Encephalopathies Flashcards

1
Q

How does magnetic resonance imaging (MRI) work?

A
  • patient is placed in a magnetic field to produce a net magnetization (spinning hydrogen atoms/protons)
  • radiofrequency pulses are administered to displace protons
  • as protons relax back to original energy states, radiofrequency energy is released at variable intensities recorded by a receiver coil and converted into images
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2
Q

What is T1 and T2 relaxation? How does the tissue alter images?

A

T1 = spin-lattice relaxation, longitudinal relaxation measure of the time taken for spinning protons to realign with the external magnetic field

T2 = spin-spin relaxation, transverse relaxation time taken for spinning protons to lose phase coherence among the nuclei spinning perpendicular to the main field

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3
Q

What is the difference between T1-weighted images and T2-weighted images?

A

T1 = water is dark, fat is bright = white matter brighter than gray matter

T2 = water is bright and fat is dark = gray matter brighter than white matter

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4
Q

What is the most common intermediate-weighted image?

A

FLAIR - fluid attenuation inversion recovery, where free water is suppressed

(also: STIR, T2, CINE)

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5
Q

What kind of test is cerebrospinal fluid analysis? What are the 2 ways of collection? What can affect interpretation?

A

very sensitive, very nonspecific

  1. CISTERNAL - atlanto-occipital cerebrospinal fluid collection between the occipital protuberance/arch of the axis (C2 vertebrae) and the wings of the atlas (C1 vertebra)
  2. LUMBAR - dorsal spinous process of L6

hemorrhage affects cell and protein counts

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6
Q

What are 5 degenerative brain disorders?

A
  1. lysosomal storage diseases
  2. leukodystrophy/spongy degeneration
  3. neuronal vacuolation - Rottweilers
  4. multisystem neuronal degeneration/abiotrophy
  5. canine cognitive dysfunction
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7
Q

What is canine cognitive dysfunction? What is the cause?

A

analog of human Alzheimer’s disease common in elderly dogs (and sometimes cats!)

beta-amyloid accumulation, vascular changes, meningeal thickening, and brain atrophy resulting in compensatory hydrocephalus —> neurochemical changes by altered neurotransmitter concentrations

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8
Q

What are 7 aspects of the pathophysiology of canine cognitive disorder?

A
  1. cerebrovascular disease
  2. toxic beta-amyloid deposition
  3. oxidative brain damage
  4. neuronal mitochondrial dysfunction
  5. excitotoxic (glutamate) brain damage
  6. impaired neuronal glucose metabolism
  7. astrocyte and microglial dysfunction
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9
Q

What are the clinical signs of canine cognitive disorder indicative of? How is it diagnosed?

A

progressive forebrain dysfunction —> clients report pet acting “senile”

history, signalment, excluding other causes, MRI features

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10
Q

What are the 4 clinical features of canine cognitive disorder?

A
  1. anxiety
  2. abnormal sleep/wake cycle
  3. decreased interaction with owners
  4. apparent confusion
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11
Q

What are 6 general MRI imaging characteristics of canine cognitive disorder?

A
  1. generalized cerebral atrophy
  2. enlarged compensatory lateral ventricles
  3. prominent sulci
  4. widened CSF space
  5. medial temporal lobe atrophy
  6. leukoaraiosis - neuroimaging abnormalities of the white matter
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12
Q

How can aging differences in the brain be differentiated from those with canine cognitive disorder?

A

interthalamic adhesion thickness is significantly smaller in patients with CCD

  • 5.0 mm or less is consistent with CCD
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13
Q

CCD, MRI:

A
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14
Q

What secondary effect is commonly seen in the brain in canine cognitive disorder and Alzheimer’s disease? What is the likely cause?

A

microhemorrhages (macrohemorrages common with age?)

amyloid deposition

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15
Q

What is the most commonly prescribed treatment for canine cognitive disorder? What are 4 other options?

A

Selegiline

  1. antioxidant-fortified diet - b/d
  2. Gabapentin, Pregabalin
  3. Carprofen
  4. environmental enrichment
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16
Q

What is the proposed mechanism of Selegiline in the treatment of canine cognitive disorder?

A

increases brain dopamine levels and catecholamine levels

17
Q

What are some foods that have been identified to prevent Alzheimer’s in humans?

A
  • high intake of plant-based foods
  • antioxidants
  • probiotics
  • soy beans
  • omega-3 PUFA
  • whole grains
  • fruits, vegetables, nuts
  • medium-chain triglyceride-rich foods
  • fish

(suspected to be similar in dogs!)

18
Q

What are some foods that have been identified to increase risk of Alzheimer’s development in humans?

A
  • read meat or poultry
  • refined sugar
  • processed foods
  • high fat dairy products

(suspected to be similar in dogs!)

19
Q

What are 4 options for commercial diets for CCD? What ingredients are seen in these diets?

A
  1. Purina Bright Minds 7+, no Rx needed
  2. Purina NeuroCare
  3. Hills b/d
  4. Re-Juvenate, no Rx needed

vitamin E, C, B, arginine, EPA, DHA, MCT, carnitine, a-lipoic acid, vegetable extracts

20
Q

Neutraceuticals and drugs used for CCD treatment:

A
21
Q

What 3 mechanisms of Levetiracetam are thought to help for CCD treatment?

A
  1. improved synaptic function
  2. mitochondrial effects
  3. decreased glutamate release
22
Q

How are medium-chain triglycerides (MCTs) thought to improve patients with CCD?

A

improve cognition by increasing ketone levels

23
Q

Chinese herbs for CCD:

A
24
Q

What are CogniCaps? What has their use improved?

A

combination of Eastern Chinese herbals and Western conventional nutraceuticals

normalization of sleep/wake cycles most consistent

25
Q

What environmental enrichment is recommended in patients with developing CCD? How does this help?

A
  • task-oriented toys
  • exercise
  • social interactions

increases cognitive reserve - brain’s ability to improvise and find alternate ways of getting a job done; mind’s and brain’s resistance to damage