Neurology Flashcards
Grades for classic disc extrusion
Grade 1
- pain without neurologic deficits
- palpation of spinal cord: pain
Grade 2
- pain + paresis + ataxia
- different grades of paraparesis, can walk
- proprioceptive deficits present
Grade 3
- pronounced paraparesis
- cannot walk without support
- voluntary movements only with support
Grade 4
- paraplegia
- no voluntary movements even with support
Grade 5
- grade 4 + problems with urination
- bladder overflow
Grade 6
- grade 5 + loss of deep pain sensation
diagnosis for degenerative disease of disc
- based upon NE we perform:
o diagnostic imaging: native radiography, contrast radiography, CT, MRI
o CSF (rarely)
treatment of disc
Conservative
- only grade 1 and grade 2 owners should sign that they were warned that surgery has better outcome for higher grades
- cage confinement - small cage: 3-4 weeks
- wait for fibrosis and cicatrisation
- should offer hospitalisation
- medications: 0.5-1mg/kg sid prednisolone + PPI
Surgically
neurapraxia
- Temporary loss of sensory and motoric function due to stop in impulse conduction
axonotmesis
- Detachment of axons from neuron body, with distal Wallerian degeneration, Schwann envelop and endoneurium are preserved: regeneration 1mm/day
neurotmesis
- Complete detachment, can but it doesn’t have to be regeneration, frequently results in neuroma formation
degenerative myelopathy
Thoracolumbal part of spine
slowly, progressive adult-onset neurodegenerative disease causing paralysis
predisposition of degenerative myelopathy
dogs usually > 5 yr, extremely rare in young GSH
cause of degenerative myelopathy
inherited disease
pathogenesis of degenerative myelopathy
Progressive loss of myeline, slowly progressive clinical signs: from loss of proprioception to further deficits.
signs of degenerative myelopathy
slowly progressive muscular atrophy. late in course of disease: faecal and/or urinary incontinence. Severe symptoms after 6-12mo
diagnosis of degenerative myelopathy
- clinical signs + exclusion of other possible disease
- neurology: signs of dragging of nails, difficulty jumping, asymmetric signs of loss of coordination and weakness in the pelvic limbs (do proprioception test, spunal reflexes, cranial nerve)
- CSF: normal or slightly increased proteins
- myelography, CT and MRI: normal findings
- definitive diagnosis: histopathology: IgG, C3 complement
treatment of degenerative myelopathy
- Aminokaproic acid: 15mg/kg PO tid
- Vitamin E 20000IJ sid, Vitamin B12
- Glucocorticoids only for acute worsening
- Intensive physiotherapy
prognosis of degenerative myelopathy
long-term poor; most dogs are nonambulatory by 10-12 months after onset of signs
monitoring of degenerative myelopathy
clinical signs are monitored by the neurologic examination
predisposition of disconspondilitis
young animals or larger breeds, more common in cats
cause of discospondilitis
: trauma and iatrogenic, S. aureus, a. pseudintermedius, brucella canis…
signs of discoponsidilitis
pain, neurologic deficits, signs of infection, NE: pain upon palpation +/- neurologic deficits, anorexia, depression, reluctance to move, lameness, paresis/ataxia
diagnosis of discospondilitis
X-ray, urine and blood culture, CSF, contrast radiography, MRI
treatment of discosponsilidit
ATB (4-8weeks), cephalexin, analgesia, surgically: disc curettage, decompression and stabilisation, NSAIDs
prognosis of discospondilitis
early diagnostics and adequate TH: good. Chronic course of the disease, fungi, neurologic symptoms: guarded to poor
monitoring of discospondilitis
repeat blood and urine culture, repeat radiographs
differentials of discpondilitis
meningitis/myelitis, intervertebral disc disease, spondylitis, trauma, neoplasia
definition of epilepsy
disease of brain characterised by enduring predisposition to generate epileptic seizures. 2 unprovoked > 24 hr apart
- most common neurological disease
a neurological disorder marked by sudden recurrent episodes of sensory disturbance, loss of consciousness, or convulsions, associated with abnormal electrical activity in the brain.
