Neuro pt.1 Flashcards
T/F: a neurological exam is sufficient for evaluation of a neurologic patient.
F: need to perform a physical exam as well
5 parts of the neuro exam
- gen observations ( mentation, gait, posture)
- cranial nerves
- postural rxns
- segmental reflexes
- palpation and pain
2 areas responsible for proper mentation
- Reticular Formation
2. Cerebral cortex
Levels of mentation
- appropriate
- obtundation ( any decrease in mentation)
- stuporous (responds to noxious stimuli only)
- comatose (unresponsive to everything)
Classifying gait abnormalities
- partial/ complete
- ataxia
- lameness
- involuntary movement
Posture Classificiation
- Decerebrate
- Decerebellate
- Schiff-Sherington
Decerebrate Posture
- extension of neck, thoracic, and hind limbs
- opisthotonus
- comatose mentation
Decerebellate Posture
- extension of neck and thoracic limbs
- flexion of hind limbs
- appropriate mentation
Schiff-Sherington Posture
- thoracolumbar myelopathy
- n mentation and thoracic limbs
Postural Reactions
- proprioceptive pathways require intact spinal tract, thalamus, cerebrum, and intact motor fxn
- not great for lesion localization
Cranial Intumescence
C5 - T3
Lumbar Intumescence
L4 - S3
Biceps Reflex
- musculocutaneous nerve
-
Triceps Reflex
- radial nerve
-
Patellar Reflex
- femoral nerve
- L4, 5, 6
Gastrocnemius Reflex
- sciatic nerve
- L6, 7, S1
When do we test nociceptive reaction
- only in animals that don’t have voluntary movement
Cutaneous Trunci Reflex
- C8 - T1
What are the 6 distinct cerebral corticol regions
- Olfactory Region
- Frontal Lobe
- Parietal Lobe
- Temporal Lobe
- Occipital Lobe
- Limbic System
Olfactory Region
- CN 1
- olfactory tract, bulbs, pyriform lobe
- only sensory info not processed by thalamus
Frontal Lobe
- behaviour, planning, judgement
- contains primary motor cortex, motor association cortex
Parietal Lobe
- primarily somatisensory
Basal Nuclei
- Striatum ( caudate nucleus)
- globus pallidus
- subthalamic region
- substatia gyri
Cerebral White Matter
- corona radiata
- internal capsule
- inter-thalamic adhesion
Medial Lemniscal Pathway
- proprioception: consious
Motor Pathways
- corticospinal, rubrospinal, vestibulospinal
Function of the Cerebrum
- Personality
- Thought
- receive sensory input & plans the action
- consciousness
Cerebral Dysfunction
- change in mentation
- behavioural abn
- abn movement: pacing, circling, head pressing
- proprioceptive deficits
- central blindness, hemi-inattention
- seizures
Blindness
- Check PLR (2, 3) and menace (2, 7)
- Central Blindness -> vision loss only (intact PLRS), contralateral loss of vision
Hemi-inattention
- neglect or decreased awareness of contralteral environment or body
Hydrocephalus
- congenital or acquired
- dilateion of ventricles, frequently the lateral vent
- treatment
- -> congenital (dec CSF production)
- -> acquired ( treat underlying cause)
9/10 Rule for Cerebral Disease
- symmetrical, diffuse signs = degenerative, metabolic, nutritional, toxic
- lateralized = lesion, mass, inflammatory
Cause of Primary Brain Injury
- parenchymal damage
- vascular disruption
Cause of Secondary Brain Injury
- Edema/ Inflammation
- hypoxia
- ischemia/ neurotoxicity
- neuronal death
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
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
ICP Dynamics ( Immediate and Chronic buffering)
Immediate --> stretch of Dura --> displacement of CSF or blood Chronic --> dec. ECF space --> brain atrophy (think hydrocephalus)
Effects of decreased Cranial Blood Flow
- dec CBF –> dec perfusion –> PP = MAP - ICP **
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
Order of cerebral tissue sensitivity to hypoxia
endothelium, neurons, glia
- neurons (grey matter)
- glia (white and grey)
- endothelium (BBB)
Intercranial Hypertension Effects
- mental deterioration
- brainstem dysfunction
- loss of motor control
- abn postures
- herniation of cerebellum or brainstem
Transtentorial Herniation
- midbrain compression:
- -> RAS: stupor to coma
- -> CN3: mydriasis w/ no PLR, strabismus
Foramen Magnum Herniations
- compression of cerebellum and brainstem
- -> stupor to coma
- -> resp. arrest, hypoventilation
- -> CN 10 defecits
How to assess ICP
- on serial examination via imaging or invasive measurement
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)
How to relieve ICP pharmaceutically?
