Neurology Flashcards
Where would the lesion be with a LMN bladder? Causes? Clinical sings?
Lesion: sacral SC or pelvic nerve
Causes: IVDD, cauda equine syndrome, congenital malformation of the sacrum (manx cats), SI luxations, sacrococcygeal fractures, spinal tumors, LS disease
Clinical signs: Urine scalding, UTIs, overflow incontinence
Large, turgid bladder that is easily expressed
Where would the lesion be with a UMN bladder? Causes? Clinical sings?
Lesions: lesions above the sacral spinal cord. Incomplete reflex detrusor contraction and spasticity of the EUS incomplete emptying
Causes: IVDD, tumors, trauma
Clinical Signs:
Large turgid bladder
Impaired stream of urine
Overflow incontinence
Automatic bladder: involuntary micturition when threshold capacity of the bladder is reached
Concurrent paresis/paralysis
What’s second line tx for status epilepticus in dogs
Keppra- IV
Phenobarbital - IV or CRI –> superior in dogs
Fosphenytoin - IV
What are the 4 stages of status epilecticus?
- Impending – neurotransmitter release, ion channel opening/closing –> 1st line tx
- Established – GABA R decrease, internalization of GABA R units, NMDAR and AMPAR up-regulation –> 2nd line tx
- Refractory – excitatory and inhibitory neuropeptides release/imbalance, +/- BBB drug transporters unregulated –> 3rd line tx
- Super refractory – gene expression alterations –> likely minimally to non-responsive
When can electroencephalogram be useful?
Non convulsive status epilepticus
Seizure termination would be - epileptiform discharged
Define status epilepticus
Continuous seizure activity or >1 sequential seizure without full recovery of consciousness in between with a duration >30mm
Best non-IV tx of SE in DOGS
Intranasal midazolam
What are the steps to follow for 3rd line seizure management
3rd line - anesthetic medications used for controlling seizure activity
- Ketamine IV bolus, followed by CRI
If ketamine doesn’t work – dexmedetomidine IV bolus and CRI - Propofol IV bolus, possibly followed by CRI – CAUTION in cats
- Anesthetic barbiturates (pentobarbital or soium thiopental) IV bolus and CRI
- Inhalation anesthesia
What’s the MOA of dexmedetomidine? How is it neuroprotective?
MOA: alpha2 adrenoreceptor agonist –> decreased excitatory neurotransmitters via suppression of sympathetic NS + NE release in amygdala, hippocampus and cerebral cortex
Neuroprotective – decreasing cerebral metabolic and oxygen demands, decreasing brain edema via VASOCONSTRICTION and contributing to maintaining normal mean arterial pressure
SE: decreased resp, bradycardia, cardiac arrhythmias, hypothermia
MOA of ketamine and SE
MOA: NMDA-receptor antagonist –> reduced release of glutamate
Also increased blood pressure
SE: vomiting, vocalization, salivation
MOA of propofol and SE
MOA: potentiates GABA by decreasing rate of dissociation of GABA from its receptors –> prolonged binding = influx of Cl –> hyperpolarization of postsynaptic cell membrane
-Interacts with glycine (agonist) and NMDA (antagonist) receptors as well as Ca channels
SE: CV and resp depression, pain at injection site, loss of gag reflex
Why do we have to be cautious with cats and propofol
Can cause Heinz body anemia
MOA and SE of anesthetic barbiturates (pentobarbitone and sodium thiopentone)
MOA: GABA receptor agonists
-Neuroprotective effect by decreasing intracellular Ca and Na, glutamate release and cerebral oxygen consumption
SE: resp and CV depression, hypotension, hypothermia, cardiac toxicity (sodium thiopentone), vocalizations and seizure-like movements in recovery
Tx for patients with supra refractory seizures
Hypothermia
IV magnesium and allopregnanolone
MOA of Mg for anti seizure
MOA: inhibit NMDA receptor and Ca channels, increase cerebral blood flow via vasodilation
Use of hypothermia for seizures
Decreases excitatory neurotransmittets, Ca, glutamate-induced excitotoxicity, cerebral metabolic rate
Normalizes ICP
What retrogene mutation is associated with TL IVDD is chondrodystrophic breeds?
FGF-4 on chromosome 12 –> leads to early chondrioid metaplasia, degeneration, mineralization of nucleus pulpous
How can MRI help with prognosis of TL IVDD?
Presence and extent of intramedullary T2 hyper intensity, T2 hypo intensity, and attenuation of CSF signal on HASTE/T2 sequences – associated with worse locomotor outcome and development of myelomalacia
What’s the sensitivity of CT for IVDD? What makes it less accurate
81-100% sensitivity for cchondrodystrophic dogs w mineralized disks
Distinguishes between chronically extruded material
Less accurate if >5yo and <7kg
Does not provide insight on severity of parenchymal injury
When would CT be the first line advanced imaging in TL IVDD
Suspect acute TL-IVDE - low likelihood of missing compressive surgical lesion
Fenestration at which sites is not recommended for IVDD?
Routine fenestration of L4-5 and more caudal sites
Fenestration at T10-11 or above - not recommended due to low rate of disk extrusion at these sites
What medications can be used to aid in urination post op TL surgery
Alpha receptor antagonists - prazosin, phenoxybenzamine, alfuzosin, tamsulosin or centrally acting muscle relaxant (diazepam)
bethanecol use not recommended - unwanted cholinergic effects
What are clinical findings in a dog with suspected progressive myelomalacia
Ascending paralysis
Hypoventilation
Loss of segmental spinal reflexes
Cranial migration of CTR caudal border
Decreased abdominal tone
Horners syndrome
Diffuse pain
Thermodysregulation
Malaise
Lesions where in the SC are more likely to develop myelomalacia
Lumbar intumescensce
Name clinical biomarkers for evaluation of progressive myelomalacia
Serum pNfn - increases
Myelography - diffuse intraparenchyman constrast
SSTSE CSF:L2 ratio >7.4 – sensitivity 100%, specificity 75%
What nerve(s) affected with medial strabismus
CN VI
What nerve(s) affected with ventrolateral strabismus
CN III
Menace CN involved
CN II - afferent
CN VII - efferent
What nerve(s) affected with dropped jaw
Bilateral CN V
What nerve(s) affected with ptosis
CN III
What nerve(s) affected with diminished to absent PLRs
CN III
What nerve(s) affected with atrophy to trapezius
CN XI
What nerve(s) affected with masticayoty muscle atrophy
CN V
What nerve(s) affected with dorsomedial strabismus in a cat
CN IV
What nerve(s) affected with atrophy of the tongue
CN XII
What nerve(s) affected with deviation of the nasal philtrum (contralateral)
CN VII
CN responsible for PLR
CN II - response to light
CN responsible for pupil constriction
CN III (oculomotor)
Name neuro signs associated with cerebellar disease
-Intention tremors of head, neck, eyes
-Opisthotonus and extensor rigidity of all limbs with hips flexes
-Truncal sway
-Head tilt
-Hypermetria/spastic gait
-Spinal reflexes: normal to exaggerated
-CN: menace deficit (ipsilateral), anisocoria (rare)
Neuro signs associated with prosencephalic disease
-Mentation: seizures, abnormal behavior, propulsive activity, depression to coma
-Posture/gait: head turn, normal gait (unless parachute lesion), propulsive circling (ipsilateral to lesion), aimless wandering, head pressing
-Posture rxns: contralateral deficits
-Contralateral hypalgesia
-CN contralateral menace deficits with normal or abnormal PLRs
Neuro signs associated with. mid to caudal brainstem disease
-Mentation: depression-coma
-Posture/gair: UMC tetraparesis/plagia and GP deficits; vestibular ataxia, opisthotonos (BS lesion)
-Postural reactions: ipsilateral deficits (pons, medulla), contralateral deficits (rostral midbrain)
-Muscle mass, spinal reflexes: normal to increased x4
-CN: anisocoria (III), dropped jaw, atrophy of muscles mastication (CN V), facial hypalgesia (V), head tilt (VIII), resting or positional nystagmus (VIII), dysphagia (IX, X), tongue paresis/paralysis (XII)
Resp or cardiac abnormalities
Describe what you would see in pelvic limbs, thoracic limbs, other in a C1-C5 lesion
Postural reactions: delayed to absent x4
Thoracic limb: UMN paresis; GP deficits, normal withdrawal
Pelvic limb: UMN paresis; GP deficits, normal to increased spinal reflexes
Severe lesions: Spastic tetraplegia, horners syndrome (ipsilateral miosis), resp complications
Describe what you would see in pelvic limbs, thoracic limbs, other in a C6-T2 lesion
Postural reactions: delayed to absent x4
Thoracic limb: LMN paresis (short and choppy gait); reduced withdrawal
Pelvic limb: UMN paresis; long stranded gait, normal to exaggerated spinal reflexes
Severe lesions: Flacid LMN paralysis in TL, spastic paraplegic HL, horners syndrome (T1-T3), resp complications
Describe what you would see in pelvic limbs, thoracic limbs, other in a T3-L3 lesion
Posture reactions: normal thoracic, delayed to absent hindlimb
Thoracic limbs: normal
Pelvic: UMN paresis, GP deficits, long strides gait, normal to exaggerated spinal reflexes
Severe: spastic paraplegic, schiff-sherrington in TL
Describe what you would see in pelvic limbs, thoracic limbs, other in a L4-S3 lesion
Postural reactions: delayed to absent PL
Thoracic limbs: normal
Pelvic: LMN paresis (short and choppy), GP deficits, reduced patellar (L4-L6) or withdrawal reflexes (L6-S1)
Severe: flaccid paraplegia in PL - flaccid ants and tail with reduced to absent sensation to perineum
Describe the pathway for Horners syndrome
1st order neurons originate in rostral brainstem –> cervical spinal cord —> (synapse with second order neurons - preganglionic) –> cell bodies in T1-T3 –>. course up the vagosympathetic trunk –> synapse with3rd order (post-ganglionic) in cranial cervical ganglion –> project to eye and adnexa
Summary: brainstem –> cervical SC (synapse–>preganglionic)–> T1-T3–>vagosymptathetic trunk–>postganglionic cranial cervical ganglion–>eye
Describe CS of horners
Miosis
3rd eyelid prolapse
Ptosis
Enophthalmos
What breed is predisposed to horners
goldens
If you’re testing for horners with phenylephrine –> mydriasis within 20min. Where is the lesion?
Post ganglionic
If you’re testing for horners with phenylephrine –> mydriasis after 20min. Where is the lesion?
Preganglionic
Where are the majority of the idiopathic HS located
post ganglionic
most will resolve in 3-4months on its own
Agent that causes botulism
Clostridium botulinum type C (dogs and cats)
Gram positive, motile, anaerobic spore forming bacilli
Presentation of botulism
Rapidly progressive symmetric LMN paresis, +/- CN deficits
No sensory nerve deficits
No hyperesthesia
Parasympathetic system affected
Ascending paralysis
Cats can present with urinary incontinence and when the forelimbs are affected have spasm of the triceps muscle that results in caudal extension of the limb with carpal flexion (different than dogs)
Dogs can still wag their tails :)
Mechanism of infection with botulism
Toxin ingested → survives in acid stomach conditions → absorbed into bloodstream from the SI → travels to peripheral cholinergic synapses → inhibits release of Ach → ascending symmetrical flaccid paralysis, megaesophagus, signs of autonomic dysfunction
Cleaves membrane associated SNARE proteins → type C toxin affects membrane, not vesicle SNARE proteins
Prevents release of Ach (pre-synaptic)
Mechanism of acquired MG
Immune mediated destruction of POST synaptic ACH receptors
CD4+ T-cell activation of B-CellG
Gold standard to diagnose MG
Ach receptor antibodies test
Diagnostic:
-Dog: >0.6
-Cat: >0.3
Tx of MG
Anticholinestarase therapy. – pyridostigmine bromine (inhibits acetylcholinesterase)
Where’s the toxin in tick paralysis
PRE synaptic
Prevents Ach release
Causative agent of tetanus
Clostridium tetani - Gram positive, motile, anaerobic spore forming bacilli
Produced 2 toxins – toxin that causes problems is Tetanospasmin
Toxin for tetanus and botulism have similar composition: 2 polypeptide chains (heavy chain and light chain) joined by disulfide bond
Heavy chain attached to presynaptic nerve terminal
L chain is zinc-dependent matrix metalloproteinase
Presentation for tetanus
Presentation: progressive muscle stiffness and rigidity
Facial muscle contraction, ears pulled towards each other
Stiff stilted gait, sew horse stance
Lockjaw
Laryngeal and pharyngeal involvement → dysphagia, dyspnea
⅓ of dogs have cryptogenic tetanus (no wound)
Describe the pathophysiology of tetanus
Tetanospasmin toxin is released from C. tetani
Toxin enters into motor axon at NMJ → travel retrograde up to spinal cord → inhibits the inhibitory interneurons (Renshaw cells) in the spinal cord (level of the ventral horn) –> Toxin enters inhibitory interneurons in brain and spinal cord → interferes with GABA and glycine inhibitory neurotransmittersT
Tx for Tetanus
Supportive care, nutrition, +/- tracheostomy
Clean wound
Abx recommended
Metronidazole - recommended as first line
Penicillin G - second line, as can antagonize GABA
Antitoxin has high risk of anaphylaxis