predisposition of epilepsy
dogs, cats, in farm and horses but very rare: St Bernard, Irish setter, dachshund, Pitbull, beagle, GSD, lab, retriever, bermese
pathophysiology of epilepsy
- disbalance between inhibitory + excitatory influences on brain cell function
- abrupt spontaneous depolarisation
seizure
any sudden, short lasting, transient event
epileptic seizure
manifestation of excessive synchronous epileptic activity of neurons in brain usually self-limiting
reactive seizure
in response to transient disturbance in function (toxic/metabolic) from normal brain
convulsive seizure
- tonic-clonic = grand mal
- tonic (generalised rigidity)
- clonic (without tonic phase)
- myoclonic = jerky movements
non-convulsive seizure
- atonic = “drop attacks” sudden and general loss of muscle tone
idiopathic epilepsy
genetic epilepsy); gene that causes the epilepsy is identified/confirmed
- (suspected genetic epilepsy): prevalence in the breed, genealogical analysis and/or familial accumulation of epileptic individuals
- (epilepsy of unknown cause): structural epilepsy must be excluded
- Age 6 moth-6yrs
- Form: mostly generalised tonic-clonic, if they are partial they are uniform
- Mode of inheritance: autosomal recessive or polygenic recessive
- breeds: beagles, GSD, lab, wolfhound
diagnosis of epilepsy
- 3 levels of confidence when we’re dealing with idiopathic epilepsy:
o Tier 1: >2 seizures minimally 24hrs apart, dog 6mo-6y, normal neurological and physical examination, normal routine blood work and urinalysis
o Tier 2: tier 1 + bile acids + MRI head + CSF
o Tier 3: tier 1 and 2 + EEG abnormalities - Further diagnostics is indicated always when:
o Patient is not of the typical age
o There are neurological deficits between the seizures
o When the beginning of the epilepsy were either status epilepticus or cluster seizures
o There’s inadequate response to therapy (therapy with 1st medication was unsuccessful)
structural epilepsy
seizures provoked by intracranial/cerebral pathology (vit D)
- vascular, inflammatory, ananomaly, metabolic, idiopathic, neoplastic, degenerative
focal epileptic seizue
- lateralising signs (originating from one hemisphere)
generalised seizure
- bilateral involvement: may occur alone or evolve from a focal epileptic seizure
o convulsive: Tonic-clonic, Tonic (generalised rigidity), clonic (without tonic phase), myoclonic
o non-convulsive: atonic (drop attack)
phases of epileptic seizure
Prodome
- In some animals long term changes in disposition: indicates forthcoming ictus hours to days earlier: eg. Restlessness, anxiousness, attention – seeking behaviour
Ictus/fit:
- Seizure activity, followed by postictal phase. Consists of: generalised epileptic seizure alone, focal seizure alone, or focal epileptic seizure that evolves into a generalised seizure
Postictal:
- Period in which brain restores its normal function, lasts from very short to several hours to day
Interictal:
- Time elapsed between two seizures
signs of epilepsy
- circling, head pressing, blindness, decreased proprioception
diagnosis of epilepsy
- physical exam, lab work and diagnostic image
o CNS hypoxia, hypoglycaemia, HE, electrolyte disturbances, uraemia, hyperlipidaemia, intestinal parasites, exogenous toxins
treatment of epilepsy
- 1st = phenobarbital, potassium bromide, imepitoin
- 2nd = levetiracetam, zonisamide, gabapentin, pregabalin
- 3rd = topiramate, felbamate, valproic acid, lacosamide, rufinamide
- emergency:
o Only IV: Diazepam, midazolam, phenobarbitone, levetiracetam, thiopental, propofol, inhalation anaesthesia (isoflurane) - emergency seizure protocol
o IV access
o boluses of diazepam
o boluses of phenobarbital
o kepra
o anaesthesia – propofol/thiopental - phenobarbital
o liver metabolism
o maintain concentration 75-150umol/L
o side effects are euthyroid sick syndrome, pancreatitis
o 2.5-3mg/kg BID - imepitoin
o 100/400mg tablets
o 10-30mg/kg BID PO
o liver metabolism
o side effects: lethargy, PUPD, increased appetite - potassium bromide
o 20mg/kg BID PO
o kidney excretions
o side effects = ataxia, pruritic, constipation, PUPD - levetiracetam (kepra)
o 20mg/kg TID/QID PO
o kidney excretion
o side effects = mild sedation, vomiting - benzodiazepines