Mannitol: 3 mech of actions:
- inc. plasma volume and blood viscocity
- osmotic diuresis in 30-60 minutes
- free radical scavenger
- - only use mannitol if needed
Hypertonic Saline
- less likely to lead to hypovolemia than mannitol
Acute Brain Injury (prognosis)
- okay scoring w/ improvement w/in first 48hrs w/ no serious lesions = guarded but likely to recover fully
Seizure Thresholds
- sum total of events that regulate neuronal excitability
T/F: seizures are clinical signs of forebrain disease.
T
Causes of neuronal hyperexcitability (seizures)
- increased excitatory post-synaptic potentials
- decreased inhibitory post-synaptic potentials
- change in ion channels or [ion]
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)
Possible mechanisms of seizures
- ion channel abnormailities
- synapse remodeling
- extracellular [ion] change
- loss of inhibitory neurons
- loss of excitatory –< inhibitory neurons
What tool do you use to measure seizure activity
EEG
Stages of seizures
- Prodrome: change in mentation
- Aura: just prior to seizure, repetitive motions/ movement occuring, but not seizuring yet
- Ictus: seizure event
- Post-Ictal: period after seizure; possible mentation/ behaviour change present
Seizure Types:
- Focal - occurs in a specific part of the brain w/ regionalized signs
- Generalized - bilateral involvement/ loss of consciousness
Idiopathic Epilepsy
- onset age (6 mnths - 6 years)
- normal on the neuro exam
- mri unremarkable
- r/o reactive seizures
Diagnostic Plans for Seizures
- signalment matters
- minimum database
- MRI, CT, CSF
Poor Seizure Control
- if you aren’t effectively controlling it, maybe it’s not a seizure
- poor classification: make sure to treat underlying cause
3 branches of CN V
- ophthalmic (sensory only)
- maxillary (sensory only)
- mandibular (sensory and motor)
CN V anatomy of motor pathway
- nucleus in pons
- mandibular n. exits skull through oval foramen
- innervates muscles of mastication (masseter, temporalis)
CN V anatomy of sensory pathway
- trigeminal ganglion contains cell bodies
- all sensory axons enter the brainstem at the pons
Testing CN V (Cutaneous sensation)
- corneal reflex (5 ophth., 6 +/- 7)
- Palpebral reflex (5 ophth. + max., 7)
- trigeminofacial reflex (5 ophth. + max, 7)
- Noxious stimuli (requires cortical processing)
Testing CN V (Motor function)
- paresis/ paralysis
- atrophy
- symmetry
- dropped jaw
Localizing CN V lesions
- intracranial –> brainstem, pons, rostral medulla
- brainstem signs are ipsilateral: obtundation, CP defecits, cerebellar signs - Extracranial signs –> no brainstem signs
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
Idiopathic Trigeminal Neuropathy (Diagnosis)
- (-) 2M myofibril serology
- MRI + CSF check
Idiopathic Trigeminal Neuropathy (treatment)
- self resolving in a few months
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
CN VII
- motor - facial expression
- sensation - concave surface of skin on pinna; taste to rostral 2/3 of tongue
- exits skull via stylomastoid foramen
Testing of CN VII
- Reflexes –> menace, corneal, palpebral, trigeminal
- motor –> facial symmetry
- parasymp. fxn –> STT
- cutaneous sensation –> pinna
- taste
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
Localization of CN VII deficiency
Intracranial: all pathways involved, ipsilateral CN VII paresis/ paralysis
Intercranial/ Interossseous: no brainstem signs, +/- middle ear signs, +/- Horner’s
Idiopathic Facial Nerve Paralysis
- Cocker spaniels
- acute, usually unilateral
- Pathology: no inflammation, degeneration, of myelinated fibers
- Prognosis: good –> weeks to months for recovery
Fx of the Vestibular System
- maintain steady visual image
- maintain steady body position
Clinical Signs of Vestibular Dz
- nystagmus
- head tilt
- strabismus
- ataxia
- vomiting
Nystagmus
- named for the fast phase
- “running away from the lesion”
- Direction, Association w/ head position, eye-coordination
Heat Tilt
