Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VET433A > Week 2-3 - Neuro > Flashcards

Week 2-3 - Neuro Flashcards

1
Q

Contraindications of KBr for seizure management (3)

A
  1. Renal dz (b/c KBr is eliminated via the kidneys)
  2. Hx of pancreatitis (since KBr can cause pancreatitis in dogs)
  3. Rapid control of seizures needed (b/c KBr has a long elimination half life at ~24 days, so it reaches steady state at 3-4 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Zonisamide - adverse effects: (6)

A
  1. Sedation and ataxia - self-limiting within first two weeks of therapy, worse in large breeds
  2. GI upset - hyperemia, v/d
  3. Immune-mediated keratoconjuncitvitis sicca (KCS), polyarthropathy (b/c sulfonamide derivative)
  4. Renal tubular acidosis (b/c sulfonamide derivative)
  5. Decreased T4
  6. Acute hepatic necrosis (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Zonisamide - contraindications: (1)

A
  1. Pre-existing keratoconjuncitivitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Levetiracetam - metabolism:

A

-70-90% excreted in urine (bioavailability is nearly 100%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Levetiracetam - adverse effects (2):

A
  1. Sedation and ataxia
  2. Anorexia in cats

usually uncommon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Levetiracetam - contraindications: (1)

A
  1. Poor efficacy as a monotherapy for epilepsy (EXCEPT for feline audiogenic reflex seizure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Levetiracetam – what does the honeymoon period refer to?

A

Honeymoon period – great response to drugs in the beginning, then fades away

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is refractory epilepsy?

A

When there is a failure of adequate trails of two tolerate, appropriately used anti-epileptic drugs (AEDs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When should a second AED be added? (4)

A

ACVIM Panel recommends:
1. appropriate drugs and maximal level of first AED for a minimum of 3mo
2. >50% increase in seizure frequency over 3mo
3. new onset of status epilecticus or cluster seizures
4. present of drug toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When do we start AED (anti-epileptic drug) therapy? (4)

A
  1. identifiable structural lesion OR hx of encephalopathy/trauma
  2. acute, repetitive seizures (3 or more generalized seizures in 24 hrs, status epilecticus)
  3. 2 or more seizure events within 6 months
  4. prolonged, severe, or unusual post-ictal period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What diagnostics should you recommend for a seizing patient? (4)

A
  1. minimum database (CBC, chem, UA, 3-view thoracic rads, abdominal US)
  2. intracranial imaging (MRI - gold standard)
  3. CSF analysis
  4. EEG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When are seizures considered an EMERGENCY? (3)

A
  1. status epilecticus
    a. ictus 5 min or more
    b. 2 or more seizures without regaining consciousness
  2. cluster seizures (3 or more generalized seizures within 24 hours)
  3. failure to regain consciousness within 1-2 hours of ictus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Status epilecticus risks: (2)

A
  1. intoxication (bromethelin, caffeine, chocolate, etc. – toxins in the CNS)
  2. idiopathic epilepsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Status epilecticus: How does Ca2+ contribute to primary brain injury?

A

NEURONAL DEATH via excitatory neurotoxicity –> an influx of Ca2+ is BAD – it causes cells to apoptose, adds oxidative stress, causes dendritic remodeling, inflammation, and necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Status epilecticus: How/why does cerebral edema contribute to primary brain injury?

A

during a seizure, higher metabolic demands increases cerebral blood flow (200%-700%)

  1. hyperperfusion – BBB disruption
  2. if metabolic demands are not med, then LACTATE is made – BBB disruption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The 2 Phases of Status Epilecticus

A

Phase I: Compensated status epilecticus
-increase in autonomic activity
-elevated catecholamines, endogenous steroids
-hypertension, tachycardia, hyperglycemia, hyperthermia, ptyalism (drooling)
-temperature will increase

Phase II: Uncompensated status epilecticus
-~30 min following continuous ictus – cerebrovascular auto regulation fails, ICP rises
-hypotension, hypoglycemia, hyperthermia, hypoxia

…ultimately leading to:
-respiratory failure
-metabolic acidosis
-hyponatremia
-hyperkalemia