o diazepam PO, IV, PR
o midazolam IV
o dogs = only for status epilepticus
o cats = maintenance and emergency therapy
when to stop therapy and how to
- when to stop therapy
o if no seizures for 1-2 years and patient is good decrease - how to stop therapy
o very slowly gradually decreasing first drug by 20%, if seizures restart, increase dose to lowest at which there were no seizures
prognosis of epilepsy
can be good with the correct treatment
differential of epilepsy
Syncope, narcolepsy/cataplexy, neuromuscular weakness, paroxysmal movement disorder (Doberman), myasthenia gravis, painful foci
proprioception
- Awareness of the position and movements of the body and limbs
- Necessary for maintaining the upright position
- Receptors in joints, tendons, muscles and inner ears cerebral cortex (conscious proprioception)
- Testing the proprioception- confirms neurologic problem, but we have to perform complete neuroexam to determine the neurolocalisation
- If there are no neurologic deficits established during neurological exam, still patient can have problem in forebrain: weakness of the neurological exam in vet med
- First 48hr after the seizures neurologic deficits can be mere consequence of neuronal exhaustion during the seizure activity: if the owners cannot afford diagnostic imaging the neurologic exam should be repeated: if the deficits persist: they are the consequence of physical lesion in the brain: further diagnostics: CSF, MRI/CT
additional diagnosis procedures in large animal
- Physical, orthopaedic and neurological exam
- CSF tap and analysis:
o Atlanto-occipital site: anaesthesia: 5cm deep, 18G needle (8.9cm): foals 1-2ml, adult: 5ml
o Lumbosacral site: sedation In stock, 13cm deep, 18 G needle (15-20cm) - Diagnostic imaging: radiography, myelography, CT, ultrasound, MRI
- Electrodiagnostic
equine degenerative myeloencephalopathy (EDME) and equine neuroaxonal dystrophy (NAD) predisposition
EDME: vitamin E responsible disease with familial predisposition
Predisposition: Arabian, quarter horse, Welsh pony and haflinger
cause of EDME and NAD
unknown, genetic familial predisposition, triggers by environmental factors (Vit E)
pathogenesis of EDME and NAD
from birth up to 3 years, mostly 6-12months
signs of EDME and NAD
symmetric ataxia, abnormal stance at rest, prominent hypermetria when walked with elevated head, proprioceptive deficits
diagnosis of EDME and NAD
observation of typical histological findings: neuronal fibre degeneration, spheroids, neuronal loss, astrogliosis and lipofuscinosis, CSF, serology (decreased Vit E)
treatment of EDME and NAD
d-a-tocopherol (RRR-alpha-tocopherol) most bioactive isoform of Vit E
prognosis of EDME and NAD
slowly progressive condition which may stabilise as animal matures, many severely affected animals are often euthanised
differential of EDME and NAD
cervical spinal cord compression, herpes virus 1 myeloencephalopathy, spinal trauma/infections, West Nile virus
cervical vertebral stenotic myelopathy CVSM predisposition
- Common cause of ataxia in horses and other animals
- Most common non-infectious cause of spinal ataxia
Predisposition: male horses, younger than 7yr, mostly thoroughbreds
cause of CVSM
abnormalities in the vertebral bodies, dorsal lamina and/or articular processes dynamic or static stenosis of the vertebral canal focal compression of the spinal cord
pathogenesis fo CVSM
narrowing of cervical vertebral canal compression on the spinal cord (static or dynamic stenosis)
signs of CVSM
ataxia and weakness, wobbler syndrome, gait abnormalities, proprioceptive abnormalities
diagnosis of CVSM
- history: other gait abnormalities (from trauma etc), chronic history
- physical exam: toe dragging, focal sweating, palpable abnormalities, reluctance to raise/lower head
- neurological exam and sway or slap tests
- blood and CSF analysis, myelography, Contrast enhanced CT, MRI (dogs, poor result in equine)
Neurological exam - should have: normal mentation and attitude, normal cranial nerve function and normal spinal reflexes
- slap test: thoracolaryngeal reflex: adductory movement of arytenoid cartilage
- standing horse: wide base stance, abnormal limb placement
- gait: UMN, paresis, general proprioceptive ataxia
types of CVSM
Type 1
- vertebral Colum fixed in flexed position at position of malarticulation/malposition (usually C2/C3) uncommon form, present at birth
Type 2
- young horse, mid-cervical region, thoroughbreds, multifactorial: gender inheritance, diet, trauma, rate of growth, fixation between vertebrae, malformation of articular processes (osteochondrosis)
Type 3
- older horses, wedging of the vertebral canal, periarticular proliferations
treatment of CVSM
Conservative (mostly dynamic)
- confine in stall for 6 months, check Ca + P, feed and water horse in elevated position, intra-articular injection of steroids into cervical articular facets (older)
Surgery
- ventral interbody fusion (both static and dynamic)
prognosis of CVSM
guarded for return to usefulness, more guarded with static stenosis
differential of CVSM
equine protozoal myeloencphlitis, trauma, equine herpes virus 1, viral encephalitis, brain abscess, neoplasia, HE, fractures
equine hepatic encephalopahty predisposition
Neurologic disorder: associated with liver failure
Predisposition: adult horses: acute/chronic liver failure, foal PSS
cause of equine hepatic encephalopathy
Theiler’s disease (flavivirus), alkaloid toxicosis, all causes of chronic fibrosis, poisoning with phosphide, iron toxicosis, cassia occidentalis seed ingestion, neoplasia etc
pathogenesis of equine hepatic encephalopathy
ammonia passes the BBB by diffusion increased metabolism by astrocytes accumulation of glutamine cytotoxic edema
inflammation and ammonia – induced free radicals vasogenic edema
signs of equine hepatic encephalopathy
depression, anorexia, frequent yawning, ataxia, head pressing, blindness, circling, coma, decreased muscle tone of lower lip, cortical blindness + mydriasis
- icterus, colic, photosensitisation, weight loss, laryngeal paralysis, dysphagia, gastric impaction-rupture
diagnosis of equine hepatic encephalopathy
- Increased: liver derived enzymes, bilirubin, serum bile acids, lactate, ammonia
- Prolonged PT and APTT
- Decreased: albumins and BUN, glucose
treatment of equine hepatic encephloatphy
- supportive treatment: prevent MODS
- propulsive signs: sedation with detomidine
- seizure: phenobarbital
- intranasal oxygen if necessary
- diazepam: causes astrocyte swelling
- potassium supplementation if necessary
- cerebral edema: mannitol/hypertonic saline
- supplementation with branched AA: valine, leucine and isoleucine
prognosis of equine hepatic encephalopathy
- Evaluating the HE: those with HE 5x larger chances to die within 6 mo
- Increased fibrinogen and decreased creatinine: poor prognostic factors
differential equine hepatic encephalopathy
primary enteric hyperammonaemia syndrome and inherited ammonia metabolic deficit (morgan horse), head trauma, organophosphate poisoning, equine protozoal myeloencephilitis (EPM), viral encephalitides, intracranial abscesses, hyponatreamia, heavy metal toxicosis
listeriosis treatment
- antibiotics: oxytetracycline, penicillin, trimethoprim-sulpha
- single injection of dexamethasone
- extended nursing care
signs of tetra paresis and tetraplegia
- mild: patient is ambulatory
- moderate: patient isn’t ambulatory, but can maintain sternal position
- severe: patient is not ambulatory, lies in lateral recumbency
diagnosis of tetraparesis and tetraplegia
- Haematology, biochemistry + urinalysis: for ruling out – determining the metabolic causes
- Additional lab: thyroid hormones, frucosamine, carnitine, pyruvate, lactate: mostly for some muscular disease
- Rx/US: to exclude other disease
- Serologic tests of PCR: for determination of specific causative organism
- Special genetic test (neuromuscular lab: prof. diane Shelton)
- CSF analysis: to exclude other diseases (positive: if nerve roots are involved or if the disease affects both CNS and PNS)
- electrodiagnostics: EMG, MNCV, SNCV, F waves, BAER
- histopathology: muscles, nerves
- EMG
predisposition for myasthenia gravis
congenital 6-12weeks old, acquitted all ages, akita, GSD, newfoundland, great dane
cause of myasthenia gravis
Acquired: most common autoimmune neurologic disease with autoantibodies against NMJ (nerve muscle junction) with reported onset 6 months and older
