaris procyonis. but note that 70% of cases are idiopathic.

Question 262

EME is more common in small or large breeds?

Answer 262

large

Question 263

greyhound nonsuppurative meningoencephalitis affects dogs of what age?

Answer 263

<12 months

Question 264

there is an association between greyhound meningoencephalitis and XX

Answer 264

dog leukocyte antigen class II haplotype

Question 265

what c/s are seen with greyhound nonsuppurative meningoencephalitis?

Answer 265

forebrain (mentation and behavior changes, blindness) and brainstem (head tilt, circling, ataxia)

Question 266

what areas of the brain are typically affected in greyhound meningoencephalitis?

Answer 266

rostroventral cerebrum, particularly olfactory lobes and bulbs

Question 267

what bacteria are common in bacterial meningoencephalitis?

Answer 267

staph, strep, pasteurella multocida (especially cats), actinomycetes, nocardia, bactericides, peptostreptococcus, fusobacterium, eubacterium, e coli, klebsiella. gram negatives most common.

Question 268

what are the 2 classical clinical features of bacterial meningoencephalitis?

Answer 268

fever and cervical hyperesthesia

Question 269

describe the CSF of an acute bacterial meningoencephalitis

Answer 269

suppurative, often with degenerate and toxic neutrophils. proteins levels elevated. +/- intracellular bacteria

Question 270

what antibiotics are good for treatment of bacterial meningitis?

Answer 270

ampicillin - crosses inflamed BBB. if gram negative infection: enrofloxacin or 3rd generation cephalosporin. if anaerobic: metronidazole

Question 271

name 6 fungal organisms that can invade the CNS

Answer 271

cryptococcus, coccidioides, blastomyces, histoplasma, aspergillus, phaeohyphomycosis (cladosporium)

Question 272

what is the most common fungal organism associated with meningoencephalitis in dogs and cats?

Answer 272

cryptococcus neoformans

Question 273

in cases of cryptococcus, what extra neural areas are most commonly infected?

Answer 273

eyes, nasal and frontal sinuses (head region)

Question 274

in cases of coccidioidomycosis, what extra neural areas are most commonly infected?

Answer 274

pulmonary system

Question 275

compare and contrast the clinical progression of bacterial and fungal meningoencephalitis

Answer 275

bacterial is usually fast and progressive; fungal is usually a slow progression

Question 276

which fungal organism are you most likely to find in CSF

Answer 276

cryptococcus

Question 277

what types of cells do you see in CSF of fungal meningoencephalitis patients?

Answer 277

mix of mononuclear cells and neutrophils; may also see eosinophils

Question 278

testing CSF and/or serum for antibodies is most reliable for which 3 fungal agents?

Answer 278

cryptococcus, coccidioides, blastomyces

Question 279

what anti fungal medication(s) can cross the BBB?

Answer 279

fluconazole, flucytosine (5-fluorocytosine)

Question 280

what is the most common viral brain infection in dogs?

Answer 280

distemper (paramyxovirus)

Question 281

what is the most common viral infection of the brain in cats?

Answer 281

FIP (coronavirus)

Question 282

what is the most common route for viral infection of the brain?

Answer 282

inhalation

Question 283

what viral agents can cause a meningoencephalitis?

Answer 283

distemper, FIP, FIV, rabies, canine herpesvrisu, feline parvovirus, feline borna disease virus, pseudorabies, west nile; in rare cases - canine adenovirus (infectious canine hepatitis virus), canine parainfluenza, canine parvovirus

Question 284

list 4 neurotropic viruses

Answer 284

distemper, rabies, pseudorabies, feline borna disease; these have predilection for neuronal and glial cells

Question 285

myoclonus of one or more limbs and/or muscles of the head is relatively specific for what disease?

Answer 285

canine CNS distemper

Question 286

FIP infection of the CNS is more common with the dry or wet form of the disease?

Answer 286

non effusive form

Question 287

what are the two forms of rabies? which species is most likely to get each?

Answer 287

furious - cats. paralytic - dogs.

Question 288

what is the characteristic histologic pattern in FIP in the brain?

Answer 288

pyogranulomas

Question 289

what is the characteristic histologic pattern of neurologic distemper?

Answer 289

demyelinating brainstem lesions

Question 290

if using antibody titers to diagnose viral neurologic disease, what condition should be met to suggest infection rather than exposure or vaccination?

Answer 290

CSF titers higher than serum titers

Question 291

what is the characteristic CSF of a patient with CNS viral disease?

Answer 291

mononuclear (lymphocytic) pleocytosis with elevated protein EXCEPT FIP - predominant cell is neutrophil, with variable numbers of lymphocytes and macrophages

Question 292

what is the typical clinical progression of a patient with pseudorabies

Answer 292

dead d/t respiratory failure within 48 hours of onset of c/s

Question 293

what two rickettsial diseases can cause encephalopathy in dogs?

