Exam 3 Flashcards
Lecture 1
Brain
Identify common clinical signs of forebrain dysfunction
Forebrain disease (Cerebral)
- Alterations in behavior or mental status
-Dull, depressed, not themselves
-Mild alterations - Walking in circles/pacing
- Central blindness: contralateral phenomenon
-Blind but intact pupil responses PLR - Seizures
- Decrease in facial sensation (contralateral)
- Postural reaction deficits (contralateral)
How an animal sees:
Light - optic nerve - optic chasm - crosses over to - optic tract - synapse in lateral genicula - to white matter - optic radiation to visual cortex
Pupils:
-Synapse occurs somewhere else, going down towards optic motor nerves.
C/S
-Mild incoordination
-Walk well
-Circle towards their problem
-Usually no gait deficits
-Head pressing
-Compulsive pacing: obstinate progression
Describe the organization of the motor system
Brain Functional Divisions
- Cerebrum
- Diencephalon
-Thalamus
-Hypothalamus
-Optic nerves - Brainstem
-Midbrain
-Pons
-Medulla - Cerebellum
- Vestibular System
Explain the relative location of sensory vs. motor tracts within the spinal cord
UMN
-Located entirely within the CNS
-Descend from brain to every segment of spinal cord
initiate voluntary movement
Both excitatory and inhibitory influence on LMN to maintain muscle tone and reflex arcs
LMN
-Located in CNS and PNS
-Involved with reflex arc (sensory and motor)
-Carry out motor function
UMN
- Pyramidal systems (motor cortex)
-Human mostly
-Corticospinal tract: major fiber system. - Extrapyramidal system (basal nuclei)
-Basal nuclei tract that is major is the
-Rubrospinal tracts
GAIT in an animal is from Rubrospinal tracts from BASAL NUCLEI where voluntary moment originates (not the cortex as humans)
Basal nuclei - Red nucleus of the midbrain in dogs
-Group of little neurons that live deep in the brain
-Biggest role in gait
-Red nucleus receives input from the motor cortex, then the rub-spinal tract for execution of voluntary movement
Cerebrum Lobes
Which lobe is in charge of conscious perception of proprioception?
What is crossover?
Frontal: motor areas
Piriform: smell, olfactory bulbs
Occipital: vision
Pariental - Somatosensory: consciousness and proprioception
Temporal - Hearing and balance, vestibular input
Limbic system: function of storing memories creating memories. Hypothalamus, amygdala.
Important:
Somatosensory cortex (from parietal lobe) function
Important for both brain and spinal diseases
Conscious perception of touch, pain, pressure, temperature
Conscious perception of Propioception
Hypothesize what clinical signs a lesion within each spinal cord segment will result in
Describe certain neuroanatomical gait abnormalities
Diencephalon divisions
and C/S when lesions
-Chief sensory integration center of nervous system
ARAS: Influenced by sleep centers in pons and medulla
Ascending Reticular Activating System
-Runs through entire brainstem and into thalamus
-Carries afferents going to thalamic nuclei
-Awakens and prepares the cerebral cortex “Switchboard”
-Accepts what is needed for consciousness and rejects what is irrelevant
Hypothalamus
-Visceral motor activity: autonomic nervous system
-Influenced by olfaction and limbic systems ex: stomach cramps prior to finals
- Superoptic neurons produce ADH and Oxytocin
- Paraventricular also produces them
C/S
-Similar to cerebral
-Circling to either side
-Visual impairment
-Possible endocrine dysfunction: PU/PD, abnormal eating patterns
-Behavioral problems (limbic)
-Temperature regulation
-Non-specific pain
Midbrain
ARAS
Red Nucleus
Nerves in Midbrain
- Oculomotor (CN III) nuclei: somatic movement of eyeball as well as constriction of pull - autonomic
- Trochlear (CN IV): innervates dorsal oblique muscle
- Tectotegmentospinal tract: sympathetic innervation of the eye (dilate)
Possibly hypothalamus
C/S
-Severe gait abnormalities
-UMN paresis and ataxia
-Abnormal mentation: disruption of ARAS. Stupor or coma
-“Decerbrate rigidity” inhibition removed, hyperextension of limbs, overwhelming amount of stimuli
Pons
More ARAS
Motor nucleus of Trigeminal (CN V)
Sensory nuclei Trigeminal CN V
Pontine micturition center (PMC) controlling urination
C/S
-Same as midbrain
-Marked mentation change
-Gait disturbance
-Dysfunction of CN V: muscles of mastication atrophy due to tumor
-Possible dysuria.
Medulla
CN VI-XII come out of here
and Vestibular Nuclei
-ARAS
-Respiratory center
-Autonomic control of HR and BP
-Medial longitudinal fasciculus: assess head trauma. It is a highway. Vestibular information comes through CN VIII and eyes move accordingly
-Medullary reticular formation gives raise to medullary reticulospinal tract (UMN tract)
-Nucleus ambiguous: poorly arranged system. Larynx, pharynx, and esophagus
C/S
-Alterations in consciousness
-Autonomic dysfunction: abnormal HR, RR, BP
-Respiratory problems (UMN for respiration): Cheyne-Stokes respiration
-UMN Paresis
Cerebellum
Does not initiate movement
Regulates, range, rate and force of our movement.
Anatomically
1. Cerebellar cortex
2. Medulla
3. Nuclei
Histology
Folium
-Outside: thick layer germinal cells (grow)
-Molecular layer
-Granular layer
Dividing and migrating during gestation = Hypoplasia or abiotrophy (wear out faster, preprogrammed)
Sections
Spinocerebellum: regulates our muscle tone. Unconscious movement
Vestibulocerebellum: eye movement, balance
C/S
-Intention tremor is the most common: bob head movement, can’t control overcorrection of movements
-Hypermetric movement: ataxia, GOOSE STEPPING
-Truncal sway
-Disequilibrium
-Ipsilateral menace deficits
Lecture 2
Spinal Cord
Gray matter inside
White matter outside
Opposite of brain: gray matter outside, white matter inside
Hypothesize what clinical signs a lesion within each spinal cord segment will result in
C8: T1 nerve already
L5: sacral nerve segments already
Motor: UMN tracts descend in white matter of spinal cord to synapse on LMN in the gray matter of spinal cord
Those facilitory to flexors = walking
a. Corticospinal
b. Rubospinal
c. Medullary reticulospinal
Those facilitory to extensors = standing
a. Vestibulospinal, pontine reticulospinal
Balance system helps weight bearing
Sensory
Ascending fibers for proprioception and pain are located mainly dorsally and laterally
Lesions
-Usually affect both: ascending proprioception fibers as well as descending UMN
-Ataxia and Paresis commonly seen
UMN interference over LMN
-Release of muscle inhibition
-Ex: Exaggerated patellar reflex
-Loss of check and balance system
Spinal Cord Lesions
Clinically Important LMN
-C6-T2
-L4-S3
C/S
-Paresis or plegia
-Depressed or absent spinal reflexes
-Decreased muscle tone
- C1-C5 section
-Descending UMN tracts to all 4 limbs
-Ascending GP and nociception from all 4 limbs
-Origins of Phrenic nerve C5-C7 (diapraghm)
-Descending sympathetic fibers to the eye
-Nerves that cause pupil dilation are in the cervical region
Lesion C/S
-Gait affected in all 4 limbs (tetra or hemi)
-UMN signs to all 4 limbs: Increased tone, hyperactive spinal reflexes, patellar reflexes
-Delayed postural reactions (proprioception deficits) in all 4 limbs
-UMN bladder
-Rarely respiratory difficulty
-Rarely Horner’s syndrome: sympathetic fibers that innervate the eye
- C6-T2 section
-Descending UMN to all 4 limbs
-Ascending general proprioceptive fibers and nociception from all 4 limbs
LMN to the front limb
-Pre-ganglionic sympathetic fibers
-LMN of phrenic nerve
-Lateral thoracic nerve: innervates the cutaneous trunci muscle
Lesions C/S
-Gait affected in all 4 limbs
-Delayed postural reactions in all 4
-LMN signs to FORELIMBS: decreased muscle tone, decreased reflexes.
-UMN to HINDLIMBS: normal to hyperactive reflexes in rear
-UMN bladder
-Horner’s and phrenic nerve dysfunction possible but less likely
Two engine gait: two different motors working the legs
-Difficulty bearing weight in the FRONT LIMBS
-SLOW backend
- T3-L3 section
-Descending UMN to REAR LIMBS only
-Front legs normal
-Ascending general proprioceptive and nociception from rear limbs
-Hypogastric nerve = L1-L4: bladder function
-Boder cells: confusing cells, live here. They go back upstream and provide inhibition to front legs = EXTENSION and RIGIDITY FRONT limbs
Schiff-Sherrington phenomenon
C/S
-Gait affected in hind limbs
-Normal postural reactions and reflexes in forelimbs
-UMN to hindlimb: normal to hyperactive reflexes, possible crossed extensor reflex.