Congenital: too few acetylcholine receptors
types of myasthenia gravis
- Focal MG
o facial muscles: weakness
o muscles of pharynx and larynx: dysphagia, aphonia, salvation
o muscles of oesophagus: megaoesophagus +/- aspiration pneumonia - Generalised
o episodic muscle weakness that improves after rest
o all other parameters of the N-exam should be normal: proprioception, spinal reflexes, muscle mass and tone - Acute fulminant MG (exists in dog and cat only)
o very progressive Tetraparesis, ventroflexion of the neck
o large overdistended urinary bladder
o megaoesophagus + respiratory muscle weakness
signs of myasthenia gravis
thymoma associated disease (part of paraneoplastic syndrome), thiourylene medications (methimazole), seronegative MG, weakness, lameness, collapse, drooling, tremors, change of bark
diagnosis of myasthenia gravis
history, physical and neurological exam (normal), blood + urine (normal)
- electrodiagnostics: EMG + NCV normal, SFEMG (single fibre electromyography): most reliable
- pharmacological testing: tensilon response
- measure acetylcholine receptor antibodies (>0.6nmol/L dog, >0.3nmol/L cat)
- tensilon test = give 0.1mg/kg if MG will see improvement in signs within 5-10 mins
treatment of myasthenia gravis
- removing underlying cause (dogs: remove thymoma)
- increasing available Ach
o pirdostigmine bromide (1-3mg/kg PO q8rh), neostigmine – metilsulphate - immunosuppressive
o corticosteroids: prednisolone (0.5-1mg/kg PO BID), azatioprin (2mg/kg/day), cyclosporin (5-6mg/kg q12), mikofenolate
diseases associated with MG
- hypoadrenocortism, thrombocytopenia, autoimmune diseases, med: methimazole (cats
prognosis of MG
generalised: mostly favourable on medication, spontaneous remissions possible. Form with megaoesophagus. Fulminant form: prognosis is poor
differentials of MG
: causes of weakness exacerbated by exercise (cardiovascular conditions, severer respiratory conditions, neoplasia) causes of megaoesophagus
what dont you give to MG
don’t give ATB that block NM endoplate: aminoglycosides, penicillin, tetracycline
predisposition of SRMA
dogs (most common), age, purebred, familiar predisposition, gender, typically 6-18months, large breed dogs, beagle, bernese, mountain
cause of SRMA
viruses, bacteria, parasites, fungi, immune mediated, idiopathic
signs of SRMA
mimic cervical disc extrusion, lethargy, anorexia, pyrexia, cervical rigidity and pain, arched back, reluctance to move rigidity, spinal pain, fever
diagnosis of SRMA
- no specific diagnostic test
- history, clinical + neurological exam, lab work, urinalysis, X-ray, US, CT, MRI, CSF analysis, brain biopsy
- Lab work: leucocytosis (with left shift) CRP increased
- WBC in CSF, failure to isolate infect agent from CSF, response to steroid therapy measure IgG, IgA + IgM
CSF sampling - general anaesthesia + aseptic technique
- analysis: volume, cell number, protein concentration, increased CRP, bacterial culture, cytology
acute and chronic form of SRMA
Acute form: classic, fulminating symptoms are episodic and recurrent
Chronic form: protracted, meningeal fibrosus
treatment of SRMA
immunosuppression (prednisone), gastric protectants
prognosis of SRMA
acute = excellent, chronic = not so good
differential of SRMA
infection (discospondylitis, encephalitis, polyarthritis, osteomyelitis, polymyositis) wobbler syndrome, trauma, neoplasms
sleep disorder
- sleep: complex physiological process driven by an active neurobehavioral state maintained by the CNS
- factors affecting sleep:
o feeding frequency
o daily owner schedule
o age and housing
o ither animals, light, temp etc - Phases: rapid eye movement (REM), non-rem/slow wave sleep (SWS)
- pattern: wake, transition to SWS, REM, brief state of wakefulness, re-entering cycle and SWS again
- PSG = polysomnography concomitant EEG, electrooculogram (EOG)+ EMG = hypnogram
- Wake states:
o dog = 7-8 h (days) = diurnal 5h (night)
o cat = 42% day = nocturnal, 53% night
diagnosis of sleep disorder
history, videos, lab, x-ray and US, MRI and CSF to exclude primary CNS disease
geriatric changes in sleep
- In dogs >9 years: the amount of activity decreases (lower locomotor activity), more daytime sleep, decrease in REM phase sleep, fragmented sleep during the day (more naps) and increased night time wakefulness
- May be normal: symptoms of age-related behavioural/physical changes, can be linked to the cognitive dysfunction syndrome (CDS), or some diseases
- When related to CDS: delay in peak activity (circadian rhythm shift) treat the underlying CDS
REM sleep behaviour disorder
- During REM most muscles become atonic
- Localised muscular activity remains
- In REM sleep disorder: no muscle atonia is present: often violent limb movements, chewing to biting of the bedding or even another dog/owner
- DG: hypnogram
- TH: potassium bromide 44mg/kg/day in 78% of patients, clomipramine 1mg/kg q 12 h (up to 4mg/kg)
sleep apnoea
- Disordered respiration and episodes of oxygen desaturation particularly in REM sleep frequently causing awakening
- Hypersomnolence: excessive daytime sleepiness
- English bulldogs: natural model
nacrolepsy
chronic sleep disorder of neurological origin, deficits in hypocretin neurotransmission
- Characterised by excessive daytime sleepiness and/or very pronounced cataplexic attacks (sudden loss of muscle tone)
- Dogs are natural model for humans
o Familial (initial onset: before 6mo of age)
o Or sporadic, sporadic observed is 17 breeds, initial onset: 7weeks- 7yr
signs of narcolepsy
- Cataplexy: from transient loss of skeletal muscle tone or muscle weakness to complete paralysis and collapse lasting from few seconds to few minutes (no excessive salivation or incontinence should be present)
- If longer catapeltic episode: dogs will get up and resume normal activity or go into normal sleep
diagnosis of narcolepsy
- Rule of other episodic events: seizures or syncope (cataplexy can be induced by positive emotional experiences: engaging play or giving food reward)
- Measuring the concentration of hypocretin-1 peptide in the CSF, familial narcolepsy with mutation on receptor: can have normal values
treatment of narcolepsy
- Avoiding the inciting course: giving food separately: time or place, not playing
- Unbreakable food bowls, elevated water bowls
- Tricyclic antidepressants: imipramine, clomipramine, desipramine: serotonin/noradrenaline reuptake inhibitor: venlafaxine: alpha-2 adrenergic antagonists: yohimbine
cognitive dysfunction syndrome (CDS)
Neurological basis
- decreased brain mass, meningeal thickening
- accumulation of lipofuscin, emergence of apoptotic bodies
- amyloid-beta accumulation
Signs: DISHA: disorientation, altered interaction, sleep-wake cycle alteration, house soiling, activity changes
Diagnostics: neuropsychological test for deficits in memory and learning, testing spatial memory
Therapy: diet and supplements, mental stimulation, selegiline (selective monoamine oxidase B inhibitor), propentofylline (xanthine derivative), no drugs for cats yet
separation related distress (SRD) signs
- some dogs feel in the absence of a person to whom they are highly attached
Signs: vocalisation, destruction, house-soiling, pacing, salivation, escaping, aggression
diagnosis of SRD
behavioural questionnaire, video evidence
treatment of SRD
avoiding triggers, calm patient behaviour is rewarded, gradual departures, fluoxetine, clomipramine, amitrip, alprazolam, trazodone, clonidine, gabapentin, melatonin
differential of SRD
OCD, gastro intestinal disease, anxiety
OCD
- obsession: recurrent or persistent thoughts, impulses or images that are experiences as intrusive and inappropriate thus causing marked anxiety and distress
- CD: behaviours usually brought on by conflict but are subsequently show the outside the original context
signs of OCD
- cats: wool or fabric eating, pica, excessive grooming, hyperesthesia, tail chasing
- dogs: spinning, tail chasing, self-mutilation, fly biting, flank sucking
Cave: - Neuropathic pain: damage to axon or stroma of sensory neurones
- Feline idiopathic cystitis
- IBD
- Mini schnauzer: “checking behaviours” also gastrointestinal disease should be on DDx list
- FIV: pica in cats
- FIP chronic: licking the concrete, carpeting or other cats
- Feline symmetric alopecia (FSA): thorax, flanks, ventral abdomen and/or pelvic region result of excessive grooming: abdominal pain?, arthritis
therapy of OCD
