Neuro pt.2 Flashcards
spinal cord
How do we classify myelopathies
- across the diameter of the spinal cord (partial or transverse)
- along the length of neuroaxis (focal, multifocal, diffuse)
General rules of spinal disease
- Neuro signs are similar regardless of underlying causes
2. severity of signs variable w/in a region of localization
6 parts of the neuro exam
- mentation
- cranial nerves
- gait
- postural rxns
- segmental reflexes
- 3 P’s (palpation, painfulness, pain perception)
T/F: mentation and cranial nerves should be normal with a myelopathy
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Intervertebral Disk Disease
- the most common spinal cord disorder
Function of a normal intervertebral disk
- compression resistance for the vertebrae
- maintaining disk space between vertebrae
Anatomy of a normal IVD (3 parts)
- annulus fibrosis –> annular, fibrous ring that surrounds the pulp and serves to keep the pulp in place. comprised of lamelae to provide strength
- nucleus pulposus –> distributes biomechanical load.. the jelly filling
- cartilagenous endplates –> supplies nutrients to the annulus and nucleus
Two types of IVDD
- Type 1 = Chondroid degeneration –> extrusion
2. Type 2 = Fibroid degeneration –> protrusion
Type 1 IVDD (signalment)
- small breeds 1-6 yrs old
- large breeds any age (less common)
- cats (rare)
Type 1 IVDD
- acute onset
- can be progressive or not
- usually painful
Type 1 IVDD (clinical signs)
- pain
- paresis
- ataxia
- hyperesthesia
- incontinece
- loss of pain sensation
- lameness
Type 1 IVDD (imaging)
- narrow disc spaces
- in situ calcification
- calcification in foramen
Type 1 IVDD (Diagnosis)
- imaging via MRI (loss of disc hydration, deviation of spinal cord, loss of CSF/ epidural fat)
Type 1 IVDD (medical management) (indications, treatment, prongosis)
Indications: pain only, ambulatory, non-amb. but good motor fxn
Treatment: rest/ confinement, analgesia, NSAIDs
Prognosis: ok in not severe; recurrence common
Type 1 IVDD (Surgical management) (indications, benefits, goals, techniques)
Indications: any severe grade, rapid progression, failed medical management, severe pain
Benefits: great outcome, low recurrence rates, faster resolution of pain
Goals: decompression, control hemorrhage, disc fenestration
Techniques: hemilaminectomy, ventral slot
Type 1 IVDD ( post-op management)
- nursing care
- rehabilitation
When to refer a Type 1 IVDD
- when it’s grade 0-3 always
Type 1 IVDD (lookout for this)
- dogs w/out deep pain perception might be having a peracute decline associated w/ myelomalacia (~10-15%) which is 100% fatal
Progressive Hemorrhagic Myelomalacia
- myelomalacia = necrotic spinal cord
- Ascending/ descending form caused by severe, acute SCI w/ infarctio, ischemia, and hem. necrosis
- 100% fatal d/t resp. paralysis
Progressive Hemorrhagic Myelomalacia (Diagnosis)
- fever, inappetance, pain
- diffuse, progressing, myelopathy
- LMN signs develop above/ below
- Imaging sometimes helps
Type 2 IVDD
- fibrocartilage degeneration + torsional biomechanical stress
- separation of annular fibers
- bulging/ protrusion of annulus –> SC compression and meningeal irritation
Type 2 IVDD (Signalment)
- older, larger breed dogs (most common)
Type 2 IVDD (History)
- chronic (> 2 weeks)
- reluctance to do strenuous activity
- myelopathy (variable progression)
- +/- lameness, incontinence
Type 2 IVDD ( Clinical Signs)
- paraparesis or tetraparesis
- ataxia
- pain w/ palpation
- +/- lameness, incontinence
Type 2 IVDD (diagnosis)
- radiography (narrow disc space, end-plate sclerosis, osteophyte production, spondylosis)
- CT
- MRI (gold standard)
Type 2 IVDD (Medical treatment)
Indications: mild disease, slowly progressing, non-painful, continent
Treatments: anti-inflammatories, physical rehab, supportive care
Prognosis: variable
Type 2 IVDD (Surgical Treatment)
Indications: mod-severe myelopathy, short hx or acute onset, deterioration of signs , painful
Prognosis: good if short hx, focal lesion, pain in main finding and not at risk for degenerative myelopathy
Acute Non-compressive Nucleus Pulposus Extrusion (ANNPE)
- tear in annulus fibrosis (from high impact forces) causing extrusion of normal nucleus pulposus
- typically peracute injury (high impact injury)
ANNPE (clinical signs + diagnosis)
Clinical signs: paresis/ paralysis, ataxia, +/- LMN signs, +/- hyperesthesia
Diagnosis: MRI
ANNPE (Treatment)
- medical – crate rest, time, physical therapy
- if compressive, consider surgery (ventral slot or hemilaminectomy)
ANNPE (prognosis)
- intact nociception = good
T/F: all animals w/ CSM (Cervical Spondylomyelopathy) have some degree of stenosis.
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Disc-Associated CSM
- 1* affecting C5-7
- mostly ventral compression (can be assymetric)
- Risk Factor: vertebral canal stenosis
Disc-Associated CSM (Treatment)
Medical: - milder cases, cost restraint - crate rest, analgesics, NSAIDs, physical rehab - guarded prognosis Surgical: - severe pain, focal lesion - decompressive surgery - good prognosis
Osseous-Associated CSM
- growth malformation of vertebrae (enlarged articular facets, bony proliferation)
- primarily the caudal cervical vertebrae
- typically dorso-lateral compression
OA-CSM (typical exam findings)
- cervical pain, ataxia, tetraparesis, +/- hypermetria
OA-CSM (progression)
- pelvic limbs hit first
- often acute decline
OA-CSM (Imaging)
MRI:
– evaluate spinal cord parenchyma = increased intensity w/in spinal cord indicates chronicity
T/F: the treatment for OA-CSM is the same as DA-CSM
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Atlanto-axial Instability (AAI)
instability of C1-2 joint leading to injury of the cranial cervical spinal cord
AAI (pathogenesis)
- malformation of C1-2
- malformation of dens
- ligamentous abnormalities
- trauma
AAI (Signalment)
- toy/ mini breeds
AAI (Clinical Signs)
- cervical pain
- tetraparesis or palegia
- brainstem signs
- seizure-like episodes
AAI (Treatment)
Medical:
- Indications: immature bones, v small patient, resolving mild signs, cost. concerns
- Tx: splinting/ bandaging, medication, crate rest
Surgery:
- Indications: mod-severe neuro defects, recurrent cervical pain, unresponsive to medical tx
- Tx: Dorsal or ventral approach
GME (Progression, Diagnosis)
Progression: acute, progressive, may wax and wane, most commonly encephalitis, can cause myelitis
Diagnosis: MRI, CSF (pleocytosis, rule out infection), histopath
GME (Treatment, Prognosis)
Treatment: immune suppression (steroids, pred, dex)
Prognosis:
short term - good/ fair
long term - guarded
SRMA (Steroid Responsive Meningitis Arteritis)
- young, large breed dogs
- progression: acute/ progressive, mainly cervical pain
- Clinical sings: no neuro deficits, cervical pain
SRMA (diagnosis)
- rule out other dz via CBC/ Chem/ Rads/ US/ w/ n MRI
- CSF analysis - neutrophilic pleocytosis, high protein
SRMA (treatment)
- immune suppression
Meningitis/ Myelitis (clinical signs and diagnosis)
Clinical Signs: acute onset pain/ hyerpesthesia, +/- myelopathy or CN signs
Diagnosis: MRI, CSF, culture (blood, urine, CSF, tissue)
Meningitis/ Myelitis (CSF analysis findings)
- neutrophilic pleocytosis
- high protein, low glucose
- +/- xanthochromia
Meningitis/ Myelitis (treatment)
- Antibiotics
- meticulous monitoring
- short course corticosteroids for inflammation control
When is it safe/ ok to assume that meningitis is inflammatory and not infectious?
(-) culture
(-) organism
no systemic infection/ signs
minimal contrast enhancing on MRI
Epidural Empyema
- spinal abscess
- occurs following: discospondylitis, foxtail, CNS infection, paraspinal abscess
Epidural Empyema (Clinical Signs, Diagnosis, Tx)
Clinical Signs - very painful, fever, lethargy , progressive signs
Diagnosis, clinical signs, inflammatory leukogram, imaging
Treatment: abx, surgical drainage if necessary
Discospondylitis
- infection of the intervertebral disc and adjacent endplates
- one of the few causes of disc space widening
Discospondylitis (pathogenesis)
- primary disease
- hematogenous
- foreign body
- extension of dz
- penetrating wound
- immunosuppresion
Discospondylitis (common organisms)
- staph aureus
- Strep
- E. coli
- Brucella
Discospondylitis (signalment)
- large/ giant breeds
- young to middle aged
- males > females
Discospondylitis (Hx)
- chronic, progressive pain
Discospondylitis (clinical signs)
- spinal pain, kyphoses, panting, lethargy
Discospondylitis (Diagnosis)
- imaging
- culture (lesion, disc, surgical site)
- cytology
- serology
Discospondylitis (treatment)
- abx
- exercise restriction
- analgesics
Fibrocartilage embolism
- infarction of the spinal cord
- obstruction of the arterial supply by fibrocartilage
FCE (signalment)
- young to middle aged
- large breed (especially active dogs during exercise)
- peracute/ acute onset
Are dogs with an FCE painful?
not usually
FCE (Diagnosis)
- signalment, hx, neuro exam
- MRI and CSF
- rule out other causes
- histopath ( gold standard)
FCE (treatment and prognosis)
Treatment - supportive care, physical therapy
Prognosis - depends on location and severity; UMN lesions usually are good prognosis while LMN are guarded
Degenerative Myelopathy
- slowly progressive degeneration of specific spinal cord tracts and nerve roots in T3-L3
- hits the pelvic limbs “hard and fast” (sturgers)
Degenerative Myelopathy (Signalment and Hx)
Signalment: middle - older age, 3 breeds over-represented (GSD, Boxer, Corgi)
Hx - chronic myelopathy, slowly progressive, non-painful
Degenerative Myelopathy (Clinical Signs)
- paraparesis
- non-painful
- symmetrical
- retain continence
- may affect L4-6
Degenerative Myelopathy (Treatment, Prognosis)
Tx: no known treatment
Prognosis: poor to grave longterm
A dog is genetically tested for Degenerative Myelopathy and comes back as AA (affected). What does this tell you?
- the animal is AT RISK for developing this disease
- it does not tell you that they will develop this disease or that they currently have it
Spinal Cord Neoplasias (signalment0
- usually older animals
- younger animals have certain predispositions
Acute Spinal Cord Injury (ASCI)
- traumatic vertebral fracture luxation
- acute hemorrhage
- acute IVD extrusion
- FCE
- Congenital vertebral instability
- acute inflammation
Acute Spinal Cord Injury ( When to refer)
- rapid change in neuro status
- onset of paralysis
- ventilation problems
- it’s all about deep pain sensation
What is important about prognosis with all neuro dz
- it’s all about the neuro exam and not what you find/ don’t find on imaging
Acute Spinal Cord Injury ( primary concern)
- don’t make things worse
Is it possible to differentiate pathology affecting the Cauda Equina and LMN pelvic lesions?
No
T/F: all sacral and caudal nerve roots pass over the L7-S1 disc space before exiting out the foramen
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Cauda Equina Syndrome (clinical signs)
Motor: - Tail - Anus - Pelvic Limb - Bladder Sensory Abnormalities - (-) conscious proprioception - change to body sensation (parasthesia, anesthesia, etc) Psuedoexaggeration fo patellar reflex \+/- Apparent Pain
What is psuedoexaggeration of the patellar reflex?
loss of antagonism of muscles innervated by the femoral nerve by muscles related to sciatic nerve
Cauda Equine Syndrome (Diagnosis)
- rule out other myelopathies
- Hx, PE, NE, CT, MRI, CSF, Myelogram, Dynamic radiographs
Lumbosacral Vertebral Canal Stenosis (cause)
Acquired in large breed dogs Stenosis is 2* to all or one of the following: - type 2 disc protrusion - hypertrophy/ plasia of ligaments - thickening of vertebral arch/ facets - +/- instability
Lumbosacral Vertebral Canal Stenosis ( signalment, Hx)
Signalment:
- male, large breed dogs (GSD)
Hx:
- slowly progressive, trouble rising
Lumbosacral Vertebral Canal Stenosis (Diagnosis, Prognosis)
Diagnosis:
- orthopedic exam, spinal radiographs, CT, MRI
Prognosis:
- mild signs = good
Lumbosacral Vertebral Canal Stenosis (Treatment)
Medically – only if minor signs
Surgical – dorsal laminectomy +/- internal stabilization
Discospondylitis
- bacterial or fungal infection of the intervertebral disc and adjacent vertebral body
Discospondylitis (Physical Exam and Neuro Exam)
- fever
- marked spinal pain
- no neuro deficits
Discospondylitis (Imaging)
- neoplasia will not cross disc space
- end-plate destruction, collapse of IV disc
Discospondylitis (prognosis)
- good for bacterial
Type 1 myofibers
- postural muscles
- “slow” twitch, oxidative metabolism
- appears dark on pH4.3 stain
Type 2 myofibers
- movement muscles
- “fast twitch”, glycolytic metabolism
- appears light on pH4.3 stain
T/F: myofiber type is determined by the type of innervation of the motor neuron
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T/F: a de-nervation, re-nervation event can cause signficiant portions of a muscle to change myofiber type
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3 ways to classify neuromuscular disease.
- neuropathies
- “junction”-opathies
- myopathies
Clinical Signs of Neuromuscular Disease
Focal or generalized weakness
Functional: gait abnormalities, paresis/ paralysis, exercise-induced weakness
Physical: muscle atrophy/ hypotrophy/ hypertrophy
Cervical Ventroflexion: classical sign in cats
Megaesophagus
Diagnostic approach to NM disease
Hx
PE, NE, minimum database
Functional Testing: Electromyography
Biopsy: muscle, nerve
Electromyography (decreased insertional activity)
decreased muscle mass
Electromyography (increased insertional activity)
hyperexcitable muscle
Electromyography (fibrillation potentials and positive sharp waves)
- popping
- rain on tin roof
Electromyography (complex repetitive discharge)
- motorcycle idling
Electromyography ( myotonic potentials)
- pathognomonic for myotonia congenita
- sounds like an air horn/ dive bomber
Nerve and Muscle Biopsy
- be smart about how you do this (would like a functional nerve post-biopsy, etc.)
