Consensus Neuro Sc

Front 1

What is hypoxic ischemic brain injury

Back 1

a. Reduction of cerebral blood flow and oxygenation during the antepartum, peripartum, or postnatal period
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Front 2

What are the risk factors for development of hypoxic brain injury

Back 2

a. Prolonged dystocia, premature placental separation, and need for resuscitation after cesarean section
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Front 3

Clinical findings that support hypoxic ischemic injury in a fetus include what

Back 3

a. Abnormal fetal heart rate, depressed infant, fetal academia
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Front 4

Reduction in cerebral blood flow and oxygen delivery causes what

Back 4

a. Switch to anaerobic metabolism, leading to depletion of high energy phosphate reserves, lactate accumulation; break down of cellular barriers and cytotoxic edema and intracellular calcium accumulation. Eventual prevention of electron passage to cytochrome c oxidase in the phase of hypoxia-> superoxide
5

Front 5

What role does glutamate play

Back 5

a. Exictatory neurotransmitter that is released in response to calcium. Important trophic factor for young brain development
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Front 6

What are microglia

Back 6

a. Resident immune cells of the brain believed to be derived from monocytes that become activated under pathological states and believed to play a central role in neonatal hypoxic ischemic injury
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Front 7

What modality provides the most information regarding hypoxic ischemic encephalopathy

Back 7

a. MRI
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Front 8

What are the four major categories of neuropathology seen in hypoxic ischemic encephalopathy

Back 8

a. Selective neuronal necrosis, parasagittal cerebral injury, periventricular leukomalacia, and focal ischemic brain necrosis (stroke)
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Front 9

What treatment has shown the most promise in this syndrome

Back 9

a. Cooling (hypothermia) as it can delay cell death and result in cells surviving versus apoptosis, reduces cellular metabolic demands, attenuate neurons that are excitatory (sometimes just the brain is cooled as 70% of heat comes from the brain in newborn)
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Front 10

What are five other alternative therapies that may be beneficial and are being evaluated currently

Back 10

a. Desferrioxamine (iron chelator and serves as free radical scavenger), erythropoietin as it can be neuroprotective), anticonvulsants, melatonin (free radical scavenger), and xenon (neuroprotective and antagonizes glutamate)
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Front 11

FIP results because of infection of what cell

Back 11

a. Mutant feline coronavirus infection of macrophages
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Front 12

What percentage of cats with FIP will develop neurologic signs

Back 12

a. ¼-1/3 of noneffusive FIP cats will
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Front 13

What are the common neurologic deficits that can be seen in cats

Back 13

a. Dementia, pica, seizures, inappropriate elimination, incontinence, and compulsive licking, ataxia, hyperesthesia, reduced consciousness, caudal paresis, cerebellar-vestibular signs, or cranial nerve deficits (ophthalmic lesions are common and include anterior uveitis, keratic precipitates, anisocoria, retinitis.
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Front 14

Anatomically, what do the lesions look like in the CNS

Back 14

a. Ependymitis, thickening and opacification of the meninges, and ventricular dilation. Pathogenesis through complement activation and deposition of C3 on affected surfaces, DIC, vessel necrosis, and effusion. Antibody production can mediate and even enhance the disease
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Front 15

What is the definitive lesion in FIP

Back 15

a. Pyogranuloma resulting from immune-mediated phenomenon- most commonly affecting the serosal, pleural, meningeal, ependymal, or uveal membranes
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Front 16

What is a general rule of thumb regarding injuries to the spinal cord

Back 16

a. Primary injury is often less damaging than the secondary injury afterwards that develops over 48 hours
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Front 17

What are the 3 different therapeutic windows after injury:

Back 17

a. Biochemical and vascular events, influence of inflammatory cells, and axonal regeneration
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Front 18

Acute injury to the spinal cord causes what

Back 18

a. Systemic and vascular abnormalities that allow for decreased perfusion and necrosis of the injured segment of the spinal cord-> fundamental causes for secondary damage to the spinal cord
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Front 19

Decreased perfusion to the spinal cord likely results from what

Back 19

a. Loss of autoregulation (maintaining systemic blood flow may help mitigate some of this), destruction of the microvasculature, thrombus formation, and vasospasm induced by increased intracellular calcium concentrations , release of vasoactive chemicals (affect grey matter first before white matter)
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Front 20

What drugs have been used in human medicine to help improve spinal cord blood flow

Back 20

a. Calcium channel antagonists, NSAID, free radical scavengers, and opioid antagonists such as naloxone
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Front 21

Increases in intracellular calcium concentrations cause what impact to the cells

Back 21

a. Activation of intracellular proteases, phospholipase A2, impairment of mitochondrial function, spasm of smooth muscle, and binding of phoshpates by calcium depleting energy sources
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Front 22

How does free radical production cause secondary damage to the spinal cord

Back 22

a. Lipid peroxidative damage to membranes. Pretreatment with vitamin E and selenium has been shown to be beneficial but not clinically producible.
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Front 23

What steroid has been proposed for its free radical scavenging actions

Back 23

a. Methylprednisolone as it is a free radical scavenger and has neuroprotective effects but timing of the medication is imperative and at a certain dosage. DMSO had significant side effects so not recommended
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Front 24

Why are NMDA antagonists proposed to potentially be beneficial

Back 24

a. NMDA receptors interact with excitatory amino acids such as glutamate and aspartate and result in cellular swelling
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Front 25

Why is naloxone potentially beneficial in spinal cord damage

Back 25

a. Helps to offset endorphin mediated local ischemia to the injured spinal cord
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Front 26

What effects does thyroid releasing hormone have

Back 26

a. Neurotrophic effects, influences on plasticity, and facilitation of motor neuron firing. Has increased side effects but some of these are mitigated by new generation drugs
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Front 27

What are microglial cells

Back 27

a. Endogenous phagocytic cells of the CNS and can release potentially cytotoxic chemicals such as hydrogen peroxide, nitric oxide, proteinases, and cytokines interleukin I and TNF alpha within minutes after inducing cerebral ischemia
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Front 28

What substances are likely to attenuate effects of excitatory amino acids

Back 28

a. Gangliosides
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Front 29

What is not recommended as treatment for improving cerebral perfusion

Back 29

a. CSF drainage
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Front 30

What is syringomyelia

Back 30

a. Where fluid-filled cavities develop in the spinal cord
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Front 31

What is the consensus on how syringomyelia develops

Back 31

a. Is not a consensus yet, the exact mechanism is still debated and it is unknown whether the syrinx develops because of increased pressure in the subarachnoid space or because increased pressure in the spinal cord. The source of fluid is also debateable and unclear if CSF fluid of ECF fluid
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Front 32

What are the most common clinical signs

Back 32

a. Pain localized to the cervical region, could worsen at night, can seem overly sensitive to touch to the lateral side of the head, neck, shoulder, or sternum. Affected dogs scratch at one area
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Front 33

Are signs of the patient matched to the size of the syrinx

Back 33

a. No but damage to the dorsal horn is a key feature and predictive of more severe pain (where sensory information to the brain comes from, expression of substance P is expressed here too)
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Front 34

What other CNS deficits might be seen in affected dogs

Back 34

a. Thoracic limb weakness and muscle atrophy and pelvic ataxia and weaknes, facial paralysis, and deafness
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Front 35

How is syrinogmyelia diagnosed

Back 35

a. MRI
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Front 36

How is syringomyelia treated

Back 36

a. Not treated in small or asymptomatic patients ; medical management includes pain medications, NSAIDS, medications to reduce CSF production, and corticosteroids
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Front 37

When is surgical treatment indicated

Back 37

a. When medical management does not control pain or when neurologic symptoms worsen or are severe
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Front 38

What medications are used to reduce CSF production

Back 38

a. Proton pump inhibitors (may not be able to use long term), carbonic anhydrase inhibitors such as azetazolamide (increased adverse effects), lastly furosemide
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Front 39

What benefits do steroids offer

Back 39

a. Decrease CSF pressure, modulate pain through substance P
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Front 40

What is the most common surgery performed on dogs

Back 40

a. Suboccipital decompression
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Front 41

What are lysosomal storage diseases

Back 41

a. Deficiency in enzyme (s) within the lysosomal catabolic pathyway
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Front 42

What are the main subgroups of lysosomes

Back 42

a. Glycoproteinoses, oligosaccharidoses, sphingolipidoses, mucopolysaccharidoses, and proteinosis
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Front 43

Therapies for lysosomal storage disease are directed at what

Back 43

a. Single enzyme deficiencies with enzyme replacement, bone marrow transplant, and gene replacement protocols
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Front 44

Do these diseases have a gender predilection and do they manifest only at young age

Back 44

a. No and no
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Front 45

What kind of neurological signs may be seen with these disorders

Back 45

a. Behavioral changes, loss of learned behavior, vacancy, ataxia, proprioceptive deficits, apparent blindness, deafness, seizure activity -> see tremors, ataxia, dysmetria, nystagmus, progression to paresis and paralysis
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Front 46

What are some other common signs that might be seen

Back 46

a. Ocular manifestations, skeletal abnormalities such as deformation of long bones, development of dysostoses multiplex-> if multifocal neurologic disease is seen then lysosomal storage diseases should be among the differential diagnoses
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Front 47

What is the most useful diagnosis in these diseases

Back 47

a. Muscle biopsy; lysosomal enzyme analysis, and molecular genetic testing
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Front 48

What is a phenotype:

Back 48

a. Physical manifestation of a trait (influenced by more than the genetics)
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Front 49

What is a genotype

Back 49

a. Genetic makeup of an individual with respect to the gene being considered (the alleles)
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Front 50

What is an allele

Back 50

a. One of alternate forms of a gene or locus
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Front 51

What is segregation

Back 51

a. Separation of alleles during meiosis which determines which allele is passed to an offspring
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Front 52

What is recombination

Back 52

a. 2 copies of a chromosome may cross over during meiosis which results in exchange of genetic material and a new combination of alleles
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Front 53