apply obedience training, SSRI (fluoxetine), TCA (clomipramine), identify and remove sources of stress
forms of vestibular syndrome
central, peripheral and paradoxical
signs of vestibular syndrome
lack of facilitation of the extensor muscles on one side loss of balance with the normal side
head tilt
vestibular ataxia
nystagmus
strabismus
cranial nerve deficits
nausea + vomiting
head tilt
o If patient has cerebellar involvement: head may be tilted to the side opposite of the lesion
vestibular ataxia
o 3 forms (vestibular, cerebellar, sensorics proprioceptive)
o wide based stance, loss of balance on side of lesion
o head and body can sway
o patients circle
o presence of paresis
nystagmus
o rhythmic involuntary movement of the eyes
o equal movement on both sides = pendular nystagmus
not a sign of vesitibular disease (Siamese, birman, himalyan, and other breeds)
o fast phase toward one side and slow toward other = jerk nystagmus
strabismus
o ventral deviation of the ocular globe on the side of lesion when the head is in extension = positional strabismus
o can be seen with both central and peripheral VD
treatment of vestibular syndrome
- fluid therapy: for vomiting and not drinking patients
- maropitant, meclizine (antivertigo)
paradoxical syndrome
- cerebellum is inhibitory to ipsilateral vestibular nuclei
- maropitant = 1mg/kg SID PO cat, 2.8mg/kg SID PO dog
- meclizine 12.5-25mg/kg SID PO
- with loss of inhibition from a cerebellar lesion the vestibular nuclei appear to be ‘hyper” on that side
o head tilt is away from lesion
peripheral VD
otitis interna/media
nasopharyngeal polpys
otitis interna/ media cause
- very common cause of peripheral VD
- facial nerve (VII) involvement and horner’s syndrome are often present
Cause: - common cause: dog = otitis externa, cats = nasopharynx from eustachian tube
- bacteria: staph, strep, pseudomonas + proteus, Malassezia (yeast)
otitis interna/ media signs
- shaking head, scratching, rubbing on furtnirue + vestibular signs appear
diagnosis of Otitis interna/ media
- otoscopic exam (intact membrane doesn’t rule out otitis), myringotomy, thyroid evaluation, radiography, CT, MRI
therapy of otitis interna/media
- ATB according to culture, rarely bulla osteotomy
prognosis of otitis interna/media
- good but head tilt may persist and if CN VII is damaged: persistent facial paralysis, central clinical signs favourable
nasopharyngeal polylps
- Pedunculated growths resulting from chronic inflammation
- Originate from: auditory tube, nasopharynx or lining of the tympanic bulla
- Can be congenital in cats (1-5y)
signs of nasopharyngeal polyps
- Upper respiratory signs (sneezing, stridor) and/or pharyngeal signs (dysphagia, gagging)
therapy for nasopharyngeal polyps
- When in bulla: bulla osteotomy
- Per-endoscopic trans-tympanic traction of polyps
idiopathic VD
- Very common disease, especially in dogs
- Acute to peracute onset of peripheral vestibular signs:
o Aetiology: unknown: abnormalities in the endolymph flow
o Often dramatic signs (neuroexam difficult to perform)
o Common: nausea, vomiting, anxiety
o Should be NO signs of central involvement nor middle ear disease (CN VII, Horner’s) - Usually unilateral, rarely bilateral (cats)
hypothyroidism
diagnosis of idiopathic VD
we should exclude other diseases: most patients significantly improve within 72hrs complete recovery 2-3 weeks, mild residual deficits possible
therapy of idiopathic VD + Prognosis
symptomatic and supportive
physical therapy
prognsosi = good
hypothyroidism VD
- Middle age to older dogs, mild to moderate signs
- Energy metabolism disturbance, axonal transport, segmental demyelination
- Concomitant facial nerve involvement, lethargy (DDx: central VD)
- Diagnosis: hormonal test + improvement or resolution within 2 mo
- Ototoxicosis/iatrogenic trauma
o For topic meds.. always check the tympanic membrane
o Aminoglycosides, loop diuretics, cisplatin, chlorhexidine - Congenital
o GSD, English cocker spaniel, Doberman, fox terrier, siamese - Neoplasia
o Carcinomas (ear canal), fibrosarcoma, osteosarcoma, lymphoma
central VD
inflammatory diseases
infections diseases
- canine distemper, FIP
non-infectious disease
- neoplasia,, CVA, meningeoencephalitisi
diagnosis of central VD
CT, MRI, CSF analysis, BAER
