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Neurology Flashcards

1
Q

Grades for classic disc extrusion

A

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

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2
Q

diagnosis for degenerative disease of disc

A
  • based upon NE we perform:
    o diagnostic imaging: native radiography, contrast radiography, CT, MRI
    o CSF (rarely)
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3
Q

treatment of disc

A

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

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4
Q

neurapraxia

A
  • Temporary loss of sensory and motoric function due to stop in impulse conduction
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5
Q

axonotmesis

A
  • Detachment of axons from neuron body, with distal Wallerian degeneration, Schwann envelop and endoneurium are preserved: regeneration 1mm/day
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6
Q

neurotmesis

A
  • Complete detachment, can but it doesn’t have to be regeneration, frequently results in neuroma formation
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7
Q

degenerative myelopathy

A

Thoracolumbal part of spine

slowly, progressive adult-onset neurodegenerative disease causing paralysis

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8
Q

predisposition of degenerative myelopathy

A

dogs usually > 5 yr, extremely rare in young GSH

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9
Q

cause of degenerative myelopathy

A

inherited disease

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10
Q

pathogenesis of degenerative myelopathy

A

Progressive loss of myeline, slowly progressive clinical signs: from loss of proprioception to further deficits.

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11
Q

signs of degenerative myelopathy

A

slowly progressive muscular atrophy. late in course of disease: faecal and/or urinary incontinence. Severe symptoms after 6-12mo

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12
Q

diagnosis of degenerative myelopathy

A
  • 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
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13
Q

treatment of degenerative myelopathy

A
  • Aminokaproic acid: 15mg/kg PO tid
  • Vitamin E 20000IJ sid, Vitamin B12
  • Glucocorticoids only for acute worsening
  • Intensive physiotherapy
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14
Q

prognosis of degenerative myelopathy

A

long-term poor; most dogs are nonambulatory by 10-12 months after onset of signs

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15
Q

monitoring of degenerative myelopathy

A

clinical signs are monitored by the neurologic examination

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16
Q

predisposition of disconspondilitis

A

young animals or larger breeds, more common in cats

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17
Q

cause of discospondilitis

A

: trauma and iatrogenic, S. aureus, a. pseudintermedius, brucella canis…

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18
Q

signs of discoponsidilitis

A

pain, neurologic deficits, signs of infection, NE: pain upon palpation +/- neurologic deficits, anorexia, depression, reluctance to move, lameness, paresis/ataxia

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19
Q

diagnosis of discospondilitis

A

X-ray, urine and blood culture, CSF, contrast radiography, MRI

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20
Q

treatment of discosponsilidit

A

ATB (4-8weeks), cephalexin, analgesia, surgically: disc curettage, decompression and stabilisation, NSAIDs

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21
Q

prognosis of discospondilitis

A

early diagnostics and adequate TH: good. Chronic course of the disease, fungi, neurologic symptoms: guarded to poor

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22
Q

monitoring of discospondilitis

A

repeat blood and urine culture, repeat radiographs

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23
Q

differentials of discpondilitis

A

meningitis/myelitis, intervertebral disc disease, spondylitis, trauma, neoplasia

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24
Q

definition of epilepsy

A

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.

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25
Q

predisposition of epilepsy

A

dogs, cats, in farm and horses but very rare: St Bernard, Irish setter, dachshund, Pitbull, beagle, GSD, lab, retriever, bermese

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26
Q

pathophysiology of epilepsy

A
  • disbalance between inhibitory + excitatory influences on brain cell function
  • abrupt spontaneous depolarisation
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27
Q

seizure

A

any sudden, short lasting, transient event

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28
Q

epileptic seizure

A

manifestation of excessive synchronous epileptic activity of neurons in brain usually self-limiting

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29
Q

reactive seizure

A

in response to transient disturbance in function (toxic/metabolic) from normal brain

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30
Q

convulsive seizure

A
  • tonic-clonic = grand mal
  • tonic (generalised rigidity)
  • clonic (without tonic phase)
  • myoclonic = jerky movements
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31
Q

non-convulsive seizure

A
  • atonic = “drop attacks” sudden and general loss of muscle tone
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32
Q

idiopathic epilepsy

A

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

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33
Q

diagnosis of epilepsy

A
  • 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)
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34
Q

structural epilepsy

A

seizures provoked by intracranial/cerebral pathology (vit D)
- vascular, inflammatory, ananomaly, metabolic, idiopathic, neoplastic, degenerative

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35
Q

focal epileptic seizue

A
  • lateralising signs (originating from one hemisphere)
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36
Q

generalised seizure

A
  • 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)
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37
Q

phases of epileptic seizure

A

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

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38
Q

signs of epilepsy

A
  • circling, head pressing, blindness, decreased proprioception
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39
Q

diagnosis of epilepsy

A
  • physical exam, lab work and diagnostic image
    o CNS hypoxia, hypoglycaemia, HE, electrolyte disturbances, uraemia, hyperlipidaemia, intestinal parasites, exogenous toxins
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40
Q

treatment of epilepsy

A
  • 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
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41
Q

when to stop therapy and how to

A
  • 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
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42
Q

prognosis of epilepsy

A

can be good with the correct treatment

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43
Q

differential of epilepsy

A

Syncope, narcolepsy/cataplexy, neuromuscular weakness, paroxysmal movement disorder (Doberman), myasthenia gravis, painful foci

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44
Q

proprioception

A
  • 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
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45
Q

additional diagnosis procedures in large animal

A
  • 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
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46
Q

equine degenerative myeloencephalopathy (EDME) and equine neuroaxonal dystrophy (NAD) predisposition

A

EDME: vitamin E responsible disease with familial predisposition
Predisposition: Arabian, quarter horse, Welsh pony and haflinger

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47
Q

cause of EDME and NAD

A

unknown, genetic familial predisposition, triggers by environmental factors (Vit E)

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48
Q

pathogenesis of EDME and NAD

A

from birth up to 3 years, mostly 6-12months

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49
Q

signs of EDME and NAD

A

symmetric ataxia, abnormal stance at rest, prominent hypermetria when walked with elevated head, proprioceptive deficits

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50
Q

diagnosis of EDME and NAD

A

observation of typical histological findings: neuronal fibre degeneration, spheroids, neuronal loss, astrogliosis and lipofuscinosis, CSF, serology (decreased Vit E)

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51
Q

treatment of EDME and NAD

A

d-a-tocopherol (RRR-alpha-tocopherol) most bioactive isoform of Vit E

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52
Q

prognosis of EDME and NAD

A

slowly progressive condition which may stabilise as animal matures, many severely affected animals are often euthanised

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53
Q

differential of EDME and NAD

A

cervical spinal cord compression, herpes virus 1 myeloencephalopathy, spinal trauma/infections, West Nile virus

54
Q

cervical vertebral stenotic myelopathy CVSM predisposition

A
  • 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
55
Q

cause of CVSM

A

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

56
Q

pathogenesis fo CVSM

A

narrowing of cervical vertebral canal  compression on the spinal cord (static or dynamic stenosis)

57
Q

signs of CVSM

A

ataxia and weakness, wobbler syndrome, gait abnormalities, proprioceptive abnormalities

58
Q

diagnosis of CVSM

A
  • 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
59
Q

types of CVSM

A

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

60
Q

treatment of CVSM

A

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)

61
Q

prognosis of CVSM

A

guarded for return to usefulness, more guarded with static stenosis

62
Q

differential of CVSM

A

equine protozoal myeloencphlitis, trauma, equine herpes virus 1, viral encephalitis, brain abscess, neoplasia, HE, fractures

63
Q

equine hepatic encephalopahty predisposition

A

Neurologic disorder: associated with liver failure
Predisposition: adult horses: acute/chronic liver failure, foal PSS

64
Q

cause of equine hepatic encephalopathy

A

Theiler’s disease (flavivirus), alkaloid toxicosis, all causes of chronic fibrosis, poisoning with phosphide, iron toxicosis, cassia occidentalis seed ingestion, neoplasia etc

65
Q

pathogenesis of equine hepatic encephalopathy

A

ammonia passes the BBB by diffusion  increased metabolism by astrocytes  accumulation of glutamine  cytotoxic edema
inflammation and ammonia – induced free radicals  vasogenic edema

66
Q

signs of equine hepatic encephalopathy

A

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

67
Q

diagnosis of equine hepatic encephalopathy

A
  • Increased: liver derived enzymes, bilirubin, serum bile acids, lactate, ammonia
  • Prolonged PT and APTT
  • Decreased: albumins and BUN, glucose
68
Q

treatment of equine hepatic encephloatphy

A
  • 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
69
Q

prognosis of equine hepatic encephalopathy

A
  • Evaluating the HE: those with HE 5x larger chances to die within 6 mo
  • Increased fibrinogen and decreased creatinine: poor prognostic factors
70
Q

differential equine hepatic encephalopathy

A

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

71
Q

listeriosis treatment

A
  • antibiotics: oxytetracycline, penicillin, trimethoprim-sulpha
  • single injection of dexamethasone
  • extended nursing care
72
Q

signs of tetra paresis and tetraplegia

A
  • mild: patient is ambulatory
  • moderate: patient isn’t ambulatory, but can maintain sternal position
  • severe: patient is not ambulatory, lies in lateral recumbency
73
Q

diagnosis of tetraparesis and tetraplegia

A
  • 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
74
Q

predisposition for myasthenia gravis

A

congenital 6-12weeks old, acquitted all ages, akita, GSD, newfoundland, great dane

75
Q

cause of myasthenia gravis

A

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

76
Q

types of myasthenia gravis

A
  • 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
77
Q

signs of myasthenia gravis

A

thymoma associated disease (part of paraneoplastic syndrome), thiourylene medications (methimazole), seronegative MG, weakness, lameness, collapse, drooling, tremors, change of bark

78
Q

diagnosis of myasthenia gravis

A

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

79
Q

treatment of myasthenia gravis

A
  • 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
80
Q

diseases associated with MG

A
  • hypoadrenocortism, thrombocytopenia, autoimmune diseases, med: methimazole (cats
81
Q

prognosis of MG

A

generalised: mostly favourable on medication, spontaneous remissions possible. Form with megaoesophagus. Fulminant form: prognosis is poor

82
Q

differentials of MG

A

: causes of weakness exacerbated by exercise (cardiovascular conditions, severer respiratory conditions, neoplasia) causes of megaoesophagus

83
Q

what dont you give to MG

A

don’t give ATB that block NM endoplate: aminoglycosides, penicillin, tetracycline

84
Q

predisposition of SRMA

A

dogs (most common), age, purebred, familiar predisposition, gender, typically 6-18months, large breed dogs, beagle, bernese, mountain

85
Q

cause of SRMA

A

viruses, bacteria, parasites, fungi, immune mediated, idiopathic

86
Q

signs of SRMA

A

mimic cervical disc extrusion, lethargy, anorexia, pyrexia, cervical rigidity and pain, arched back, reluctance to move rigidity, spinal pain, fever

87
Q

diagnosis of SRMA

A
  • 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
88
Q

acute and chronic form of SRMA

A

Acute form: classic, fulminating symptoms are episodic and recurrent
Chronic form: protracted, meningeal fibrosus

89
Q

treatment of SRMA

A

immunosuppression (prednisone), gastric protectants

90
Q

prognosis of SRMA

A

acute = excellent, chronic = not so good

91
Q

differential of SRMA

A

infection (discospondylitis, encephalitis, polyarthritis, osteomyelitis, polymyositis) wobbler syndrome, trauma, neoplasms

92
Q

sleep disorder

A
  • 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
93
Q

diagnosis of sleep disorder

A

history, videos, lab, x-ray and US, MRI and CSF to exclude primary CNS disease

94
Q

geriatric changes in sleep

A
  • 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
95
Q

REM sleep behaviour disorder

A
  • 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)
96
Q

sleep apnoea

A
  • Disordered respiration and episodes of oxygen desaturation particularly in REM sleep  frequently causing awakening
  • Hypersomnolence: excessive daytime sleepiness
  • English bulldogs: natural model
97
Q

nacrolepsy

A

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

98
Q

signs of narcolepsy

A
  • 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
99
Q

diagnosis of narcolepsy

A
  • 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
100
Q

treatment of narcolepsy

A
  • 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
101
Q

cognitive dysfunction syndrome (CDS)

A

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

102
Q

separation related distress (SRD) signs

A
  • some dogs feel in the absence of a person to whom they are highly attached
    Signs: vocalisation, destruction, house-soiling, pacing, salivation, escaping, aggression
103
Q

diagnosis of SRD

A

behavioural questionnaire, video evidence

104
Q

treatment of SRD

A

avoiding triggers, calm patient behaviour is rewarded, gradual departures, fluoxetine, clomipramine, amitrip, alprazolam, trazodone, clonidine, gabapentin, melatonin

105
Q

differential of SRD

A

OCD, gastro intestinal disease, anxiety

106
Q

OCD

A
  • 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
107
Q

signs of OCD

A
  • 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
108
Q

therapy of OCD

A

apply obedience training, SSRI (fluoxetine), TCA (clomipramine), identify and remove sources of stress

109
Q

forms of vestibular syndrome

A

central, peripheral and paradoxical

110
Q

signs of vestibular syndrome

A

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

111
Q

head tilt

A

o If patient has cerebellar involvement: head may be tilted to the side opposite of the lesion

112
Q

vestibular ataxia

A

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

113
Q

nystagmus

A

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

114
Q

strabismus

A

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

115
Q

treatment of vestibular syndrome

A
  • fluid therapy: for vomiting and not drinking patients
  • maropitant, meclizine (antivertigo)
116
Q

paradoxical syndrome

A
  • 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
117
Q

peripheral VD

A

otitis interna/media
nasopharyngeal polpys

118
Q

otitis interna/ media cause

A
  • 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)
119
Q

otitis interna/ media signs

A
  • shaking head, scratching, rubbing on furtnirue + vestibular signs appear
120
Q

diagnosis of Otitis interna/ media

A
  • otoscopic exam (intact membrane doesn’t rule out otitis), myringotomy, thyroid evaluation, radiography, CT, MRI
121
Q

therapy of otitis interna/media

A
  • ATB according to culture, rarely bulla osteotomy
122
Q

prognosis of otitis interna/media

A
  • good but head tilt may persist and if CN VII is damaged: persistent facial paralysis, central clinical signs favourable
123
Q

nasopharyngeal polylps

A
  • Pedunculated growths resulting from chronic inflammation
  • Originate from: auditory tube, nasopharynx or lining of the tympanic bulla
  • Can be congenital in cats (1-5y)
124
Q

signs of nasopharyngeal polyps

A
  • Upper respiratory signs (sneezing, stridor) and/or pharyngeal signs (dysphagia, gagging)
125
Q

therapy for nasopharyngeal polyps

A
  • When in bulla: bulla osteotomy
  • Per-endoscopic trans-tympanic traction of polyps
126
Q

idiopathic VD

A
  • 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

127
Q

diagnosis of idiopathic VD

A

we should exclude other diseases: most patients significantly improve within 72hrs  complete recovery 2-3 weeks, mild residual deficits possible

128
Q

therapy of idiopathic VD + Prognosis

A

symptomatic and supportive
physical therapy

prognsosi = good

129
Q

hypothyroidism VD

A
  • 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
130
Q

central VD

A

inflammatory diseases

infections diseases
- canine distemper, FIP

non-infectious disease
- neoplasia,, CVA, meningeoencephalitisi

131
Q

diagnosis of central VD

A

CT, MRI, CSF analysis, BAER

Internal (12 decks)

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