-Delayed postural reactions in hinblimbs
-UMN bladder/sphincter: rigid bladder and spinchter
-Possible Schiff-Sherrington phenomenon
- L4-S3 section
-UMN to rear limbs only
-GP and nociception from rear limbs only and pain fibers
-LMN to the rear limbs
-L4-L6 femoral nerve
-L6-S1(2) Sciatic nerve
-S1-S3 - pudendal nerve
-S1-S3 - pelvic nerve
C/S
-Gait affected (variably) in hind limbs only
-Normal postural reactions and reflexes in forelimbs
-LMN sings to hindlimb: decreased spinal reflexes, decreased muscle tone, tail, anal sphincter.
-Delayed (variable) postural reactions in hindlimb
-LMN Bladder/sphincter: impact on the bladder, different than UMN
S1-S3 Section
C/S
Plantigrade stance
-Forelimbs normal
-Gait may be normal
-Posture could be normal or plantigrade in hindlimb
-LMN anal sphincter
-LMN bladder
Cd1-5
-LMN tail
-Bladder should be normal
-Anal tone should be normal
-Rare Cd spinal cord segment disease
Lecture 3
Determine whether or not neurologic disease is present
Perform the major parts of the neurologic examination
Define what is normal vs. abnormal response
Assess severity of dysfunction
Neurologic Exam
Goals
-Nervous system disease present?
-Recognize/interpret abnormal signs
-Localize lesion
-Assess severity of dysfunction
-Differential diagnosis
-Tentative prognosis
Neuroanatomic diagnosis»_space; etiologic diagnosis
Localization - differentials - diagnostic plan
- History: time course of the disease. Acute vs. chronic. Static, improving, progressing
- Observation: Mention, Posture, Gait.
-Bright, alert, responsive, depression/dull, conscious but inactive.
-Severe signs: obtunded (sleeps when undisturbed), Stupor: touch, noise does not cause arousal. Strong stimuli to respond. Coma (unconscious), Demented: inappropriate. - Postural reactions: sensory inputs from receptors in limbs, and body, visual system, vestibular system.
-Abnormal: wide-based stance, leaning, head tilt, schiff-sherrington posture, decerebrate rigidity.
-Increased muscle tone (usually extensors): Sign of UMN disease
-Decreased muscle tone: LMN disease
Gait, very complex
-Basal nuclei (& motor cortex) initiation of movement
-Cerebellum: coordination how much movement gets released
-Vestibular system: gravity
-Spinal cord: takes information down to peripheral nerves and neuromuscular functions
Forebrain lesions: rarely cause gait abnormality. It is midbrain or caudal.
- Spinal reflexes (myotatic & withdrawal)
- Cranial nerves
- Palpation
- Sensory perception
Indications
Changes in
-Behavior/attitute/onset of seizures
-Balance
-Gait
-Strength/endurance
-Muscle tone/symmetry
Definitions related to Gait
Circling
Not a localizing sign by itself
Forebrain lesion
-Wide circles
-Generally towards the lesion
Vestibular Dysfunction
-Tight circles
-Head tilt usually present
Animals usually circle toward the lesion
Ataxia
-Lack of coordination
- Vestibular ataxia: loss of orientation of body with respect to gravity. Drift, lean, fall, roll.
- Cerebellar ataxia: not weak, very uncoordinated, trunk sway, hypermhtric.
- Propioceptive ataxia: disruption of ascending proprioceptive fibers. Spatial information fails to reach the brain . Limbs crossing over, scuffing digits, standing, don’t know where to put the leg, delay in the protraction (forward movement of the leg).
Postural Reactions
-It is a Complex responses that maintain normal upright body position when pushed/moved
-Does NOT specifically localize region
-Good for abnormalities in nervous system
-Often first abnormality test, may notice deficits prior to overt gait problems
-Very sensitive not very specific
-Assess for ASYMMETRY!!
Requires ALL
-Sensory systems
-Spinal cord
-Cortical integration (somatosensory cortex)
-Motor system UMN & LMN
-Neuromuscular junction to flip the switch back over
Examples
-Propioceptive positioning (paw placement test)
-Hopping
-Hemiwalking: used for large animals
Spinal Reflexes
Which is the best in forelimb, hindlimb?
-Independent of higher brain centers
-Does not require any activation of brain
-Does not necessarily indicate patient can feel pain
-Most reliable forelimb
-Most reliable sciatic reflex withdrawal
-Reflex intact even with cord transection
-Evaluates: Component of reflex arc (sensory and motor) The integrity of the spinal cord segments
-Influence of descending UMN pathways on arc
-Help us localize spinal lesions!
- Myotatic (stretch) reflexes
-Monosynaptic: one connection, one nerve up, one nerve down - Flexor (withdrawal) reflexes: multi synaptic. Recruits more muscle fibers to get the leg pulled back
Forelimb Reflexes
-Flexor (withdrawal): all limb flexor mm. All nerves from C6-T2
Hindlimb Reflexes
-Patellar: Femoral; L4-L6
-Sciatic: Sciatic; L6-S1
-Withdrawal: Sciatic; L6-S2
-Cutaneous trunci: Lateral thoracic; C8-T1
UMN
-Increased muscle tone
-Normal to hyperreflexia
LMN
-Flaccid muscle tone
-Decreased to absent reflexes
Tips for Spinal Reflexes
-Perform with animal lateral recumbency
-Pelvic limb first, then thoracic
-Myotatic reflexes first, then flexor
-Do one side, then flip to other side
Patellar Reflex
Which nerve is tested?
Withdrawal Reflex
Hold the pinch on the toes
Forelimb Withdrawal reflex
What nerves/spinal cord?
Test objective: “Cutaneous trunci is absent caudal to …?”
Perineal (Anal) Reflex
Nerve evaluated
-Pudendal (S1-S3)
-Perineal (S1-S3)
Cranial Nerves
Which cranial nerves are not usually tested?
-CNI and CN XI
-Most test are reflex arcs
-Some are responses: implication that requires cortex
1. Menace response
2. Nasal sensation
Consistency order is key
Which cranial Nerves are usually assess during neurological exam?
- Menace Response
CN II, VII - Cortical, cerebellum
-Move hand toward one eye, opposite eye is covered
-Blinking is the normal response
-Not present in puppies and kittens until about 3 mts
Requires contralateral cortical input
- Palpebral Reflex & Facial Sensation
CN V, VII - Cortical
-Medial cantos of the eye
-Afferent: CN V (ophthalmic branch)
-Efferent: CN VII
- Pupillary Light Reflex
CN II, III
What are the branches of the trigeminal nerve?
Which are we testing with Nasal Sensation test?
Nasal sensation test the ophthalmic brach +/- maxillary
-Contralateral, so cortex somatosensory test too.
Pupillary Light Reflex
What are we testing?
Afferent: CN II (optic n)
Efferent: CN III (oculomotor nn)
Assessment of the pupil size and symmetry
Swinging light test: Direct PLR = what is happening in the ipsilateral eye
Indirect = what is going on in the opposite eye
Physiological Nystagmus
What is being tested? Afferent, Efferent
-Oculocephalic Reflex & Oculovestibular Reflex
Test for connection of MLF which is the connection between CN VIII, CN III, IV, VI.
Afferent: CN VIII (Vestibulocochlear) - Gravity
Efferent: CN III, IV, VI
Abnormal signs
-Spontaneous (resting)
-Positional (inducible)
Orientation
-Horizontal
-Rotary
-Vertical
Direction
-Of the FAST PHASE
Gag Reflex & Jaw Tone & Tongue
Gag Reflex
Caudal Brainstem
Afferent: IX, X
Efferent: IX, X, (XI), (XII) back of the throat
Abnormal: no jaw tone usually
Jaw Tone
From Trigeminal nerve
Lesions: atrophy of temporals/masseter muscles, loss of jaw tone, dropped jaw (bilateral)
Tongue
From CN XII (Hypoglossal nn)
General Somatic Efferent
Neurological Exam
Palpation
Spinal Palpation
-Hyperesthesia = increased sensitivity to stimulation
-Perform from caudal to cranial
-Vertebral column (start at L7)
-Press spinous process and epaxial muscles
-Gently flex and extend neck
-Squeeze transverse process
Neurological exam
Sensation
Evaluated by
-Cranial nerves
-Spinal reflexes
-Propioceptive positioning
-Spinal palpation
Still to be evaluated: superficial pain and deep pain
Perform if needed and always last
Nociception
-Perception of noxious stimuli Afferent information.