RISK FOR SUDDEN DEATH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Systemic effects of Status Epilecticus (3)

A
  1. Kidneys: poor perfusion + muscle death –> lead to acute renal failure
  2. Skeletal muscle: death of muscle secondary to hyperthermia
  3. Heart: arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Convulsive status epilecticus (CSE) characteristics: (3)

A
  1. generalized tonic/clonic movements
  2. impaired consciousness
  3. +/- autonomic manifestations

majority of dogs/cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Non-convulsive status epilecticus (NCSE) characteristics: (3)

A
  1. EEG evidence of seizure activity without clinical appearance associated with CSE
  2. may occur before or after convulsive seizures are present
  3. could be for patient with prolonged period of impaired consciousness following CSE tx

EEG necessary to rule out NCSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Goals of seizure treatment/status epilecticus: (4)

A
  1. stop the seizure
  2. prevent further seizures
  3. manage seizure complications
  4. manage underlying conditions causing seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which 1st line anti-epileptic drug should be administered in an emergency? (2)

A

BENZODIAZEPINES

  1. Diazepam: IV (0.5mg/kg) or per rectum (1-2mg/kg)
  2. Midazolam: IV or IN (0.2-0.5mg/kg)

midaz>diaz, midaz more favorable

20lb dog = 0.5mL midazolam IV/IN; 1mL diazepam IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What other aspects should you consider when trying to STOP THE SEIZURE (emergency setting)? (5)

A
  1. establish IVC access
  2. check electrolytes
  3. supply flow-by O2, bc PaO2 <50 increases ICP (and we don’t want increased ICP)
  4. if hyperthermic, cool down! (stopping seizure will help this)
  5. blood pressure - if elevated ICP, reduce it (hypertonic saline, mannitol, keep head elevated over 30 degrees)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

I’ve given 2-3 benzodiazepine boluses and started CRI AND loaded with a a long-acting AED. Patient is still seizing. Now what?

A

Patient is refractory!

  1. Propofol – GABAa receptor agonist/inhibits NMDA receptors
    -modulates slow Ca2+ ion channels
    -administer as CRI bc half life is very short
  2. IF STILL SEIZING – add inhalant anesthetic gases
    -iso/sevo - GABAa recepter agonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Cushing’s Reflex?

A

It’s a reflex in response to increased ICP. Increased ICP decreases cerebral blood flow, so ischemia occurs. Ischemia causes systemic hypertension (increases mean arterial pressure) to try and improve blood flow. Baroreceptors sense the increased MAP and have a reflex bradycardia.

Ultimately results in
-increased systolic BP
-low HR
-low RR (?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Trigeminal nerve is which CN? What are its branches?

A

CNV

a. opthalmic - (sensory)
b. maxillary (sensory)
c. mandibular (motor - for mastication, sensory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Mandibular nerve exits the skull through _____ foramen.

A

OVAL foramen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the muscles of mastication? (3)

A

There are 5, but the ones we should know are:

  1. masseter
  2. termporalis
  3. pterygoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

All sensory axons for CNV enter the _______ ___ ___ ____.

A

brainstem at the pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

CNV Testing: Cutaneous Sensation methods: (4)

A
  1. Corneal reflex: moist Q-tip, gently touch cornea, observe retraction of globe/eye blink
    -afferent: CNVa (ophthalmic)
    -efferent: CNVI +/- CNVII
  2. Palbebral reflex: touch lateral and medial canthus of eyes, observe eye blink
    -afferent: CNVa and CNVb (ophthalmic and maxillary)
    -efferent: CNVII
  3. Trigeminofacial reflex: Touch area of maxillary vibrissae, observe for eye blink
    -afferent: CNV (ophthalmic and maxillary)
    -efferent: CNVII
  4. Noxious responses:
    -requires cortical processing (not just reflex)
    -afferent: CNV
    -blunt stimulation of nasal mucosa (CNVa and CNVb)
    -Noxious stimulus to the lateral maxilla at the level of the canine tooth (CNVb –> lead to efferent CNVII)
    -Noxious stimulus to the lateral mandible at the level of the canine tooth (CNVc –> lead to efferent CNVII)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

CNV Testing: Motor Function: (3)

A
  1. paresis/paralysis: ability to close mouth and pretend food, difficult to see if unilateral
  2. atrophy: mastication muscles, eyes may be sunken in due to atrophy of pterygoid m.
  3. symmetry and tone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical signs of CNV Dysfunction (Sensory, 6 and Motor, 3)

A

SENSORY Dysfunction:
1. decreased sensation (hypesthesia, anesthesia)
2. decreased or absent reflexes (palpebral, corneal, trigeminofacial)
3. reduced facial sensation
4. corneal ulcer
5. abnormal (paresthesia, hyperesthesia)
6. rubbing or pawing at face

MOTOR Dysfunction
1. masticatory muscle paresis or paralysis
-unilateral—difficult to detect clinically
-bilateral—dropped jaw, inability to close mouth, drooling, difficulty in prehending food
2. masticatory muscle atrophy (masseter, temporalis, pterygoids)
-severe neurogenic atrophy (unilateral or bilateral), “caved in head”
3. trismus (difficulty opening mouth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Localizing a CNV lesion (2)

A
  1. Intracranial: brainstem - pons and rostral medulla
    -motor and sensory dysfunction
    -brainstem signs:
    -CN deficits, esp CNVII and CNVIII
    -ipsilateral hemiparesis
    -obtundation
    -CP deficits
    -cerebellar signs
  2. Extracranial
    -signs vary
    -NO brainstem signs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How to diagnose a CNV lesion?

A
  1. hx
  2. clinical signs
  3. advanced imaging (MRI preferred over CT)
  4. CSF analysis
  5. +/- skull radiographs
  6. for dogs: +/- type 2M antibody serology (for masticory muscle myositis - MMM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CNV Disease: Idiopathic Trigeminal Neuropathy

A

IDIOPATHIC: Idiopathic Trigeminal Neuropathy

-aka trigeminal neuritis
-don’t know underlying dz
-common in dogs, uncommon in cats
-ACUTE onset - dropped jaw, inability to close mouth
-dysphagia, drooling
-sensation usually normal
-atrophy common, may be unilateral
-+/- Horner’s syndrome, facial paralysis associated

DIAGNOSIS
-hx, clinical signs
-negative serology for type 2M antibody (rule out MMM)
-MRI + CSF (may see enhancement of trigeminal nerve(s) and masticatory muscle atrophy on MRI)
-diagnosis of exclusion
-electrophysiology and muscle biopsy (not common), biopsy difficult

TX
-supportive care - tube feeding, fluids
-corticosteroids NOT recommended

PROGNOSIS
-usually resolves within 2-6 weeks

RULE OUT DDX:
-Masticatory muscle myositis (MMM) – usually don’t have dropped jaw though, usually have trismus, not unilateral, may have muscle swelling or pain
-neoplasia: lymphoma, round cell neoplasia
-infection: rabies
-trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

CNV Disease: Infection: Rabies

A

-predilection for brainstem: most common clinical signs:
-pharyngeal paralysis: (nucleus ambiguous (CN IX and X))
-dropped jaw (motor nucleus of CN V)
-clinical signs are progressive once neurological signs are apparent
-obtain a thorough history from ALL animals with a hx of DROPPED JAW, including
vaccination history, and environment (re: exposure) history, remember, this is a zoonotic
disease

-incubation: 7 days to 1 year

-recovery rare once CS develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

CNV Disease: Neoplasia and Trauma

A

NEOPLASIA

  1. intracranial
    -primary and secondary neoplasia
  2. extramedullary
    -lymphoma
    -malignant peripheral nerve sheath tumor
    -squamous cell carcinoma and parotid adenocarcinoma.

-a good minimum database is important. Prognosis generally poor but varies with type of neoplasia.

TRAUMA

-signs are acute, and other cranial nerves such as the facial nerve, may also be involved
-resolution of signs depends on the severity of the injury

37
Q

CNVII Functions

A

-motor: facial expression
-sensory: concave surface of skin on pinna
-taste to rostral 2/3 of tongue
-parasympathetic fibers to lacrimal and salivary glands

38
Q

CNVII and CNVIII exits brainstem at _____ _______ _______

A

INTERNAL ACOUSTIC MEATUS

39
Q

CNVII exits the skull at the _______ foramen.

A

Stylomastoid

40
Q

CNVII Testing - Which reflexes? (4)

A
  1. Menace (A: CNII, E: CNVII)
  2. Corneal (A: CNVa, E: CNVII)
  3. Palpebral (A: CNVa/b, E: CNVII)
  4. Trigeminofacial (A: CNVa/b, E: CNVII)
41
Q

CNVII Motor Dysfunction

A

-inability to close eye
-dropping ear, eyelid, lip
-widening of palpebral fissure
-NO nostral flare
-facial spare (rare)

42
Q

CNVII Sensory Dysfunction

A

-impaired taste
-reduced or absent sensation on medial surface of pinna
-hyperacusis (hypersensitivity to normal sound)

43
Q

What is CNVII’s parasympathetic function? How does an autonomic dysfunction of CNVII present?

A

-Lacrimation (Schirmer tear test)
-presents as dry eye and nose – can lead to corneal ulcers

44
Q

Localization of CNVII lesions?

A
  1. Intracranial - brainstem
    -motor, sensory, and parasympathetic involved
    -ipsilateral CNVII paresis/paralysis
    -reduced/absent lacrimation, taste
    -other brainstem signs (obtundation, CP deficits, etc)

INTEROSSEOUS NERVE
CN VII paresis/paralysis (reduced to absent reflexes)
-No brainstem signs
-+/-taste sensation
-+/-lacrimation
-CN VIII signs +/-
-Signs of middle ear disease may be present (+/- vestibular signs, signs of Horner’s syndrome)

  1. Extracranial
    -CS depend on localization of lesion along nerve
    -NORMAL lacrimation and taste
45
Q

CNVII Diagnosis plan

A

-CS
-hx, PE, NE
-Schirmer tear test, taste test
-electrodiagnostics (BAER to evaluate CNVIII, EMG, NCV) - not common
-MRI + CT
-skull rads
-CSF analysis
-otoscopic exam

46
Q

Ddx of CNVII Neuropathies:

A
  1. IDIOPATHIC: Idiopathic Facial Nerve Paralysis
    -dogs and cats (cocker spaniels)
    -acute, usually unilateral
    -reduced tear production
    -+/- Ipsilateral peripheral vestibular signs
    -localization: peripheral, proximal to geniculate ganglion
    -pathology: no inflammation, degeneration of myelinated fibers
    -diagnosis of EXCLUSION
    -MRI and CSF
    -prognosis: good - weeks to months (contracture with chronicity)
    -Tx/therapy - eye ointment to prevent exposure keratitis, monitor for KCS/corneal ulcers
    -NO corticosteroids
  2. INFECTIOUS: Otitis Media/Interna
  3. NEOPLASIA:
    -Lymphoma
    -Compression or invasion of facial nerve caused by tumors of surrounding tissue
    (adenomas, adenocarcinomas, squamous cell carcinoma, osteosarcoma, fibrosarcoma etc)
    especially of the middle ear and petrous temporal bone
    -Brainstem neoplasia may affect the facial nerve (meningioma)
  4. TRAUMA
    -bite wounds to head
  5. METABOLIC
    -Hypothyroid facial neuropathy in dogs
    -Existence is suspected, but NOT proven
  6. INFLAMMATION
    -May be associated with polyradiculoneuritis, brachial plexus neuritis
  7. MOTOR UNIT DZ
    -myasthenia gravis
47
Q

Function of the vestibular system? (2)

A

-maintain steady visual image
-maintain steady body position

48
Q

Function of the middle ear?

A

-sound conduction and amplification

-NO vestibular part of middle ear – (no middle ear dz with vestibular dz)

49
Q

Function of the Inner Ear?

A

-fxn: balance and equilibrium

-has auditory and vestibular components

-bony labyrinth - perilymph - semicircular canals vestibule
-membranous labyrinth - endolymph - semicircular ducts, utriculus/saaculus

50
Q

In the vestibular pathway, axons project to: (2)

A
  1. vestibular nuclei (in brainstem) - rostral, caudal, medial and lateral; located lateral to the 4th ventricle)
  2. Vestibular portion of the cerebellum (flocculonodular lobe and fastigial nuclei)

cells of origin - lateral vestibular nucleus

51
Q

What is peripheral vestibular dz?

A

-Dz of the receptors or vestibular nerve (issues with the ear – labyrinth or vestibular nerve itself)

nystagmus: horizontal or rotary ONLY (fast phase away from lesion
-non-positional
-conjugate
strabismus: ventral or ventrolateral
-dysconjugate
-ipsilateral to lesion

CNVII deficits are in peripheral OR central vestibular dz – but if more, then it’s CENTRAL dz

associated problems:
-facial nerve/CNVII paresis/paralysis
-Horner’s syndrome
-otitis externa, media-interna
-pain on palpation of bulla/TMJ
-pharyngeal pain

52
Q

What is central vestibular dz?

A

Brain issue – dz of the vestibular nuclei (in brainstem), vestibular part of the cerebellum (the floculonodular lobe and the caudal cerebellar penduncles) and pathways
-paradoxical

-nystagmus: can be anything, BUT vertical, positional, dysconjugate ALWAYS central dz ( but CAN BE horizontal/rotary, non-positional, conjugate)

-altered level of consciousness - usually decreased bc of RAS in brainstem

-CN deficits (esp. CNV)

-long tract signs:
–Ascending tracts (sensory). Particularly postural deficits such as loss of conscious
proprioception ipsilateral to the lesion.
–Descending tracts (motor). Paresis or paralysis ipsilateral to the lesion.

-Cerebellar signs
Dysmetria, hypermetria, intention tremor may be present if areas of the cerebellum other than the vestibulocerebellum are involved in the disease process

-seizures

53
Q

Clinical signs of Vestibular Dz (6)

A
  1. Nystagmus (pendular - congenital, or jerk) – named for fast phase (fast phase is away from lesion)
    -conjugate or dysconjugate
    -horizontal/rotary or vertical (usually central)
    -positional or non-positional
  2. Strabismus
  3. Head tilt (leaning/rolling)
    -circling but NO head tilt … not likely vestibular
    -tilt towards lesion
  4. Tight circling
    -tilt towards lesion
  5. Ataxia
  6. Nausea +/- vomiting, salivating

vestibular signs are almost always IPSILATERAL to lesion

54
Q

What is bilateral peripheral vestibular dz?

A

-No normal or abnormal nystagmus
-Crawling, crouching posture, often falling or staggering to either side
-Characteristic wide head excursions from side to side
-Symmetrical ataxia with preservation of strength
-Flexion of the neck ventrally when suspended by the pelvis

55
Q

What is central paradoxical vestibular dz?

A

special form of central vestibular disease, and is termed paradoxical because the vestibular signs are directed to the side OPPOSITE the lesion.

-Head tilt AWAY from the lesion
-Positional ventral strabismus on the side AWAY from the lesion.
-Fast phase of nystagmus TOWARDS the side of the lesion.

need other neurological deficits to recognize
-brainstem signs (CP deficits, paresis, CN deficits) will be ipsilateral to the lesion and will reflect the TRUE laterality of the lesion

Lesions causing paradoxical vestibular disease are usually destructive lesions such as neoplasms or inflammatory disease and often involve the caudal cerebellar peduncle and/or flocculonodular lobe.

Paradoxical signs are probably due to loss of cerebellar inhibition of the vestibular output on the
side of the lesion

56
Q

When is the auditory system developed in dogs?

A

Normal hearing developed by 4-5 weeks of age in dogs

57
Q

What are the types of deafness? (2)

A
  1. Peripheral Deafness
    a) Conductive deafness: Failure of sound transmission to the inner ear caused by abnormalities
    within the external or middle ear cavity
    b) Sensorineural deafness: Failure of sound transduction by the spiral organ or failure of
    propagation of nerve impulses in the auditory (VIII) nerve
  2. Central
    This is RARE. Due to the extensive crossing over of pathways at several levels, lesions causing
    central deafness must involve both temporal lobes, or the pathways in the brainstem bilaterally
58
Q

How is metronidazole related to central vestibular disease?

A

Doses of metronidazole over 50-60 mg/kg daily have been associated with acute onset of vestibular signs, often with a marked vertical nystagmus and ataxia. Other CNS signs
such as seizures may be apparent

Injury to purkinje cells in cerebellum

59
Q

What are the 6 lobes of the brain?

A
  1. Frontal - behavior, planning, judgement - contains primary motor cortex
  2. Olfactory - smell – sensory info does NOT go through thalamus
  3. Parietal - somatosensory - pain, position, temperature, vibrations
  4. Temporal - auditory
  5. Occipital - vision
  6. Limbic - contain hypothalamus, amygdala, etc. - emotion, memory, instinct (4 F’s)
60
Q

What is MUO?

A

Meningoencephalitis of unknown origin

MUO describes GME and NME/NLE

GME - granulomatous meningoencephalomyelitis (back of brain dz)
NME/NLE - necrotizing disease

61
Q

What are the 3 clinical forms of GME (granulomatous meningoencephalomyelitis)?

A
  1. ocular
  2. focal (50% of cases)
  3. multifocal

brainstem dz is common for GME

62
Q

Typical signalment of GME?

A

-typically young breeds
-young to middle-aged
-female>male

63
Q

Clinical signs of GME?

A

-vestibular
-long tract signs (postural reaction deficits and paresis)
-cerebellar
-CN deficits
-seizures

64
Q

MRI and Pathology for GME

A

-focal vs. multifocal
-variable lesion pattern
-can be normal

-lymphoplasmacytic inflammation
–ENCEPHALITIS and/or MYELITIS
–perivascular cuffing

65
Q

Typical signalment for NME (Necrotizing Meningoencephalitis)

A

-small breeds (pug, chihuahua, maltese, pekingnese) - PUG encephalitis
-young (median age 18mo)
-female>male

Pugs can inherit genes for NME – homozygous carriers have 1:8 risk of NME
–genetic test

66
Q

Clinical Signs of NME (Necrotizing Meningoencephalitis)

A
  1. predominantly cerebral
    -seizures
    -mentation changes
    -behavioral changes
    -compulsivity, pacing
  2. often asymmetric - circling

seizures is common for NME/NLE

67
Q

MRI and Pathology for NME

A

-lymphoplasmacytic inflammation
–MENINGITIS AND ENCEPHALITIS
–necrosis and cavitation

68
Q

Typical Signalment for Necrotizing Leukoencephalitis (NLE)

A

-small breeds (yorkie, frenchie, Pomeranian) – YORKIE Encephalitis
-young to middle-aged
-no sex predilection

69
Q

MRI and Pathology of NLE

A

-lymphoplasmacytic inflammation
–deep white matter encephalitis
–no meningitis
–necrosis and cavitation

70
Q

CSF Analysis in Inflammatory Brain Diseases (4)

A

-pleocytosis (>5 cells)
-elevated protein
-infectious dz testing negative
-can be normal

71
Q

Definitive diagnosis of Inflammatory Brain Disease

A

-biopsy
-$$$

72
Q

Tx for Inflammatory Brain Disease

A

Immunomodulation
–corticosteroids most widely used
–slowly taper meds once in remission

Adjunctive Immunomodulatory therapies
–to reduce corticosteroid use
–increase treatment efficacy

3 treatment groups:
1. corticosteroids alone
2. corticosteroids + radiation therapy
3. corticosteroids + 1 (or more) adjective drug

73
Q

Risk factors for Inflammatory Brain Disease

A

Dz is NOT associated/not risk factors for IBD:
-BCS
-Season
-Time since last vaccination

NO IDEA what the issue is/risk factors are

we know it’s an auto-immune dz, so do we vaccinate or not?

74
Q

Prognosis for Inflammatory Brain Disease

A

Postive:
-younger age at diagnostics
-focal dz
-referral within 7 days within onset of signs

Negative:
-seizures, altered mentation
-mass effect, brain herniation on MRI

Outcome:
-33% mortality rate despite tx
-out of remaining 65%, 2/3 will relapse
-survival at one month likely predicts long-term survival

75
Q

Origin of Primary Brain Tumors

A

-Neural Tube - astrocytomas, oligodendroglioma
-Neural Crest - meningioma, schwannoma

76
Q

Meningiomas

A

-from neural crest
-most common primary tumor in dogs and cats
-median age
-dog: goldens, boxer, min schnauzer
-cat: domestic shorthair

cellular origin: arachnoid vill(?)

extra-axial tumors - surface oriented (outside the brain)

77
Q

Glioma

A

-from neural tube
-second most common primary brain tumor in dogs, rare in cats

-astrocytoma FROM astrocytes (supporting cells of CNS)
-oligodendroglioma FROM oligodendrocytes (mylenating cell of the CNS)

-median age
-dog: boxer, boston terrier, bulldog, pitbull
–dogs 50% of gliomas
–boxers 50% of all oligodendroglioma

-intra-axial tumor – from within brain parenchyma

78
Q

Secondary Brain Tumors (does not originate from brain)

A

50% of all intracranial neoplasia in dogs

metastatic
-hemangiosarcoma (common in dog)
-lymphoma (younger animals, can be primary) (common in cat)

invasive
-pituitary tumor (common in cat)

79
Q

Clinical signs with Brain Tumors

A

CATS
-behavioral changes
-seizures
-altered mentation
-circling
-non-specific lethargy, anorexia

DOGS
-seizures
-circling
-ataxia
-head tilt
-altered mentation

80
Q

Diagnosis of Brain tumors - what do you need? (4)

A
  1. minimum database
  2. imaging (skull rads, CT, MRI, PET)
  3. CSF analysis
    -intracranial neoplasia = normal cell count + elevated protein
    -usually not super helpful
  4. biopsy
81
Q

What is myoclonus?

A

a sudden lightning-like involuntary movement of short duration caused by muscle activity

usually focal but can be multifocal

82
Q

What is a tremor?

A

Rhythmical oscillatory movement of a body part, mourned an axiom resulting from alternate or synchronous contraction of antagonistic muscle groups

83
Q

What is an action tremor?

A

tremor that occurs during voluntary contraction of skeletal muscle

postural and kinetic tremors!

84
Q

What is a postural tremor?

A

An action tremor that occurs in a body part that is voluntarily maintained against gravity (eg. standing)

85
Q

What is a kinetic tremor?

A

an action tremor that occurs during directed voluntary movement

intention tremor – amplitude increases during pursuit of target

86
Q

How does Lysosomal Storage Diseases cause tremors?

A

-rare
-affect CNS - cause tremors
-metabolic by-products accumulate in neurons due to enzyme deficiency
-dz most likely inherited
-young animals <1 year
-many dz affect cerebellum
-genetic testing
-BW and UA
-no effective therapies
-poor prognosis

87
Q

Cerebellar has 3 cortex layers:

A
  1. molecular (superficial)
  2. purkinje (intermediate)
  3. granular (deep) – cerebellar nuclei, a lot of neurons
88
Q

Cerebellar embryology

A

-from metencephalon

-2 germinal cell migration groups
1. purkinje layer and cerebellar nuclei migrate (don’t divide, just migrate)
2. external germinal layer – goes to surface of cerebellum and divides to 10-12 layers thick, stops diving then migrates into cerebellum, forms the granular cell layer (deep)

late in gestation, post-natal

89
Q

Clinical signs of cerebellum dysfunction

A
  1. ataxia
  2. dysmetria
  3. vestibular signs
  4. menace reaction deficits
  5. postural reaction deficits
  6. anisocoria
  7. increased muscle tone +/- hyperflexia

CS are IPSILATERAL to lesion

VET433A (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions