Neuro pt.1 Flashcards
(154 cards)
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
2
Q
5 parts of the neuro exam
A
- gen observations ( mentation, gait, posture)
- cranial nerves
- postural rxns
- segmental reflexes
- palpation and pain
3
Q
2 areas responsible for proper mentation
A
- Reticular Formation
2. Cerebral cortex
4
Q
Levels of mentation
A
- appropriate
- obtundation ( any decrease in mentation)
- stuporous (responds to noxious stimuli only)
- comatose (unresponsive to everything)
5
Q
Classifying gait abnormalities
A
- partial/ complete
- ataxia
- lameness
- involuntary movement
6
Q
Posture Classificiation
A
- Decerebrate
- Decerebellate
- Schiff-Sherington
7
Q
Decerebrate Posture
A
- extension of neck, thoracic, and hind limbs
- opisthotonus
- comatose mentation
8
Q
Decerebellate Posture
A
- extension of neck and thoracic limbs
- flexion of hind limbs
- appropriate mentation
9
Q
Schiff-Sherington Posture
A
- thoracolumbar myelopathy
- n mentation and thoracic limbs
10
Q
Postural Reactions
A
- proprioceptive pathways require intact spinal tract, thalamus, cerebrum, and intact motor fxn
- not great for lesion localization
11
Q
Cranial Intumescence
A
C5 - T3
12
Q
Lumbar Intumescence
A
L4 - S3
13
Q
Biceps Reflex
A
- musculocutaneous nerve
-
14
Q
Triceps Reflex
A
- radial nerve
-
15
Q
Patellar Reflex
A
- femoral nerve
- L4, 5, 6
16
Q
Gastrocnemius Reflex
A
- sciatic nerve
- L6, 7, S1
17
Q
When do we test nociceptive reaction
A
- only in animals that don’t have voluntary movement
18
Q
Cutaneous Trunci Reflex
A
- C8 - T1
19
Q
What are the 6 distinct cerebral corticol regions
A
- Olfactory Region
- Frontal Lobe
- Parietal Lobe
- Temporal Lobe
- Occipital Lobe
- Limbic System
20
Q
Olfactory Region
A
- CN 1
- olfactory tract, bulbs, pyriform lobe
- only sensory info not processed by thalamus
21
Q
Frontal Lobe
A
- behaviour, planning, judgement
- contains primary motor cortex, motor association cortex
22
Q
Parietal Lobe
A
- primarily somatisensory
23
Q
Basal Nuclei
A
- Striatum ( caudate nucleus)
- globus pallidus
- subthalamic region
- substatia gyri
24
Q
Cerebral White Matter
A
- corona radiata
- internal capsule
- inter-thalamic adhesion
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Medial Lemniscal Pathway
- proprioception: consious
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Motor Pathways
- corticospinal, rubrospinal, vestibulospinal
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Function of the Cerebrum
- Personality
- Thought
- receive sensory input & plans the action
- consciousness
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Cerebral Dysfunction
- change in mentation
- behavioural abn
- abn movement: pacing, circling, head pressing
- proprioceptive deficits
- central blindness, hemi-inattention
- seizures
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Blindness
- Check PLR (2, 3) and menace (2, 7)
| - Central Blindness -> vision loss only (intact PLRS), contralateral loss of vision
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Hemi-inattention
- neglect or decreased awareness of contralteral environment or body
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Hydrocephalus
- congenital or acquired
- dilateion of ventricles, frequently the lateral vent
- treatment
- -> congenital (dec CSF production)
- -> acquired ( treat underlying cause)
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9/10 Rule for Cerebral Disease
- symmetrical, diffuse signs = degenerative, metabolic, nutritional, toxic
- lateralized = lesion, mass, inflammatory
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Cause of Primary Brain Injury
- parenchymal damage
| - vascular disruption
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Cause of Secondary Brain Injury
- Edema/ Inflammation
- hypoxia
- ischemia/ neurotoxicity
- neuronal death
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Secondary Acute Brain Injury
- 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
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ICP Dynamics/ Monroe-Kellie doctrine
- intracranial contents are in a rigid container
- Brain 80&, Blood 10%, CSF 10%
- If one volume inc., the others must decrease
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ICP Dynamics ( Immediate and Chronic buffering)
```
Immediate
--> stretch of Dura
--> displacement of CSF or blood
Chronic
--> dec. ECF space
--> brain atrophy (think hydrocephalus)
```
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Effects of decreased Cranial Blood Flow
- dec CBF --> dec perfusion --> PP = MAP - ICP **
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What is the Cushing's Response
- 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
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Order of cerebral tissue sensitivity to hypoxia
| endothelium, neurons, glia
- neurons (grey matter)
- glia (white and grey)
- endothelium (BBB)
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Intercranial Hypertension Effects
- mental deterioration
- brainstem dysfunction
- loss of motor control
- abn postures
- herniation of cerebellum or brainstem
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Transtentorial Herniation
- midbrain compression:
- -> RAS: stupor to coma
- -> CN3: mydriasis w/ no PLR, strabismus
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Foramen Magnum Herniations
- compression of cerebellum and brainstem
- -> stupor to coma
- -> resp. arrest, hypoventilation
- -> CN 10 defecits
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How to assess ICP
- on serial examination via imaging or invasive measurement
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Treatment of Brain Trauma (6 steps/ actions)
- 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)
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How to relieve ICP pharmaceutically?
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
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Acute Brain Injury (prognosis)
- okay scoring w/ improvement w/in first 48hrs w/ no serious lesions = guarded but likely to recover fully
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Seizure Thresholds
- sum total of events that regulate neuronal excitability
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T/F: seizures are clinical signs of forebrain disease.
T
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Causes of neuronal hyperexcitability (seizures)
- increased excitatory post-synaptic potentials
- decreased inhibitory post-synaptic potentials
- change in ion channels or [ion]
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Major neurotrasmitters (seizures)
Glutamate: excitatory w/ both Ionotropic and metabotropic
Gaba: inhibitory w/ post-synaptic (A linked to Cl) and pre-synaptic (B linked to K)
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Possible mechanisms of seizures
1. ion channel abnormailities
2. synapse remodeling
3. extracellular [ion] change
4. loss of inhibitory neurons
5. loss of excitatory --< inhibitory neurons
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What tool do you use to measure seizure activity
EEG
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Stages of seizures
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
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Seizure Types:
1. Focal - occurs in a specific part of the brain w/ regionalized signs
2. Generalized - bilateral involvement/ loss of consciousness
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Idiopathic Epilepsy
- onset age (6 mnths - 6 years)
- normal on the neuro exam
- mri unremarkable
- r/o reactive seizures
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Diagnostic Plans for Seizures
- signalment matters
- minimum database
- MRI, CT, CSF
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Poor Seizure Control
- if you aren't effectively controlling it, maybe it's not a seizure
- poor classification: make sure to treat underlying cause
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3 branches of CN V
1. ophthalmic (sensory only)
2. maxillary (sensory only)
3. mandibular (sensory and motor)
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CN V anatomy of motor pathway
- nucleus in pons
- mandibular n. exits skull through oval foramen
- innervates muscles of mastication (masseter, temporalis)
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CN V anatomy of sensory pathway
- trigeminal ganglion contains cell bodies
| - all sensory axons enter the brainstem at the pons
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Testing CN V (Cutaneous sensation)
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)
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Testing CN V (Motor function)
- paresis/ paralysis
- atrophy
- symmetry
- dropped jaw
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Localizing CN V lesions
1. intracranial --> brainstem, pons, rostral medulla
- brainstem signs are ipsilateral: obtundation, CP defecits, cerebellar signs
2. Extracranial signs --> no brainstem signs
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Idiopathic Trigeminal Neuropathy
- common in dogs
- acute onset dropped jaw, inability to close mouth
- sensation is normal
- atrophy common (may be unilateral)
- +/- Horner's syndrome
- Facial paralysis
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Idiopathic Trigeminal Neuropathy (Diagnosis)
- (-) 2M myofibril serology
| - MRI + CSF check
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Idiopathic Trigeminal Neuropathy (treatment)
- self resolving in a few months
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Rabies
- enveloped RNA virus
- clinical signs = death
- incubation: 7 days - 1 year
- pathology: hits the motor nucleus in CN 5 to cause a dropped jaw
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CN VII
- motor - facial expression
- sensation - concave surface of skin on pinna; taste to rostral 2/3 of tongue
- exits skull via stylomastoid foramen
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Testing of CN VII
- Reflexes --> menace, corneal, palpebral, trigeminal
- motor --> facial symmetry
- parasymp. fxn --> STT
- cutaneous sensation --> pinna
- taste
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CN VII (clinical signs of deficiency)
- 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
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Localization of CN VII deficiency
Intracranial: all pathways involved, ipsilateral CN VII paresis/ paralysis
Intercranial/ Interossseous: no brainstem signs, +/- middle ear signs, +/- Horner's
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Idiopathic Facial Nerve Paralysis
- Cocker spaniels
- acute, usually unilateral
- Pathology: no inflammation, degeneration, of myelinated fibers
- Prognosis: good --> weeks to months for recovery
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Fx of the Vestibular System
- maintain steady visual image
| - maintain steady body position
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Clinical Signs of Vestibular Dz
- nystagmus
- head tilt
- strabismus
- ataxia
- vomiting
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Nystagmus
- named for the fast phase
- "running away from the lesion"
- Direction, Association w/ head position, eye-coordination
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Heat Tilt
- named for most ventral side
| - rolling towards the lesion
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Strabismus
- ipsilateral to lesion
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Peripheral vs Central Vestibular Disease
- 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)
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Paradoxical Vestibular Disease
