Neurology Flashcards
supposed to be under ettinger notes (496 cards)
1
Q
define “resting membrane potential”
A
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.
2
Q
what pump is most responsible for formation of the resting membrane potential?
A
Na/K ATPase
3
Q
what is equilibrium potential?
A
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+)
4
Q
what is the resting membrane potential for neurons?
A
-65 mV
5
Q
what is a channelopathy? give an example in cats and an example in dogs
A
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
6
Q
what is the threshold for voltage-gated Na channels to open, beginning the action potential?
A
-55 mV
7
Q
how does phenytoin prevent seizures?
A
enhance inactivation of sodium channels, making it less likely that an action potential will be propagated
8
Q
how do pyrethrins increase tremors and seizures?
A
block sodium channel inactivation, increasing action potential generation
9
Q
what two factors influence the speed at which the action potential travels down an axon?
A
axonal diameter and myelin
10
Q
what is the name for an unmyelinated area on a nerve? how do ions flow in these areas?
A
node of ranvier. ions flow in a saltatory fashion.
11
Q
how does polyradiculoneuritis cause weakness?
A
demyelination increases capacitance of axonal membrane, slowing the conduction velocity and potentially blocking propagation of action potential
12
Q
describe the basic process of neurotransmitter release
A
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
13
Q
how does botulism toxin cause weakness?
A
binds to one of the vesicle docking proteins, preventing release of acetylcholine at the neuromuscular junction
14
Q
what are the two receptor types at the post-synaptic cell?
A
ionotropic: regulate ion channels. Metabotropic: act through second messengers.
15
Q
what are the three families of ionotropic receptors?
A
1) nicotinic ACh, GABA, and glycine; 2) glutamate; 3) ATP or purine P2X receptors
16
Q
is ACh excitatory or inhibitory? explain.
A
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.
17
Q
What is the function of acetylcholinesterase?
A
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
18
Q
How does myasthenia gravis cause weakness?
A
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.
19
Q
what is the mechanism behind the treatment for myasthenia gravis?
A
acetylcholinesterase inhibitors prolong the interaction of ACh with the receptor and reverse c/s
20
Q
Is GABA excitatory or inhibitory? explain.
A
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.
21
Q
how does phenobarbital stop seizures?
A
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
22
Q
how does diazepam stop seizures?
A
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
23
Q
what is the major excitatory neurotransmitter in the CNS?
A
glutamate
24
Q
discuss the mechanism of glutamate function
A
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)
25
List the metabotropic receptors
muscarinic acethylcholine receptors, metabotropic glutamate receptors, GABA-B receptors, serotonin receptors, receptors for norepinephrine, epinephrine, histamine, dopamine, neuropeptides, and endocannabinoids
26
how do metabotropic receptors work?
through second messenger systems such as G-proteins; because of this, they produce a longer influence on function
27
contrast what happens when ACh binds to an M2 versus M1 muscarinic ACh receptor
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.
28
describe long-term depression
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.
29
What dog breed has a mutation in the mGluR1 gene? what does this cause?
Coton de Tulear. they have impaired motor learning and severe cerebellar ataxia.
30
discuss dopamine and adenosine's actions on cAMP
stimulating D2 dopamine receptor decreases cAMP and increases arousal. stimulating adenosine receptor increases cAMP and decreases arousal.
31
how does fluoxetine work/
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.
32
describe the role of kinesins and dyneins
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)
33
explain the difference between temporal and spacial summation
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
34
what is an interneuron?
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
35
what is a renshaw cell and what does it do?
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
36
how does tetanus toxin cause tetany?
it blocks glycine release (from renshaw cells), resulting in excessive excitation of the motor neurons
37
what is lateral inhibition?
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
38
what is the reticular activating system?
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.
39
crossed extensor reflex: what is it, and when do you see it?
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
40
recumbency can be associated with disease in which three areas? what sets each apart?
brainstem, cervical spinal cord, diffuse neuromuscular disease. brainstem is the only that affects sensorium.
41
alteration in sensorium is due to disease where?
ascending reticular activating system (ARAS) and/or limbic system components of the cerebrum or rostral brainstem (diencephalon)
42
describe decerebrate rigidity
opisthotonus with rigid extension of the neck and all four limbs; associated with midbrain or rostral cerebellar lesions
43
describe decerebellate rigidity
from severe cerebellar lesions; characterized by opisthotonus with extensor rigidity of the limbs, but hips flexed
44
describe pleurothotonus
deviation fo the head and neck to one side; may be present with mid to rostral brainstem or cerebral lesions
45
what are the two key UMN pathways that function in gait generation?
reticulospinal and rubrospinal
46
what are the two main general propioceptive pathways?
spinocerebellar and conscious proprioceptive
47
what is the modified frankel score?
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
48
unilateral pros encephalic lesions result in ipsi or contralateral postural reaction deficits? menace? sensory deficits?
contralateral for all
49
unilateral brainstem lesions cause ipsi or contralateral postural reaction deficits?
ipsi
50
unilateral spinal cord lesions cause ipsi or contralateral postural reaction deficits?
ipsi
51
what are the parts of the LMN unit?
cell body, nerve root, peripheral nerve, NMJ, muscle
52
the patellar reflex test is mediated by what nerve? what spinal cord segments?
femoral nerve, L4-L7
53
the biceps reflex is mediated by what nerve? what spinal cord segments?
musculocutaneous nerve; C6-C8
54
the triceps reflex is mediated by what nerve? what spinal cord segments?
radial nerve; C7-T2
55
the forelimb withdrawal involves which nerves? which spinal cord segments?
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
56
the pelvic withdrawal involves which nerves? which spinal cord segments?
sciatic nerve; L6-S1
57
dogs with sciatic nerve paralysis can still support weight if which nerve is intact?
femoral
58
discuss the sensory innervation of the pelvic paw
peroneal nerve - dorsal surface; tibial nerve - plantar surface; saphenous (branch of femoral, L4-6) - medial
59
what happens if the medial surface of the paw is stimulated in a pet with a pure sciatic injury?
animal will flex the hip because of intact innervation of the iliopsoas muscle, but stifle, tarsus, and digits will not flex
60
the perineal reflex is mediated by what nerve?
branches of the sacral and caudal segments of the spinal cord through the pudendal nerve
61
discuss the pathway for noxious stimuli
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
62
cranial nerve I: name and function
olfactory. smell
63
cranial nerve II: name and function
optic. vision and response to light
64
cranial nerve III: name and function
oculomotor. motor to extra ocular muscles; parasympathetic to pupil
65
cranial nerve IV: name and function
trochlear. motor to dorsal oblique muscle
66
cranial nerve V: name and function
trigeminal. motor to muscles of mastication (mandibular), sensory to face (ophthalmic and maxillary)
67
cranial nerve VI: name and function
abducent. motor to lateral rectus and retractor bulbi
68
cranial nerve VII: name and function
facial. motor to muscles of facial expression; parasympathetic to lacrimal glands; sensory (taste) to rostral tongue
69
cranial nerve VIII: name and function
vestibulocochlear. balance, hearing
70
cranial nerve IX: name and function
glossopharyngeal. sensory and motor to pharynx
71
cranial nerve X: name and function
vagus. sensory and motor to pharynx, larynx, and viscera
72
cranial nerve XI: name and function
accessory. motor to trapezius
73
cranial nerve XII: name and function
hypoglossal. motor to tongue muscles
74
menace response: pathway? anything notable? Tests ipsi or contralateral?
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)
75
indirect PLR occurs because optic nerve fibers cross where?
optic chasm and pretectal nucleus
76
PLR tests what cranial nerves?
optic nerve and oculomotor nerve
77
what are the potential causes of ptosis?
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.
78
ventrolateral strabismus is associated with dysfunction of what?
oculomotor nerve
79
medial strabismus is associated with dysfunction of what?
abducent nerve
80
eyeball extorsion (outward rotation) is seen with dysfunction of what?
trochlear nerve
81
describe the pathway for physiologic nystagmus
cranial nerve VIII -> brainstem -> vestibular nuclei -> medial longitudinal fascicles -> abducent and oculomotor neurons (for abduction and adduction of the eyeball, respectively)
82
a positional, ventrolateral strabismus is associated with what?
vestibular disease
83
palpebral reflex tests what nerves?
sensory branches (ophthalmic - medial, maxillary - lateral) of trigeminal nerve; facial nerve
84
what would you see on a physical exam with unilateral versus bilateral mandibular nerve dysfunction?
uni/bi: muscle atrophy of temporals and masseter muscles. bi: dropped jaw, excessive drool
85
nasal hypalgesia indicates a problem where?
ipsilateral trigeminal nerve (ophthalmic branch) OR contralateral prosencephalic lesion (via nociceptive pathways that project to contralateral thalamus and somesthetic cerebral cortex)
86
the gag reflex tests which CN?
glossopharyngeal, vagus, hypoglossal
87
dysphagia can be seen with dysfunction of what CN?
IX and X
88
what are the two parts of the prosencephalon?
cerebrum, thalamus
89
what are the three parts of the brainstem?
midbrain, medulla oblongata, pons
90
the thalamus belongs to which neuroanatomic region?
prosencephalon
91
midbrain belongs to which neuroanatomic region?
brainstem
92
medulla belongs to which neuroanatomic region?
brainstem
93
pons belongs to which neuroanatomic region?
brainstem
94
what type of circling do you see with disease in the prosencephalon?
wide, ipsilateral
95
prosencephalic disease: postural reaction deficits or ipsi or contralateral?
contralateral
96
prosencephalic disease: describe spinal reflex deficits
normal (no deficit)
97
prosencephalic disease: cutaneous sensation deficit
contralateral (often facial/nasal) hypalgesia
98
prosencephalic disease: menace deficits are contra or ipsi?
contralateral
99
prosencephalic disease: PLRs or normal or abnormal? ipsi or contra?
normal if optic radiation or occipital cortex; abnormal if optic chasm, optic tracts; if abnormal, contralateral
100
prosencephalic disease: what changes might you see/hear about that aren't part of the typical neuro exam?
abnormalities in thirst, appetite, thermoregulation, electrolyte and water balance, sleep patterns
101
brainstem disease: discuss posture/gait
UMN tetra paresis/plegia and proprioceptive deficits; vestibular ataxia with pontine or medullary lesions; opisthotonus with midbrain lesions
102
brainstem disease: postural reaction deficits are ipsi or contralateral?
ipsi if pons and medulla (caudal brainstem); contralateral of rostral midbrain (i think this is very rare - check with AT's notes)
103
brainstem disease: what cranial nerves could be affected?
3-12
104
what are the two parts of the prosencephalon? what is included in each of these?
telencephalon (cerebral hemispheres), diencephalon (epithalamus, thalamus, hypothalamus)
105
the gait is normal or abnormal with procencephalon disease? why?
normal - the UMNs responsible for gait generation are located in midbrain, pons, and medulla
106
describe adverse syndrome
AKA semi-neglect; pet ignores all sensory input perceived from its environment that is CONTRAlateral to prosencephalic lesion
107
central vestibular disease: postural reactions are contra or ipsilateral?
ipsilateral
108
vestibular disease: head tilt is contra or ipsilateral?
ipsilateral (toward lesion)
109
where do lesions have to be to get a paradoxical head tilt? is it ipsi or contralateral?
caudal cerebellar peduncle or flocculonodular lobules of cerebellum; contralateral
110
with vestibular disease, is nystagmus towards or away from lesion?
peripheral vestibular disease - FAST phase is AWAY from lesion. central disease - unreliable (either way or changing)
111
facial nerve disorder is seen with peripheral or central vestibular disease?
both
112
describe Horner's syndrome as seen with a brainstem lesion
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
113
describe sensorium with peripheral and central vestibular lesions
unaffected with peripheral; dull to comatose with central if ARAS is affected
114
discuss the rebound phenomenon
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
115
cerebellar disease: head tilt is ipsi or contra?
head tilt away from lesion (paradoxical)
116
cerebellar disease: menace deficit is ipsilateral or contralateral?
ipsilateral (bilateral if diffuse disease)
117
cerebellar disease: postural reaction deficits are ipsi or contralateral?
ipsilateral
118
what pupillary change can you see with cerebellar disease?
anisocoria
119
Horner's disease is seen with lesions in what spinal cord segments?
C1-C5 (UMN) (ipsilateral), T1-T3 (ipsilateral)
120
LMN cell bodies for the limbs are located where?
ventral grey matter of the cervicothoracic (C6-T2) and lumbosacral (L4-S3) intumescences
121
ascending and descending pathways compose which area of the spinal cord?
white matter (more superficial than the LMN cell bodies in the grey matter)
122
the classic 2-engine gait is seen with lesions where?
C6-T2 (short and choppy FL, long strided HL)
123
discuss schiff-sherrington syndrom
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.
124
discuss spinal shock
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).
125
T3-L3 lesions that produce LMN signs in pelvic limbs WITHOUT schiff-sherrington syndrome is most commonly seen with which disease?
fibrocartilaginous embolic myelopathy (FCEM)
126
what are the differentials for a diffuse CNS localization?
dysmyelinogenesis, diffuse meningitis (idiopathic tremor syndrome, disseminated granulomatous meningoencephalomyelitis, infectious meningitis) and toxicoses (molds, algae, ethylene glycol)
127
describe cushing's reflex
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
128
what are the three places the brain tissue can herniate?
falx cerebri (lateral) or tentorium (caudal) or through the foramen magnum
129
what are the three types of brain edema?
cytotoxic, vasogenic, interstitial
130
discuss cytotoxic brain edema
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
131
discuss vasogenic brain edema
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.
132
describe interstitial edema
accompanies obstructive hydrocephalus, causing compartmentalized CSF to cross ependymal linings and creating extracellular periventricular interstitial brain edema
133
how do you treat cytotoxic, interstitial, and vasogenic edema?
cytotoxic and interstitial edemas - treat underlying cause; vasogenic - osmotic and corticosteroid therapy
134
what makes up the BBB?
endothelial cells, basement membranes, neighboring perivascular pericytes, glial cells (astrocytes, microglia) and neurons
135
in T1 weighted MRI, fat is bright or dark? water is bright or dark?
bright fat. dark water
136
in T2 weighted MRI, fat is bright or dark? water is bright or dark?
bright water. dark fat. edema is apparent as increased signal.
137
what is the purpose of the FLAIR MRI sequence?
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
138
what is the purpose of the STIR MRI sequence?
short-tau inversion recovery: allow for fat suppression
139
what is the purpose of the T2* MRI sequence?
gradient echo (GRE) T2W: detect artifact from blood products that are formed in hemorrhage
140
what is the purpose of the DWI MRI sequence?
diffusion weighted imaging: can aid in ID'ing issues like cytotoxic edema associated with ischemic infarction
141
discuss hypo- and dysmyelinogenesis
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
142
what clinical signs do you see with leukodystrophy?
general proprioceptive ataxia and upper motor neuron paraparesis, which progress to tetra paresis +/- signs of cerebellar involvement and seizures
143
what are the histopathologic changes seen in leukodystrophy?
myelin degeneration w/o producing vacuolation, that is replaced by severe astrogliosis or Rosenthal fibers (astrocytic processes); widespread throughout brain and spinal cord
144
describe myelinolysis
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.
145
compare and contrast myelinolysis in the afghan hound and dutch kooiker
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
146
what is spongy degeneration?
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)
147
what symptoms may you see in spongiform leukoencephalomyelopathy?
cerebellar ataxia, seizures, opisthotonus; c/s occurs w/in 1-9 mo's of age, progressive
148
describe central axonopathy
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
149
what are the c/s of central axonopathy?
general proprioceptive or cerebellar ataxia and UMN paresis
150
what is the treatment for neurodegenerative disease?
currently there is none
151
describe neonatal encephalopathy with seizures (NEWS)
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)
152
what is subacute necrotizing encephalopathy? what c/s does it cause?
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
153
what c/s do you see in mitochondria encephalopathy in alaskan husky puppies?
acute proprioceptive ataxia, seizures, behavior changes, central blindness, tetra paresis, facial sensation deficits
154
what is the purpose of cellular malonic acid?
regulate use of carbohydrates or fatty acids as energy in fed versus fasted states, respectively
155
cobalamin is a necessary cofactor in the conversion of what to what?
methylmalonyl CoA to succinyl CoA (part of the kreb's cycle)
156
what is imerslund-grasbeck syndrome?
selective cobalamin malabsorption
157
what symptoms might you see with cobalamin malabsorption syndrome?
altered mentation, inappetence, seizures associated with hyperammonemia and blood dyscrasias; these resolve with cyanocobalamin supplementation
158
how do you diagnose cobalamin malabsorption syndrome?
high urinary methylmalonic acid and low serum cobalamin
159
cobalamin deficiency with elevated urine MMA and neurologic signs in cats is due to what?
deficiency of intrinsic factor (which is necessary for absorption of cyanocobalamin), GI disease
160
why do cats with GI disease develop D-lactic acidosis?
excessive bacterial production of the D isoform in intestines
161
what is the difference between the D and L isoforms of lactate?
D isn't detected by most routine lactate assays, but is more likely to produce encephalopathy
162
what is lysosomal storage disease?
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.
163
what substrates are found within lysosomes that help in catabolism?
sphingolipids (a component of myelin), oligosaccharides, mucopolysaccharides, glycoproteins, proteins
164
what c/s do you commonly see with lysosomal storage diseases?
cerebellar signs of dysmetria, truncal ataxia, nystagmus at first, progressing to UMN weakness, behavioral abnormalities, seizures
165
if you suspect a lysosomal storage disease, what are some diagnostic options?
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
166
what is a neuronal ceroid lipofuscinosis? what is another name for it?
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.
167
what c/s might you see with a neuronal ceroid lipofuscinosis?
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)
168
what options do you have for diagnosis of neuronal ceroid lipofuscinosis?
cross-sectional imaging shows generalized brain atrophy, but definitive diagnosis requires recognition of auto fluorescent material in the brain or other tissues. DNA testing.
169
treatment for neuronal ceroid lipofuscinosis?
none. symptomatic therapy for seizures and behavior changes.
170
intra-axial tumors come from what types of cells? give tumor examples.
neuroepithelial cells. astrocytoma, oligodendroglioma, gliomatosis cerebri, medulloblastoma/primitive neuroectodermal tumor (PNET), ependymoma, choroid plexus tumor
171
astrocytoma comes from what type of cell? intra- or extra- axial?
neuroepithelial, intra-axial
172
oligodendroglioma comes from what type of cell? intra- or extra- axial?
neuroepithelial, intra-axial
173
gliomatosis cerebri comes from what type of cell? intra- or extra- axial?
neuroepithelial, intra-axial
174
medulloblastoma / primitive neuroectodermal tumors come from what type of cell? intra- or extra- axial?
neuroepithelial, intra-axial
175
ependymoma comes from what type of cell? intra- or extra- axial?
neuroepithelial, intra-axial
176
choroid plexus tumor comes from what type of cell? intra- or extra- axial?
neuroepithelial, intra-axial
177
extra-axial tumors come from what cells? list tumor examples
meninges: meningioma, granuloma cell tumor
178
meningioma is intra- or extra-axial?
extra-axial
179
what is the most common primary brain tumor in dogs?
meningiomas (50% of primary brain tumors)
180
what is the second most common primary brain tumor in dogs?
gliomas (30-40% of primary brain tumors)
181
what is the most common primary brain tumor in cats?
meningiomas (60%)
182
what is the second most common primary brain tumor in cats?
gliomas
183
what primary brain tumors have a potential for extraneural spread?
meningioma, PNET, malignant glioma, histolytic tumor, choroid plexus tumor
184
where do meningiomas metastasize to? how common is this?
lung, pancreas - rare
185
rank in order of median age for development in dogs: glioma (astrocytoma, oligodendroglioma), meningioma, choroid plexus tumor
choroid plexus tumor (5-6y), glioma (8y), meningioma (10-14y)
186
what breeds have increased risk of primary intracranial neoplasia?
boxer, boston terrier, golden retriever, french bulldog, rat terrier
187
over expression of this growth factor is common in primary brain tumors in dogs
VEGF
188
young cats with this storage disease have a high incidence of meningioma
mucopolysaccharidosis type I
189
in terms of signalment of those developing primary brain tumors, how are dogs and cats different
cats are older, whereas dogs can be younger
190
in cats with meningiomas, are males or females more commonly affected?
males
191
what tumor location is most likely to press to the brain by direct extension?
nasal tumors (through cribriform plate)
192
what tumor types can invade the brain by direct extension?
otic SCC, pituitary tumor, calvarial tumor (osteochondrosacoma, chondrosarcoma, multilobular osteochondrosarcoma), nerve sheath tumor (CN V tumor)
193
secondary neoplasia accounts for X% of all canine intracranial tumors
50%
194
what is the most common tumor to metastasize to the brain in dogs?
hemangiosarcoma
195
metastases most commonly affect what part of the brain?