Answer 293

RMSF, ehrlichiosis

Question 294

what protozoal organisms can cause encephalopathy/

Answer 294

neospora (dog); toxoplasma (dog, cat)

Question 295

what verminous organism can cause encephalopathy in a cat?

Answer 295

cuterebra

Question 296

what medications are recommended for treatment of protozoal meningoencephalitis?

Answer 296

clindamycin or sulfonamides combined with trimethoprim or pyrimethamine

Question 297

what 3 antibiotics can be used to treat rickettsial meningoencephalitis?

Answer 297

doxycycline, enrofloxacin, chloramphenicol

Question 298

how do you treat cuterebra in cats?

Answer 298

ivermectin; premedicate with diphenhydramine and glucocorticoids. follow with 2 weeks of clavamox

Question 299

describe neuroaxonal dystrophy

Answer 299

primary disorder of axonal transport, characterized by swellings within the axons called “spheroids”

Question 300

what symptoms do togs affected by neuroaxonal dystrophy show?

Answer 300

cerebellar ataxia and tetra paresis

Question 301

what is “multiple systems degenerations”?

Answer 301

when the cerebellum and basal ganglia are involved in a disease process. the basal ganglia (caudate nucleus, substantia nigra) are important in movement

Question 302

what is the primary clinical sign of polymicrogyria?

Answer 302

cortical blindness (seen in standard poodles)

Question 303

cerebellar hypoplasia is seen in cats following in utero or early neonatal infection with what infectious agent?

Answer 303

feline panleukopenia virus; possibly also canine parvovirus

Question 304

in intraventricular obstructive hydrocephalus, where is the blockage of CSF flow through the ventricular system seen?

Answer 304

most commonly - connection between 3rd and 4th ventricle (mesencephalic aqueduct). also seen at connection between lateral ventricle and 3rd ventricle (interventricular foramen)

Question 305

in extraventricular hydrocephalus, where is the obstruction?

Answer 305

subarachnoid space or arachnoid villi; entire ventricular system and subarachnoid space will dilate.

Question 306

what are the c/s and physical features of hydrocephalus?

Answer 306

behavioral changes, ataxia, visual deficits, seizures; enlarged and dome-shaped calabria, persistent cranial sutures and fontanelle, ventrolateral strabismus (congenital hydrocephalus)

Question 307

describe medical treatment for hydrocephalus

Answer 307

anti-epileptics; diuretics (furosemide), carbonic anhydrase inhibitors (acetazolamide); PPI (omeprazole) +/- steroids to decrease CSF production

Question 308

what is chiari-like malformation?

Answer 308

herniation of cerebellar semis and medulla into or through foramen magnum and indention of the cerebellum by the occipital bone

Question 309

what is syringohydromyelia?

Answer 309

formation of fluid-filled cavities within the spinal cord, most commonly in the cervical region

Question 310

what are c/s of syringohydromyelia secondary to chiari-like malformation?

Answer 310

proprioceptive ataxia, postural reaction deficits, neuropathic pain, scratching of ear / neck / shoulder, vocalization, facial rubbing

Question 311

what is cataplexy?

Answer 311

sudden loss of muscle tone

Question 312

what gene is affected in dogs with familial narcolepsy?

Answer 312

hypocretin-receptor-2 (Hcrtr 2)

Question 313

what is the most sensitive and specific diagnostic tool for diagnosing the sporadic form of narcolepsy?

Answer 313

measuring concentration of hypocretin-1 peptide in CSF. note: patients with familial form will have normal levels.

Question 314

what are the c/s of cognitive dysfunction syndrome?

Answer 314

DISHA: Disorientation, altered Interactions with owners/other pets, Sleep-wake cycle alterations, Housesoiling, Activity changes; can also see agitation/anxiety, altered responsiveness to stimuli, altered interest in appetite/self-hygiene, decreased ability to perform previously trained commands

Question 315

what is the only drug approved for treating cognitive dysfunction syndrome?

Answer 315

selegiline

Question 316

what are the symptoms of optic neuritis?

Answer 316

acute loss of vision - typically bilateral and associated with mydriatic and unresponsive pupils

Question 317

what are the possible causes for optic neuritis?

Answer 317

infectious (distemper, mycotic, protozoal), immune-mediated (GME) meningoencephalitidies, neoplasms (meningioma, glioma, pituitary tumors)

Question 318

describe the ERG of patients with optic neuritis

Answer 318

normal

Question 319

in dogs where you are considering optic neuritis, what other disease presents similarly?

Answer 319

SARDS

Question 320

what symptoms are associated with dysfunction of cranial nerve I?

Answer 320

inability to smell

Question 321

what symptoms are associated with dysfunction of cranial nerve II?

Answer 321

blindness

Question 322

what symptoms are associated with dysfunction of cranial nerve III?

Answer 322

abnormal eye position, pupil size, or PLR

Question 323

what symptoms are associated with dysfunction of cranial nerve IV?