- CN deficits, CP deficits, hemiparesis will reflect the true laterality of the lesion
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Clinical signs of auditory disease
- impairment of hearing
- apparent behavioural problems
- may be difficult to assess if unilateral
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Types of Peripheral Auditory Disease
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
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Diagnostic Testing of Auditory Disease
- 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
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Congential Aplasia/ Hypoplasia of the Cochlear Duct
- sensorineural deafness
- white and merle coloration (genetic condition)
- diagnose with BAER
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Degenerative Auditory Disease
- senile degeneration of ossicles or spiral organ
- progressive loss
- Dx: based on hx and BAER
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Peripheral Vestibular Dz (Infection)
Otitis media - interna
- usually bacterial, sometimes fungal
- Tx: abx therapy, surgery may be required
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T/F: Cats (aged 1-5 years) may develop an inflammatory polyp in the middle ear that requires surgical excision to correct.
T
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Canine Idiopathic Vestibular Disease
- don't have CN VII or sympathetic signs
- acute, peracute loss of vestibular signs preceeded by vomiting
Tx: supportive care
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Feline Idiopathic Vestibular Dz
- unknown cause
| - only on the east coast
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Central Vestibular Disease (Thiamine)
- causes a polioencephalomalacia (grey matter)
| - Tx: supportive, diet change
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Metronidazole toxicity
- injury to purkinje cells in cerebellum
| - prognosis: good if dx made early
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Clinical signs of multifocal brain disease
- obtundation
- compulsion
- hypermetria, cervical dorsiflexion
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GME (granulomatous meningioencephalomyelitis)
- can cause ocular lesions
- focal (`50% of cases) - brainstem, cervical spinal cord, cerebellar, cerebrum
- multifocal
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GME (clinical signs)
- vestibular
- long tract signs (paresis, postural rxn deficits)
- cerebellar
- cranial nerve deficits
- seizures
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GME (signalment)
- typically small breeds, middle-aged, female > males
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NME (necrotizing meningioencephalitis )
- young (<18mnths), small breed dogs, female > males
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NME ( clinical signs)
- predominantly cerebral ( seizures, mentation, behaviour)
- often asymmetric --> circling
- Lymphoplasmacytic inflammation (meningitis, encephalitis, necrosis and cavitation)
- Pugs
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NLE (Necrotizing Leukoencephalitis)
- small breeds, young-middle-aged, no sex difference
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NLE (clinical signs)
- cerebral white matter
- brainstem (vestibular, long tract, CN deficits)
- Lymphoplasmacytic inflammation (deep white matter encephalitis, no meningitis)
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Eosinophilic Meningioencephalitis
- large breeds, young, males
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Diagnosis of Inflammatory Brain Disease
- MRI
| - CSF analysis (hypercellular, hyperprotein)
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Treatment of Inflammatory Brain Disease
- immunomodulation (corticosteroids w/ adjunctive therapies for drug sparing effects)
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Brain Tumors (stats)
- 50% of brain tumors in dogs are 2*, only 10% in cats
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Meningioma
- most common 1* tumor in dogs & cats
- signalment: older animals
- Cellular origin: arachnoid villi
- extra-axial tumor (outside the brain)
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Gliomas
- 2nd most common 1* tumor in dogs and cats
- signalment: middle aged
- Breed: brachycephalics
- intra-axial tumors
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Choroid Plexus tumors
- commonly met w/in the ventricular system
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Clinical signs w brain tumors (Cats)
- behaviour change
- seizures
- altered mentation
- circling
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Clinical signs w/ brain tumors (dogs)
- seizures
- circling
- ataxia
- head tilt
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Albuminocytologic dissociation
- CSF analysis resulting in normal cell count and hyperprotein
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Treatment options for Brain tumors
- palliative w/ corticosteroids
- surgical ressection
- radiation therapy
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Define: Myoclonus
a sudden involuntary movement of short duration caused by muscle contractions and pauses in muscle activity
- usually focal
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Define: Tremor
rhythmically oscillatory movement of a body part around an axis
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Define: Action Tremor
- occurs during voluntary contraction of skeletal muscle
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Define: Postural tremor
- occurs in a body part that is voluntarily maintained against gravity
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Define: Kinetic tremor
- occurs during directed voluntary movement
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Define: Intention tremor
- increased amplitude during the pursuit of a target