- named for most ventral side
- rolling towards the lesion
Strabismus
- ipsilateral to lesion
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)
Paradoxical Vestibular Disease
- CN deficits, CP deficits, hemiparesis will reflect the true laterality of the lesion
Clinical signs of auditory disease
- impairment of hearing
- apparent behavioural problems
- may be difficult to assess if unilateral
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
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
Congential Aplasia/ Hypoplasia of the Cochlear Duct
- sensorineural deafness
- white and merle coloration (genetic condition)
- diagnose with BAER
Degenerative Auditory Disease
- senile degeneration of ossicles or spiral organ
- progressive loss
- Dx: based on hx and BAER
Peripheral Vestibular Dz (Infection)
Otitis media - interna
- usually bacterial, sometimes fungal
- Tx: abx therapy, surgery may be required
T/F: Cats (aged 1-5 years) may develop an inflammatory polyp in the middle ear that requires surgical excision to correct.
T
Canine Idiopathic Vestibular Disease
- don’t have CN VII or sympathetic signs
- acute, peracute loss of vestibular signs preceeded by vomiting
Tx: supportive care
Feline Idiopathic Vestibular Dz
- unknown cause
- only on the east coast
Central Vestibular Disease (Thiamine)
- causes a polioencephalomalacia (grey matter)
- Tx: supportive, diet change
Metronidazole toxicity
- injury to purkinje cells in cerebellum
- prognosis: good if dx made early
Clinical signs of multifocal brain disease
- obtundation
- compulsion
- hypermetria, cervical dorsiflexion
GME (granulomatous meningioencephalomyelitis)
- can cause ocular lesions
- focal (`50% of cases) - brainstem, cervical spinal cord, cerebellar, cerebrum
- multifocal
GME (clinical signs)
- vestibular
- long tract signs (paresis, postural rxn deficits)
- cerebellar
- cranial nerve deficits
- seizures
GME (signalment)
- typically small breeds, middle-aged, female > males
NME (necrotizing meningioencephalitis )
- young (<18mnths), small breed dogs, female > males
NME ( clinical signs)
- predominantly cerebral ( seizures, mentation, behaviour)
- often asymmetric –> circling
- Lymphoplasmacytic inflammation (meningitis, encephalitis, necrosis and cavitation)
- Pugs
NLE (Necrotizing Leukoencephalitis)
- small breeds, young-middle-aged, no sex difference
NLE (clinical signs)
- cerebral white matter
- brainstem (vestibular, long tract, CN deficits)
- Lymphoplasmacytic inflammation (deep white matter encephalitis, no meningitis)
Eosinophilic Meningioencephalitis
- large breeds, young, males
Diagnosis of Inflammatory Brain Disease
- MRI
- CSF analysis (hypercellular, hyperprotein)
Treatment of Inflammatory Brain Disease
- immunomodulation (corticosteroids w/ adjunctive therapies for drug sparing effects)
Brain Tumors (stats)
- 50% of brain tumors in dogs are 2*, only 10% in cats
Meningioma
- most common 1* tumor in dogs & cats
- signalment: older animals
- Cellular origin: arachnoid villi
- extra-axial tumor (outside the brain)
Gliomas
- 2nd most common 1* tumor in dogs and cats
- signalment: middle aged
- Breed: brachycephalics
- intra-axial tumors
Choroid Plexus tumors
- commonly met w/in the ventricular system
Clinical signs w brain tumors (Cats)
- behaviour change
- seizures
- altered mentation
- circling
Clinical signs w/ brain tumors (dogs)
- seizures
- circling
- ataxia
- head tilt
Albuminocytologic dissociation
- CSF analysis resulting in normal cell count and hyperprotein
Treatment options for Brain tumors
- palliative w/ corticosteroids
- surgical ressection
- radiation therapy
Define: Myoclonus
a sudden involuntary movement of short duration caused by muscle contractions and pauses in muscle activity
- usually focal
Define: Tremor
rhythmically oscillatory movement of a body part around an axis
Define: Action Tremor
- occurs during voluntary contraction of skeletal muscle
Define: Postural tremor