Answer 323

abnormal eye position

Question 324

what symptoms are associated with dysfunction of cranial nerve V?

Answer 324

rubbing or pawing at face, loss of muscle mass on head, dropped jaw - flaccid inability to close the mouth

Question 325

what symptoms are associated with dysfunction of cranial nerve VI?

Answer 325

abnormal eye position

Question 326

what symptoms are associated with dysfunction of cranial nerve VII?

Answer 326

drooping of ear or cheek, deviation of the nose, drooling; dry eye

Question 327

what symptoms are associated with dysfunction of cranial nerve VIII?

Answer 327

abnormal head position, abnormal eye movements, vertigo; deafness

Question 328

what symptoms are associated with dysfunction of cranial nerve IX?

Answer 328

difficulty eating or swallowing

Question 329

what symptoms are associated with dysfunction of cranial nerve X?

Answer 329

loss of voice, coughing, regurgitating

Question 330

what symptoms are associated with dysfunction of cranial nerve XI?

Answer 330

difficult to appreciate

Question 331

what symptoms are associated with dysfunction of cranial nerve XII?

Answer 331

tongue deviation or paralysis; difficulty eating

Question 332

cavernous sinus and orbital fissure syndromes are defined by clinical dysfunction of what nerves?

Answer 332

2 or more of the following: III, IV, VI, and ophthalmic or maxillary branches of V

Question 333

what c/s are seen with cavernous sinus and orbital fissure syndromes?

Answer 333

external and internal ophthalmoplegia, reduced corneal sensitivity, neurotrophic keratitis, ptosis

Question 334

what is the most common cause of cavernous sinus or orbital fissure syndromes?

Answer 334

neoplasia, although infectious causes have been reported, particularly in cats

Question 335

what is the most common cause of dropped jaw in dogs?

Answer 335

idiopathic trigeminal neuritis

Question 336

what is the treatment for idiopathic trigeminal neuritis?

Answer 336

supportive care with assisted feeding. affected dogs usually recover within 2-4 weeks.

Question 337

what 3 generalized neuropathies / neuromuscular diseases can have facial nerve paralysis?

Answer 337

MG, acute polyradiculoneuritis, tick paralysis

Question 338

the esophagus is innervated by…

Answer 338

vagus and internal branch of the accessory nerves

Question 339

the larynx is innervated by…

Answer 339

branches of the vagus nerve

Question 340

what are the 4 parts of horner’s syndrome?

Answer 340

miosis, ptosis, protrusion of the 3rd eyelid, enophthalmos

Question 341

describe the oculosympathetic pathway affected in horner’s syndrome

Answer 341

first order (UMN) neurons originate in rostral brainstem, travel down cervical spinal cord to synapse on 2nd order (pregnaglionic) neurons, which have their cell bodies in T1-T3 spinal segments. second order axons cause up vagosympathetic trunk to synapse on 3rd order (post-ganglionic) neurons in cranial cervical ganglion, which then project to eye and adnexa.

Question 342

describe the test to differentiate between 2nd order and 3rd order lesions (pre and post ganglionic) leading to horners

Answer 342

topical phenylephrine: mydriasis within 20 minutes = post-ganglionic. mydriasis >20 minutes = pre-ganglionic.

Question 343

what are the components of the central vestibular system?

Answer 343

the 4 pairs of vestibular nuclei adjacent to the wall of the fourth ventricle on the dorsal part of the pons and medulla, and the fastigial nucleus and flocculonodular lobe of the cerebellum

Question 344

most axons from the vestibular nuclei project to (1) the spinal cord via the (contra/ipsi)lateral XXX tract to influence extensor tone by facilitation on (contra/ipsi)lateral extensor muscles and inhibition on the (contra/ipsi)lateral flexor muscles and to (2) the XXX, which synapses in the nuclei of CN XX, XX, and XX to adjust the position of the eyes in relation to the position of and movement of the head

Answer 344

most axons from the vestibular nuclei project to (1) the spinal cord via the ipsilateral lateral vestibulospinal tract to influence extensor tone by facilitation on ipsilateral extensor muscles and inhibition on the ipsilateral flexor muscles and to (2) the medial longitudinal fasciculus, which synapses in the nuclei of CN 3, 4, and 6 to adjust the position of the eyes in relation to the position of and movement of the head

Question 345

head tilt is seen in what type of lesion? head turn is seen in what type of lesion?

Answer 345

vestibular / forebrain

Question 346

small circles are seen with a lesion in what area?

Answer 346

vestibular

Question 347

pendular nystagmus is seen in what breeds?

Answer 347

siamese, himalayan, birman

Question 348

in vestibular diseases, the physiologic nystagmus may reduced XX eye(s) when the head is turned toward/away from the side of the lesion

Answer 348

both eyes / toward

Question 349

in vestibular disease, fast phase of nystagmus is towards or away from lesion?