cerebrum
196
secondary neoplasia accounts for X% of all feline intracranial tumors
22%
197
what is the most common tumor to metastasize to the brain in cats?
lymphoma (renal, in particular) and pituitary tumors
198
what is the most common c/s associated with a brain tumor in dogs? cats?
seizures in dogs; altered mentation in cats
199
what is the difference between intra- and extra-axial brain tumors?
extra-axial arise from outside the brain (meninges, calvaria, ventricles). intra-axial arise from within the brain parenchyma
200
a tumor that has come to the brain via hematogenous spread is usually located where?
at the gray-white matter interface
201
what CSF finding is typical for an intracranial neoplasm?
albuminocytologic disassociation: increased protein concentrations and a normal to mild increase in total nucleated cell count
202
what tumor type is associated with the most marked elevation in CSF total protein?
choroid plexus tumors
203
discuss prognosis with surgical removal of meningiomas in cats versus dogs
MST dogs 7mo, MST cats 36mo
204
what tumor is most amenable to surgical removal?
meningioma near the brain surface and noninvasive (which is why cats have a better prognosis - less likely to be invasive)
205
what acute adverse effects of radiation can you see with RT of brain tumors?
cerebral edema linked to BBB disturbance, which may result in demyelination and responds to corticosteroids
206
what delayed adverse effects of radiation can you see with RT of brain tumors?
focal CNS radiation necrosis, severe vascular lesions
207
what is the survival time for gliomas after imaging diagnosis?
<80 days
208
supratentorial versus infratendorial tumors: which has a longer MST?
supratentorial has a longer MST
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?
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
210
measurement of anti-epileptic drug concentrations takes place after establishment of a steady-state concentration based on X elimination half-lifes
5
211
a drop of X% or more in the trough serum concentration of anti-epileptic drugs is an indicator of poor administration compliance
20%
212
describe the target and transporter hypotheses for drug-related mechanisms of epilepsy refractory to medicaitons
Target: genetic or disease-related alterations in cellular targets of AEDs. Transporter: postulates altered transport of drugs across the BBB
213
describe metabolic tolerance in terms of refractory epilepsy
increasing the drug dosage does not result in a parallel increase in serum drug concentration
214
what factors are associated with reduction in seizures in epileptic dogs taking AEDs?
female gender, neutering, no history of cluster seizures, older age at onset
215
of epileptic dogs taking AEDDs, what dog breeds are least likely to go into remission or have a >50% in seizure reduction?
border collie, GSD, staffordshire terrier
216
what are the risk factors for euthanasia amongst epileptic dogs?
younger age of onset, high initial seizure frequency, poor seizure control, episodes of status epilepticus
217
define a transient ischemic attack
cerebrovascular accident where c/s resolve within 24 hours
218
what is the most common CVA recognized in dogs?
nonhemorrhagic ischemic infarcts
219
what are the most common sites for ischemic stroke in dogs?
cerebellum, striatocapsular region, thalamus
220
lacunar thalamic/midbrain infarcts are more common in large or small breed dogs?
large
221
why are miniature schnauzers at increased risk of CVAs?
hyperlipidemia
222
what diseases predispose dogs to nonhemorrhagic ischemic stroke/
metabolic disorders (hypothyroidism, pheochromocytoma, hypertension) or hypercoagulopathy (DM, HAC, renal disease, PLN)
223
what diseases predispose dogs to hemorrhagic ischemic stroke?
coagulopathy, hypertension, sepsis, inflammation, metastasis (hemangiosarcoma)
224
what parasite has been reported in dogs with hemorrhagic strokes?
angiostrongylus vasorum
225
discuss feline ischemic encephalopathy
cerebral infarction syndrome; usually involves the middle cerebral artery. some cases have been associated with aberrant migration of Cuterebra larvae.
226
use of what drug in brachycephalic breeds predisposes them to global ischemia?
ketamine
227
use of mouth gags in cats has been associated as a risk factor of developing what?
cerebral ischemia, hearing loss, and blindness. blood flow through maxillary arteries is occluded, which can lead to further vision and hearing loss
228
when does watershed infarction develop?
when cerebral blood flow is lowered below the point of compensation by cerebral auto regulatory mechanisms, causing widespread bilateral brain dysfunction
229
what are the most common c/s seen in CVAs?
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
230
ischemic stroke in dogs most commonly involves what blood vessel? what c/s may this cause?
middle cerebral artery (70%) - signs of sensory hemi-neglect and contralateral motor deficits
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
24 hours
232
how long is the window of opportunity for instituting supportive care therapy after a CVA?
6 hours
233
what is a penumbra?
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.
234
identification of this condition in dogs with non-traumatic intracranial hemorrhage is a poor prognostic indicator
hypertension
235
in dogs with intracranial hemorrhage and multiple lesions >5 mm, this infection was the only concurrent conditional with a good outcome
angiostrongylus vasorum
236
for animals with multifocal/diffuse encephalopathy, what types of diseases should be highest on the differential list?
inflammatory, metabolic, multifocal/metastatic neoplasia, toxins
237
list 4 differentials for degenerative disorders that can cause multifocal/diffuse brain dysfunction
lysosomal storage dz, cognitive dysfunction syndrome, leukodystrophy/spongy degeneration, neuronal vacuolation and spinocerebellar degeneration in Rottweilers and boxers
238
list 6 differentials for anomalous disorders that can cause multifocal/diffuse brain dysfunction
COMS, intracranial arachnoid cyst, congenital hydrocephalus, neuronal migration disorder, atlanto-occipital overlap, dandy-walker syndrome
239
what is dandy-walker syndrome? it has been associated with a mutation in what receptor?
agenesis of the cerebellar vermis and hydrocephalus; mutation in VLDR, encoding the very low density lipoprotein receptor (seen in a eurasier dog)
240
list 8 differentials for metabolic disorders that can cause multifocal/diffuse brain dysfunction
hepatic encephalopathy, hypoglycemia, electrolyte-associated encephalopathy, endocrine (hypothyroidism, hyperthyroidism), renal encephalopathy, kernicterus, mitochondrial encephalopathy, organic acidurias
241
what two vitamin deficiencies can cause multifocal/diffuse brain dysfunction
thiamine; cobalamin (border collies)
242
what three inflammatory/noninfectious diseases can cause multifocal/diffuse brain dysfunction
GME, NME, EME
243
list 9 toxins that can cause multifocal/diffuse brain dysfunction
bromethalin, marijuana, metaldehyde, TCA, brunfelsia, lead, methylxanthine overdose, nicotine, salt intoxication (including paintballs)
244
what types of cells are found in increased numbers in the brain and/or spinal cord in GME?
mononuclear cells: lymphocytes, macrophages, plasma cells
245
what type of immune reaction is GME suspected to be?
delayed-type (T-cell mediated) hypersensitivity
246
In GME, are lesions in the grey or white matter?
white
247
what are the 3 clinical forms of GME?
focal, multifocal/disseminated, ocular
248
what is the typical signalment of a GME patient?
young to middle-aged (median of 5yo) female dogs of small breeds (poodle, terrier)
249
what c/s are most common in GME patients?
seizures, cerebellovestibular dysfunction, cervical hyperesthesia
250
describe the CSF of a GME patient
mononuclear pleocytosis, variable % of neutrophils and elevated protein level
251
list 4 drugs used for treatment of GME
prednisone, procarbazine, cytosine arabinoside, cyclosporine
252
necrotizing encephalitis involves grey or white matter?
both
253
NME lesions are found where?
cerebrum, with consistent meningeal involvement
254
NLE lesions are found where?
brainstem, cerebrum; less consistent involvement of meninges and cerebral cortex than NME (ie mainly white matter)
255
what types of cells are commonly found in necrotizing encephalitis?
necrotic nonsuppurative inflammatory lesions.
256
clinical signs of dysfunction in what neuro localization predominate in dogs with necrotizing encephalitis?
forebrain: seizures, circling, obtunded, head pressing, visual deficits with normal PLR; can also see neck pain
257
in addition to c/s of XX dysfunction and XX, yorkies with NLE often show c/s of XX dysfunction
forebrain, neck pain; brainstem (i.e. central vestibular disease)
258
describe the typical CSF associated with NME and NLE
mononuclear pleocytosis. mononuclear cells in NME are mostly lymphocytes; in NLE are a mixture of lymphocytes and monocytes
259
eosinophilic meningoencephalitis typically has inflammation where?
meninges
260
what does the CSF typically look like in an EME case?
eosinophilic pleocytosis with >10% eosinophils
261
what infectious agents have been reported to cause EME?
cryptococcus neoformans, neospora caninum, baylisascaris procyonis. but note that 70% of cases are idiopathic.
262
EME is more common in small or large breeds?
large
263
greyhound nonsuppurative meningoencephalitis affects dogs of what age?
<12 months
264
there is an association between greyhound meningoencephalitis and XX
dog leukocyte antigen class II haplotype
265
what c/s are seen with greyhound nonsuppurative meningoencephalitis?
forebrain (mentation and behavior changes, blindness) and brainstem (head tilt, circling, ataxia)
266
what areas of the brain are typically affected in greyhound meningoencephalitis?
rostroventral cerebrum, particularly olfactory lobes and bulbs
267
what bacteria are common in bacterial meningoencephalitis?
staph, strep, pasteurella multocida (especially cats), actinomycetes, nocardia, bactericides, peptostreptococcus, fusobacterium, eubacterium, e coli, klebsiella. gram negatives most common.
268
what are the 2 classical clinical features of bacterial meningoencephalitis?
fever and cervical hyperesthesia
269
describe the CSF of an acute bacterial meningoencephalitis
suppurative, often with degenerate and toxic neutrophils. proteins levels elevated. +/- intracellular bacteria
270
what antibiotics are good for treatment of bacterial meningitis?
ampicillin - crosses inflamed BBB. if gram negative infection: enrofloxacin or 3rd generation cephalosporin. if anaerobic: metronidazole
271
name 6 fungal organisms that can invade the CNS
cryptococcus, coccidioides, blastomyces, histoplasma, aspergillus, phaeohyphomycosis (cladosporium)
272
what is the most common fungal organism associated with meningoencephalitis in dogs and cats?
cryptococcus neoformans
273
in cases of cryptococcus, what extra neural areas are most commonly infected?
eyes, nasal and frontal sinuses (head region)
274
in cases of coccidioidomycosis, what extra neural areas are most commonly infected?
pulmonary system
275
compare and contrast the clinical progression of bacterial and fungal meningoencephalitis
bacterial is usually fast and progressive; fungal is usually a slow progression
276
which fungal organism are you most likely to find in CSF
cryptococcus
277
what types of cells do you see in CSF of fungal meningoencephalitis patients?
mix of mononuclear cells and neutrophils; may also see eosinophils
278
testing CSF and/or serum for antibodies is most reliable for which 3 fungal agents?
cryptococcus, coccidioides, blastomyces
279
what anti fungal medication(s) can cross the BBB?
fluconazole, flucytosine (5-fluorocytosine)
280
what is the most common viral brain infection in dogs?
distemper (paramyxovirus)
281
what is the most common viral infection of the brain in cats?
FIP (coronavirus)
282
what is the most common route for viral infection of the brain?
inhalation
283
what viral agents can cause a meningoencephalitis?
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
284
list 4 neurotropic viruses
distemper, rabies, pseudorabies, feline borna disease; these have predilection for neuronal and glial cells
285
myoclonus of one or more limbs and/or muscles of the head is relatively specific for what disease?
canine CNS distemper
286
FIP infection of the CNS is more common with the dry or wet form of the disease?
non effusive form
287
what are the two forms of rabies? which species is most likely to get each?
furious - cats. paralytic - dogs.
288
what is the characteristic histologic pattern in FIP in the brain?
pyogranulomas
289
what is the characteristic histologic pattern of neurologic distemper?
demyelinating brainstem lesions
290
if using antibody titers to diagnose viral neurologic disease, what condition should be met to suggest infection rather than exposure or vaccination?
CSF titers higher than serum titers
291
what is the characteristic CSF of a patient with CNS viral disease?
mononuclear (lymphocytic) pleocytosis with elevated protein EXCEPT FIP - predominant cell is neutrophil, with variable numbers of lymphocytes and macrophages
292
what is the typical clinical progression of a patient with pseudorabies
dead d/t respiratory failure within 48 hours of onset of c/s
293
what two rickettsial diseases can cause encephalopathy in dogs?
RMSF, ehrlichiosis
294
what protozoal organisms can cause encephalopathy/
neospora (dog); toxoplasma (dog, cat)
295
what verminous organism can cause encephalopathy in a cat?
cuterebra
296
what medications are recommended for treatment of protozoal meningoencephalitis?
clindamycin or sulfonamides combined with trimethoprim or pyrimethamine
297
what 3 antibiotics can be used to treat rickettsial meningoencephalitis?
doxycycline, enrofloxacin, chloramphenicol
298
how do you treat cuterebra in cats?
ivermectin; premedicate with diphenhydramine and glucocorticoids. follow with 2 weeks of clavamox
299
describe neuroaxonal dystrophy
primary disorder of axonal transport, characterized by swellings within the axons called "spheroids"
300
what symptoms do togs affected by neuroaxonal dystrophy show?
cerebellar ataxia and tetra paresis
301
what is "multiple systems degenerations"?
when the cerebellum and basal ganglia are involved in a disease process. the basal ganglia (caudate nucleus, substantia nigra) are important in movement
302
what is the primary clinical sign of polymicrogyria?
cortical blindness (seen in standard poodles)
303
cerebellar hypoplasia is seen in cats following in utero or early neonatal infection with what infectious agent?
feline panleukopenia virus; possibly also canine parvovirus
304
in intraventricular obstructive hydrocephalus, where is the blockage of CSF flow through the ventricular system seen?
most commonly - connection between 3rd and 4th ventricle (mesencephalic aqueduct). also seen at connection between lateral ventricle and 3rd ventricle (interventricular foramen)
305
in extraventricular hydrocephalus, where is the obstruction?
subarachnoid space or arachnoid villi; entire ventricular system and subarachnoid space will dilate.
306
what are the c/s and physical features of hydrocephalus?
behavioral changes, ataxia, visual deficits, seizures; enlarged and dome-shaped calabria, persistent cranial sutures and fontanelle, ventrolateral strabismus (congenital hydrocephalus)
307
describe medical treatment for hydrocephalus
anti-epileptics; diuretics (furosemide), carbonic anhydrase inhibitors (acetazolamide); PPI (omeprazole) +/- steroids to decrease CSF production
308
what is chiari-like malformation?
herniation of cerebellar semis and medulla into or through foramen magnum and indention of the cerebellum by the occipital bone
309
what is syringohydromyelia?
formation of fluid-filled cavities within the spinal cord, most commonly in the cervical region
310
what are c/s of syringohydromyelia secondary to chiari-like malformation?
proprioceptive ataxia, postural reaction deficits, neuropathic pain, scratching of ear / neck / shoulder, vocalization, facial rubbing
311
what is cataplexy?
sudden loss of muscle tone
312
what gene is affected in dogs with familial narcolepsy?
hypocretin-receptor-2 (Hcrtr 2)
313
what is the most sensitive and specific diagnostic tool for diagnosing the sporadic form of narcolepsy?
measuring concentration of hypocretin-1 peptide in CSF. note: patients with familial form will have normal levels.
314
what are the c/s of cognitive dysfunction syndrome?
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
315
what is the only drug approved for treating cognitive dysfunction syndrome?
selegiline
316
what are the symptoms of optic neuritis?
acute loss of vision - typically bilateral and associated with mydriatic and unresponsive pupils
317
what are the possible causes for optic neuritis?
infectious (distemper, mycotic, protozoal), immune-mediated (GME) meningoencephalitidies, neoplasms (meningioma, glioma, pituitary tumors)
318
describe the ERG of patients with optic neuritis
normal
319
in dogs where you are considering optic neuritis, what other disease presents similarly?
SARDS
320
what symptoms are associated with dysfunction of cranial nerve I?
inability to smell
321
what symptoms are associated with dysfunction of cranial nerve II?
blindness
322
what symptoms are associated with dysfunction of cranial nerve III?
abnormal eye position, pupil size, or PLR
323
what symptoms are associated with dysfunction of cranial nerve IV?
abnormal eye position
324
what symptoms are associated with dysfunction of cranial nerve V?
rubbing or pawing at face, loss of muscle mass on head, dropped jaw - flaccid inability to close the mouth
325
what symptoms are associated with dysfunction of cranial nerve VI?
abnormal eye position
326
what symptoms are associated with dysfunction of cranial nerve VII?
drooping of ear or cheek, deviation of the nose, drooling; dry eye
327
what symptoms are associated with dysfunction of cranial nerve VIII?
abnormal head position, abnormal eye movements, vertigo; deafness
328
what symptoms are associated with dysfunction of cranial nerve IX?
difficulty eating or swallowing
329
what symptoms are associated with dysfunction of cranial nerve X?
loss of voice, coughing, regurgitating
330
what symptoms are associated with dysfunction of cranial nerve XI?
difficult to appreciate
331
what symptoms are associated with dysfunction of cranial nerve XII?
tongue deviation or paralysis; difficulty eating
332
cavernous sinus and orbital fissure syndromes are defined by clinical dysfunction of what nerves?
2 or more of the following: III, IV, VI, and ophthalmic or maxillary branches of V
333
what c/s are seen with cavernous sinus and orbital fissure syndromes?
external and internal ophthalmoplegia, reduced corneal sensitivity, neurotrophic keratitis, ptosis
334
what is the most common cause of cavernous sinus or orbital fissure syndromes?
neoplasia, although infectious causes have been reported, particularly in cats
335
what is the most common cause of dropped jaw in dogs?
idiopathic trigeminal neuritis
336
what is the treatment for idiopathic trigeminal neuritis?
supportive care with assisted feeding. affected dogs usually recover within 2-4 weeks.
337
what 3 generalized neuropathies / neuromuscular diseases can have facial nerve paralysis?
MG, acute polyradiculoneuritis, tick paralysis
338
the esophagus is innervated by...
vagus and internal branch of the accessory nerves
339
the larynx is innervated by...
branches of the vagus nerve
340
what are the 4 parts of horner's syndrome?
miosis, ptosis, protrusion of the 3rd eyelid, enophthalmos
341
describe the oculosympathetic pathway affected in horner's syndrome
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.
342
describe the test to differentiate between 2nd order and 3rd order lesions (pre and post ganglionic) leading to horners
topical phenylephrine: mydriasis within 20 minutes = post-ganglionic. mydriasis >20 minutes = pre-ganglionic.
343
what are the components of the central vestibular system?
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
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
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
345
head tilt is seen in what type of lesion? head turn is seen in what type of lesion?
vestibular / forebrain
346
small circles are seen with a lesion in what area?
vestibular
347
pendular nystagmus is seen in what breeds?
siamese, himalayan, birman
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
both eyes / toward
349
in vestibular disease, fast phase of nystagmus is towards or away from lesion?
away from the lesion (if central lesion, can be toward lesion)
350
a resting nystagmus rate of >XX beats per minute is XX% specific and XX% sensitives of peripheral vestibular disease
66bpm. 95% specific, 85% sensitive
351
do you see facial nerve involvement with central or peripheral vestibular disease?
both
352
horner's syndrome is more common with central or peripheral vestibular disease?
peripheral
353
paradoxical vestibular syndrome can be seen with lesions where?
flocculonodular lobe of the cerebellum, caudal cerebellar peduncle, rostral and medial vestibular nuclei in the medulla
354
what 2 qualities for nystagmus suggest a central vestibular lesion?
vertical nystagmus or nystagmus with fast phase toward lesion
355
otitis media/interna: what is the most common cause in dogs? in cats?
dogs: extension from otitis external. cats: ascending infection from nasopharynx (via Eustachian tube)
356
most common bacteria seen in otitis interna/media?
staphylococcus, streptococcus, pseudomonas, proteus, malassezia pachydermatis (yeast)
357
how long should you treat with antibiotics for otitis interna/media?
4-6 weeks
358
most common signalment for nasopharyngeal polyps?
young cat (1-5yo)
359
what symptoms can you see with a nasopharyngeal polyp?
signs of middle/inner ear disease, upper respiratory signs (sneeze, stridor), pharyngeal signs (gagging, dysphagia)
360
idiopathic vestibular disease is seen in what age cat? dog?
cats of all ages; old dog
361
idiopathic vestibular disease is more often unilateral or bilateral?
in dogs, unilateral; bilateral is especially seen in cats (still unilateral most common)
362
in a cat in northeastern US/canada in summer and early fall that has developed idiopathic vestibular disease, what is one potential differential?
migration of Cuterebra larvae through ear canal
363
how does hypothyroidism lead to vestibular disease?
deficit in energy metabolism with disturbance in axonal transport and possible segmental demyelination
364
list 4 ototoxic drugs
aminoglycosides (mostly streptomycin), loop diuretics, chlorhexidine, cisplatin
365
what tumors can you see in the ear canal and middle ear?
ceruminous glad adenocarcinoma, SCC, fibrosarcoma, osteosarcoma, chondrosarcoma, lymphoma (cats mainly) - most carry guarded to poor prognosis
366
what infectious diseases have been reported to cause central vestibular disease?
canine distemper virus, FIP, RMSF, ehrlichiosis, cryptococcus, toxoplasma, neospora, rabies, cuterebra
367
what is the most useful antemortem diagnostic for distemper?