- occurs in a body part that is voluntarily maintained against gravity
Define: Kinetic tremor
- occurs during directed voluntary movement
Define: Intention tremor
- increased amplitude during the pursuit of a target
Dysmyelination/ Hypomyelination
- congenital, noted when starting to walk
- action tremor
- no neuro deficits
- Tx: none
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
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
Primary orthostatic tremor in Great Danes
- progressive generalized tremors (only when standing)
- n physical and neuro exam
- cause unknown
Fx of cerebellum
- coordinate movement initiated elsewhere
3 layers of the cerebellar cortex
- molecular
- perkinje
- granular
Sings of Cerebellar Disease
All signs are ipsilateral
- ataxia
- dysmetria
- vestibular signs (may be paradoxical)
- (-) menace
- (-) postural rxn
- anisocoria (rarely)
Acute Decerebellation
- dysfunction of cerebellum, often d/t trauma
- can show opisthotonus (but will be conscious)
Cerebellar Abiotrophy
- spontaneous, premature neuronal death
- age of onset varies with breed
- MRI will maybe show small cerebellum
Cerebellar Hypoplasia
- usually from in vitro viral infections, toxin, genetic
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
Mech to stop a seizure
- enhancment of inhibitory processes via faciliated activity of GABA
- reduction of excitatory tranmission
- modulation of membrane conductance ( Na or Ca)
Realistic objectives of AEP/ ACP
- control frequency, severity, duration of seizures while minimizing adverse effects
- won’t necessarily stop seizures from occurring
T/F: not all seizures require therapy
T
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
Monotherapy
- use of a single ACD
- newer ACDs may not be more effective/ better
- ~70% of epileptic patients are responsive to AED monotherapy
What are the “big 4” drugs to treat seizures
- Phenobarbital
- Bromide
- Zonisamide
- Levetiracetum
Phenobarbital (moa)
- increased GABA-A activity
- inhibition of voltage Ca channels
Phenobarbital (efficacy)
- up to 85% seizure free
- no serious side effects in cats
- first line drug for dogs and cats
Phenobarbital (adverse effects)
- PUPD
- polyphagia
- weight gain
- transient sedation
Phenobarbital (monitoring)
- PE/NE every six months
- [phenobarbital] at least every year to check < 35
Toxicity/ Efficacy is not a number
yes
Bromide (pharma)
- 3-4 month to steady state
- safe w/ liver disease
- dose q24hr
Bromide (moa)
- incompletely understood
- appears to involve GABA-A channels
Bromide (Dosing)
- KBr is dosed higher than NaBr
Bromide ( Adverse Effects)
- PUPD
- polyphagia
- weight gain
- transient sedation
Zonisamide
- oral formulation only
- efficacy: best used as adjunctive
- side effects: sedation, ataxia, dec. appetite
- MOA: not super sure
Levetiracetum (keppra) (moa)
- binding to synaptic vessicular protein to dec NT release
Levetiracetum (keppra) (pharma)
- oral, IV, IM, rectal admin
- 100% bioavailability
- rapid absorption and effective in status
Bezodiazepines
- not good for maintenance
- useful in emergency situations
- can be given rectally
- do not give to cats – Fatal idiosyncratic necrotizing hepatopathy
When to start a 2nd drug
- dose is maxed out on drug #1
- combo therapy useful in 70% of refractory epilepsy
What is Status Epilepticus
- seizures that occur for > 5 min.
- consciousness not recovered between ictus
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)
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)
T/F: you do not need bloodwork prior to giving any dose of anticonvulsant
T
Systemic complications of SE
- hyperthermia (DIC, etc)
- progressive and irreversible brain damage and intracranial hypertension
Cluster Seizures
- several seizures close together w/in 24 hours
- predictable pattern
- prioritize seizure control
- minimize # and severity
- tolerate adverse effects in short term
Prognosis of SE
- almost all dogs can be stabilized and will recover
- have hope