Answer 349

away from the lesion (if central lesion, can be toward lesion)

Question 350

a resting nystagmus rate of >XX beats per minute is XX% specific and XX% sensitives of peripheral vestibular disease

Answer 350

66bpm. 95% specific, 85% sensitive

Question 351

do you see facial nerve involvement with central or peripheral vestibular disease?

Answer 351

both

Question 352

horner’s syndrome is more common with central or peripheral vestibular disease?

Answer 352

peripheral

Question 353

paradoxical vestibular syndrome can be seen with lesions where?

Answer 353

flocculonodular lobe of the cerebellum, caudal cerebellar peduncle, rostral and medial vestibular nuclei in the medulla

Question 354

what 2 qualities for nystagmus suggest a central vestibular lesion?

Answer 354

vertical nystagmus or nystagmus with fast phase toward lesion

Question 355

otitis media/interna: what is the most common cause in dogs? in cats?

Answer 355

dogs: extension from otitis external. cats: ascending infection from nasopharynx (via Eustachian tube)

Question 356

most common bacteria seen in otitis interna/media?

Answer 356

staphylococcus, streptococcus, pseudomonas, proteus, malassezia pachydermatis (yeast)

Question 357

how long should you treat with antibiotics for otitis interna/media?

Answer 357

4-6 weeks

Question 358

most common signalment for nasopharyngeal polyps?

Answer 358

young cat (1-5yo)

Question 359

what symptoms can you see with a nasopharyngeal polyp?

Answer 359

signs of middle/inner ear disease, upper respiratory signs (sneeze, stridor), pharyngeal signs (gagging, dysphagia)

Question 360

idiopathic vestibular disease is seen in what age cat? dog?

Answer 360

cats of all ages; old dog

Question 361

idiopathic vestibular disease is more often unilateral or bilateral?

Answer 361

in dogs, unilateral; bilateral is especially seen in cats (still unilateral most common)

Question 362

in a cat in northeastern US/canada in summer and early fall that has developed idiopathic vestibular disease, what is one potential differential?

Answer 362

migration of Cuterebra larvae through ear canal

Question 363

how does hypothyroidism lead to vestibular disease?

Answer 363

deficit in energy metabolism with disturbance in axonal transport and possible segmental demyelination

Question 364

list 4 ototoxic drugs

Answer 364

aminoglycosides (mostly streptomycin), loop diuretics, chlorhexidine, cisplatin

Question 365

what tumors can you see in the ear canal and middle ear?

Answer 365

ceruminous glad adenocarcinoma, SCC, fibrosarcoma, osteosarcoma, chondrosarcoma, lymphoma (cats mainly) - most carry guarded to poor prognosis

Question 366

what infectious diseases have been reported to cause central vestibular disease?

Answer 366

canine distemper virus, FIP, RMSF, ehrlichiosis, cryptococcus, toxoplasma, neospora, rabies, cuterebra

Question 367

what is the most useful antemortem diagnostic for distemper?

Answer 367

PCR of urine or CSF

Question 368

what % of cats with the dry form of FIP have neurologic signs?

Answer 368

1/4 to 1/3

Question 369

what are the most common primary tumors affecting the vestibular components of the CNS in dogs?

Answer 369

meningioma, nerve sheath tumor of trigeminal nerve (affecting brainstem or CN VIII by extension), choroid plexus tumor in the 4th ventricle

Question 370

what are the most common primary tumors affecting the vestibular components of the CNS in cats?

Answer 370

meningioma, lymphoma

Question 371

what is the most common location for CVA in dogs?

Answer 371

cerebellum - in areas supplied by rostral cerebellar artery

Question 372

define a TIA

Answer 372

episode of brief, focal neurologic deficit secondary to embolism, vascular constriction, or spasms that resolve within 24 hours (most resolve within minutes to a few hours)

Question 373

what drug can cause vestibular signs?

Answer 373

metronidazole

Question 374

describe signs of metronidazole toxicity as seen in dogs and cats

Answer 374

dogs: central vestibular signs +/- cerebellar signs (intention tremors, hypermetria), vertical nystagmus, anorexia/vomiting.
cats: forebrain disturbance (seizure, blindness, ataxia)

Question 375

why does metronidazole cause vestibular signs?

Answer 375

interacts with GABA receptors in the cerebellum and vestibular nuclei

Question 376

what vitamin deficiency can lead to vestibular disease?

Answer 376

thiamine (B1)

Question 377

describe signs of thiamine deficiency in cats

Answer 377

vestibular and ocular nuclei are affected: vestibular signs, dilated and unresponsive pupils, ventroflexion of head/neck

Question 378

thiamine deficiency can occur in patients fed what types of diets

Answer 378

high in thiamin’s (raw fish) or canned food subjected to excessive heat, food that uses sulfur dioxide used as a preservative

Question 379

what malformation seen in cavies can cause vestibular disease?

Answer 379

COMS

Question 380

describe post anesthetic vestibular syndrome in cats

Answer 380

most between 3-6 months of age; normal anesthetic recovery; vestibular signs within 2-24 hours after recovery; may have salivation and nausea. recovery takes 48 hours to 10 weeks; most normal within a week

Question 381

disc-associated compression leading to cervical spondylomyelopathy is seen most commonly in what breed? age?

Answer 381

doberman; middle-aged

Question 382

disc-associated compression leading to cervical spondylomyelopathy is caused by what?

Answer 382

intervertebral disc protrusion with or without hypertrophy of the dorsal longitudinal ligament or ligament flavor

Question 383

disc-associated compression leading to cervical spondylomyelopathy most commonly affects which disc spaces?

Answer 383

C5-6 and C6-7

Question 384

osseous compression leading to cervical spondylomyelopathy is most commonly seen in what breed? age?

Answer 384

giant breed (great dane); young adult

Question 385

cervical spondylomyelopathy: describe the gait

Answer 385

gait deficits primary affect pelvic limbs; two engine gait is common; cervical hyperesthesia is not a common finding

Question 386

what is the gold standard for diagnosis of cervical spondylomyelopathy?

Answer 386

MRI

Question 387

discuss the basic pathophysiology of degenerative lumbosacral stenosis

Answer 387

chronic progressive intervertebral disc degeneration, with subsequent protrusion of L7-S1 intervertebral disc into the vetebral canal along with proliferation of the soft tissues surrounding the caudal equina, such as hypertrophy of the interarcuate ligament (ligament flavor), the joint capsule, and epidural fibrosis

Question 388

what is the main clinical sign seen with lumbosacral stenosis?

Answer 388

pain

Question 389

describe the gain of a dog with lumbosacrall stenosis

Answer 389

pelvic limb weakness without proprioceptive ataxia and a stiff gait (note: many will still have proprioceptive deficits in pelvic limbs)

Question 390

surgical treatment of lumbosacral stenosis is less successful in dogs with what clinical signs?

Answer 390

fecal or urinary incontinence

Question 391

degenerative myelopathy affects primarily what area of the spinal cord?

Answer 391

thoracolumbar

Question 392

mutation in what gene has been proposed as being related to development of degenerative myelopathy?

Answer 392

superoxide dismutase 1 (SOD1)

Question 393

describe degenerative myelopathy

Answer 393

a primary central axonopathy restricted to the spinal cord that begins in the thoracic spinal cord and ascends and descends along the cord. axon and myelin degeneration of the cord occurs in all funiculi but primarily in the dorsal aspect of the lateral funiculi and dorsal funiculi

Question 394

clinical signs of degenerative myelopathy are those of a myelopathy localized to what cord segments?

Answer 394

T3 - L3

Question 395

degenerative myelopathy is painful or not painful?

Answer 395

not painful

Question 396

what 2 breeds are the most commonly affected with degenerative myelopathy?

Answer 396

GSD, boxer

Question 397

describe the typical MRI of a patient with degenerative myelopathy

Answer 397

normal

Question 398

how can steroids help in diagnosis of DM?

Answer 398

CCS typically lead to improvement in dogs with chronic compressive myelopathies (i.e. IVDD) but won’t help dogs with degenerative myelopathy

Question 399

what is the best treatment for DM?

Answer 399

physical therapy

Question 400

what is the prognosis for DM?

Answer 400

poor - most dogs euthanized within 6-12 months

Question 401

discuss the difference between Hansen type I and II IVDD

Answer 401

type I: herniation of nucleus pulpous through annular fibers and extrusion of nuclear material into spinal canal. Associated with chondroid disc degeneration. Disc extrudes through dorsal annulus. Affects chondrodystrophic breeds, acute onset.
type II: annular protrusion caused by shifting of central nuclear material, associated with fibroid disc degeneration. Annulus fibrosis slowly protrudes into spinal canal. More common in older, on-chondrodystrophic breeds of dog.

Question 402

what are the 2 most common infectious causes of meningomyelitis?

Answer 402

canine distemper virus and protozoa

Question 403

what is the most common non-infectious inflammatory cause of meningomyelitis?

Answer 403

SRMA

Question 404

increased expression of this molecule on polymorphonuclear cells appears to be an important factor in the pathogenesis of SRMA

Answer 404

CD11a

Question 405

describe the CSF of a patient with SRMA

Answer 405

marked neutrophilic pleocytosis (non-degenerative) and protein elevation

Question 406

elevated IgA in serum and CSF for a diagnosis of SRMA has a sensitivity of XX and specificity of XX

Answer 406

91%, 78%

Question 407

what is the major canine acute phase protein?

Answer 407

CRP

Question 408

what is the #1 most common agent associated with canine discospondylitis?

Answer 408

staphylococcus (pseudintermedius or aureus - coagulase-positive)

Question 409

what 6 infectious agents are the most commonly associated with canine discospondylitis?

Answer 409

staphylococcus, streptococcus, e coli, actinomycetes, brucella canis, aspergillus

Question 410

young female german shepherd are predisposed to discospondylitis due to what infectious agent?

Answer 410

aspergillus

Question 411

basset hounds contract discospondylitis due to what infectious agent most commonly?

Answer 411

systemic tuberculosis

Question 412

what sites are the most commonly affected with discospondylitis?

Answer 412

L7-S1, caudal cervical, mid-thoracic, and thoracolumbar spine

Question 413

what are good empiric antibiotics for discospondylitis?

Answer 413

clavamox, cephalexin

Question 414

what peripheral nerves arise in the ventral horn of the spinal cord, and exit via the ventral root?

Answer 414

motor and sympathetic

Question 415

what peripheral nerves arise in the dorsal root ganglion, adjacent to the spinal cord, and enter the cord via the dorsal root?

Answer 415

sensory fibers

Question 416

autonomic dysfunction leads to what clinical signs?

Answer 416

vomiting, regurgitation, diarrhea, ileus, urinary retention, incontinence, impaired lacrimation and salivation, pupillary dysfunction

Question 417

in diabetic neuropathy, which predominates - axonal changes or demyelination?

Answer 417

demyelination

Question 418

thyroid hormone deficiency leads to axonal damage or demyelination?

Answer 418

both

Question 419

what is the most common cranial nerve neoplasm?

Answer 419

trigeminal nerve sheath tumor

Question 420

describe c/s on neospora in an adult dog

Answer 420

paresis of 1+ limbs, muscle atrophy, reduced muscle tone, muscle pain, postural reaction deficits, reduced/absent segmental spinal reflexes, head tilt, dysphagia, tongue paresis

Question 421

what is the classical presentation of neospora in puppies?

Answer 421

paraparesis, which leads to a non-ambulatory state characterized by rigid extension of the pelvic limbs associated with muscle contractors

Question 422

how are puppies infected with neospora?

Answer 422

transplacentally

Question 423

ingestion of raw meat is a risk factor for toxoplasma or neospora?

Answer 423

both

Question 424

treatment of choice for toxoplasma?

Answer 424

clindamycin&raquo_space; suflonamides, pyrimethamine, doxy, minocycline

Question 425

treatment of choice for neospora?

Answer 425

clindamycin or potentiated sulfonamides, with or without pyrimethamine

Question 426

can acute polyradiculoneuritis lead to respiratory musculature failure?

Answer 426

yes

Question 427

describe c/s of acute polyradiculoneuritis

Answer 427

acute, ascending, flaccid tetra paresis. usually starts in pelvic limbs. can progress to involve cranial nerves and respiratory musculature. segmental spinal reflexes reduced to absent. intact sensation +/- hyperesthesia

Question 428

where is the inflammation in acute polyradiculoneuritis?

Answer 428

peripheral nerves and ventral nerve roots

Question 429

antibodies to XXX have been found in some dogs with acute polyradiculoneuritis

Answer 429

anti-GM2 ganglioside antibodies

Question 430

what diagnostic can differentiate acute polyradiculoneuritis fro tick paralysis, botulism, elapid envenomation, and fulminant MG?

Answer 430

electrophysiologic testing:

EMG - spontaneous activity seen

Question 431

what is the treatment for acute polyradiculoneuritis?

Answer 431

supportive care. NOT steroids.

Question 432

describe the distribution of brachial plexus neuritis

Answer 432

thoracic limbs, bilateral but asymmetric

Question 433

axonal regeneration occurs at a rate of XX per day

Answer 433

1-2 mm

Question 434

what toxins have been associated with peripheral neuropathies?

Answer 434

heavy metal (mercury, thallium, lead),
antibiotics (lasalocid, nitrofurantoin, salinomycin),
pesticides (organophosphates),
organic solvents and chemicals (acrylamide, hexacarbon),
vitamin (pyridoxine - Vitamin B6),
chemotherapy (vincristine, vinblastine, cisplatin)

Question 435

what are the parts of the neuromuscular junction?

Answer 435

presynaptic motor nerve terminal
synaptic cleft
post-synaptic muscle end plate

Question 436

what neurotransmitter(s) are used in neuromuscular junctions?

Answer 436

acetylcholine

Question 437

what is the safety factor of neuromuscular transmission?

Answer 437

the muscle membrane potentials produced by nerve depolarization greatly exceed what is required for muscle fiber contraction

Question 438

tick paralysis is a presynaptic or postsynaptic condition?

Answer 438

presynaptic

Question 439

what ticks are associated with tick paralysis?

Answer 439

dermacentor (N America), ixodes (australia)

Question 440

what is the pathophysiology of tick paralysis?

Answer 440

neurotoxin from female tick salivary gland interferes with ACh release from pre-synpatic nerve terminal via a calcium-mediated mechanism

Question 441

what is the treatment for tick paralysis?

Answer 441

remove the tick

Question 442

what are the symptoms of tick paralysis?

Answer 442

acute, rapidly progressive, ascending flaccid paresis/tetraplegia; diminished/absent spinal reflexes, decreased muscle tone. cranial nerve defects uncommon, but may have mild facial and masticatory muscle weakness and dysphonia; respiratory paralysis is possible

Question 443

what is different about australian tick paralysis than north american?

Answer 443

cats affected as well as dogs (US - just dogs). autonomic dysfunction, urinary dysfunction, CHF d/t diastolic dysfunction. pupillary dilation. pulmonary edema, aspiration pneumonia, progressive hypoventilation. cranial nerve deficits, horner’s. may decline for days after tick removal.

Question 444

in australian tick paralysis, what two medications can be used to treat autonomic signs?

Answer 444

phenoxybenzamine and acepromazine

Question 445

what type of bacteria is clostridium botulinum?

Answer 445

gram positive anaerobe

Question 446

where is clostridium botulinum found?

Answer 446

ubiquitous in soil, water, GI tracts of mammals and fish

Question 447

how do most pets develop botulism?

Answer 447

ingest pre-formed botulinum neurotoxin in spoiled or uncooked meat; the toxin may rarely be produced in vivo after liver or GI infection (AKA toxico-infection)

Question 448

what is toxico-infection as it relates to botulinum?

Answer 448

animals getting botulism by toxin being produced in vivo after liver or GI infection

Question 449

what is the most common botulinum toxin in dogs?

Answer 449

botulinum neurotoxin type C (BoNT-C)

Question 450

what is the pathophysiology of botulism?

Answer 450

botulism toxin blocks release of ACh at pre-synaptic terminal of skeletal muscle and cholinergic autonomic synapsis by irreversible enzymatic cleavage of Soluble N-ethylmaleimide-sensitive factor activating protein receptor (SNARE) proteins, which are needed for docking synaptic ACh vesicles to pre-synaptic membranes.

Question 451

botulism is a pre- or post-synaptic disease?

Answer 451

presynaptic

Question 452

what are the symptoms of botulism?

Answer 452

progressive acute tetra paresis accompanied by autonomic signs (ileus, tachy- or bradycardia, mydriasis, urianry retention) +/- cranial nerve deficits (decreased palpebral reflex, megaesophagus, diminished PLR)

Question 453

how do you diagnose botulism?

Answer 453

demonstrate BoNT in feces, blood, stomach contents, food source; gold standard - mouse inoculation test

Question 454

what is the treatment for botulism?

Answer 454

supportive. antibiotics only if toxico-infection is a possibility

Question 455

what antibiotics should you avoid in botulism? why?

Answer 455

aminoglycosides, ampicillin - may potentiate neuromuscular blockade

Question 456

is antitoxin helpful for botulism?

Answer 456

most products don’t contain antibodies against BoNT-C = not useful for dogs. antitoxins can’t bind toxin after it’s entered nerve terminals, but can bind circulating toxin

Question 457

what are the elapid snakes?

Answer 457

eastern (micrurus fulvius) and Texas (Micrurus tener) coral snakes; tiger (Notechis scutatus), brown (Pseudonaja), and red-bellied black snakes (pseudechis porphyriacus) in Australia; cobra, krait, mamba

Question 458

elapid snake envenomation is pre- or post-synaptic?

Answer 458

either: can bind to AChR on postsynaptic membrane or cause pre-synpatic inhibition of ACh release (depends on the snake)

Question 459

describe c/s of elapid snake envenomation

Answer 459

flaccid tetraparesis/plegia, hypotonia, reduced/absent segmental spinal reflexes, hypoventilation; cranial nerves commonly affected (ptyalism, dysphagia, dysphonia, facial paresis); hemoglobinuria, myoglobinuria (these set the snake bite apart from other NMJ/peripheral nerve disease!); vomiting, hypotension, depression, hypothermia, bleeding coagulopathy, ventricular arrhythmia

Question 460

treatment for elapid snake envenomation?

Answer 460

supportive, antivenin

Question 461

acquired MG is an autoimmune disorder characterized by production of autoantibodies against ___

Answer 461

nicotinic AChR on the post-synaptic muscle terminal

Question 462

what is the age distribution of acquired MG?

Answer 462

bimodal: <4 or >9 years of age

Question 463

what c/s are associated with acquired generalized MG?

Answer 463

choppy, stilted gait after exercise. pelvic limbs, then thoracic limbs. fatiguable palpebral reflex. Segmental spinal reflexes normal. pharyngeal/laryngeal dysfunction - ptyalism, dysphonia. megaesophagus, regurgitation. Cervical ventroflexion d/t weakness (cat > dog)

Question 464

what c/s are associated with fulminant MG?

Answer 464

severe diffuse weakness that doesn’t improve with rest, non ambulatory tetra paresis, lateral recumbency, spinal reflexes normal to decreased, regurgitation, aspiration pneumonia, respiratory muscle weakness, urine retention

Question 465

what cancer has been associated with fulminant MG?