-Heat, pain, pressure, chemical
-Often difficult to differentiate from superficial and deep pain perception
Pain is a conscious, emotional sensation which means it requires input from the brain
Perform test
-Use the least noxious stimulus possible
-Fingers before hemostats
-Skin/webbing between toes, nailed, or last digit
-Normal response indicates deep pain perception. Withdrawal of limb (unless LMN location)
-Behavioral response: anxiety, vocalization, attempt to escape
-Turning head, attempt to bit
-Increase in respiration or pupil dilation
-withdrawal of the limb only does NOT indicate pain perception
-If voluntary movement in its limbs = 99% of the time will have nociception
-Do not unduly harm the animal by crushing its toes
Neuro Exam Light version
- Mentation
- Paw placement +/- reflexes
- Menace response +/- PLR, palpebral reflex
Lecture 4
Identify key points from neurological case history
Assimilate exam findings
Assign a neurolocalization based on all findings
Generate a brand differential list based on sign-time graph
Sign-time graph
Severity vs. time
- Congenital/anomalous
- Neoplastic
- Degenerative
- Inflammatory, Toxic
- Traumatic, vascular
Case 1
Forebrain disease?
1.Mental status: QAR
2.Walking in circles: no
3.Seizures: No seizures
4.Central blindness: No central blindness
5.Decreased facial expression: (contralateral) No
6.Postural reaction deficits: proprioceptive ataxia both rear limbs. Moderate to severe paraparesis. Normal postural reactions in front limbs. Very delayed paw replacement and hopping bilaterally in rear.
Gait
-Forelimbs: normal
-Rear limbs: exaggerated patellar reflexes bilaterally. Cutaneous trunci absent bilaterally caudal to L1
-CN: normal
-Spain pain elicited on palpation at thoracolumbar junction
Arched back, walking as if drunk
Conclusions
-Gait affected: midbrain or caudal to it because forebrain does not cause gait abnormalities
-Lesion location: caudal to foramen magnum bc mentation normal
-Caudal to T2 bc forelimbs normal
-Lesion is T3-L3
Dx:
-Intervertebral Disc Herniation
-Degeneration
Case 1B
Gait
-Affected rear limbs
-1 year history of wobbly rear limbs
-No improvement steroids, pain meds.
-Absent paw replacement and hopping bilaterally
-Rear normal patellar reflexes bilateral, normal withdrawal bilaterally.
-Cutaneous trunci absent caudal to T13
Conclusions
-Location: T3-L3
-Degenerative: chronic, progressive, non-painful thoracolumbar myelopathy in an old-aged dog.
-Degenerative, Neoplastic, Infectious.
-DX: Fluid accumulation in Spine “diverticulum”
Case 2
-6 yo beagle
-No history of trauma
-Screamed and reluctance to move
-Screams when approached
Neuro PE
-Ambulatory with mild tetra paresis and proprioceptive ataxia 4 limbs
-Slightly delayed paw replacement and hopping 4 legs
-All spinal reflexes normal
-Marked pain and hyperesthesia elicited on gentle flexion of the neck
Conclusions:
-Lesion location: C1-C5, caudal to foramen magnum bc mentation was normal
-Acute onset, painful disease resulting in cervical myelopathy in a middle-aged dog
-DX: IVD herniation
Case 3
Signalment: 6 yo, female spayed west highland white terrier
History
-Recumbent in backyard 4 days earlier, unable to walk
-Static over past 4 days
-Left thoracic and pelvic limbs: voluntary movement
PE
-Urine scald in inguinal region
-No other significant abnormalities
Neuro PE
-Dog falls to the right when placed on feet
-No motor function seen on right
-Absent proprioception right front and hind, slightly delayed on left rear and front
-Reflexes: most significant 0-1 withdrawal right thoracic limb
-No pain on spinal palpation or neck flexion
Conclusion
-Lesion location: C6-T2
-Acute onset, non-progressive, non-painful, asymmetrical.
-DX: Stroke, Ischemic myelopathy
Case 4 highlights
Signalment
History: fallen down stairs, depressed
PE: collapsing trachea and locating patellas typical for breed
Neuro exam: anxious, inappropriate, slow to respond to stimuli.
-Paced around always to the right.
-Rt side: normal postural reactions
-Lft side: delayed to absent paw placement and hopping
-All spinal reflexes normal
Central blindness phenomenon
-Absent menace response (CN VII, CN II) OS, normal OD
-Normal palpebral (CN V, VII) and pupillary light reflexes (CN II, III) UO
-Nasal sensation blunted (CN V, CN I, CN VII) left, normal right.
-Normal oculi-vestibular movements
-Normal gag reflex.
Conclusions
-Lesion: Intracranial
-Circling and compulsive to the right: forebrain right side affected
-Acute onset behavioral changes. Progressively more severe despite medication
-DX: Meningioencephalitis, Asymmetrical Brain, Right-sided.
Case 5 highlights
PE
-Noticeably decreased muscle tone and moderate muscle atrophy
Neuro exam
-QAR
-Lateral recumbency
-Flaccid paralysis/tetraplegia with absent muscle tone
-Unable to bark, can move mouth
-Can move head slightly
-Absent postural runs and spinal reflexes in all 4 limbs
-CN normal
Conclusion
-DX: diffused LMN or neuromuscular disease
1. Absent spinal reflexes in all 4 limbs
2. Widespread flaccid paralysis with muscle atrophy
3. Aphonia (inability to bark)
Acute, idiopathic polyradiculoneuritis, AKA Coonhound paralysis
-Ddx: tick paralysis, coral snake bite, botulism, fulminant myasthenia gravis
Case 6 highlights
Conclusion
-Orthopedic disease
Case 7 highlights
signalment: 8mt old female intact Yorkshire terrier
-Thin 3/9
-Innapropriate mental behavior
-Normal gate
-Paces
-Propioception delayed, hopping delayed in all four limbs
-spinal reflexes normal
-CN: absent menace (CN II, CN VII), normal palpebral and PLR OU.
Conclusion
-Insidious onset, minimally progressive disease showing forebrain signs in a young, toy-breed.
-Lesion: forebrain (cerebrum)
-Ddx: degenerative, anomalous, metabolic, nutritional, infectious.
-DX: Congenital Hydroencephalus
Case 10 highlights
History
-Slowly progressive gains abnormality since 2.5 yo. (3.5 yo Golden retriever)
Neuro exam
-Truncal sway
-Intention tremors
-Cerebellar ataxia (marked)
-No paresis noticed
-Hyperactive reflexes
-No cranial nerve abnormalities
Conclusion
-Slowly progressive onset of severe cerebellar deficits in a young, mature dog
-Cerebellum dysfunction/deficits
-DX: Neosporosis (neospora caninum). Degenerative, infectious
Case 12
DX: Clot older dog, Disk herniation with compression of caudal equine L7-S1
-Slow, insidious onset of hair abnormalities in an older dog, large breed
-Pain elicited when tail elevated
-Location: L4-S3
-Decreased withdrawal bilaterally hind limbs = caudal to T2
-slightly increased patella reflexes bilaterally: means L4-L6 Femoral ok.
-L7-S1: SCIATIC problem
Case 13
Old German Shepherd
DX: degenerative myelopathy
Slow insidious onset of gait abnormality in al older large-breed dog. No pain elicited
-Hip dysplasia history
-PE: normal
-Neuro exam: wide based stance in pelvic limbs. Truncal ataxia, thoracic limbs appear normal. Severe paraparesis with marked proprioceptive ataxia. Paw replacement absent in both hind limbs. Hemiwalking pelvic.
-Cutaneous trunci absent caudal to T13
-Location: T3-L3
-Patellar reflex normal (L4-L6 Ok)
Lecture 6 Seizures and Epilepsy
Understand what conditions can mimic seizure activity
Compare different types of seizures and epilepsies
Develop a clear understanding of how to diagnose primary (idiopathic) epilepsy
Describe what aspects of epilepsy management need to be expressed to clients
1 What is a seizure?
2 What is nor a seizure?
- Clinical manifestation of excessive and or hyper synchronous neural activity
-originate from forebrain (cerebrum/thalamus)
Types
A. Generalized
B. Focal
- Seizures are NOT
-syncope
-Narcolepsy/cataplexy
-Acute vestibular dysfunction
-Animals sleeping/dreaming
-Tremors (can be confusing)
-Movement disorders
Seizures Definitions/Stages
- Prodrome: before onset of seizure
-Changes in behavior, anxiousness, seeking attention, hiding
-Can last several days - Aura: initial manifestation of seizure
-Drooling, vomiting, pacing, whining, barking,
-Seconds to minutes in duration prior to full seizure - Ictus: actual phase event per EEG.
-Seconds to minutes in duration - Postictal phase: abnormal behavior, disorientation, deep sleep, weakness, confusion, blindness, sensory and motor dysfunction.