What is the locus

Back 53

a. Location of a gene or genes on a chromosome; often used as a vague proxy for gene in gene mapping studies before the specific gene is identified
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Front 54

What is the codon

Back 54

a. 3 nucleotide code for an amino acid or the initiation or stop of the protein translation
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Front 55

What is the variant

Back 55

a. Variation in the DNA sequence of an individual from the reference sequence. Could be disease causing mutation or it could be neutral
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Front 56

What is a single neucleotide polymorphism

Back 56

a. Variants where only a single nucleotide is substituted, most common type of variant
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Front 57

What is a frame shift

Back 57

a. Deletion or insertion of any number of nucleotides not divisible by 3 shifting the reading frames of the codon which follow. In turn, changes the subsequent amino acid sequence and location of the stop codon
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Front 58

What are missense mutations

Back 58

a. Change a codon so that a different amino acid is specified , alters protein structure
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Front 59

What is a nonsense mutation

Back 59

a. Changes amino acid specifying codon to a premature stop codon resulting in a truncated nonfunctional protein
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Front 60

What is a phenocopy

Back 60

a. A phenotype that is very similar to the trait under investigation but has a different cause. Sometimes it is from an acquired disease that imitates the signs of a hereditary disease
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Front 61

What is the explanation for a homozygous mutant allele being present but the animal is not effected

Back 61

a. Because incomplete penetrance
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Front 62

Should all heterozygous breeding animals be taken out of a breeding pool when detected by DNA tests

Back 62

a. No, should just use discretion in breeding those animals however
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Front 63

What are the common signs of canine meningitis

Back 63

a. Cervical pain and rigidity are common in meningitis, hyperesthesia manifested by reluctance to walk, arched spine, and resistance to passive manipulation of the head, neck, and limbs. Vomiting and nausea from increased ICP
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Front 64

What is steroid responsive suppurative meningitis

Back 64

a. Most common form of meningitis diagnosed in most veterinary hospitals, most often in large dogs less than 2 yrs of age -> fever, cervical rigidity, and vertebral pain. Diagnosed with CSF showing increased protein and neutrophilic pleocytosis, waxing and waning course. Rapidly responds to steroids. Proposed immune etiopathogenesis
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Front 65

How does vasculitis manifest as meningitis

Back 65

a. Severe necrotizing vasculitis of the CNS is recognized in Beagles, Bernese Mountain Dogs, German Short-haired pointers. Young dogs are more commonly affected -> classical signs of fever, cervical rigidity, and spinal pain are seen. Progression to more severe signs if no therapy is instituted sucha s paralysis, blindness, and seizures. Treatment with steroids is effective in some dogs. Necropsy will show leptomeningitis with severe arteritis. Vasculitis syndromes are commonly caused by immune complex deposition
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Front 66

What is pyogranulomatous meningoencephalomyelitis

Back 66

a. Acute rapidly progressive disorder in mature pointers. Despite therapy, many dogs are euthanized (antibiotic therapy will help but does not stop progression. Steroids have not been tried in this disease)
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Front 67

What is granulomatous meningoencephalomyelitis

Back 67

a. Progressive granulomatous disease of the CNS has been recognized primarily in young dogs of small breeds such as poodles and terriers. There are focal, disseminated, and ocular forms which can often occur together. Has a rapid onset and 25% of cases progress to death in a week in the disseminated case. CSF shows pleocytosis consisting of lymphocytes, monocytes, and occasional plasma cells. Most cases progress despite treatment with steroids and prognosis for permenant recovery is poor. Lesions predominate in white matter
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Front 68

Bacterial meningitis can result from what sources

Back 68

a. Local extension of local tissues such as eyes, ears, sinuses, nasal passages, or areas of osteomyelitis. Hematogenous spread from endocarditis, prostatitis, metritix, discospondylitis, Pyoderma, and pneumonia
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Front 69

What bacteria are implicated in bacterial meningitis

Back 69

a. Staph aureus, staph epidermis, pasturella multocida, actinomyces, and nocardia
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Front 70

How are clinical signs different in these dogs vs. other cause for meningitis

Back 70

a. Often very sick and can have shock, hypotension, DIC, predominant CSF with neutrophilic pleocytosis. Blood cultures are best way to diagnose but not always positive
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Front 71

What antibiotics get good penetration in the CSF

Back 71

a. Chloramphenicol (bacteriostatic), trimethoprim, sulfonamides, and metronidazole. Ampicillin likely gets in the CSF when there is inflammation
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Front 72

What biochemical changes might be evident in a dog with distemper meningitis

Back 72

a. CBC with lymphopenia, distemper inclusions in circulating lymphocytes, lymphocytic pleocytosis in CSF
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Front 73

What other infectious disease processes are known to cause meningitis

Back 73

a. Toxoplasmosis, parvovirus, acanthamoeba castellani, Cryptococcus neoformans, Aspergillosis , blastomycosis, Histoplasmosis, coccidioides immitis, RMSF, ehrlichia canis, dirofilaria immitis, toxocara canis, angiostrongylus cantonensis, ancylostoma caninum, Cuterebra, and prototheca