PCR of urine or CSF
368
what % of cats with the dry form of FIP have neurologic signs?
1/4 to 1/3
369
what are the most common primary tumors affecting the vestibular components of the CNS in dogs?
meningioma, nerve sheath tumor of trigeminal nerve (affecting brainstem or CN VIII by extension), choroid plexus tumor in the 4th ventricle
370
what are the most common primary tumors affecting the vestibular components of the CNS in cats?
meningioma, lymphoma
371
what is the most common location for CVA in dogs?
cerebellum - in areas supplied by rostral cerebellar artery
372
define a TIA
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)
373
what drug can cause vestibular signs?
metronidazole
374
describe signs of metronidazole toxicity as seen in dogs and cats
dogs: central vestibular signs +/- cerebellar signs (intention tremors, hypermetria), vertical nystagmus, anorexia/vomiting.
cats: forebrain disturbance (seizure, blindness, ataxia)
375
why does metronidazole cause vestibular signs?
interacts with GABA receptors in the cerebellum and vestibular nuclei
376
what vitamin deficiency can lead to vestibular disease?
thiamine (B1)
377
describe signs of thiamine deficiency in cats
vestibular and ocular nuclei are affected: vestibular signs, dilated and unresponsive pupils, ventroflexion of head/neck
378
thiamine deficiency can occur in patients fed what types of diets
high in thiamin's (raw fish) or canned food subjected to excessive heat, food that uses sulfur dioxide used as a preservative
379
what malformation seen in cavies can cause vestibular disease?
COMS
380
describe post anesthetic vestibular syndrome in cats
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
381
disc-associated compression leading to cervical spondylomyelopathy is seen most commonly in what breed? age?
doberman; middle-aged
382
disc-associated compression leading to cervical spondylomyelopathy is caused by what?
intervertebral disc protrusion with or without hypertrophy of the dorsal longitudinal ligament or ligament flavor
383
disc-associated compression leading to cervical spondylomyelopathy most commonly affects which disc spaces?
C5-6 and C6-7
384
osseous compression leading to cervical spondylomyelopathy is most commonly seen in what breed? age?
giant breed (great dane); young adult
385
cervical spondylomyelopathy: describe the gait
gait deficits primary affect pelvic limbs; two engine gait is common; cervical hyperesthesia is not a common finding
386
what is the gold standard for diagnosis of cervical spondylomyelopathy?
MRI
387
discuss the basic pathophysiology of degenerative lumbosacral stenosis
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
388
what is the main clinical sign seen with lumbosacral stenosis?
pain
389
describe the gain of a dog with lumbosacrall stenosis
pelvic limb weakness without proprioceptive ataxia and a stiff gait (note: many will still have proprioceptive deficits in pelvic limbs)
390
surgical treatment of lumbosacral stenosis is less successful in dogs with what clinical signs?
fecal or urinary incontinence
391
degenerative myelopathy affects primarily what area of the spinal cord?
thoracolumbar
392
mutation in what gene has been proposed as being related to development of degenerative myelopathy?
superoxide dismutase 1 (SOD1)
393
describe degenerative myelopathy
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
394
clinical signs of degenerative myelopathy are those of a myelopathy localized to what cord segments?
T3 - L3
395
degenerative myelopathy is painful or not painful?
not painful
396
what 2 breeds are the most commonly affected with degenerative myelopathy?
GSD, boxer
397
describe the typical MRI of a patient with degenerative myelopathy
normal
398
how can steroids help in diagnosis of DM?
CCS typically lead to improvement in dogs with chronic compressive myelopathies (i.e. IVDD) but won't help dogs with degenerative myelopathy
399
what is the best treatment for DM?
physical therapy
400
what is the prognosis for DM?
poor - most dogs euthanized within 6-12 months
401
discuss the difference between Hansen type I and II IVDD
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.
402
what are the 2 most common infectious causes of meningomyelitis?
canine distemper virus and protozoa
403
what is the most common non-infectious inflammatory cause of meningomyelitis?
SRMA
404
increased expression of this molecule on polymorphonuclear cells appears to be an important factor in the pathogenesis of SRMA
CD11a
405
describe the CSF of a patient with SRMA
marked neutrophilic pleocytosis (non-degenerative) and protein elevation
406
elevated IgA in serum and CSF for a diagnosis of SRMA has a sensitivity of XX and specificity of XX
91%, 78%
407
what is the major canine acute phase protein?
CRP
408
what is the #1 most common agent associated with canine discospondylitis?
staphylococcus (pseudintermedius or aureus - coagulase-positive)
409
what 6 infectious agents are the most commonly associated with canine discospondylitis?
staphylococcus, streptococcus, e coli, actinomycetes, brucella canis, aspergillus
410
young female german shepherd are predisposed to discospondylitis due to what infectious agent?
aspergillus
411
basset hounds contract discospondylitis due to what infectious agent most commonly?
systemic tuberculosis
412
what sites are the most commonly affected with discospondylitis?
*L7-S1*, caudal cervical, mid-thoracic, and thoracolumbar spine
413
what are good empiric antibiotics for discospondylitis?
clavamox, cephalexin
414
what peripheral nerves arise in the ventral horn of the spinal cord, and exit via the ventral root?
motor and sympathetic
415
what peripheral nerves arise in the dorsal root ganglion, adjacent to the spinal cord, and enter the cord via the dorsal root?
sensory fibers
416
autonomic dysfunction leads to what clinical signs?
vomiting, regurgitation, diarrhea, ileus, urinary retention, incontinence, impaired lacrimation and salivation, pupillary dysfunction
417
in diabetic neuropathy, which predominates - axonal changes or demyelination?
demyelination
418
thyroid hormone deficiency leads to axonal damage or demyelination?
both
419
what is the most common cranial nerve neoplasm?
trigeminal nerve sheath tumor
420
describe c/s on neospora in an adult dog
paresis of 1+ limbs, muscle atrophy, reduced muscle tone, muscle pain, postural reaction deficits, reduced/absent segmental spinal reflexes, head tilt, dysphagia, tongue paresis
421
what is the classical presentation of neospora in puppies?
paraparesis, which leads to a non-ambulatory state characterized by rigid extension of the pelvic limbs associated with muscle contractors
422
how are puppies infected with neospora?
transplacentally
423
ingestion of raw meat is a risk factor for toxoplasma or neospora?
both
424
treatment of choice for toxoplasma?
clindamycin >> suflonamides, pyrimethamine, doxy, minocycline
425
treatment of choice for neospora?
clindamycin or potentiated sulfonamides, with or without pyrimethamine
426
can acute polyradiculoneuritis lead to respiratory musculature failure?
yes
427
describe c/s of acute polyradiculoneuritis
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
428
where is the inflammation in acute polyradiculoneuritis?
peripheral nerves and ventral nerve roots
429
antibodies to XXX have been found in some dogs with acute polyradiculoneuritis
anti-GM2 ganglioside antibodies
430
what diagnostic can differentiate acute polyradiculoneuritis fro tick paralysis, botulism, elapid envenomation, and fulminant MG?
electrophysiologic testing:
| EMG - spontaneous activity seen
431
what is the treatment for acute polyradiculoneuritis?
supportive care. NOT steroids.
432
describe the distribution of brachial plexus neuritis
thoracic limbs, bilateral but asymmetric
433
axonal regeneration occurs at a rate of XX per day
1-2 mm
434
what toxins have been associated with peripheral neuropathies?
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)
435
what are the parts of the neuromuscular junction?
presynaptic motor nerve terminal
synaptic cleft
post-synaptic muscle end plate
436
what neurotransmitter(s) are used in neuromuscular junctions?
acetylcholine
437
what is the safety factor of neuromuscular transmission?
the muscle membrane potentials produced by nerve depolarization greatly exceed what is required for muscle fiber contraction
438
tick paralysis is a presynaptic or postsynaptic condition?
presynaptic
439
what ticks are associated with tick paralysis?
dermacentor (N America), ixodes (australia)
440
what is the pathophysiology of tick paralysis?
neurotoxin from female tick salivary gland interferes with ACh release from pre-synpatic nerve terminal via a calcium-mediated mechanism
441
what is the treatment for tick paralysis?
remove the tick
442
what are the symptoms of tick paralysis?
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
443
what is different about australian tick paralysis than north american?
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.
444
in australian tick paralysis, what two medications can be used to treat autonomic signs?
phenoxybenzamine and acepromazine
445
what type of bacteria is clostridium botulinum?
gram positive anaerobe
446
where is clostridium botulinum found?
ubiquitous in soil, water, GI tracts of mammals and fish
447
how do most pets develop botulism?
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)
448
what is toxico-infection as it relates to botulinum?
animals getting botulism by toxin being produced in vivo after liver or GI infection
449
what is the most common botulinum toxin in dogs?
botulinum neurotoxin type C (BoNT-C)
450
what is the pathophysiology of botulism?
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.
451
botulism is a pre- or post-synaptic disease?
presynaptic
452
what are the symptoms of botulism?
progressive acute tetra paresis accompanied by autonomic signs (ileus, tachy- or bradycardia, mydriasis, urianry retention) +/- cranial nerve deficits (decreased palpebral reflex, megaesophagus, diminished PLR)
453
how do you diagnose botulism?
demonstrate BoNT in feces, blood, stomach contents, food source; gold standard - mouse inoculation test
454
what is the treatment for botulism?
supportive. antibiotics only if toxico-infection is a possibility
455
what antibiotics should you avoid in botulism? why?
aminoglycosides, ampicillin - may potentiate neuromuscular blockade
456
is antitoxin helpful for botulism?
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
457
what are the elapid snakes?
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
458
elapid snake envenomation is pre- or post-synaptic?
either: can bind to AChR on postsynaptic membrane or cause pre-synpatic inhibition of ACh release (depends on the snake)
459
describe c/s of elapid snake envenomation
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
460
treatment for elapid snake envenomation?
supportive, antivenin
461
acquired MG is an autoimmune disorder characterized by production of autoantibodies against ___
nicotinic AChR on the post-synaptic muscle terminal
462
what is the age distribution of acquired MG?
bimodal: <4 or >9 years of age
463
what c/s are associated with acquired generalized MG?
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)
464
what c/s are associated with fulminant MG?
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
465
what cancer has been associated with fulminant MG?
thymoma
466
what muscles are most commonly involved in focal MG?
ocular, facial, esophageal, pharyngeal, laryngeal
467
what endocrine diseases have been associated with MG?
hypothyroidism, hypoadrenocorticism, methimazole treatment for hyperthyroidism
468
what non-endocrine diseases have been associated with MG?
thymoma, polymyositis, masticatory myositis
469
what is the gold standard for diagnosis of acquired MG?
anti-AChR autoantibodies in serum (note: species-specific assay)
470
what age does congenital MG show up at?
6-9 weeks of age
471
why are Gammel Dansk Honsehund (GDH) dogs different when it comes to congenital MG?
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.
472
how do you diagnose congenital MG?
quantification of AChR in muscle biopsy
473
why are miniature dachshunds different when it comes to congenital MG?
spontaneously resolve by 6 months of age
474
what is the protein dynamin 1 (DNM1) important for?
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.
475
what infectious disease causes cerebellar hypoplasia?
feline panleukopenia virus
476
what is the most common diffuse cerebellar disorder in cats?
feline panleukopenia virus
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?
earlier than last 3 weeks: hydranencephaly
last 3 weeks: cerebellar hypoplasia
first 3 weeks of life: cerebellar hypoplasia
478
what should you note about vaccinating a pregnant cat for feline panleukopenia virus?
vaccination with a modified live FPV vaccine during pregnancy can result in clinically ffected kittens
479
what is feline spongiform encephalopathy? how do cats contract it?
prion-induced disease; contracted by eating BSE-contaminated food
480
what are the symptoms of feline spongiform encephalopathy?
chronic progressive symptoms - abnormal behaviors ataxia, muscle tremors, hypersalivation, dilated and unresponsive pupils, hyperesthesia
481
what is the most common infectious CNS disease in cats?
FIP
482
what are the most common symptoms seen in CNS FIP?
altered mental status, menace response deficits, vestibular syndrome, seizures, ataxia, paresis
483
what is the most common cause of myelopathy in cats younger than 2 years of age?
FIP
484
what type of neurologic disease is FeLV associated with?
chronic degenerative myelopathy
485
what c/s are seen with FIV in the CNS?
abnormal behavior, facial twitching, ataxia, seizures, sleep disorders, intention tremors
486
what type of virus is feline borna disease virus?
negative-stranded RNA virus
487
what are the reservoirs of feline borna disease virus?
birds and rodents
488
what are the c/s of feline borna disease virus?
ataxia, postural reaction deficits, abnormal behavior, absent/decreaesd menace
489
how do you diagnose feline borna disease virus?
serum titers and RT-PCR in serum and CSF are supportive
490
what is gurltia paralysans?
neurotropic metastrongylid nematode of domestic cats in south america
491
what are the c/s of gurltia paralysans?
pelvic limb proprioceptive ataxia, paraparesis, paraplegia, LS hyperesthesia, fecal or urinary incontinence, tail paralysis
492
how do you diagnose gurltia paralysans?
histopathology via detection of adult G. paralysans in the spinal cord
493
treatment for gurltia paralysans?
no treatment
494
what is feline hippocampal necrosis?
seizure disorder characterized by epileptic events and interictal abnormal behavior
495
treatment for feline hippocampal necrosis/
anti epileptic medications. immunosuppressives sometimes recommended
496
what is feline orofacial pain syndrome? what breed is it common in?
a pain disorder characterized by acute behavioral signs of oral discomfort +/- tongue mutilation.
most common in Burmese