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Dysmyelination/ Hypomyelination
- congenital, noted when starting to walk
- action tremor
- no neuro deficits
- Tx: none
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Generalized Tremor Syndrome of Dogs
- 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
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Lysosomal Storage Disease
- 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
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Primary orthostatic tremor in Great Danes
- progressive generalized tremors (only when standing)
- n physical and neuro exam
- cause unknown
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Fx of cerebellum
- coordinate movement initiated elsewhere
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3 layers of the cerebellar cortex
- molecular
- perkinje
- granular
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Sings of Cerebellar Disease
All signs are ipsilateral
- ataxia
- dysmetria
- vestibular signs (may be paradoxical)
- (-) menace
- (-) postural rxn
- anisocoria (rarely)
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Acute Decerebellation
- dysfunction of cerebellum, often d/t trauma
| - can show opisthotonus (but will be conscious)
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Cerebellar Abiotrophy
- spontaneous, premature neuronal death
- age of onset varies with breed
- MRI will maybe show small cerebellum
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Cerebellar Hypoplasia
- usually from in vitro viral infections, toxin, genetic
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Vascular Disease (cerebellum)
- 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
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Mech to stop a seizure
1. enhancment of inhibitory processes via faciliated activity of GABA
2. reduction of excitatory tranmission
3. modulation of membrane conductance ( Na or Ca)
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Realistic objectives of AEP/ ACP
- control frequency, severity, duration of seizures while minimizing adverse effects
- won't necessarily stop seizures from occurring
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T/F: not all seizures require therapy
T
131
When to recommend therapy for seizures
- hx of status epilepticus
- has ictus > 2 min
- 2+ isolated seizures over 6-8 wks
- 2+ seizures within the past 24 hours
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Monotherapy
- use of a single ACD
- newer ACDs may not be more effective/ better
- ~70% of epileptic patients are responsive to AED monotherapy
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What are the "big 4" drugs to treat seizures
1. Phenobarbital
2. Bromide
3. Zonisamide
4. Levetiracetum
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Phenobarbital (moa)
- increased GABA-A activity
| - inhibition of voltage Ca channels
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Phenobarbital (efficacy)
- up to 85% seizure free
- no serious side effects in cats
- first line drug for dogs and cats
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Phenobarbital (adverse effects)
- PUPD
- polyphagia
- weight gain
- transient sedation
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Phenobarbital (monitoring)
- PE/NE every six months
| - [phenobarbital] at least every year to check < 35
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Toxicity/ Efficacy is not a number
yes
139
Bromide (pharma)
- 3-4 month to steady state
- safe w/ liver disease
- dose q24hr
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Bromide (moa)
- incompletely understood
| - appears to involve GABA-A channels
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Bromide (Dosing)
- KBr is dosed higher than NaBr
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Bromide ( Adverse Effects)
- PUPD
- polyphagia
- weight gain
- transient sedation
143
Zonisamide
- oral formulation only
- efficacy: best used as adjunctive
- side effects: sedation, ataxia, dec. appetite
- MOA: not super sure
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Levetiracetum (keppra) (moa)
- binding to synaptic vessicular protein to dec NT release
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Levetiracetum (keppra) (pharma)
- oral, IV, IM, rectal admin
- 100% bioavailability
- rapid absorption and effective in status
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Bezodiazepines
- not good for maintenance
- useful in emergency situations
- can be given rectally
- do not give to cats -- Fatal idiosyncratic necrotizing hepatopathy
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When to start a 2nd drug
- dose is maxed out on drug #1
| - combo therapy useful in 70% of refractory epilepsy
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What is Status Epilepticus
- seizures that occur for > 5 min.
| - consciousness not recovered between ictus
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Therapeutic goals for Status Epilepticus
- stop the seizures
- ensure survival
- prevent recurrence
- reduce chance of CNS damage ( SE requires 200-700% cerebral blood flow to maintain metabolsm)
150
Anticonvulsant therapy for SE
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)
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T/F: you do not need bloodwork prior to giving any dose of anticonvulsant
T
152
Systemic complications of SE
- hyperthermia (DIC, etc)
| - progressive and irreversible brain damage and intracranial hypertension
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Cluster Seizures
- several seizures close together w/in 24 hours
- - predictable pattern
- - prioritize seizure control
- - minimize # and severity
- - tolerate adverse effects in short term
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Prognosis of SE
- almost all dogs can be stabilized and will recover
| - have hope
