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Specialty Boards Prep > Deck 11 > Flashcards

Deck 11 Flashcards

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1
Q

True or false — EEGs are representations of just neuronal activity

A

False — glial cells can also contribute to the EEG, both directly and indirectly via modulation of neurons

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2
Q

Describe the concept of sink-source.

A

Sink refers to where an ion (positive or negative) moves into a neuron via ion channels, creating a relative lack of that ion’s charge in the extracellular space.

Source refers to where similar ions now leave the neuron to go back into the extracellular space.

Together sink-source creates a dipole, often within the neurons themselves (one end has more of one charge, while the other end has less of it).

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3
Q

Neurons in what layers of the cerebral cortex are responsible for generating EEG signal?

A

3, 5 and 6

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4
Q

Neurons in gyri or sulci generate more EEG signal? Why?

A

Gyri because the orientation of the neurons (and subsequent dipole) enable one part of the dipole to be closer to the recording electrode than the other. In sulci, the positive and negative ends of the dipole are equidistant from the recording electrode, so no signal is generated.

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5
Q

What is a paroxysmal depolarizing shift?

A

This is the cellular correlate of an epileptic seizure. This involves prolonged depolarization of the neuron, resulting in opening of NMDA and calcium channels, followed by prolonged hyperpolarization due to potassium channel opening.

A group of neurons that undergo a paroxysmal depolarizing shift will generate an epileptic focus, and a spike on a scalp electrode.

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6
Q

Explain the convention for naming electrodes for EEG.

A

The letters are in reference to the lobe of the cerebral cortrex (Fp - prefrontal, F - frontal, or C for central, etc)

The left-sided electrodes are odd numbers, and right-sided are even, and midline ones are Z.

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7
Q

Where should the reference electrode be placed and what is common mode rejection?

A

The reference electrode should be placed somewhere electrically inert from the signals you are recording.

Common mode rejection refers to getting rid of signal that is affecting both the active and reference electrode — this signal goes out the ground electrode (which can be placed anywhere).

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8
Q

Where is the CZ electrode placed in EEG? The reference electrode?

A

CZ — halfway between the nasion and occipital protuberance (often corresponds well with the vertex)

Reference — nasion

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9
Q

Which type of montage is more likely to be impacted by artifacts — referential or bipolar?

A

Referential — if something impacts the reference electrode, then all the channels will be impacted.

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10
Q

What is the goal activation procedures, and what are two examples?

A

Activation procedures are meant to induce an epileptic waveform on EEG in susceptible patients. Examples include hyperventilation (limited value in vetmed) and photic stimulation.

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11
Q

What are these EEG artifacts?

A

A — muscle
B — blinking
C — ECG

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12
Q

What three criteria need to be met for a signal to have originated from the cortex?

A

Field — recorded by multiple electrodes
Lag — there will be a latency difference between electrodes (shortest for the closest ones)
Gradient — closest electrode will have tallest amplitude

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13
Q

Explain the main ways to determine the source of signal using referential and bipolar montages.

A

Referential — typically the signal arose from near the electrode with the largest amplitude signal.

Bipolar — signal arose from the area where phase reversal occurs

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14
Q

What are two explanations for phase reversal on a referential montage? How can you distinguish them?

A
  • contamination of the reference electrode with signal
  • recording of a tangetial dipole

You can distinguish between them by switching the location of your reference. If the phase reversal goes away, then it was due to reference contamination.

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15
Q

Complete the chart.

A
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16
Q

What are the stages of the sleep? What background waves happen in each stage?

A

Wakefulness — alpha and beta
Drowsiness (N1) — theta
Sleep (N2) — theta
Deep sleep (N3) — delta
REM — similar to beta

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17
Q

What are three normal waveforms that can be seen during sleep? What stage of sleep is each seen in?

A
  • vertex waves — N1
    (small positive deflection, followed by large negative deflection)
  • sleep spindles — N2 and N3
    (brief run of small amplitude waves)
  • K complexes — N2 and N3
    (bi-triphasic waves with negative deflection followed by positive deflection)
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18
Q

What is burst suppression?

A

This is when then EEG background is suppressed for 50-99% of the recording.

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19
Q

What are the three main sporadic epileptiform discharges? What are their characteristics?

A

Spikes, sharp waves and spike-waves.

Spikes and sharp waves are similar in morphology with a tall negative deflection — the only difference is that spikes are 20-70 ms, and sharp waves are 70-200ms.

Spike-waves are a spike followed by a negative wave of >200 ms duration.

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20
Q

What percent of non-epileptic humans have interictal SEDs on EEG? Epileptic patients?

What are the clinical implications of this?

A

Non-epileptic: 1-4%
Epileptic: 50%

A normal interictal EEG does not rule out epilepsy!

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21
Q

What were the classic MRI findings in this paper? What was the one main difference in more acutely affected patients?

A

T1 and T2W hypointensity with STIR hyperintensity of the end plates and vertebral body, with end plate erosion.

T2W and STIR hyperintense, contrast enhancing discs.

Large amount of epidural and paravertebral extension.

In acutely affected patients, the boney changes involved a T2W hyperintensity, likely due to edema.

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22
Q

What are the signal characteristics of the middle ear effusion in cases of presumed tensor veli palatini dysfunction?

A

T1 and T2 hyperintense — this is probably because the fluid is high in protein.

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23
Q

What are the origins and insertions of the tensor veli palatini muscle? What is its specific function and when does it normally perform this function?

A

Origin — muscular process of temporal bone
Insertion — hamulus of pterygoid bone

It opens the normally closed nasopharyngeal orifice of the auditory tube via stretching of the soft palate. This occurs when swallowing happens.

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24
Q

How much more likely is a non-fenestrated disc than a fenestrated disc to experience herniation?

A

26.2 times

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25
What were the confirmed / suspected recurrence rates in this paper? What were the reported complications?
- confirmed — 2.3% - suspected — 10% Iatrogenic introduction of disc material into vertebral canal and subluxation / instability
26
Classic EDX findings of HCSMA in Brittany spaniels
Decreased M wave amplitude but maintained conduction velocity — later disease states can cause reduced velocities too.
27
What is the genetic defect in HCSMA cases? Human equivalent?
SOD1 Amyotrophic lateral sclerosis
28
Mechanism of action of VNS
GVA stimulation of solitary nucleus, and the solitary nucleus projects to cortical and subcortical areas to interrupt seizure activity
29
Baclofen MOA
GABA(B) agonism — decreases excitatory XTR release by blocking calcium influx at pre-synaptic terminal
30
Breeds at risk for congenital myasthentic syndrome and which one gets a pre-synaptic form? Post-synaptic form?
Mini dachshund, Labs, Golden, Spinx and Devon Rex cats, springer spaniel, Brahman calves Presynaptic is Gammel Danske Honsehund, and post-synaptic is the JRT.
31
Distinguishing features between granulomas, and gliomas.
All more common in granulomas: Contralateral brain changes Dural contact Meningeal contrast enhancement T2 hypointensity
32
What is the most common cause of myelopathy in young cattle?
Discospondylitis
33
What’s the most common cause of myelitis in cattle?
Rabies
34
Most common location for disc herniation causing nerve root signature?
C6-7
35
Angle of shunt placement into the lateral ventricle? Antibiotics used post-op per shores?
30 degrees, and angled cranially. 2 weeks of metronidazole and Clavamox
36
Degree of dislocation is prognostic in dogs but not cats cats luxate dorsally
37
Auto-antibodies implicated in limbic encephalitis
VGKC LGI-1
38
Which LSD can cause radiographic changes?
Mucopolysaccharidosis — due to abnormal growth plates
39
What is the bulbocavernosus reflex?
Squeezing of the glans penis leading to contraction of the anal sphincter. Similar pathway as to the perineal reflex.
40
Why does spinal shock recover more quickly in animals versus people?
In humans, the corticospinal tracts insert directly onto the LMN cell bodies in the spinal cord, whereas in animals they generally insert into the dorsal grey horn and then use interneurons to influence the LMN cell bodies.
41
What is the timeline for recovering reflexes in experimental spinal shock in dogs?
Perineal reflex — 15 minutes Patellar reflex — 30 min to 2 hours Withdrawal reflex — 12 hours Obvious spasticity — 24 to 48 hours
42
Spinal shock occurs due a sudden interruption of _________________.
Descending supraspinal input
43
Why do reflexes return after spinal shock? Why do they become hyper-reflexive?
They return due to denervation hypersensitivity, and increase due to new synapse formations onto the LMNs.
44
Two other things can be dramatically impacted during spinal shock — what are they and what are the clinical implications of their dysfunction?
1. The autonomic nervous system also develops decreased tone — if spinal shock occurs in the neck, then the loss of TL spinal cord function means loss of sympathetic tone to the thoracic and abdominal viscera, leading to unopposed vagal tone to the heart, which can cause bradycardia and hypotension. 2. The spinal cord autoregulatory system is compromised, and the perfusion to the cord becomes directly dependent on MAP. Be sure that these patients are normotensive to ensure appropriate spinal cord perfusion.
45
What drives the movement of CSF?
Pulsation of the intracranial arteries
46
Is pressure higher in the spinal cord or in the syrinx? What is the significance of this?
It is higher in the syrinx. The significance is that syringes likely don’t form due to “sucking” of CSF into the syrinx.
47
What are the main principles to explain syringomyelia?
1. Syringomyelia is caused by repeated mechanical distension of the spinal cord. 2. Cavitation arises from extracellular fluid originating from the high-pressure microcirculation of a spinal cord (not from CSF in the low-pressure SAS).
48
True or false — the fluid in a syrinx is derived from CSF.
False — current evidence suggests that it is a derivative of extracellular fluid
49
Explain this photo.
This photo is demonstrating the pathogenesis of SM in COMS. With cerebellar herniation, flow of CSF out of the FM is decreased, particularly at the dorsal SAS. The ventral SAS at the FM is narrowed as well, but now, all CSF has to flow through here (because the dorsal potion is obstructed with cerebellum). The ventral CSF flows faster because the channel width is decreased. However, nothing happens to the spinal cord immediately caudal to the FM because this SAS in this area is all under high pressure due to the presence of normal vertebral canal narrowing at the C2-3 disc space. However, because less CSF is getting into the SAS caudal to the C2-3 disc, the SAS caudally has lower pressure. The presence of low pressure in the SAS distends the spinal cord a little bit. And then, additionally, the space for CSF flow at the C2-3 disc is smaller, meaning that the CSF has to flow faster. Via the Venturi effect (Bernoullis law), this fast flow also lowers the pressure in the downstream SAS more, contributing to spinal cord distention. This explains why SM doesn’t usually affect the spinal cord until after C2-3. It could also account for the occurrence of SM in the cranial thoracic cord because of normal slight narrowing at C7-T1.
50
True or false — the vascular compliance is increased in COMS patients. How does this contribute to SM formation? How does this explain the significance of Vasalva maneuvers in SM patients?
False — the vascular compliance is decresed in COMS patients (there is less give to the vessels). This means that the pressure in the vessels during systole is higher, and therefore a more intense CSF pulse pressure wave is generated during systole, which when there is obstruction to CSF flow, perpetuates SM formation via the Venturi effect. Valsava maneuvers (coughing, abdominal straining) result in higher pressure in these non-compliant vessels. This can perpetuate signs even more. This might be why some SM patients cry when picked up by their bellies (a pseudo-Valsava maneuver).
51
Per this article, what is the first line medication used to medically manage SM in dogs?
Furosemide
52
What type of axons are spared in complete spinal cord injuries?
Sub-pial axons
53
Per this review article, does timing of decompression matter?
Yes — “prompt decompression improves outcomes”
54
What are some examples of secondary spinal cord injury in the acute phase of SCI?
- hemorrhage - rapid changes of intracellular ions - excitotoxicity - free radical production - inflammation
55
What is TRMP4?
This is a gene that is normally expressed at low levels within the CNS, but is unregulated in endothelial cells after SCI. It encodes for ion channels — excessive ion entry into endothelial cells causes cell swelling / death, promoting secondary hemorrhage.
56
What are two mechanisms for extracellular glutamate accumulation in the damaged spinal cord? What does this accumulation lead to?
Directly released from damaged neurons and failure of damaged astrocytes to recycle it. Glutamate then binds to NMDA and AMPA receptors on neurons and oligodendrocytes, allowing influx of sodium (and calcium) into the cells. This, along with failure of NaKATPase pumps, contributes to the formation of cytotoxic edema.
57
What is the recommended way to assess the feline menace response?
Standing from behind them, without covering the contralateral eye.
58
What is the proposed MOA of polyethylene glycol in treatment of acute SCI?
It is known as a fusogen, that targets damaged cell membranes and seals them. This helps prevent intracellular leak of ions.
59
“Basic factors such as _________, _________, and _________ remain central to effective therapy for acute SCIs.” — Olby
Blood pressure, oxygenation and spinal cord decompression
60
What were the main findings of this article?
- recurrence rate of cervical disc herniations is similar between medically and surgically managed dogs (~30% in both) - recurrence in medically managed dogs tended to be the site of initial herniation, whereas this rarely happened in surgically managed cases.
61
Describe the “claw sign”.