-Minutes to 48 hours - Interictal period: Time between seizures
- Cluster Seizures
- Status epilepticus = increased mortality
- What can happen during a seizure?
- 2 or more seizures within 24 hours
- Seizures lasting more than 5 minutes
-Repeated without full return to consciousness in between
-Associated with worse prognosis - Hyperthermia, hypoventilation, hypoxia, hypertension, possible neurotoxicity, neuronal cell death, increased ICP
Generalized Seizure
-The entire brain is involved
-Tonic/clonic most common: bilateral compulsive tonic and clonic muscle contractions.
-Reflects involvement of both cerebral hemispheres: motor manifestations are bilateral
-Impaired consciousness
+/- autonomic signs
Common complications
-Urination/defecation/hypersalivation
-vocalization due to pain but inability to control it
-Biting tongue
-Head trauma
-Aggression
Partial (focal) Seizure
-Abnormal activity in one specific area of the forebrain
-Motor, autonomic, or behavioral signs all possible
Simple
- if consciousness not altered, can respond to stimuli
Complex
-If consciousness is impaired: fear aggression, whining, appearance of hallucinations
Arise from FOCAL AREAS of FOREBRAIN
-Paroxysmal changes in motor function: facial-muscle twitching, single-limb movements (Contralateral cerebrum)
-Paroxysmal changes in vegetative or sensory function: fly biting, licking, bug-hunting, anxiety, restlessness. Excessive unmotivated vocalization, autonomic signs.
What are some causes of seizures?
What are the classification of animal Epilepsy?
- Idiopathic (primary) epilepsy
-No recognized underlying metabolic or structural cause
-Most common
-Genetic or hereditary possible
- Symptomatic (secondary) epilepsy
-Metabolic or structural brain disorders
- Probably symptomatic (cryptogenic) epilepsy
-Metabolic or structural brain disorders that are present yet undetectable
- Reactive seizures
-disturbances in systemic metabolism or toxicosis Ex: hepatic encephalopathy, xylitol, or chocolate toxicity.
-No structural brain disease
-Not considered a true epilepsy
Idiopathic Epilepsy
Most common cause in dogs
What are the breeds dispositions?
-Spontaneous seizures, most often during rest/sleep.
-Quick and uneventful recovery
-Initial frequency: q 4-6mts
-Increase in frequency and severity over time if untreated
-Stressors are very common in humans
NORMAL interictal period and NORMAL neurological exam
-Border collies, Australian shepherd, Labrador Retriever, Pitbull, Boxers, etc.
-onset ~1-5 yo (6 months to 6 years)
-Usually generalized tonic-clonic: may be focal that proceed to generalized tonic/clonic
Idiopathic Epilepsy diagnosis
Signalment
History: very important
-Vaccination, travel, trauma, exposure to toxins?
-Medical, surgical history
Seizure description
-Onset
-Frequency
-Duration
-Characteristic of poetical phase
PE
and Blood pressure
-Heart murmurs, other sigs of cardiac disease (syncope)
-Hypertension
-Minimum database: CBC, CHEM, UA, BP
-BG, Creatinine
-Other lab tests: bile acids, rule out PSS, liver disease. T4, ACTH stim.
-Addison’s (hypoglycemia) Cushing’s (Increased BP, hypercuagulable)
Imaging
-Thoracic radiographs, Abdominal, Ultrasound abdomen
Testing for brain disease
-MRI, CT
-CSF
-Infectious disease tests
-EEG
Seizures Therapy
- Maintenance: control of the seizures. Decrease in severity, duration, frequency. Maintain quality of life for pet and owner
-Surgery: cortical resection vs. corpus collasum division
-Vagal nerve stimulation: expensive and limited data
-Acupuncture
-Ketogenic diet
-Cannabidiol (CBD)
- Emergency tx: stop the seizure
Treatment recommended when
-Symptomatic epilepsy
-Seizures occurring more than once every 2-3 mts
-Status or cluster seizures
-Prolonged postictal periods
-If the client can not deal with it
Client Education
-Treatment is lifelong
-Anticonvulsants daily
-Periodic monitoring
-Emergencies will happen
-Keep seizure log
-Drugs have cost and side effects
-Do not alter drug doses
-Be cautious of other drugs/supplements
Management Mistakes
-Failure to obtain diagnosis
-Insufficient drug doses
-Owner non-compliance
-Use of wrong drug
-Setting unrealistic expectations
Treating seizures Drugs
- Idiopathic epilepsy
-Most respond well to combination therapy
-Small % may be refractory even with multiple medications
-If seizure free for >1yr: weaned slowly
-Diazepam (oral): NEVER CATS
Anticonvulsants
-Phenobarbital
-Bromide
-Zonisamide
-Levetiracetam
-Topiramate
-Diazepam: short half life and tolerance
-Clonazepam: short half life and tolerance
Others
-Gabapentin: usually used as pain medication. binds to alpha2 subunit of Ca channels
-Pregabalin
-Felbamate: inhibits excitatory transmission (NMDA) start slow
-Carbamazepine: voltage gated Na channels
Rescue Protocol
Cluster seizures
If 3 seizures in a 24 hr period, Initiate
If 4, rescue repeat
If 5, seek immediate veterinary care
Reminder: status epileptics seizures >5 minutes
-Diazepam injectable, PR
-Midazolam injectable, PR
-Additional dose of patient’s daily med
-Clorazepate course: 1 mg/kg BID until seizure free for 24hrs
Lecture 7
Recognize the individual components of the vestibular system
Explain the normal function of the vestibular system in regards to coordinated limb and eye movements
Differentiate the common signs associated with peripheral vs. central vestibular disease
Understand just how paradoxical vestibular disease occurs
List the most causes of peripheral and central vestibular disease
Vestibular system - Neuroanatomy
Functions
-Maintain balance (general proprioception, visual system)
-Stabilize images during head movement
-Coordinate posture, movements, and ocular position with respect to the influence of gravity
Abnormalities C/S
-Head/body posture
-Gait
-Occular movements
Anatomy
-Labyrinth
-Bony - perilymph: the bone
-Menbranous - endolymph: inside the bone
- Macula of saccule: vertical
- Macula of utricle: horizontal
- Cristae of SCC: rotational
Provide continuous tonic input
Stimulation of one side = inhibition of the other
Peripheral anatomy of CN VIII
- Distal Portion
-CN VIII receptors to vestibular portion
-Within petrous temporal bone
- Proximal portion
-Travels through acoustic meatus with CN VII
-Enters brainstem on rostral medulla
-Very close to CN V on pons and CN VII on medusa
Central Vestibular Structures
- Vestibular nuclei
- Cerebellar components
Others
-Other CN nuclei
-Medial longitudinal fasciculus: pathway from vestibular nuclei to LMNs in motor nuclei of CN III, IV, and VI. Coordinate, conjugate eye movements as the head changes.
-Descending spinal cord tracts
-Vomiting center: less of a problem in vet med
-Conscious perception of orientation: thought to ascend through thalamus to temporal bone
Central Vestibular Projections & Vestibulospinal Tract
- Spinal cord
- Rostral brainstem
- Cerebellum: projects continuous inhibitory impulses back to vestibular nuclei. Helps maintain position of head, trunk, and limbs when body moves
-Crucial fo “paradoxical vestibular syndrome”
Vestibulospinal tract
-Travels to all segments of ipsilateral spinal cord, including cervical
Causes:
-Fascilitation of ipsilateral extensor mm.
-Inhibition of ipsilateral flexor mm.
-Inhibition of contralateral extensor mm.
Eye Movement
AKA Physiologic Nystagmus oculi-cephalic reflex.
VS helps stabilize image on retina
-Information from semicircular canals
-Movement of head induces compensatory eye movement
-Vestibular neurons - motor nuclei CN III, CN IV, and CN VI.
Normal: Turning the head to the RIGHT
-Contraction of Left lateral rectus and Right medial rectus “slow phase”
-Reset is the “fast phase” and it is controlled by higher centers not the vestibular system.
