Encephalopathies Flashcards
How does magnetic resonance imaging (MRI) work?
- 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
What is T1 and T2 relaxation? How does the tissue alter images?
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
What is the difference between T1-weighted images and T2-weighted images?
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
What is the most common intermediate-weighted image?
FLAIR - fluid attenuation inversion recovery, where free water is suppressed
(also: STIR, T2, CINE)
What kind of test is cerebrospinal fluid analysis? What are the 2 ways of collection? What can affect interpretation?
very sensitive, very nonspecific
- CISTERNAL - atlanto-occipital cerebrospinal fluid collection between the occipital protuberance/arch of the axis (C2 vertebrae) and the wings of the atlas (C1 vertebra)
- LUMBAR - dorsal spinous process of L6
hemorrhage affects cell and protein counts
What are 5 degenerative brain disorders?
- lysosomal storage diseases
- leukodystrophy/spongy degeneration
- neuronal vacuolation - Rottweilers
- multisystem neuronal degeneration/abiotrophy
- canine cognitive dysfunction
What is canine cognitive dysfunction? What is the cause?
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
What are 7 aspects of the pathophysiology of canine cognitive disorder?
- cerebrovascular disease
- toxic beta-amyloid deposition
- oxidative brain damage
- neuronal mitochondrial dysfunction
- excitotoxic (glutamate) brain damage
- impaired neuronal glucose metabolism
- astrocyte and microglial dysfunction
What are the clinical signs of canine cognitive disorder indicative of? How is it diagnosed?
progressive forebrain dysfunction —> clients report pet acting “senile”
history, signalment, excluding other causes, MRI features
What are the 4 clinical features of canine cognitive disorder?
- anxiety
- abnormal sleep/wake cycle
- decreased interaction with owners
- apparent confusion
What are 6 general MRI imaging characteristics of canine cognitive disorder?
- generalized cerebral atrophy
- enlarged compensatory lateral ventricles
- prominent sulci
- widened CSF space
- medial temporal lobe atrophy
- leukoaraiosis - neuroimaging abnormalities of the white matter
How can aging differences in the brain be differentiated from those with canine cognitive disorder?
interthalamic adhesion thickness is significantly smaller in patients with CCD
- 5.0 mm or less is consistent with CCD
CCD, MRI:
What secondary effect is commonly seen in the brain in canine cognitive disorder and Alzheimer’s disease? What is the likely cause?
microhemorrhages (macrohemorrages common with age?)
amyloid deposition
What is the most commonly prescribed treatment for canine cognitive disorder? What are 4 other options?
Selegiline
- antioxidant-fortified diet - b/d
- Gabapentin, Pregabalin
- Carprofen
- environmental enrichment
Neutraceuticals and drugs used for CCD treatment:
Chinese herbs for CCD:
