Brainscape's Knowledge GenomeTM

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


See full index

VET 433a - Small Animal Stream 1 > Neuro pt.1 > Flashcards

Neuro pt.1 Flashcards

1
Q

T/F: a neurological exam is sufficient for evaluation of a neurologic patient.

A

F: need to perform a physical exam as well

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

5 parts of the neuro exam

A
  1. gen observations ( mentation, gait, posture)
  2. cranial nerves
  3. postural rxns
  4. segmental reflexes
  5. palpation and pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

2 areas responsible for proper mentation

A
  1. Reticular Formation

2. Cerebral cortex

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

Levels of mentation

A
  1. appropriate
  2. obtundation ( any decrease in mentation)
  3. stuporous (responds to noxious stimuli only)
  4. comatose (unresponsive to everything)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Classifying gait abnormalities

A
  • partial/ complete
  • ataxia
  • lameness
  • involuntary movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Posture Classificiation

A
  1. Decerebrate
  2. Decerebellate
  3. Schiff-Sherington
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Decerebrate Posture

A
  • extension of neck, thoracic, and hind limbs
  • opisthotonus
  • comatose mentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Decerebellate Posture

A
  • extension of neck and thoracic limbs
  • flexion of hind limbs
  • appropriate mentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Schiff-Sherington Posture

A
  • thoracolumbar myelopathy

- n mentation and thoracic limbs

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

Postural Reactions

A
  • proprioceptive pathways require intact spinal tract, thalamus, cerebrum, and intact motor fxn
  • not great for lesion localization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cranial Intumescence

A

C5 - T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lumbar Intumescence

A

L4 - S3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Biceps Reflex

A
  • musculocutaneous nerve

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Triceps Reflex

A
  • radial nerve

-

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

Patellar Reflex

A
  • femoral nerve

- L4, 5, 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gastrocnemius Reflex

A
  • sciatic nerve

- L6, 7, S1

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

When do we test nociceptive reaction

A
  • only in animals that don’t have voluntary movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cutaneous Trunci Reflex

A
  • C8 - T1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 6 distinct cerebral corticol regions

A
  1. Olfactory Region
  2. Frontal Lobe
  3. Parietal Lobe
  4. Temporal Lobe
  5. Occipital Lobe
  6. Limbic System
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Olfactory Region

A
  • CN 1
  • olfactory tract, bulbs, pyriform lobe
  • only sensory info not processed by thalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Frontal Lobe

A
  • behaviour, planning, judgement

- contains primary motor cortex, motor association cortex

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

Parietal Lobe

A
  • primarily somatisensory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Basal Nuclei

A
  • Striatum ( caudate nucleus)
  • globus pallidus
  • subthalamic region
  • substatia gyri
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cerebral White Matter

A
  • corona radiata
  • internal capsule
  • inter-thalamic adhesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Medial Lemniscal Pathway

A
  • proprioception: consious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Motor Pathways

A
  • corticospinal, rubrospinal, vestibulospinal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Function of the Cerebrum

A
  • Personality
  • Thought
  • receive sensory input & plans the action
  • consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Cerebral Dysfunction

A
  • change in mentation
  • behavioural abn
  • abn movement: pacing, circling, head pressing
  • proprioceptive deficits
  • central blindness, hemi-inattention
  • seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Blindness

A
  • Check PLR (2, 3) and menace (2, 7)

- Central Blindness -> vision loss only (intact PLRS), contralateral loss of vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Hemi-inattention

A
  • neglect or decreased awareness of contralteral environment or body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hydrocephalus

A
  • congenital or acquired
  • dilateion of ventricles, frequently the lateral vent
  • treatment
  • -> congenital (dec CSF production)
  • -> acquired ( treat underlying cause)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

9/10 Rule for Cerebral Disease

A
  • symmetrical, diffuse signs = degenerative, metabolic, nutritional, toxic
  • lateralized = lesion, mass, inflammatory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Cause of Primary Brain Injury

A
  • parenchymal damage

- vascular disruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Cause of Secondary Brain Injury

A
  • Edema/ Inflammation
  • hypoxia
  • ischemia/ neurotoxicity
  • neuronal death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Secondary Acute Brain Injury

A
  • more delayed (minutes to days post-injury)
  • secondary to the primary injury
  • -> inflam mediators –> change in cell permeability –> cellular edema and swelling, increased extracellular glutamate triggering increased [ca] and [na] intracellularly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

ICP Dynamics/ Monroe-Kellie doctrine

A
  • intracranial contents are in a rigid container
  • Brain 80&, Blood 10%, CSF 10%
  • If one volume inc., the others must decrease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

ICP Dynamics ( Immediate and Chronic buffering)

A 
Immediate
--> stretch of Dura
--> displacement of CSF or blood
Chronic 
--> dec. ECF space
--> brain atrophy (think hydrocephalus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Effects of decreased Cranial Blood Flow

A
  • dec CBF –> dec perfusion –> PP = MAP - ICP **
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the Cushing’s Response

A
  • the body will increase MAP in response to elevated ICP tin hopes of maintaining perfusion to the brain
  • will see decreased HR d/t baroreceptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Order of cerebral tissue sensitivity to hypoxia

endothelium, neurons, glia

A
  • neurons (grey matter)
  • glia (white and grey)
  • endothelium (BBB)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Intercranial Hypertension Effects

A
  • mental deterioration
  • brainstem dysfunction
  • loss of motor control
  • abn postures
  • herniation of cerebellum or brainstem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Transtentorial Herniation

A
  • midbrain compression:
  • -> RAS: stupor to coma
  • -> CN3: mydriasis w/ no PLR, strabismus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Foramen Magnum Herniations

A
  • compression of cerebellum and brainstem
  • -> stupor to coma
  • -> resp. arrest, hypoventilation
  • -> CN 10 defecits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How to assess ICP

A
  • on serial examination via imaging or invasive measurement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Treatment of Brain Trauma (6 steps/ actions)

A
  • no corticosteroids
    1. maintain cerebral perfusion pressure (monitor MAP, PaCO2, Cerebral metabolic activity, head position)
    2. Stabilize (ABCs)
    3. Examine (neuro exam may be cursory)
    4. Determine Severity (mentation, posture, pupils)
    5. Treat 2* Brain Injury
    5. Advanged Imaging
    6. Treat Underlying Disease (if applicable)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How to relieve ICP pharmaceutically?

A

Mannitol: 3 mech of actions:

  1. inc. plasma volume and blood viscocity
  2. osmotic diuresis in 30-60 minutes
  3. free radical scavenger
    - - only use mannitol if needed

Hypertonic Saline
- less likely to lead to hypovolemia than mannitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Acute Brain Injury (prognosis)

A
  • okay scoring w/ improvement w/in first 48hrs w/ no serious lesions = guarded but likely to recover fully
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Seizure Thresholds

A
  • sum total of events that regulate neuronal excitability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

T/F: seizures are clinical signs of forebrain disease.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Causes of neuronal hyperexcitability (seizures)

A
  • increased excitatory post-synaptic potentials
  • decreased inhibitory post-synaptic potentials
  • change in ion channels or [ion]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Major neurotrasmitters (seizures)

A

Glutamate: excitatory w/ both Ionotropic and metabotropic
Gaba: inhibitory w/ post-synaptic (A linked to Cl) and pre-synaptic (B linked to K)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Possible mechanisms of seizures

A
  1. ion channel abnormailities
  2. synapse remodeling
  3. extracellular [ion] change
  4. loss of inhibitory neurons
  5. loss of excitatory –< inhibitory neurons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What tool do you use to measure seizure activity

A

EEG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Stages of seizures

A
  1. Prodrome: change in mentation
  2. Aura: just prior to seizure, repetitive motions/ movement occuring, but not seizuring yet
  3. Ictus: seizure event
  4. Post-Ictal: period after seizure; possible mentation/ behaviour change present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Seizure Types:

A
  1. Focal - occurs in a specific part of the brain w/ regionalized signs
  2. Generalized - bilateral involvement/ loss of consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Idiopathic Epilepsy

A
  • onset age (6 mnths - 6 years)
  • normal on the neuro exam
  • mri unremarkable
  • r/o reactive seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Diagnostic Plans for Seizures

A
  • signalment matters
  • minimum database
  • MRI, CT, CSF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Poor Seizure Control

A
  • if you aren’t effectively controlling it, maybe it’s not a seizure
  • poor classification: make sure to treat underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

3 branches of CN V

A
  1. ophthalmic (sensory only)
  2. maxillary (sensory only)
  3. mandibular (sensory and motor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

CN V anatomy of motor pathway

A
  • nucleus in pons
  • mandibular n. exits skull through oval foramen
  • innervates muscles of mastication (masseter, temporalis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

CN V anatomy of sensory pathway

A
  • trigeminal ganglion contains cell bodies

- all sensory axons enter the brainstem at the pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Testing CN V (Cutaneous sensation)

A
  1. corneal reflex (5 ophth., 6 +/- 7)
  2. Palpebral reflex (5 ophth. + max., 7)
  3. trigeminofacial reflex (5 ophth. + max, 7)
  4. Noxious stimuli (requires cortical processing)
63
Q

Testing CN V (Motor function)

A
  • paresis/ paralysis
  • atrophy
  • symmetry
  • dropped jaw
64
Q

Localizing CN V lesions

A
  1. intracranial –> brainstem, pons, rostral medulla
    - brainstem signs are ipsilateral: obtundation, CP defecits, cerebellar signs
  2. Extracranial signs –> no brainstem signs
65
Q

Idiopathic Trigeminal Neuropathy

A
  • common in dogs
  • acute onset dropped jaw, inability to close mouth
  • sensation is normal
  • atrophy common (may be unilateral)
  • +/- Horner’s syndrome
  • Facial paralysis
66
Q

Idiopathic Trigeminal Neuropathy (Diagnosis)

A
  • (-) 2M myofibril serology

- MRI + CSF check

67
Q

Idiopathic Trigeminal Neuropathy (treatment)

A
  • self resolving in a few months
68
Q

Rabies

A
  • enveloped RNA virus
  • clinical signs = death
  • incubation: 7 days - 1 year
  • pathology: hits the motor nucleus in CN 5 to cause a dropped jaw
69
Q

CN VII

A
  • motor - facial expression
  • sensation - concave surface of skin on pinna; taste to rostral 2/3 of tongue
  • exits skull via stylomastoid foramen
70
Q

Testing of CN VII

A
  • Reflexes –> menace, corneal, palpebral, trigeminal
  • motor –> facial symmetry
  • parasymp. fxn –> STT
  • cutaneous sensation –> pinna
  • taste
71
Q

CN VII (clinical signs of deficiency)

A
  • widening of palpebral fissure
  • inability to closer eye, drooper ear, eyelid, lip
  • impaired taste
  • hyperacusis (inc sensitivity to sound)
  • autonomic dysfx: dry eye and nose
72
Q

Localization of CN VII deficiency

A

Intracranial: all pathways involved, ipsilateral CN VII paresis/ paralysis
Intercranial/ Interossseous: no brainstem signs, +/- middle ear signs, +/- Horner’s

73
Q

Idiopathic Facial Nerve Paralysis

A
  • Cocker spaniels
  • acute, usually unilateral
  • Pathology: no inflammation, degeneration, of myelinated fibers
  • Prognosis: good –> weeks to months for recovery
74
Q

Fx of the Vestibular System

A
  • maintain steady visual image

- maintain steady body position

75
Q

Clinical Signs of Vestibular Dz

A
  • nystagmus
  • head tilt
  • strabismus
  • ataxia
  • vomiting
76
Q

Nystagmus

A
  • named for the fast phase
  • “running away from the lesion”
  • Direction, Association w/ head position, eye-coordination
77
Q

Heat Tilt

A
  • named for most ventral side

- rolling towards the lesion

78
Q

Strabismus

A
  • ipsilateral to lesion
79
Q

Peripheral vs Central Vestibular Disease

A
  • the major difference is that central will most likely show mentation changes and can also show long tract signs (proprioceptive deficits) and cerebellar signs (ipsilateral)
80
Q

Paradoxical Vestibular Disease

A
  • CN deficits, CP deficits, hemiparesis will reflect the true laterality of the lesion
81
Q

Clinical signs of auditory disease

A
  • impairment of hearing
  • apparent behavioural problems
  • may be difficult to assess if unilateral
82
Q

Types of Peripheral Auditory Disease

A

Conductive – failure of sound transmission to the inner ear caused by problems w/in the external or middle ear

Sensoineural – failure of sound transduction by the organ of Corti or failure of propagation of nerve impulses by the cochlear nerve

83
Q

Diagnostic Testing of Auditory Disease

A
  • physical and neuro exam
  • minimum database, t4
  • otoscopic exam
  • pharyngeal exam
  • palpation of bulla and TMJ
  • BAER: helps classify the type of dysfunction
  • Rads, CT, MRI
  • Myringotomy
  • Biopsy
  • CSF analysis, serology, PCR, histopath
84
Q

Congential Aplasia/ Hypoplasia of the Cochlear Duct

A
  • sensorineural deafness
  • white and merle coloration (genetic condition)
  • diagnose with BAER
85
Q

Degenerative Auditory Disease

A
  • senile degeneration of ossicles or spiral organ
  • progressive loss
  • Dx: based on hx and BAER
86
Q

Peripheral Vestibular Dz (Infection)

A

Otitis media - interna

  • usually bacterial, sometimes fungal
  • Tx: abx therapy, surgery may be required
87
Q

T/F: Cats (aged 1-5 years) may develop an inflammatory polyp in the middle ear that requires surgical excision to correct.

A

T

88
Q

Canine Idiopathic Vestibular Disease

A
  • don’t have CN VII or sympathetic signs
  • acute, peracute loss of vestibular signs preceeded by vomiting
    Tx: supportive care
89
Q

Feline Idiopathic Vestibular Dz

A
  • unknown cause

- only on the east coast

90
Q

Central Vestibular Disease (Thiamine)

A
  • causes a polioencephalomalacia (grey matter)

- Tx: supportive, diet change

91
Q

Metronidazole toxicity

A
  • injury to purkinje cells in cerebellum

- prognosis: good if dx made early

92
Q

Clinical signs of multifocal brain disease

A
  • obtundation
  • compulsion
  • hypermetria, cervical dorsiflexion
93
Q

GME (granulomatous meningioencephalomyelitis)

A
  • can cause ocular lesions
  • focal (`50% of cases) - brainstem, cervical spinal cord, cerebellar, cerebrum
  • multifocal
94
Q

GME (clinical signs)

A
  • vestibular
  • long tract signs (paresis, postural rxn deficits)
  • cerebellar
  • cranial nerve deficits
  • seizures
95
Q

GME (signalment)

A
  • typically small breeds, middle-aged, female > males
96
Q

NME (necrotizing meningioencephalitis )

A
  • young (<18mnths), small breed dogs, female > males
97
Q

NME ( clinical signs)

A
  • predominantly cerebral ( seizures, mentation, behaviour)
  • often asymmetric –> circling
  • Lymphoplasmacytic inflammation (meningitis, encephalitis, necrosis and cavitation)
  • Pugs
98
Q

NLE (Necrotizing Leukoencephalitis)

A
  • small breeds, young-middle-aged, no sex difference
99
Q

NLE (clinical signs)

A
  • cerebral white matter
  • brainstem (vestibular, long tract, CN deficits)
  • Lymphoplasmacytic inflammation (deep white matter encephalitis, no meningitis)
100
Q

Eosinophilic Meningioencephalitis

A
  • large breeds, young, males
101
Q

Diagnosis of Inflammatory Brain Disease

A
  • MRI

- CSF analysis (hypercellular, hyperprotein)

102
Q

Treatment of Inflammatory Brain Disease

A
  • immunomodulation (corticosteroids w/ adjunctive therapies for drug sparing effects)
103
Q

Brain Tumors (stats)

A
  • 50% of brain tumors in dogs are 2*, only 10% in cats
104
Q

Meningioma

A
  • most common 1* tumor in dogs & cats
  • signalment: older animals
  • Cellular origin: arachnoid villi
  • extra-axial tumor (outside the brain)
105
Q

Gliomas

A
  • 2nd most common 1* tumor in dogs and cats
  • signalment: middle aged
  • Breed: brachycephalics
  • intra-axial tumors
106
Q

Choroid Plexus tumors

A
  • commonly met w/in the ventricular system
107
Q

Clinical signs w brain tumors (Cats)

A
  • behaviour change
  • seizures
  • altered mentation
  • circling
108
Q

Clinical signs w/ brain tumors (dogs)

A
  • seizures
  • circling
  • ataxia
  • head tilt
109
Q

Albuminocytologic dissociation

A
  • CSF analysis resulting in normal cell count and hyperprotein
110
Q

Treatment options for Brain tumors

A
  • palliative w/ corticosteroids
  • surgical ressection
  • radiation therapy
111
Q

Define: Myoclonus

A

a sudden involuntary movement of short duration caused by muscle contractions and pauses in muscle activity
- usually focal

112
Q

Define: Tremor

A

rhythmically oscillatory movement of a body part around an axis

113
Q

Define: Action Tremor

A
  • occurs during voluntary contraction of skeletal muscle
114
Q

Define: Postural tremor

A
  • occurs in a body part that is voluntarily maintained against gravity
115
Q

Define: Kinetic tremor

A
  • occurs during directed voluntary movement
116
Q

Define: Intention tremor

A
  • increased amplitude during the pursuit of a target
117
Q

Dysmyelination/ Hypomyelination

A
  • congenital, noted when starting to walk
  • action tremor
  • no neuro deficits
  • Tx: none
118
Q

Generalized Tremor Syndrome of Dogs

A
  • small breeds, < 2 years of age
  • low amplitude, generalized, action tremor
  • most have n neuro exam
  • Diagnosis: n MRI, mild pleocytosis of CSF
  • Tx: most improve w/ corticosteroids
119
Q

Lysosomal Storage Disease

A
  • many affects CNS and cause tremors
  • metabolic products accumulate in neurons and other CNS tissues
  • most are inherited and < 1 year of age
  • Diagnose via genetic testing
  • Tx: euthanasia
120
Q

Primary orthostatic tremor in Great Danes

A
  • progressive generalized tremors (only when standing)
  • n physical and neuro exam
  • cause unknown
121
Q

Fx of cerebellum

A
  • coordinate movement initiated elsewhere
122
Q

3 layers of the cerebellar cortex

A
  • molecular
  • perkinje
  • granular
123
Q

Sings of Cerebellar Disease

A

All signs are ipsilateral

  • ataxia
  • dysmetria
  • vestibular signs (may be paradoxical)
  • (-) menace
  • (-) postural rxn
  • anisocoria (rarely)
124
Q

Acute Decerebellation

A
  • dysfunction of cerebellum, often d/t trauma

- can show opisthotonus (but will be conscious)

125
Q

Cerebellar Abiotrophy

A
  • spontaneous, premature neuronal death
  • age of onset varies with breed
  • MRI will maybe show small cerebellum
126
Q

Cerebellar Hypoplasia

A
  • usually from in vitro viral infections, toxin, genetic
127
Q

Vascular Disease (cerebellum)

A
  • dogs: ischemic infraction of the cerebellum; usually from rostral cerebral artery
  • wedge or rectangular lesion on MRI
  • clinical signs improve with time and supportive care
128
Q

Mech to stop a seizure

A
  1. enhancment of inhibitory processes via faciliated activity of GABA
  2. reduction of excitatory tranmission
  3. modulation of membrane conductance ( Na or Ca)
129
Q

Realistic objectives of AEP/ ACP

A
  • control frequency, severity, duration of seizures while minimizing adverse effects
  • won’t necessarily stop seizures from occurring
130
Q

T/F: not all seizures require therapy

A

T

131
Q

When to recommend therapy for seizures

A
  • hx of status epilepticus
  • has ictus > 2 min
  • 2+ isolated seizures over 6-8 wks
  • 2+ seizures within the past 24 hours
132
Q

Monotherapy

A
  • use of a single ACD
  • newer ACDs may not be more effective/ better
  • ~70% of epileptic patients are responsive to AED monotherapy
133
Q

What are the “big 4” drugs to treat seizures

A
  1. Phenobarbital
  2. Bromide
  3. Zonisamide
  4. Levetiracetum
134
Q

Phenobarbital (moa)

A
  • increased GABA-A activity

- inhibition of voltage Ca channels

135
Q

Phenobarbital (efficacy)

A
  • up to 85% seizure free
  • no serious side effects in cats
  • first line drug for dogs and cats
136
Q

Phenobarbital (adverse effects)

A
  • PUPD
  • polyphagia
  • weight gain
  • transient sedation
137
Q

Phenobarbital (monitoring)

A
  • PE/NE every six months

- [phenobarbital] at least every year to check < 35

138
Q

Toxicity/ Efficacy is not a number

A

yes

139
Q

Bromide (pharma)

A
  • 3-4 month to steady state
  • safe w/ liver disease
  • dose q24hr
140
Q

Bromide (moa)

A
  • incompletely understood

- appears to involve GABA-A channels

141
Q

Bromide (Dosing)

A
  • KBr is dosed higher than NaBr
142
Q

Bromide ( Adverse Effects)

A
  • PUPD
  • polyphagia
  • weight gain
  • transient sedation
143
Q

Zonisamide

A
  • oral formulation only
  • efficacy: best used as adjunctive
  • side effects: sedation, ataxia, dec. appetite
  • MOA: not super sure
144
Q

Levetiracetum (keppra) (moa)

A
  • binding to synaptic vessicular protein to dec NT release
145
Q

Levetiracetum (keppra) (pharma)

A
  • oral, IV, IM, rectal admin
  • 100% bioavailability
  • rapid absorption and effective in status
146
Q

Bezodiazepines

A
  • not good for maintenance
  • useful in emergency situations
  • can be given rectally
  • do not give to cats – Fatal idiosyncratic necrotizing hepatopathy
147
Q

When to start a 2nd drug

A
  • dose is maxed out on drug #1

- combo therapy useful in 70% of refractory epilepsy

148
Q

What is Status Epilepticus

A
  • seizures that occur for > 5 min.

- consciousness not recovered between ictus

149
Q

Therapeutic goals for Status Epilepticus

A
  • stop the seizures
  • ensure survival
  • prevent recurrence
  • reduce chance of CNS damage ( SE requires 200-700% cerebral blood flow to maintain metabolsm)
150
Q

Anticonvulsant therapy for SE

A

1st line –> benzodiazepine bolus w/ 3 doses
2nd line –> other IV AEDs
3rd line –> benzodiazepine CRI ( may not work if bolus didn’t work)
4th line –> propofol
5th line –> gas anesthesia (iso/ sevo)

151
Q

T/F: you do not need bloodwork prior to giving any dose of anticonvulsant

A

T

152
Q

Systemic complications of SE

A
  • hyperthermia (DIC, etc)

- progressive and irreversible brain damage and intracranial hypertension

153
Q

Cluster Seizures

A
  • several seizures close together w/in 24 hours
    • predictable pattern
    • prioritize seizure control
    • minimize # and severity
    • tolerate adverse effects in short term
154
Q

Prognosis of SE

A
  • almost all dogs can be stabilized and will recover

- have hope

VET 433a - Small Animal Stream 1 (10 decks)

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