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CVNT2 > Neurology > Flashcards

Neurology Flashcards

1
Q

how do seizures occur?

A

due to an altered balance between excitatory and inhibitory input

leading to hypersynchronisation of neurons

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2
Q

what is a seizure?

A

an abnormal, uncontrollable, hypersynchronous electrical activation of a large group of neurons

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3
Q

what are the types of seizure?

A

isolated seizure
cluster seizure
status epilepticus

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4
Q

what is an isolated seizure?

A

a seizure lasting less than 5 minutes

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5
Q

what is a cluster seizure?

A

2 or more seizures within a 24 hour period with complete recovery in-between

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6
Q

what is status epilepticus?

A

seizure lasting longer than 5 minutes

OR

2 seizures without complete recovery in-between

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7
Q

what type of seizure is an emergency?

A

status epilepticus

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8
Q

what are partial/focal seizures?

A

asymmetric - one part of the brain is affected

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9
Q

what are the signs of a partial/focal seizure?

A

facial twitching
hypersalivation
behavioural changes

consciousness maintained

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10
Q

what type of seizure produces no change in mentation?

A

simple

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11
Q

what type of seizure produces a change in mentation?

A

complex

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12
Q

what is a generalised (tonic/clonic) seizure?

A

a seizure with bilateral cerebral hemisphere involvement

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13
Q

what are the signs of a generalised (tonic/clonic) seizure?

A

autonomic signs (U/D)

loss of consciousness

identifiable pre-ictal, ictal and post-ictal phases

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14
Q

what is the pre-ictal phase? how can it be identified?

A

phase before seizure onset

may see behavioural changes, altered mentation, attention-seeking behaviour

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15
Q

what is the ictal phase? how can it be identified?

A

active seizure phase - loss of consciousness, muscle contraction, U/D, salivation

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16
Q

what is the post-ictal phase? how can it be identified?

A

minutes to days post-seizure - mainly see abnormal neurological signs and behavioural changes but will vary greatly between patients

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17
Q

what are the 2 main types of extracranial seizure triggers/causes?

A

toxins and metabolic factors

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18
Q

which toxins can lead to seizures?

A 
methaldehyde (slug bait) 
ethylene glycol (antifreeze) 
permethrin in cats 
pesticides 
ivermectin (collie breeds) 
human drugs
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19
Q

what metabolic factors can lead to seizures?

A

portosystemic shunt (blood toxins)
hypoglycaemia
hypocalcaemia

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20
Q

what are the types of intracranial factors which can cause seizures?

A

structural - brain tumour, inflammation, hydrocephalus

functional - idiopathic epilepsy

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21
Q

what is the most common cause of seizures?

A

idiopathic epilepsy

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22
Q

what age dogs are more commonly diagnosed with idiopathic epilepsy?

A

6 months - 6 years

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23
Q

how is a diagnosis of idiopathic epilepsy concluded?

A

normal inter-ictal neurological exam

normal metabolic investigation

normal MRI scan of brain

normal CSF

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24
Q

what diagnostics should be performed if a patient is experiencing seizures?

A

thorough history

blood tests 
MRI scan (IV gadolinium contrast) 
CSF analysis 
videos 
monitoring and recording

retinal exam and blood pressure measurement
if possible

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25
Q

which blood tests are performed when investigating seizures?

A 
haematology 
biochemistry 
fasted blood glucose 
pre- and post-prandial bile acids 
possibly ammonia
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26
Q

which other conditions/disorders can mimic seizures?

A 
narcolepsy/cataplexy 
fly-catching 
movement disorder 
syncope 
3rd degree AV block 
canine epileptoid cramping syndrome 
peripheral vestibular disease
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27
Q

what is narcolepsy/cataplexy? how does it present?

A

a sleep-wake disorder with flaccid collapses

loss of muscle tone but no autonomic signs

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28
Q

what is fly catching and how does it present?

A

unknown cause - dog appears to be chasing/trying to catch imaginary flies (mins-hours)
normal mentation, no autonomic signs

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29
Q

what is movement disorder? how does it present?

A

an episodic disorder - patient remains conscious and performs involuntary movements that are spontaneous and uncontrolled
neurologically normal between episodes

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30
Q

what is syncope? how does it present?

A

temporary loss of consciousness (‘fainting’) due to reduced oxygenation to the brain

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31
Q

what can cause syncope?

A

cardiac-related (most common)

neurological

hypoglycaemia
hypocalcaemia

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32
Q

how does 3rd degree AV block present?

A

prolonged hypoxic event with partial seizure-like episodes

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33
Q

what is canine epileptoid cramping syndrome? how does it present?

A

movement disorder affecting mostly border terriers

patient conscious and responsive with no autonomic signs and normal mentation

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34
Q

what is involved in emergency management of seizures?

A 
oxygen therapy 
place IV catheter (if possible) 
administer diazepam 
assess circulation and temperature 
intubate if required 
active cooling if hyperthermic 
mannitol if seizure >15 mins or suspected cerebral oedema 
collect full bloods
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35
Q

how do you triage a seizuring patient (over the phone)?

A

stay calm and reassure owner

enquire into previous history, toxin exposure, head trauma

establish how long patient has been seizuring and how many times

ask if patient is conscious and responsive

any U/D

advise to travel when safe to do so

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36
Q

what kennel considerations should be made with seizure patients?

A

minimise noise and light in kennel

bottom kennel/easily accessible

seizure plan on kennel with doses calculated/medication drawn up

sign on door to limit staff numbers/traffic

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37
Q

what steps should you take if a patient seizures?

A

stay calm and note the time, call clinician in charge for help

remove any dangers

dim lights and reduce noise as much as possible

limit handling

monitor vital signs

follow seizure plan if one in place
do not put hands in/near patients mouth!!

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38
Q

what steps should you take when the patient comes into the practice after seizuring?

A 
reassure the owner 
triage - ABC 
provide oxygen therapy 
obtain IV access ASAP 
administer anticonvulsants 
check temperature and actively cool if required 
consider mannitol 
consider intubation and CRI if frequent/extended seizures
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39
Q

what is the first line treatment for managing seizures?

A

Phenobarbital (epiphen) tablets

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40
Q

how does phenobarbital work?

A

acts on GABA receptors in the brain to increase frequency of synaptic inhibition and reduce neuronal excitability

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41
Q

what are the advantages of phenobarbital?

A

high efficacy and safety, low cost

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42
Q

what are the disadvantages of phenobarbital?

A

takes ~2 weeks for steady state plasma concentration to be reached
requires regular blood tests
many side effects

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43
Q

what are the side effects of phenobarbital?

A 
hepatotoxicity in high doses 
sedation 
polyuria/polydipsia 
polyphagia 
ataxia
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44
Q

what else can be used in first line management of seizures?

A

potassium bromide (libromide) - can be used alone or in conjunction with another antiepileptic drug

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45
Q

what are the disadvantages of potassium bromide?

A

side effects

takes ~ 4 months to achieve steady state plasma concentration

renally excreted - not good for px with renal compromise

regular blood rests required

causes lung issues in cats

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46
Q

what are the side effects of potassium bromide?

A 
gastric irritation 
nausea 
polydipsia/polyuria 
sedation 
pancreatitis (rare)
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47
Q

what is levetiracetam (keppra)?

A

used as an adjunct to other AEDs - unknown method of action

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48
Q

what are the advantages of levetiracetam?

A

primarily excreted unchanged in urine
excellent oral bioavailability
well-tolerated

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49
Q

what are the side effects of levetiracetam?

A

ataxia
vomiting
sedation

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50
Q

which drug is licensed specifically for idiopathic epilepsy?

A

imepitoin (pexion)

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51
Q

which dogs cannot take imepitoin?

A

those with seizures caused by anything other than idiopathic epilepsy
dogs with impaired hepatic/renal/cardiovascular function

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52
Q

what are the side effects of imepitoin?

A

ataxia
vomiting
polyphagia

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53
Q

what home care considerations are relevant for patients that seizure?

A

family situation
financial situation
type of property dog is living in
good communication

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54
Q

what kind of disease is polyradiculoneuritis?

A

immune-mediated musculoskeletal disease

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55
Q

how does polyradiculoneuritis present?

A

short-strided gait that progresses to tetraparesis

patient can be ambulatory or non-ambulatory

dysphonia

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56
Q

how long does it take to recover from polyradiculoneuritis?

A

within 1-4 months once signs stabilise

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57
Q

how is polyradiculoneuritis diagnosed?

A

accurate patient history

physical and neurological exam

EMG, NCV

muscle and nerve biopsies

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58
Q

how is polyradiculoneuritis treated?

A

intensive nursing care and physiotherapy

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59
Q

what is myasthenia gravis?

A

disease of neuromuscular transmission affecting the NMJ

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60
Q

what causes myasthenia gravis?

A

can be congenital or acquired

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61
Q

how does myasthenia gravis present?

A

muscle weakness and fatigue (more obvious when patient is exercising)

focal, generalised or acute

regurgitation commonly seen due to oesophageal weakness

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62
Q

how is myasthenia gravis diagnosed?

A

presumptive based on history and presentation
thoracic radiographs (megaoesophagus)
tensilon test

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63
Q

how is myasthenia gravis treated?

A

anticholinesterase therapy plus corticosteroids at immunosuppressive doses

intensive nursing care and support

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64
Q

what is polymyositis?

A

immune-mediated inflammatory myopathy

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65
Q

what causes polymyositis?

A

idiopathic but can be associated with systemic disease

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66
Q

how does polymyositis present?

A

exercise intolerance and stiffened gait

muscle weakness and atrophy

dysphonia, dysphagia, regurgitation

signs often wax and wane in initial period

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67
Q

how is polymyositis diagnosed?

A

criteria not well defined - diagnosis of exclusion

main diagnostics are clinical history, biochemistry, electrodiagnostic testing and muscle biopsy

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68
Q

how is polymyositis treated?

A

corticosteroids at immunosuppressive doses
intensive nursing care and support
azothrioprine can be used alongside steroids

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69
Q

what are the clinical signs of aspiration pneumonia?

A

coughing
tachypnoea
harsh lung sounds
crackles on auscultation

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70
Q

which neuromuscular diseases carry the most risk of aspiration pneumonia?

A

myasthenia gravis

polymyositis

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71
Q

which neuromuscular disease carries the most risk of pressure sores?

A

polyradiculoneuritis

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72
Q

which neuromuscular disease carries the most risk of contracture?

A

polyradiculoneuritis (esp in young)

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73
Q

how can you prevent severe aspiration pneumonia?

A

careful and close monitoring of patients

early administration of antibiotics

IV fluids + oxygen therapy

walking/turning patients regularly very important

feeding balls of food from a height

severe cases may require mechanical ventilation

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74
Q

how do pressure sores form?

A

recumbency leads to increased pressure over bony prominences, which then leads to ischaemia and necrosis

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75
Q

how can you prevent pressure sores?

A 
thick padded bedding 
turn every 2-4 hours 
donut bandages
physiotherapy 
monitor patients closely
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76
Q

how does muscle contracture occur?

A

recumbency and immobilisation

–> leads to adaptive shortening of the muscle and soft tissues, and inelasticity of the soft tissues

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77
Q

how is contracture treated?

A

massage
PROM
proprioceptive exercises
neuromuscular stimulation

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78
Q

what is ataxia?

A

uncoordinated gait

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79
Q

what does -paresis/-paretic mean?

A

weakness, decreased voluntary movement

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80
Q

what does -paralysis/-plegic mean?

A

no voluntary movement?

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81
Q

what does mono- mean in regards to gait?

A

one limb affected

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82
Q

what does hemi- mean in regards to gait?

A

both limbs on one side affected

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83
Q

what does para- mean in regards to gait?

A

both pelvic limbs affected

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84
Q

what does quadra/tetra- mean in regards to gait?

A

all 4 limbs affected

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85
Q

when would you perform a neurological exam on a patient?

A

seizures
behavioural changes
gait abnormalities
change in posture/positioning

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86
Q

why might you perform a neurological exam?

A

identify if nervous system involvement

identify specific location/localisation

aid diagnosis and prognosis

continuous assessment of condition/comparisons

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87
Q

what do the upper motor neurons do?

A

send signals to the lower motor neurons

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88
Q

what do the lower motor neurons do?

A

connect the CNS to the effector organ (muscle) and send a signal to make them contract

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89
Q

what factors should you assess during a neurological examination?

A

mentation

gait and posture

cranial nerve function

postural reactions

spinal reflexes

sensory evaluation

palpitation of head/spine/limbs

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90
Q

what does head tilt look like?

A

one ear is below the other

91
Q

what does head turn look like?

A

nose is turned towards body

92
Q

what does ventroflexion of the neck look like?

A

low head carriage

93
Q

what is scoliosis?

A

lateral deviation of the spine

94
Q

what is lordosis?

A

ventral deviation of the spine

95
Q

what is kyphosis?

A

dorsal deviation of the spine

96
Q

what is decerebrate rigidity?

A

extension of all limbs, head and neck

97
Q

what is decerebellate rigidity?

A

extension of the thoracic limbs, head and neck

98
Q

what are the common postural tests for spinal cord injury?

A

proprioceptive positioning (paw placement)

hopping

visual placement

tactile placing

hemi-walking

wheelbarrowing

99
Q

what spinal reflexes should be present in the thoracic limbs?

A

withdrawal reflex
extensor carpi radialis
biceps brachii and triceps reflex

100
Q

what spinal reflexes should be present in the pelvic limbs?

A

patella reflex

cranial tibial and gastrocnemius

101
Q

which spinal reflexes are part of the trunk?

A

perineal reflex

panniculus reflex

102
Q

what is the panniculus reflex?

A

pinching either side of the spinal column to see if skin twitches

103
Q

how do you perform a pain evaluation?

A

pinching/pressure applied to digits on each limb - looking for reaction from patient (turning, vocalising, trying to bite)

104
Q

what is the important thing to remember about pain evaluation?

A

it is not the same as withdrawal reflex

105
Q

what are the acute causes of spinal injury?

A

intervertebral disc disease (IVDD)

trauma (fracture/luxation)

infarction (fibrocartilagenous embolism)

106
Q

what are the chronic causes of spinal injury?

A

degenerative disc disease
degenerative myelopathy
cervical stenotic myelopathy (wobblers)

107
Q

what are the other possible causes of spinal injury (aside from primary acute/chronic)?

A 
atlanto-axial subluxation 
vertebral anomalies 
neoplasia 
inflammatory diseases 
discospondylitis
108
Q

what is discospondylitis?

A

infection of the vertebrae/vertebral disc spaces

109
Q

what additional diagnostics can be used to identify spinal disease?

A 
imaging - radiographs, CT, MRI
CSF tap (cisternal or lumbar)
110
Q

what is involved in conservative treatment for spinal cord disease?

A 
6 weeks strict rest
physiotherapy 
anti-inflammatory drugs 
analgesia 
steroid therapy
111
Q

what is involved in surgical treatment for spinal cord disease?

A

hemilaminectomy
ventral slot (upper cord)
dorsal laminectomy
spinal stabilisation/fixation

112
Q

what is a hemilaminectomy?

A

removal of compressing/problematic bone

113
Q

how does upper motor neuron disease affect bladder function?

A 
increased urethral resistance 
detrusor and urethral sphincter can contract at same time 
not able to control bladder function 
urinary retention 
kidney damage possible 
difficult to manually express 
require catheterisation 
intermittent "squirting" of urine
114
Q

how does lower motor neuron injury affect bladder function?

A

flaccid bladder, does not contract spontaneously
continues to fill, resulting in “overflow” leaking of urine
bladder muscle is overstretched
easy to manually express

115
Q

what are the nursing considerations for patients with spinal cord injury?

A 
holistic care 
enrichment 
nutrition 
turning/physio 
temperature control 
padded bedding 
excretion management 
grooming 
hygiene
116
Q

what is an intracranial disease?

A

a disease that affects the brain

117
Q

what is the skull vault?

A

a closed, inelastic compartment that doesn’t allow any room for inflammation and swelling

118
Q

what does the skull vault contain?

A

80% parenchymal tissue
10% blood
10% CSF

119
Q

what is parenchymal tissue?

A

brain tissue

120
Q

how is cerebral blood flow maintained?

A

autoregulatory mechanisms maintain cerebral blood flow over a wide range of mean arterial pressures (50-150mmHg)

121
Q

what is intracranial pressure?

A

pressure exerted between skull and intracranial tissues

normal is 5-10mmHg

122
Q

what is the effect of intracranial hypertension?

A

results in reduced cerebral perfusion pressure, reduced blood flow and secondary changes

123
Q

what triggers cushings reflex?

A

severe, acute rise in ICP

124
Q

what is cushings reflex?

A

a rise in MAP and reflex bradycardia

125
Q

what does cushings reflex indicate?

A

it is a sign of potentially life threatening increase in ICP and should be treated immediately

126
Q

what are the possible causes of intracranial disease?

A 
trauma 
inflammatory (MUO) 
infections 
neoplasia 
toxins 
seizures 
anomalous (hydrocephalous)
127
Q

what types of neoplasia can can intracranial disease?

A

meningioma
glioma
choroid plexus tumour

128
Q

which part of the neurological examination are most likely to pick up on ICP?

A

mentation (alert, obtunded, stuporous, comatose)

cranial nerve function (menace, PLR, gag, palpebral, vestibuloccular)

129
Q

what is alert mentation?

A

normal response to surroundings

130
Q

what is obtunded mentation?

A

awake but less responsive, will sleep if left

131
Q

what is stuporous mentation?

A

only responds to noxious/painful stimuli

132
Q

what is comatose mentation?

A

unconscious, unresponsive to any stimuli

133
Q

what mentation signs indicate something could be wrong with ICP?

A 
circling 
head pressing 
pacing 
head tilt 
head turn
134
Q

what is the menace response?

A

covering one eye and moving hand towards the face menacingly - animal should blink/flinch

135
Q

what is the oculocephalic reflex?

A

physiological nystagmus - eye position correction with movement

136
Q

what does absence of oculocephalic reflex indicate?

A

poor prognosis for the animal - severe brainstem damage

137
Q

what is miosis/miotic pupils?

A

constricted pupils

138
Q

what is mydriasis/mydriatic pupils?

A

dilated pupils

139
Q

what is anisocoria?

A

unequal pupil size

140
Q

which pupil status indicates a very poor prognosis?

A

mid-size fixed pupils that are unresponsive to light

141
Q

list some of the clinical signs of intracranial disease.

A

circling and ataxia

head tilt/turn

nystagmus, blindness

altered mentation/loss of consciousness/coma

seizures

cheyne-stokes respirations

loss of gag reflex and oculocephalic reflex

strabismus and non-responsive pupils

decerebrate/decerebellate posture

142
Q

what are the 3 domains of the glasgow coma score?

A

motor activity
brainstem reflexes
level of consciousness

143
Q

what glasgow coma scale score indicates a grave prognosis?

A

3-8

144
Q

what glasgow coma scale score indicates a guarded prognosis?

A

9-14

145
Q

what glasgow coma scale score indicates a good prognosis?

A

15-18

146
Q

what is the main treatment for raised intracranial pressure?

A

IV mannitol infusion

147
Q

why is mannitol used to decrease ICP?

A

hyperosmolar - reduced cerebral oedema

increases CPP and cerebral blood flow

rapid onset (minutes)

effects for 1.5-6 hours

148
Q

what should be infused after mannitol treatment?

A

isotonic fluids - mannitol has a profound diuretic effect

149
Q

what is the alternative treatment for raised ICP?

A

hypertonic saline therapy - similar osmolarity to mannitol

150
Q

in addition to mannitol, what else can be used in treatment of raised ICP?

A 
sedatives/analgesia 
anaesthesia 
mechanical ventilation 
CRI 
require intense care and monitoring
151
Q

what is involved in nursing management of raised ICP patients?

A

recumbency - turning, padding, physiotherapy, monitor/manage excretions

elevate cranial part of body 30-40°

ocular care
mouth checks

nutritional support - in sternal every 4-6 hours if conscious

152
Q

what is hydrocephalus?

A

excessive accumulation of CSF within the ventricular system

153
Q

how can hydrocephalus be caused?

A

obstruction to CSF outflow
decreased absorption of CSF
increased production of CSF

154
Q

what are the 2 types of hydrocephalus?

A

congenital - present at birth

acquired - tumour, inflammation, haemorrhage

155
Q

what are the clinical signs of hydrocephalus?

A 
behavioural changes 
slowness in learning 
loss of coordination 
visual deficits 
seizures
circling
depressed/obtunded mentation 
enlarged and dome-shaped skull 
signs can wax and wane
156
Q

how is hydrocephalus managed medically?

A

aims to reduce production of CSF - steroids (prednisolone, frusemide, omeprazole)

157
Q

how is hydrocephalus managed surgically?

A

aims to divert CSF to another location

ventriculoperitoneal shunt - tubing placed from ventricle to peritoneal cavity

158
Q

what is the prognosis for hydrocephalus?

A

dependent on cause and severity of signs - more severe = more guarded

good prognosis for infectious cause
tumour = more guarded

159
Q

what is MUO?

A

meningoencephalitis of unknown origin - inflammatory disorder of CNS

160
Q

what are the 3 types of MUO?

A

granulomatous ME
necrotising
necrotising leukoencephalitis

161
Q

why are the 3 types referred to as an umbrella term of MUO?

A

not possible to determine type in live patient

162
Q

which dogs are more prone to MUO?

A

small dogs
females more than males
>6 months of age

163
Q

what are the neurological signs of MUO?

A 
seizures 
muscle tremors 
blindness 
head tilt 
altered balance and posture
circling
164
Q

how is MUO diagnosed?

A

clinical examination
blood tests
MRI - brain
CSF analysis

165
Q

what is involved in management of MUO?

A

immunosuppressive drugs - steroids, cyclosporine, azathioprine, cytarabine
antiepileptics
nursing care

166
Q

what is the prognosis for MUO?

A

variable
seizures = poorer
better for focal lesions than multifocal
improvement within 3 months = good prognosis
patients can relapse and represent with clinical signs

167
Q

what considerations need to be taken in regards to nursing considerations of neuro patients?

A 
ambulation status/recumbency
type of surgery 
continence 
temperament 
normal routine of patient
168
Q

what type of bedding should be used for a neuro patients kennel?

A

thick bedding to prevent sores (duvet/mattress as bottom layer)

layer with incontinence pads

vet bed as top layer to wick away any urine

pad out sides of kennel for extra comfort and injury prevention

169
Q

which methods are available to help a patient empty their bladder?

A 
manual expression 
intermittent catheterisation (males only) 
in-dwelling catheterisation (larger/aggressive/nervous patients; constantly leaking urine)
170
Q

what is overflow incontinence?

A

where the patient is unaware their bladder is full - overflows and leaks urine (reflexes have been affected)

171
Q

how many times should the bladder be emptied per day?

A

ideally 4x a day

172
Q

what is the main cause of urine scalding?

A

overflow incontinence/leaky bladder

173
Q

if passing an intermittent urinary catheter, how often should this be done?

A

twice daily - always a risk of causing iatrogenic trauma with each catheter passed

174
Q

how do we monitor for UTIs in spinal injury patients?

A

monitor smell, colour and turbidity of urine

guidance must be given to owner at discharge to monitor urine and take a sample to vet for urinalysis if concerned

175
Q

how can we manage faecal incontinence patients?

A

check beds regularly

keep patient clean/dry at all times - may require regular bathing

check skin daily for changes/sore spots

apply topicals if necessary (under vet direction)

176
Q

what is a decubitus ulcer?

A

an open skin wound caused by continued pressure of skin on a firm surface - eventually causes tissue ischaemia in the skin

177
Q

where do decubital ulcers most commonly occur?

A

bony prominences e.g. ileum, ischium, hock, olecranon and feet

178
Q

how often should patients be turned in order to prevent decubitus ulcers?

A

every 4 hours as a minimum - more often for more bony breeds

179
Q

how can you prevent decubital ulcers?

A

turn every 4 hours with great care

deep padded bedding, checked regularly

keep patients clean and dry

donut bandages on elbows and hocks can help prevent

prop recumbent patients up with pillows for comfort

180
Q

which products/medications can be used to prevent and treat decubital sores?

A

clorexyderm for treatment of mild urine scalding

talc to help dry a patient after bathing

cavilon spray as a no sting barrier around anus/perineum (diarrhoea)

flamazine - antibac cream used for surface thickness sores

181
Q

what can you use to exercise the paretic/paraplegic patient?

A

sling/rear harness

foot covers

182
Q

why do we cover the hind paws when walking paretic/plegic patients?

A

to prevent trauma to the hind toes and claws (will drag along floor)

183
Q

how can we exercise the tetraparetic/plegic patient?

A

walk using a secure and supportive chest harness/sling/rear harness
may require a hoist/multiple people
cover all 4 paws

184
Q

which spinal surgery carries a higher risk of seroma?

A

hemilaminectomy - more skin movement, separation of layers of tissue and over the midline

185
Q

how is cold therapy useful post-surgery?

A

provides analgesia and decreases inflammation

186
Q

how long should cold therapy be given post-surgery?

A

15 mins 4x daily for 48-72 hours

187
Q

how can you prevent patient interference with surgical wounds?

A

primapore dressing

188
Q

why might self-mutilation happen in neuro patients?

A

can occur in deep pain negative animals due to paraesthesia, boredom or stress

189
Q

how can self mutilation be prevented?

A

use a buster collar if a patient starts to like/bite at any part of their body
look for any triggers such as a sore

190
Q

what is physiotherapy useful for post neuro surgery?

A

can help keep joints and muscles mobile as well as retrain limbs to move correctly as mobility improves

191
Q

why do physiotherapy?

A

promote recovery

prevent further complications

192
Q

how much physiotherapy is involved in recovery from acute spinal cord damage?

A

aggressive therapy 1-2 weeks after trauma

193
Q

how much physiotherapy is involved in recovery from chronic spinal cord damage?

A

low impact, low intensity long-term therapy to preserve neuromuscular function

194
Q

how can physiotherapy help with degenerative myelopathy?

A

can lead to longer survival times

195
Q

what are the benefits of physiotherapy?

A 
pain management 
improved range of motion 
reduce muscle contraction and tension 
stimulate the nVS 
improve blood perfusion 
improve cardiorespiratory capacity 
encourage relearning of motor patterns 
weight management
196
Q

how can we make sure patients are safe to undergo physiotherapy?

A

patients should be clinically stable before commencing therapy - critical surgical and medical needs should have been addressed

197
Q

how should we handle/move dogs during physiotherapy?

A

encourage natural movement
short, regular sessions
take it slow
keep spine in line (vital!)

198
Q

which patient factors will affect rehabilitation therapy program design?

A 
patient size 
temperament 
degree of disability 
location of incision(s) 
IV/urinary catheterisation 
bandages and external coaptation 
comorbidities
199
Q

which client factors will affect rehabilitation therapy program design?

A

physical abilities
financial resources
schedule and household restrictions
emotional needs and concern

200
Q

which facility factors will affect rehabilitation therapy program design?

A 
size and indoor/outdoor exercise space 
availability of lift equipment 
appropriate modalities 
facility hours 
adequate bedding and housing
201
Q

which staff factors will affect rehabilitation therapy program design?

A

availability of sufficient support staff
proper training and experience
physical ability to lift and transport patients
access to specialists

202
Q

what different components are involved in physiotherapy?

A

massage

passive range of motion (PROM)

assisted exercises

proprioceptive exercises

neuromuscular electrical stimulation

203
Q

what are the 4 types of physiotherapy massage?

A

effleurage
petrissage
percussion
vibration

204
Q

what is effleurage massage?

A

gentle contact with palm of hand - stroke towards the heart

can be used all over body

205
Q

what is petrissage massage?

A

therapist rolls, squeezes, compresses and kneads the skin and muscles to increase circulation

206
Q

what is percussion massage?

A

gentle tapping o the skin with pam or side of hand - increases blood supply and aids relaxation of the muscle

207
Q

what is vibration massage?

A

limbs are gently shaken to stimulate the whole limb

good for relaxation at the end of the massage session

208
Q

what is coupage?

A

a technique which loosens secretions and assist in airway clearance by coughing
firm cupped hands on chest - caudal to cranial

209
Q

when might we perform coupage?

A

important in recumbent patients and those suffering from pulmonary disease/aspiration pneumonia

210
Q

what is passive range of motion?

A

joint mobilisation and stretching

external forces applied to the limbs/axial skeleton - flexion/extension (normal ROM) and monitor for pain

211
Q

how often should PROM be performed?

A

3-4 times daily for 10 mins

212
Q

how should PROM be performed?

A

begin at toes and move up limbs
care with hips and shoulders
consider comorbidities (anything that may affect ROM)

213
Q

what assisted exercises can be performed as part of physiotherapy?

A

assisted standing/walking
assisted sit
three-legged standing
weight-shifting

214
Q

what proprioceptive exercises help with sensation and awareness of limbs?

A 
standing 
wobble boards 
uneven surfaces 
over poles 
weaving 
different surfaces
215
Q

why perform active exercises as part of physiotherapy?

A

improve strength

promote independence with functional activities (off lead, normal walking etc)

216
Q

what types of active exercise can be done?

A 
lead exercise - slowly and increasing gradually 
add in steps/stairs/ramps 
figure of 8, circles 
encourage sitting and then standing 
pole walking, weight shifting 
move head/neck with treats/food balls 
hydrotherapy
217
Q

which patients cannot do pool hydrotherapy?

A

ventral slot patients due to swimming position

patients in early stages of recovery

218
Q

what is e-stim?

A

neuromuscular electrical nerve stimulation applied to skeletal muscle to stimulate contraction

219
Q

how is NMES delivered? what does it do?

A

percutaneously

increases tissue perfusion and can help to slow neurogenic muscle atrophy

220
Q

what are the benefits of e-stim?

A 
increases muscle strength, ROM and muscle tone 
enhances function 
pain control (some) 
oedema reduction 
reduces muscle spasm
221
Q

how does e-stim generate effective muscle contractions?

A

1 electrode placed near motor point of muscle and other placed along the muscle body
check for muscle contraction

222
Q

how often should e-stim be used?

A

10-20 mins daily (depends on patient tolerance)

223
Q

what is the procedure for applying the e-stim?

A 
clip hair 
clean with spirit 
apply conducting gel 
place electrode on top of gel 
set contraction/rest cycle

CVNT2 (47 decks)

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