Pathologic: Lesion on left inner ear
-Left neuronal input abolished
-Right input remains
-Nystagmus has the FAST PHASE to the RIGHT
-Stimulates right vestibulospinal tract: increases tone on right
-Head and body tilt or lean LEFT
Asymmetry of input, Rt side overdoing it
Clinical Signs in General
Common to both peripheral and central disease
- Nausea +/-
- Head tilt: due to unilateral loss of antigravity muscle tone. Usually ventrally deviated ear is the side of the lesion
- Pathologic nystagmus: Distinct fast as slow phase “jerk”
-Described by direction of the fast phase. Ex: rotary nystagmus with fast phase to the right
-Can be spontaneous or induced (positional)
-Always try to induce it
-Quickly compensated for
a. Horizontal
b. Rotary
c. Vertical - Positional strabismus
-Ventrally or ventrolaterally deviated globe when head/neck is extended
-Loss of CN III, IV, VI innervation
-Ipsilateral to lesion - Vestibular ataxia
-Wide-based stance, leaning, listing, tight turning circles, falling, rolling
-Asymmetric input to vestibular tracts
-No paresis
Pendular Nystagmus
-Congenital anomaly of visual system
-SIAMESE or HIMALAYAN cats
-NOT a sign of vestibular dysfunction
Peripheral vs. Central
- Propioceptive deficits
-Usually central - Altered mentation
-Possible central - Head tilt
-Peripheral
-Central - Deficits other than CN VII or CN VIII
-Not peripheral
-Possible central - Nystagmus: both except
-Vertical: central, not peripheral
-Positional induced: Occasionally peripheral, but Yes central
-Change in direction of fast phase: Central for sure - Horner’s syndrome: both possible
Vestibular Central Disease
-Lesions usually exert REGIONAL EFFECT
-Vestibular nuclei, Ascending GP, Postural deficits
-Descending UMN: Tetra/hemiparesis
-ARAS: depressed consciousness
-CN V-XII
Paradoxical Vestibular Disease
-Caudal cerebellar peduncles
-Flocculonodular lobes of cerebellum
-Fastigial nucleus of cerebellar medulla
Remember cerebellum sends inhibitory impulses to vestibular nuclei at all times
Nystagmus: fast phase towards the lesion
Head tilt: opposite to side of true lesion
Ataxia (listing, falling, circling): opposite side of true lesion
Postural reactions deficits: Ipsilateral to the lesion
Bilateral Vestibular Disease
-More common in cats
-Usually peripheral in nature
-Absence of head tilt
-No pathologic nystagmus
-No physiological nystagmus (absent oculo-cephalic reflex)
-Crouched low to ground (can’t feel gravity, but can feel ground)
-Wide, lateral head excursions
Diseases that cause Peripheral Vestibular Dysfunction
- Otitis media/interna: can see peripheral vestibular dysfunction VIII, facial nerve deficits, Horner’s syndrome (eyelid affected) sympathetics
-Most common cause
-Unilateral or bilateral
-Preceded by head shaking, pain, smell, or nothing
-Common concurrent VII deficits and horner’s syndrome
-Otoscopy, bulla radiographs, advanced imaging.
-Tx: myringotomy, C&S, flushing, appropriate antibiotics
-VBO or TECA: ventral bulla osteotomy or total ear canal ableration
- Idiopathic (dogs vs. cats)
DOG
-2nd most common
-Geriatric
-Unknown etiology
-Usually >10 yo
-Acute onset unilateral
-Normal proprioception
-Does NOT CN VII or Horner’s syndrome
-Signs stabilize in 2-3 days, resolution 2-3 weeks
-Tx: Diazepam or Meclizine
-Rare recurrence
CAT
-Any age
-Summer and fall mts most common
-Will occasionally be bilateral in nature
-Etiology unknown
- Inflammatory polyps (cats>dogs)
Diseases that cause Central Vestibular Dysfunction
-Neurolocalization to central vestibular system is an indication for more advanced diagnostics
-MRI, CSF, BAER test
-Generally associated with rapid deterioration and death
- Hypothyroidism
-Change in CN VIII
-Pathophysiology likely multifactorial
-Increased cholesterol, triglycerides
-Ischemic infarctions associated with atherosclerotic vascular disease
-CNS demyelination
- Neoplasia
- Meningioencephalitis
-Autoimmune
-Otitis media/interna can result in abscess
- Cerebrovascular accidents
- Metronidazole toxicity
-MOA unknown
-Dose >60mg/kg/day
-Cats show more forebrain signs
Case 8
-Listing and circling to the right
-Horizontal nystagmus fast phase to left
-Manace absent on right
-Follows cotton ball OU
-PLR normal OU
-Drooping right lip
-Postural reactions all normal
-Spinal reflexes all normal
-No obvious pain or hyperesthesia
Conclusions
-Balance or vestibular dysfunction
-CN VII involvement
-Peripheral vestibular disease more likely
-Right sided peripheral vestibular problem
-Right sided CN VII problem: commonly affected with labyrinthine disease
Ddx
-Peracute, unilateral vestibular and facial nerve deficits in a middle aged cooker spaniel
-Infectious, immune, idiopathic, traumatic, vascular
DX: Idiopathic facial paralysis
DX: Infectious Otitis media/interna
Case 10
Horizontal nystagmus = peripheral but central disease is sneaky
Left ventrolateral strabismus when head elevated
Paw placement slightly delayed on left limbs
Lecture 8-9
Create a proper differential list based on DAMMIT-V and the sign-time graph concept
Understand the pathophysiology and clinical presentation of selected disease processes
Outline general treatment plans and prognoses for selected disease processes
Intracranial Diseases
- Degenerative
-Cognitive dysfunction - Anomalous/structural
-Hydrocephalus
-Chiari-like malformations (COMS) - Metabolic
-Hepatoencephalopathy - Nutritional
-Thiamine deficiency - Neoplastic
-Primary vs. secondary - Inflammatory
-Infectious
-Non-infectious - Traumatic
-Head trauma
-Hemorrhage - Toxic
-Tremorgenic
-Mycotoxins
-Metronidazole - Vascular Disease
-CVA and TIA
-Feline Ischemic encephalopathy
Degenerative diseases
Cognitive Dysfunction Syndrome
In general
-Time of onset can be young or old
-Slow but steady progression without improvement
-Signs of forebrain problems
-Poor prognosis
Pathophysiology
-Uncertain, similar to Alzheimer’s
-Changes: cerebral vascular, meningeal thickening, gloss and ventricular dilation.
-Progressive accumulation of protein B-amyloid, toxic, inhibits neuronal function
-Intraneuronal accumulation of tau protein, precursor to neurofibrulary tangles
C/S
-Dogs >9 yo
-Cats > 12 yo
-Change in obedience/response to commands
-Change in recognition of familiar people or pets
-Frequent house soiling
-Change in excitement for walks or outings
-Frequency of waking in the night
-Avoids being petted or touched
Diagnosis
-History: 1-2 years changes
-Exclusion
-MRI
-CSF
Tx
-Pharmacologic: SLEGLINE
-Diet, supplements, environment
-Toys, environmental enrichment
Anomalous/Structural
General
-Signs usually present shortly after birth
-Signs remain static although many times they present after exacerbation
-Treatments are aimed at reversing or managing nature.
Anomalous
Hydrocephalus - Developmental
-Any increase in CSF volume within the ventricular system or SA space
- Developmental
- Acquired
C/S
-PE: dome shaped head, sunset eyes, +/- persistent fontanelle (fixed strabismus)
-NE: Forebrain signs predominate, central blindness
Diagnosis
-Often presumptive based on exam
-MRI > CT > Ultrasound
Treatment
-Corticosteroids (may decrease CSF production) Prednisone or Dexamethasone
-Diuretics, but not sustainable for longterm
-Carbonic anhydrase inhibitor
-Proton pump inhibitor
-Anticonvulsants
Surgical
-Ventriculoperitoneal shunt 75% successful improvement
-Other procedures
Prognosis
-Guarded
Anomalous - Acquired
Obstructive Hydrocephalus
-Usually from blockage of normal CSF flow
Anomalous
Chiari-Like Malformations (COMS)
AKA CAudal Occipital Malformation Syndrome
-Thought to be congenital occipital bone defect
-Compression of cervicomedullary junction at foramen magnum
-Variable degrees of syringomyelia
Breeds:
-Cavalier King Charles Spaniel most common
-Brussels Griffon
-Yorkshire terrier
-French bulldog
-Mini/toy poodle
-Maltese
-Pug dog
-Pomeranian
C/S
-Highly variable
-Problem is caudal fossa, so less forebrain
-Cervical pain
-Scoliosis “Phantom” scratching
-Weakness and ataxia: C1-C5, or C6-T2
-Central vestibular signs
-Seizures only rarely
Diagnosis
-Ddx for susceptible breeds
-MRI
-Occasionally incidental finding on MRI
Treatment
-Medical: mild to 1st time signs
-Surgical: severe or recurrent signs
-Gabapentin or Pregabalin: inhibits DORSAL HORN influx Ca++
-Tramadol: synthetic opiate
-Amantadine: NMDA antagonist
-Prednisone: lowest effective dose
Surgery
-Foramen magnum decompression
-Reoperation rate high due to scarring within 5 years
Prognosis
-Overall fair to guarded
Hepatoencephalopathy
-Results from failure of liver to remove toxic substances
-Commonly secondary to:
Congenital/acquired portosystemic shunt
End-stage chronic liver disease
Acute, fulminant liver disease (LEPTO)
C/S
-Symmetrical
-Depression
-Dementia
-Pacing
-Head-pressing
-Stupor
-Coma
-Seizures
-Rarely cerebellar signs
-Ptyalism (CATS) excessive secretion of saliva
Neoplasia
1 Meningioma
- Primary
-Slow insidious onset - Secondary
-Can cause thrombosis and infarction, or hemorrhage
-Significant deficits relatively quickly - Primary Brain tumors
-Brain parenchymal cells (neurons, glial cells)
-Membranes (meninges, ependymal cells)
-Vascular elements (choroid plexus)
Signs caused by:
-Invading effects
-Peritumoral edema/inflammation
-Ischemia
-Obstructive hydrocephalus
-Hemorrhage
-Gliomas: Astrocytoma (GBM), Oligodendroglioma.