- Fixed - formalin kills tissue
- Frozen - permits assessment of enzymatic fxn
Categories of Neuropathies
- Mononeuropathies
- Multiple Mononeuropathies
- Polyneuropathies
Neuropathies: Histopath
- angular atrophy of myofibers (whatever that means)
- denervation atrophy = both type 1 and 2
- end-stage denervation = pyknotic nuclear clumps
- myofiber type grouping = chronic denervation, renervation
Tetanus
- C. tetani infection, anaerobic conditions
- toxin enters nerve and ascends to cord
- destruction of inhibitory interneuron (renshaw cell) synapse to LMN
Tetanus (diagnosis and tx)
Diagnosis: clinical signs ( tetany, risus sardonicus), Hx
Treatment: antitoxin ( can only give once), debridement, abx w/ anaerobic spectrum
Mononeuropathies
- radial neuropathy, facial paralysis, etc
- common causes: trauma, iatrogenic, idiopathic, neoplasia, inflammatory
Brachial Plexus Avulsion
musculocutaneous (C6-8) (biceps, withdrawal)
radial (C7-T1) (triceps, weight bearing)
median/ ulnar (C8-T2)
Lumbosacral Plexus Avulsion
Femoral (L4-6) (patellar reflex, weight bearing)
Sciatic (L6-S1) (gastroc reflex, withdrawal and flexion)
Pudendal (S1-3)
Acute Polyradiculoneuritis
- rapid onset flaccid tetraparesis/ plegia
- LMN signs in all 4 limbs
- often history of bite or other antigen. stimulus w/in past 2 weeks
- causes an immune mediated attack of ventral nerve root (primarily motor fxn loss) and demyelination
T/F: an animal suffering from acute polyradiculoneuritis will have intact sensory fxn but little motor abilities to react appropriately
True
Polyradiculoneuritis (Treatment, Recovery)
Tx: supportive care
Recovery: time for remyelination and axonal regrowth is weeks to months
Polyradiculoneuritis (EMG, CN)
EMG: spontaneous activity > 4-5 days
CN: rarely affected
Chronic Polyneuropathies
- often pelvic limb more affected
- generalized weakness/ LMN signs
- plantigrade/ palmigrade stance
What’s 2+2?
IDK, but maureen’s a big loserface lmao
Junctionopathies - histopath
- usually absent or non-specific
- diagnosis based on other assays
Pre-synaptic Junctionopathies ( two categories)
- decreased ACh release: inability to activate AChR (hypocalcemia, high Mg, botulism, tick paralysis, aminoglycosides)
- elevated ACh release: weakness caused by continued depolarization of post-synaptic membrane and depletion of pre-synaptic vesicles (low Mg, envenomation)
Tick Paralysis
- dermacentor, Ixodes (australia)
- salivary neurotoxin secreted by tick causes reversible interference of Ca mediated ACh release –> rapidly ascending UMN paralysis
- Diagnosis: find the tick
- Treatment: tick hunt and removal, supportive
Botulism
- ingestion of type C neurotoxin from C. botulinum
- irreversible inhibition of ACh release from cholinergic nerve terminals
CS: acute onset LMN signs, fatal tetraplegia and areflexia, mild weakness, megaesophagus/ aspiration pneumonia
Diagnosis: organism detection
Treatment: supportive care, C. botulinum antitoxin
Synaptic Cleft Disorders
- Cholinesterase Inhibitors
- inhibit breakdown of ACh prolong active at receptor
- organophosphates and carbamates **
Myasthenia Gravis (Acquired or Congenital)
Acquired: autoimmune attack against AChR resulting in depletion of receptors (dogs)
Congenital: deficiency or functional disorder of AChR (nicotinic)
Acquired MG (age range)
2-4 years, 9-13 years old
Acquired MG (History and CS)
Focal – esophageal, pharyngeal, facial weakness
Generalized – generalized weakness +/- the areas above
- exercise intolerance
- regurgittaion/ megaesophagus
- mediastinal mass (thymoma)
- acute tetraplegia
Acquired Maureen’s G-stupid (Diagnosis)
- immunological testing: gold standard, AChR antibodies
- pharmacological testing: short acting AChE inhibitor
- Electrodiagnostics: decremental response
Acquired MG (treatment)
- cholinesterase inhibitors (pyridostigmine)
Congenital MG
- onset at 6-12 weeks
- generalized weakness
- breed disposition - labs
- diagnosis - no immune testing
- treatment - variable