Answer 465

thymoma

Question 466

what muscles are most commonly involved in focal MG?

Answer 466

ocular, facial, esophageal, pharyngeal, laryngeal

Question 467

what endocrine diseases have been associated with MG?

Answer 467

hypothyroidism, hypoadrenocorticism, methimazole treatment for hyperthyroidism

Question 468

what non-endocrine diseases have been associated with MG?

Answer 468

thymoma, polymyositis, masticatory myositis

Question 469

what is the gold standard for diagnosis of acquired MG?

Answer 469

anti-AChR autoantibodies in serum (note: species-specific assay)

Question 470

what age does congenital MG show up at?

Answer 470

6-9 weeks of age

Question 471

why are Gammel Dansk Honsehund (GDH) dogs different when it comes to congenital MG?

Answer 471

disease begins at 4 months of age (older than usual) and is unresponsive to AChE-blocking drugs - thought to have presynaptic defect in neuromuscular transmission. remain stable with mild c/s.

Question 472

how do you diagnose congenital MG?

Answer 472

quantification of AChR in muscle biopsy

Question 473

why are miniature dachshunds different when it comes to congenital MG?

Answer 473

spontaneously resolve by 6 months of age

Question 474

what is the protein dynamin 1 (DNM1) important for?

Answer 474

group of enzymes that maintain synaptic vesicle formation during sustained neurotransmission (such as periods of intense physical activity. DNM1 is expressed at synaptic terminal membranes w/in CNS and is important in recycling synaptic vesicles during high-frequency neurological stimulation.

Question 475

what infectious disease causes cerebellar hypoplasia?

Answer 475

feline panleukopenia virus

Question 476

what is the most common diffuse cerebellar disorder in cats?

Answer 476

feline panleukopenia virus

Question 477

what symptoms do you get if a kitten is infected with feline panleukopenia before the last 3 weeks of gestation? in the last 3 weeks of gestation? first 3 weeks of life?

Answer 477

earlier than last 3 weeks: hydranencephaly
last 3 weeks: cerebellar hypoplasia
first 3 weeks of life: cerebellar hypoplasia

Question 478

what should you note about vaccinating a pregnant cat for feline panleukopenia virus?

Answer 478

vaccination with a modified live FPV vaccine during pregnancy can result in clinically ffected kittens

Question 479

what is feline spongiform encephalopathy? how do cats contract it?

Answer 479

prion-induced disease; contracted by eating BSE-contaminated food

Question 480

what are the symptoms of feline spongiform encephalopathy?

Answer 480

chronic progressive symptoms - abnormal behaviors ataxia, muscle tremors, hypersalivation, dilated and unresponsive pupils, hyperesthesia

Question 481

what is the most common infectious CNS disease in cats?

Answer 481

FIP

Question 482

what are the most common symptoms seen in CNS FIP?

Answer 482

altered mental status, menace response deficits, vestibular syndrome, seizures, ataxia, paresis

Question 483

what is the most common cause of myelopathy in cats younger than 2 years of age?

Answer 483

FIP

Question 484

what type of neurologic disease is FeLV associated with?

Answer 484

chronic degenerative myelopathy

Question 485

what c/s are seen with FIV in the CNS?

Answer 485

abnormal behavior, facial twitching, ataxia, seizures, sleep disorders, intention tremors

Question 486

what type of virus is feline borna disease virus?

Answer 486

negative-stranded RNA virus

Question 487

what are the reservoirs of feline borna disease virus?

Answer 487

birds and rodents

Question 488

what are the c/s of feline borna disease virus?

Answer 488

ataxia, postural reaction deficits, abnormal behavior, absent/decreaesd menace

Question 489

how do you diagnose feline borna disease virus?

Answer 489

serum titers and RT-PCR in serum and CSF are supportive

Question 490

what is gurltia paralysans?

Answer 490

neurotropic metastrongylid nematode of domestic cats in south america

Question 491

what are the c/s of gurltia paralysans?

Answer 491

pelvic limb proprioceptive ataxia, paraparesis, paraplegia, LS hyperesthesia, fecal or urinary incontinence, tail paralysis

Question 492

how do you diagnose gurltia paralysans?

Answer 492

histopathology via detection of adult G. paralysans in the spinal cord

Question 493

treatment for gurltia paralysans?

Answer 493

no treatment

Question 494

what is feline hippocampal necrosis?

Answer 494

seizure disorder characterized by epileptic events and interictal abnormal behavior

Question 495

treatment for feline hippocampal necrosis/

Answer 495

anti epileptic medications. immunosuppressives sometimes recommended

Question 496

what is feline orofacial pain syndrome? what breed is it common in?

Answer 496

a pain disorder characterized by acute behavioral signs of oral discomfort +/- tongue mutilation.
most common in Burmese