C/S
-Dogs >9 yo
-Cats >10 yo
-Dolichocephalic breeds = meningioma (Golden Retriever)
-Brachycephalic breeds = Glioma (Boxer)
-Cats = meningioma, better prognosis
Dogs: seizures, behavioral change, circling, lethargy, visual deficits, and semi-inattention (neglect) syndrome
Cats: behavioral change
Dx
-Suspicion
-Susceptible breeds
-BIOPSY only definitive surgical CT guided
-Presumptive with imaging
Tx
-Surgery
-Radiation
-Chemotherapy
Primary Brain tumors
Inflammatory Brain Disease
Many categories
Variable onset and severity
Disease will typically progress unless proper treatment is initiated
General
1. Infectious meningoencephalitis: bacterial, viral, fungal, protozoal, rickettsial, verminous
2. Meningoencephalitis of unknown etiology MUE, thought to be autoimmune
3. Neoplastic
-Diagnosis and treatment can be frustrating
-Rarely get antemortem definitive diagnosis
Sigs
-Diffuse or multifocal encephalopathy
-Forebrain or vestibular or cerebellar or all
-Variable degrees of fever and neck pain
Dx
-Referral mostly
-MRI/CT
-CSF
-Infectious disease testing
Prognosis
-Guarded
Infectious Inflammatory
Canine Distemper Virus
C/S
-Concurrent neural signs
-Hyperkeratosis
-Enamel hypoplasia
-GI disease
-Mucopurulent Năsal discharge
-Conjunctivitis
-Choriorentinitis
Pathophysiology
-Paramyxovirus
-Contact with secretions
-Migrates via macrophages to lymph nodes and organs in 1st week
-Immune response variable, can clear disease or progresses
Forms
- Young/Acute <1yo
-Forebrain signs (seizures, blindness, behavioral) - Mature and Chronic >1yo
-Leukoencephalomyelopathy: demyelinating in entire CNS.
-Cerebello-vestibular, spinal cord dysfunction (myoclonus) difficulty walking - Adult/older >5 yo
-Considered rare, mostly forebrain - Post vaccinal
Dx
-Frustrating
-Lymphopenia common
-MRI/CT
-Multiple CDV, viral antigen, serum CSF Ab, urine RT-PCR.
-Most consider results in light of patients c/s
Treatment
-Symptomatic not cure
Prognosis
-Most require euthanasia
-Some recover, depends on immune response from patient
Infectious Inflammatory
FIP
-Virulent type if feline enteric coronavirus (FECV) that hides in macrophages and forms immune complexes that deposit in a variety of tissues
- Wet/effusive: immune complex
- Dry: vasculitis and heavy accumulation of inflammatory cells
Signs
The most common infection to affect CNS of cats
-Myelopathy
-Persistent fever
-Obtundation
-Myriad of neurological signs
-Cerebellovestibular, paraparesis, and seizures
Dx
-Serology
-PCR
-No test is perfect
-MRI
-CSF: very high protein
-Diagnosis made at necropsy
Prognosis
-Usually fatal
Vax questionable
Infectious Inflammatory
Fungal
Geographical
-Cryptococcus neoformans: pigeon poop
-Coccidioides immitus (Valley fever): SW USA
-Blastomyces: usually systemic, affect eyes
-Histoplasma: daily rare. Near river valleys
-Aspergillus: more commonly causes discopondylitis. If meningeoencephalitis, likely fatal
Inflammatory
Non-Infectious
Meningoencephalitis of unknown etiology (MUE)
-SRMA
-GME
-NME
-NLE
-Little White Shaker dog disease
Steroid Responsive Meningitis/Arteritis
-Likely immune mediated
Breeds
-Bernese MD,
-Boxers
-Beagles
C/S
-Acute onset spinal pain especially cervical
-Minimal to no neurological abnormalities
Pathology
-Suppurative leptomeningitis with severe arteritis and fibrinoid necrosis of arterial wall
Dx
-Rule out other causes like IVDD, etc
-CBC leukocytosis with mature neutrophilia (not toxic neuts)
-CSF elevated protein, neutrophilic pleocytosis (mature)
Tx
-Pain medications
-Immunosuppression
-Predinosone, weaned slowly 4-6 mts
-Elevated food water dish
Px
-Excellent but relapse possible
Granulomatous Meningioencephalitis
-Fairly common idiopathic inflammatory CNS disease
-Thought to be T-cell mediated hypersensitivity reaction
C/S
-Potential triggers of autoimmune attack include infections and vaccinations
-Young to middle aged FEMALE SMALL BREED
- Ocular
- Focal
- Multifocal/dessiminated: more common
Pathology
-Predilection for white matter and brain stem
Signs
-Largely dependent on location of disease
-Common seizures and cerebella-vestibular dysfunction
Hallmark: cytopath perivascular walls
Dx
-Histopath only definitive
-Signs + suspicion + MRI + CSF + Negative infectious tests
-Presumptive antemortem diagnosis
-Mixed cell pleocytosis: macrophages/monocytes evidence of reactivity
Tx
-Multimoddal immunosuppression is recommended
-Anticonvulsants if indicated
-Corticosteroids: prednisone
Adjunctive therapy
-Cyclosporine
-Cytarabine arabinoside
-Azathioprine
-Procarbazine
-Mycofenolate mofetil
-Lomustine
-Leflunomide
Px
-Guarded
-Patients with focal disease do better
-Survival times are variable
-Early intervention helps
Necrotizing Meningioencephalitils/Leukoencephalitis
Breeds
-Pug - genetic marker
-Maltese
-Chihuaha
-Shish Tzu
-Pekingese
-Papillon
-Boston terrier
-Non-infectious
-Thought to be immune mediated
-Potential triggers
C/S
-Acute to peracture onset of forebrain signs
-Seizures predominate
-Circling, visual impairment, head pressing, altered mentation
Dx
-Compatible signs
-MRI/CT
-CSF
Tx
-Same as for GME
Px
-Poor to grave
-Therapy is unrewarding
“White Shaker Disease”
Action-related repetitive myoclonus
Signs
-Diffuse whole-body tumor
-Rarely incapacitating only when severe
Pathology
-Mild lymphocytic meningoencephalitis
Dx
-MRI
-CSF analysis
Tx
-Prednisone
Px
-Excellent
How to diagnose and treat brain inflammation without having an MRI or CSF results?
-Consider signalment
-History and clinical course
-Results of Neurologic exam
-Rule out any strongly suspicious infectious causes
-Discuss referral, pros/cons of empirical therapy
-Initiate treatment (consider status of patient)
-Closely monitor
Head Trauma
-Acute onset of variable severe signs
Common causes
-HBC
-Falls
-Kicks
-Penetrating wound
-Bites
Primary injury: concussion, contusion, laceration, bleeding
Secondary injury: minutes to hours after initial insult. Driven by cerebral ischemia, results in an increase ICP
C/S
-Gait and posture: paresis, ataxia, circling. Opisthonus (spasms of muscles causing backward arching of the head, neck, spine)
-Mental status: bright, depressed/obtunded, demented, stuporous, comatose
-Vestibular signs
-Pupils: size, symmetry, response to light
-CV system
-Respiratory rate and effort: Cheyne-Stoke’s (occurs usually during sleep, a period of fast shallow breathing followed by slow heavier breathing and apneas), Kussmaul respirations (due to metabolic acidosis usually, rapid deep breathing at a consistent pace)
-Cushing reflex: physiological nervous system response to acute elevations of intracranial pressure (ICP) resulting in Cushing’s triad of widened pulse pressure (increased systolic, decreased diastolic) bradycardia, and irregular respiration. Reflex to brainstem ischemia seen in ICP increased.
Cheyne-Stoke’s and Kussmaul respirations
Head Trauma Pupils and Prognosis
Head Trauma Response and Treatment
Medial Longitudinal Faciculus pathway assessment
-dysfunction = lower score
Treatment
-Mannitol: indicated when Cushing response - high MAP with bradycardia
-Hypertonic saline (7%): not if Na+ derangement present
-Furosemide
-Corticosteroids: CONTRAINDICATED (hyperglycemia)
-Analgesia or anti=anxiety meds if indicated
-Monitoring: serial neuro exams, recheck lab values
-Supportive care: padded bedding, rotate, nutrition, eye lube, anti-convulsants if indicated
Neurotoxicity
-Signs usually appear within minutes to hours after exposure
-C/S do not tend to wax and wane once present
Causes
Mycotoxins
-Penitrem A and
-Roquefortine produced by fungi
-Sources: garbage, moldy dairy products, walnuts, peanuts, bread and grains
C/S
-Tremors
-Anxiety
-Seizures
-Polyuria
-Elevated temp
Dx
-Degree of suspicion and compatible signs
Tx
-IV fluids, reduction of fever, and -Methocarbamol IV
Px
-Ecellent (signs abate in 2-3 days)
Metronidazole Toxicity
-Antibiotic and antiprotozoal
->60 mg/kg/day, though seen at lower doses
MOA: bind GABBA-minergic receptor in cerebellum and vestibular sytem
C/S
-Head tilt, falling, cerebella-vestibular ataxia, vertical nystagmus, tremors, rigidity, rarely seizures.
Tx
-Diazepam
-Initial IV dose
-IV fluid therapy
-Diazepam 3 days, response within 13.2 hrs, recovery 38.8 hrs
Ischemia and Vascular Disease
-Acute to parachute onset of c/s
-Recovery ultimately depends on establishment of blood and oxygen and duration of tissue ischemia
-Ischemia results in necrosis of neurons and glial cells
-Once tissue dies it is called INFARCT
-Penumbra: is the tissue around the infarct
Cerebrovascular Accident - CVA
Stroke
-Abrupt onset of focal neurologic deficits resulting from an intracranial vascular event with clinical signs lasting <24 hrs
Transient Ischemic attack
-resolves within 24 hrs and no lasting signs
- Hemorrhagic stroke
-Less common
-Neoplasia: most common
-thrombocytopenia
-Vasculitis
-Hypertension
-Idiopathic
-Vascular malformation
-DIC
Dx
-CFS may show hemorrhage
-CT
-MRI superior T2
Tx
-Tincture of time
-Underlying disease, anticonvulsants
-Steroids controversial
- Ischemic stroke
-More common
-Renal disease
-Endocarditis
-Neoplasia
-D. immitis
-Idopathic
-Hyperadrenocorticism
-Hypothyroidism, diabetes mellitus, hypercholesterolemia, chronic hypertension = Artherosclerosis
Pathology
-Hypoperfusion - anaerobic metabolism - reduced ATP - NA/K/ATPase failure - H2O into the cell - cytotoxic edema - cells depolarize - excitatory AA - Ca++ influx - Nitric Oxide and free radicals - cell death -release of inflammatory mediators.
C/S
-Forebrain
-Area of infarction
-Territorial: 3 cerebral arteries, 2 cerebellar arteries.
-Lacunar: penetrating vessels
Dx
-MRI
-CSF may be normal
Prognosis
-Ischemic > hemorrhagic
-Idiopathic cases have fair to good prognosis
Feline Idiopathic Ischemic Encephalopathy
Cuterebra Larvae
Tx
-Supportive care with anticonvulsants
-Unapproved and anecdotal tx
-Ivermectin, etc.
Lecture 10-11
Vertebral spine and disk anatomy
Intercapital ligament: T11, T12, T13
-Lacking ligament could be related to disks ruptures in those locations
Intervertebral Disk
-Annulus fibrosis (AF): made of collagen fibers. Attached to vertebral endplate on either side. Tough part that does not move
-Nucleus pulposus (NP): jelly center, remnant of developing notochord. Absorbs shock. Eccentrically placed. AF much thicker ventrally
Intervertebral Disk Diseases - IVD Degeneration
Degeneration is a normal process
Hensen type I
-Chondroid metaplasia of the NP
-NP loses water binding capacity.
-New Hayline cartilage calcifies and loses hydroelasticity
C/S
-3-6 yo but as early as 6mts
-Presents as an ACUTE EXTRUSION of nuclear material out of disk
Common sites
-C2-C3
-T10-L3: is the danger zone
-T11, T12, T13: have no inter capital ligament
Hensen Type II
-Fibroid metaplasia of the NP
-NP replaced with fibrocartilage
NO calcification
-Micro tears in the AF, causes firm disc bulge
C/S
Non-chondrodystrophic breeds, usually large breeds
->5-7 yo
-Chronic PROTRUSION of disk
What are Chondrodystrophic breeds?
-Anything with little twisted legs
-Dachshund
-Pekingese
-Shih Tzu
-Frenchie
-Beagle
-Basset hound, etc
IVDD General C/S
What is the order of loss of function?
-Spinal pain common
-Reluctance to move
-Abnormal posture
Gait
-Paresis and proprioceptive ataxia
-Scuffing toes
-Muscle spasms
-Fasciculations, especially cervical
-Bladder dysfunction (UMN vs. LMN)
Dx
-Neurolocalization is key
-Plain radiographs: proper placement a must
-CT better
-MRI best
Radiographs
-Mineralization of disk confirms degenerative process
-Narrowing or opacification in foramen
-Narrowing or wedging of disk space
-Overlapping of articular facets
-NEVER for planning surgery
Tx
A. Cervical
B. thoracolumbar
1. Conservative
2. surgical
Order of loss of function with increasing damage
- Propioception: outer most
- Voluntary motor: next inner
- Superficial pain
- Nociception: Deep Pain, last inner most
Pain Pathways (nociception)
-Small, non-myelinated
-Multisynaptic
-Multi decussations
-Loss of nociception: functional transection
If they can walk they should be able to fell deep pathways
Cervical IVDD
Common locations?
Common signs cervical?
C2-C3 most common in small breeds
C6-C7 in large breeds
-Cervical hyperesthesia
-Low head carriage
-Neck guarding
-Muscle fasciculations
-Myelopathy
Cervical IVDD Treatment
Is loss of deep pain common?
Conservative
-Mildly affected patients
-First time offenders
-Cage confinement for 3-4 weeks (annulus must heal)
-Gabapentin (MOA not fully understood, but binds to Alpha-delta units of voltage gated Ca++ channels, decreasing Ca influx, thus inhibiting release of excitatory neurotransmitters.
-Predinisone questionable
Px
-Ambulatory patients very likely to respond
-Reccurence 36%
Surgical
-Severely affected or chronic cases
-Ventral slot decompression
-Goal is to remove the perturbing material
Px
-Even tetraplegic dogs up to 83% full recovery
-Small percentage have residual pain or deficits
Thoracolumbar IVDD
Conservative treatment
-Only grades 4-5
-First time offenders
-Cons: recurrence likely
-If absent nociception only 5% chance of recovery
Tx
-Strict confinement 3-4 wks
-Medications: analgesics, Gabapentin, muscle relaxants
-Do not admin dexamethasone = urinary tract infection more likely
Surgical
-Repeat offenders 0-3 grade
-Cons: can not correct any functional damage to cord
-Only relieving compression, can’t fix neurological damage
-Hemilaminectomy, dorsal laminectomy, pediculectomy, etc.
Px - chance they can walk
Henson Type I
Intact nociception =
86-96% chondrodystrophic breeds. 78-85% non-chondrodystrophic breeds
Henson type II
-22-52%
Absent nociception
-Overall 0-76% chance of recovery
IVDD Complimentary therapy
Review
-Presence or absence of nociception is most prognostic indicator
-Absent nociception: guarded to poor
-Present nociception: 80-95%
-Myelomalacia: 5-10% occurrence, grave prognosis
Accessories
-Slings, carts, diapers, etc
Micturition - Anatomy - Bladder
3 layers of smooth muscle
- B-adrenergic and A-adrenergic receptors innervated by hypogastric nerve (SNS)
- Cholinergic (PSNS) receptors innervated by pelvic nerve (contraction)
- Stretch sensation in bladder wall transmit through pelvic nerve
Urethra
-Internal sphincter: A-adrenergic, stimulation = contraction, facilitates filling
-External sphincter: innervated by pudendal nerve (somatic motor) cholinergic
Filling phase
Pointe Micturition Center
-Hypogastric nerve: adrenergic = relaxation of bladder and contraction of internal sphincter
-Inhibition of cholinergic cell bodies of pelvic nerve = relaxation of bladder
-Pudendal nerve somatic efferents = contraction of external sphincter
Evacuation
-Pelvic nerve and pudendal nerve to the PMC
-Threshold “on/off switch”
-PMC will cause: inhibition of hypogastric nerve, facilitation of cholinergic in pelvic nerve, inhibition of pudendal nerve
-DETRUSOR REFLEX
Micturition
- Detrusor reflex (local)
- Brainstem influence
- Cortical influence (conscious potty trained) can be consciously initiated or inhibited
UMN Bladder
-Occurs when lesion between Pons and L7
-Interfere with or abolish DEXTRUSOR REFLEX
C/S
-Hallmark: Increased sphincter tone (loss of inhibitory pudendal nerve)
-Bladder feels turgid when palpated
-Very difficult to express
LMN Bladder
-Occurs with any lesion of sacral spinal cord/nerve roots/pelvic plexus
C/S
-Hallmark: decreased bladder and sphincter tone
-Easy to express
-Constant dribbling
Saddle Thrombus - CATS
-Ischemic neuromyopahty “saddle thrombus”
-Thrombus lodges in distal aorta inhibiting blood flow to the muscles and nerves of the pelvic limbs
-Acute in cats, and insidious in dogs
-Very commonly confused with disk disease, especially in dogs
Ischemic Myelopahty - Fibrocartilagenous Embolism (FCE)
-Occlusion artery/venous system that feeds the spinal cord
-Embolizing fibrocartilage from NP
-Exact mechanism unknown
Usually active, non-chondrodystrophic, large breeds
-Older cats
#1 Miniature Schnauzer in small breeds
-Acute onset, non-painful, and generally non-progressive after the first 24 hrs
-BOXERS most commonly represented
C/S
-Signs and severity highly variable
-Asymmetry
-Dependent on location and distribution within the spinal cord
Dx
-Myelography and CT
-MRI hyper intensity within cord representing edema
Tx
-Maintain spinal cord perfusion is key
-Steroids contraindicated
-Nursing care
-Physiotherapy
Px
-Usually good
-Lose of nociception, LMN signs, symmetry, owner compliance, no function at 2 weeks mark
Atlantoaxial Subluxation
-Unstable or malformed
-AA joint the “no” joint results in excessive movement of AA joint
-Ventral cord compression from cranial aspect of C2
-Transverse ligament injury most likely
Pathophysiology &
C/S
-Young <2yo
-Toy and small breed (yorkie)
-Failure of normal development (dens, ligaments)
-Predisposes to acute luxation from minor trauma
-Can also become chronic (abnormal dens, stretching of ligaments, trauma)
-Lesion: compression of spinal cord by axis C2
C/S
-Acute neck pain
-Reluctance to move
-C1-5 myelopathy: Tetraparesis and ataxia 4 limbs (very likely is going to die due to respiratory dysfunction)
-Postural deficits
-UMN to all limbs
-Animals resist flexion, DO NOT manipulate neck
Dx
-Radiographs: neutral view first, no flexion
-Increased space between dorsal lamina C1 and spinous process C2
-Extreme caution when flexed views
-Evaluate dens (CT better)
-MRI for cord
Tx
-Conservative 60% success
-External rigid splint/bandage for 6-8 weeks
-Very labor intensive
-Bandages sores/infections
-Recurrence
Atalntoaxial subluxation Treatment
Surgical
-60-90% success
-Eventual osseous fusion of AA joint
-Immediate fixation
Cons: invasive, expensive, implant failure, infection, migration
Lumbosacral Syndrome
-Degenerative LS stenosis, cauda equina syndrome
-Commonly affects adult, large breed dogs (GSD)
Pathology
-Chronic instability at LS joint (vertebral spondylosis)
-Type 2 disk disease at L7-S1
-Subluxation of the sacrum under caudal aspect of L7
-Hypertrophy of interarcuate ligament
-Facet/joint capsule hypertrophy
C/S
-Lumbosacral pain is an early indication
-Spinal lordosis or tail flexion
-Reluctance to rise, sit, climb stairs, jump.
-Lameness resembles orthopedic disease. Beware of concurrent hip dysplasia
L4-S4 myelopathy
-Urinary/fecal incontinence
-Decreased withdrawal reflexes especially at hock is common
Dx
-Radiography: may see LS spondylosis and articular facet hypertrophy
-Myelography confusing due to anatomy
-CT excellent for bony changes and
MRI for soft tissue
Tx
Non-surgical
-Forced exercise restriction
-NSAIDs or steroid
-Analgesics
-Weight loss
Surgical
-Dorsal laminectomy at LS disk space
+/- LS diskectomy
Px
-Non surgical: transient effectiveness or not at all
-Surgical 55-87% success
Pre surgical incontinence = poor post op outcome
LS disease
Degenerative Myelopathy
-Slowly progressive
-Non-inflammatory disease of spinal cord
-Axonal degeneration +/- demyelination in TL cord
Breeds
-GSD
-Pembroke Welsh corgi ~ 11 yo
-Boxer
-Chesapeake Bay
-Retriever
-Rhodesian Ridgeback
-Rare in cats
C/S
-9 yo (8-14 yo)
-Non-painful insidious onset, slowly progressive
-T3-L3 myelopathy
-Postural deficits in rear
-Normal to hyperactive rear limb reflexes
-Disuse atrophy
-Progressive to bladder incontinence, paraplegia over 6-9 mts
-Disease will proceed cranially in late stages
Dx
-Only histopath definitive
-Exclusion of other diseases
-DNA test?
Tx
-No effective treatment
Px
-Long term is poor
Cervical Spondylomyelopathy
“Wobbler Syndrome”
-Vertebral malformation
Breeds
-Labrador
-Dalmatian
-Giant breeds (great dane, mastiff)
-Doberman pincher
C/S
-Any cervical spinal cord lesion can result in “wobbly” gait
Giant Breed C/S
-Ataxia and paresis begin ~1-2 yo
-Overzealous nutrition?
-Static Compression of spinal cord and/or nerve roots
-Vertebral canal stenosis
-Disk disease rarely involved
Cervical Spondylomyelopathy
Doberman Pinscher
-6-8 yo
-Slow progressive
-Static or dynamic
Path
-IVD protrusion
-Proliferation of annulus
-Facet hypertrophy: joint capsule proliferation
-Dorsal longitudinal ligament
-Interarcuate ligament (yellow)
C/S
-Cervical pain
-Low head carriage
-Resistance to flexion
Caudal cervical spine most commonly affected
-Signs of c6-T2 myelopathy
-Classic “2 engine gait” forelimbs are choppy, short, rear limbs are slow and clumsy
Dx
-Imaging radiographs to rule out other diseases
-MRI preferred
Tx
-Conservative: exercise restriction, confinement 3-4 wks, NSAIDs, Gabapentin, Prednisone.
-Neck brace
-Improvement transient
Surgical
-Ventral slot and many others
Syringomyelia
-Both intracranial and spinal diseases associated
-Fluid within spinal cord, central canal, or mixture
-NOT CSF
Sigs
-Cervical pain
-Phantom scratching
-Myelopathy
Dx
-MRI only
Tx
-Prednisone
-Gabapentin
-Pain meds: Tramadol, Codeine
Lecture 12
Horner’s Syndrome
-Collection of signs that reflect sympathetic dysfunction, not a specific disease (loss of SNS tone)
-Control of pupillary size is a tonic balance between Constriction and dilation
Signs
-Can be partial or complete
-Unilateral or bilateral
-Miosis: dilator pupillae and celiris mm. SNS = dilation
-Ptosis: Orbital muscle: drooping of eyelid
-Enophthalmos: orbital muscle retreats globe into socket
-elevation of 3rd eyelid: orbital muscle
-Possible stuffy/crusty nostril
Conditions associated with Horner’s syndrome
-Brachial plexus damage
-Neoplasia (thyroid, PNST)
-Aggressive venipuncture
-Otitis media/interna
-CV accident stroke in the brains
-Polyps
-Mediastinal mass
-Brain disease
-Dysautonomia
Golden Retriever = Idiopathic = 50% of canine cases
Dx
-Testing supposed to be able to distinguish where in the pathway the problem is
-Unpredictable and unreliable
-Best imaging of head and neck to check for structural lesions
Pathway
UMN from hypothalamus to T1-T3 (1st order)
Preganglionic fibers from T1-T3 to CCG (2nd order)
Postganglionic fibers to the eye (3rd order)
Idiopathic Facial Nerve Paralysis
-Acute neuropathy of one or both facial nerves
-Axonal loss of some demyelination but NO INFLAMMATION
-Exact pathogenesis unknown “idiopathic” - analogue to Bell’s palsy
-Middle-aged to older animals
Breeds
#1 Crocker Spaniels
C/S
-Drooping ear, lip, and lower eyelid
-Decreased to absent palpebral reflex and menace response
-Can still see
-Excessive salivation and history of dropping food/water
-Corneal ulceration: blink and PS disruption
-Rarely mild vestibular signs
-Must rule out otitis media/interna and hypothyroidism
Tx
-Symptomatic treatment
-Corticosteroids controversial, may be not indicated
Px
-Guarded for return to full function (unlike people)
-Can go bilateral
-Contracture of muscles possible in time