A claw sign can be used to help determine if a lesion with pial contact is intra or extra-axial. Intra-axial lesions will demonstrate a positive claw sign, characterized by acute angles formed from where the lesion meets the pia.
62
Describe the “claw sign”. What tumors is it helpful in distinguishing? What was the sensitivity and specificity?
A claw sign can be used to help determine if a lesion with pial contact is intra or extra-axial. Intra-axial lesions will demonstrate a positive claw sign, characterized by acute angles formed from where the lesion meets the pia. The published paper regarding the claw sign evaluated intracranial meningiomas versus contrast enhancing gliomas with pial contact. Sensitivity - 85% Specificity - 80% (Termed moderate)
63
Do these tumors demonstrate a claw sign?
No — these are all extra-axial meningiomas with obtuse angles
64
Where is the claw sign the least accurate?
Olfactory region and caudal fossa — in these regions, a fake claw sign could be present with extra-axial lesions.
65
What is the blackout effect on MRI?
This refers to when a strongly T2 hypointense lesion (like some stages of hemorrhage) show up hypointense on DWI and ADC. It is similar in concept to T2 shinethrough.
66
What were the main findings of this study?
ADC values were low in the peripheral areas of hyperacute and acute hemorrhages….maybe this can help age hemorrhages? Hemorrhagic lesions commonly displayed a blackout effect.
67
Describe the abnormalities of this dog. What is the diagnosis?
- mydriasis (fixed in this dog) - ptosis - lateral strabismus Idiopathic oculomotor nerve palsy.
68
What breed of dog was over-represented for idiopathic oculomotor palsy?
Boxer (4/14 cases)
69
True or false — masticatory muscle changes are significantly more common in neospora cases compared to MUO cases Do these changes correlate with muscle atrophy? What do they correlate with instead?
True — these changes include multifocal T2W and T2 FLAIR hyperintensities that contrast enhance. No, it is uncommon for muscle atrophy to be noted in these dogs. Dogs with masticatory muscle changes on MRI had significantly more inflammatory CSF.
70
What were the main results of this article?
CK and AST were significantly higher in cases of neospora meningoencephalitis compared MUE. A CK value of 485, and AST value of 57 or higher correlated with a high likelihood of a neospora diagnosis.
71
What is the half life of CK?
2-4 hours
72
What are the main clinical signs of toxoplasmosis in cats and dogs?
Fever, ocular changes, respiratory difficulty and neurological/ myopathic signs.
73
Describe the lifecycle of toxoplasma.
Cats are definitive hosts, and sexual reproduction of the organism occurs in their guts. They then poop out oocysts. It takes 1-5 for these oocysts to become sporulated (infective). The sporulated oocysts are then ingested by intermediate hosts. In the intermediate hosts, the sporulated oocysts get absorbed across intestines, after which, tachyzoites are released. If the immune response of the intermediate host is sufficient, the tachyzoite infection will be controlled, and bradyzoite-containing tissue cysts will form. Ingestion of cyst containing tissues is another way for exposure, especially in humans. Cats can either be exposed to the organism by ingesting sporulated oocysts from the environment or by eating something infected with tissue cysts. Cats can also be infected transplacentally and transmammillary.
74
When do IgM toxoplasmosis titers typically become negative again?
Within 16 weeks
75
True or false — a single high IgG titer (1:10000) is indicative of an active toxoplasmosis infection.
False — some animals can have very IgG titers for a very long time after exposure.
76
What are two ways that a toxoplasmosis titer could be highly suggestive of a recent / clinically relevant infection?
- positive IgM titer (any value) - rising IgG titers (great than 4-fold increase)
77
Describe the lifecycle of neospora.
Dogs are definitive hosts — sexual reproduction occurs in their intestines, and they pass unsporulated oocysts in their feces. These become ingested by various intermediate hosts (ruminants mostly), leading to tissue cyst formation in these animals. Dogs are then exposed by ingesting tissues with cysts in them, or by ingesting reproductive tissues from animals who aborted. Pregnant dogs can pass the infection on transplacentally.
78
True or false — a single high titer for toxoplasmosis is not necessarily indicative of clinical significant infection, whereas a single high titer is indicative for neospora.
True (per Greene’s)
79
For protozoal infections, such drugs a ‘static’ and which are ‘cidal’?
Clindamycin and sulfa drugs are static, while ponazuril is cidal.
80
Per Greene’s, how the dosing of clindamycin change between treatment of toxoplasmosis versus neosporosis?
The dose used for toxoplasmosis is listed as q12, while it is q8 for neosporosis. Additionally, it is recommended to treat toxoplasmosis for 4 weeks, and neosporosis for at least 8.
81
Main route of exposure to rabies in people worldwide? In the US specifically?
Worldwide — dogs US — bats Both are most commonly via bite wounds with innoculation of infected saliva.
82
Which genotype of rabies is most common?
Genotype 1
83
Three continents where the is no dog-variant rabies virus
North America (specifically USA and Canada) Europe Australia
84
How does rabies virus make its way to the CNS from a bite wound? How does this relate to some of the initial clinical signs that can be seen?
It binds to the nicotinic acetylcholine receptors, and buds into the synaptic cleft and is taken up into the synaptic terminal of the motor neuron. From here, it travels retrograde up the nerve to the neuronal cell body, where it replicates. It then crosses retrograde across another synapse (now within the CNS), where it replicates a ton in those neurons of the spinal cord, but without causing overt histopathologic changes. This explains why lower motor neuron signs of a limb / intumescence may be seen initially.
85
What is the typical incubation for rabies in the dog /cat?
1-2 months, although it can be delayed up to 6 months after exposure.
86
What are the three forms of rabies, and what are the associated clinical signs / when they occur?
Prodromal (~2 days): fever, licking at bite site, various behavioral changes and mydriasis Furious phase (up to the next 7 days): behavioral changes with mostly aggression, foreign body ingestion, ataxia, seizures, vestibular signs. Paralytic phase (1-10 days after onset of signs): ascending LMN paralysis following involvement of the bitten extremity, can also involve pharyngeal / laryngeal muscles, precluding swallowing
87
What is the main diagnostic test (on path) to diagnose rabies?
Direct fluorescent antibody — IHC can also work.
88
Rabies virus results in (mild/moderate/severe) non-suppurative polioencephalomyeliits, despite (small/moderate/large) amounts of intraneuronal viral replication
Mild and large
89
Explain reasoning behind the timing of the bite rule in regards to rabies.
The salivary glands are always affected after the CNS has become infected. The average time between shedding of virus in the saliva and onset of clinical signs is 1-5 days in dogs/cats, although they can be delayed up to 2 weeks post-shedding in the saliva.
90
What is a common labwork finding in animals with distemper?
Lymphopenia — occurs due to massive destruction of lymphocytes by the virus
91
What are some ways that distemper virus can enter the CNS?
Virus can cross the BBB in infected lymphocytes (or as free virus if the viral load is high enough), via the choroid plexus or directly via the nasal passages.
92
When do neurologic signs occur following systemic signs in distemper?
1-3 weeks
93
Describe the “bystander” effect in regard to demyelination in distemper cases. How can distemper progress to a chronic infection?
When infected animals start regaining their lymphocyte populations, they develop a peri vascular inflammatory infiltrate. These lymphocytes produce antibodies against CDV virus. These antibodies then interact with the infected macrophages that initially brought CDV into the CNS. Upon interaction, the macrophages are activated and release reactive oxygen radicals, damaging both oligodendroglial cells and myelin. If the virus has spread throughout large parts of the CNS by the time the lymphocyte population rebounds, this can cause a fatal outcome. If the virus is not cleared by this immune response, it can continue to travel throughout the brain via glial cell networks, inciting areas of inflammation wherever it spreads to next.
94
What are the MRI findings in rabies?
T2W hyperintense, non-CE lesions in thalamus, midbrain, and basal nuclei.
95
Vaccine induced distemper primarily causes a _______________________ within the _______________.
Necrotizing polioencephalitis, brainstem
96
What is this photo demonstrating?
Intracytoplasmic AND intracytonuclear inclusions in a distemper case. The top photo shows them in a neuron, while the bottom photo is lung tissue.
97
What is the vector for tick borne encephalomyelitis virus, and what is the class of virus? What is the classic lesion distribution? What does it look like on MRI?
Ixodes ricinus Flavivirus Bilaterally symmetric polioencephalitis of brainstem, cerebellum and ventral horn On MRI, there is also involvement of the basal nuclei and hippocampus — T2 hyperintensities.
98
What are the two MRI patterns of coccidiodomycosis? Which one is more common?
Solitary granulomas with extensive edema — much more common Bilaterally symmetric frontal lobe, internal capsule and caudate nucleus T2W hyperintensity with wispy CE.
99
What were the main clinical signs of these patients? Breed predilection?
Behavior changes, compulsive pacing / circling and seizures (fits pretty well with know lesion distribution). Schnauzers
100
What was the general outcome of these patients? What was seen on follow-up MRI if available?
Good outcomes (11/13 lived) with resolution of MRI lesions, but development of frontal lobe and caudate nucleus atrophy.

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