Neurology Flashcards
1
Q
How can we classify seizures depending on their length?
A
Isolated = lasting less than 5 minutes
Cluster = 2 or more within a 24hr period, complete recovery in-between
Status epilepticus = lasting longer than 5 minutes/2 without complete recovery in-between
2
Q
What are the two types of seizure?
A
Partial/focal - simple/complex
Generalised (tonic/clonic)
3
Q
Describe partial/focal seizures.
A
Asymmetric, one part of brain affected Facial twitching Hypersalivation Behavioural changes Consciousness maintained Simple = no change in mentation / complex = change in mentation seen
4
Q
Describe generalised (tonic/clonic) seizures.
A
Bilateral cerebral hemisphere involvement
Autonomic signs
Loss of consciousness
Pre-ictal, ictal and post-ictal phases
5
Q
Describe the three phases of a seizure.
A
Pre-ictal (minutes) = behaviour changes, altered mentation, attention-seeking behaviour
Ictal (less than 5 mins) = loss of consciousness, muscle contraction, urination/defecation
Post-ictal (minutes to days) = abnormal neurological signs
6
Q
What are the extracranial causes of a seizure?
A
Toxins
Metabolic - portosystemic shunt, hypoglycaemia, hypocalcaemia
7
Q
Give some examples of toxins that may cause a seizure.
A
Methaldehyde (slug bait) Ethylene glycol (antifreeze) Permethrin in cats Organophosphates/carbamates (pesticides) Ivermectins in collie breeds Human drugs
8
Q
What are the intracranial causes of a seizure?
A
Structural - brain tumour, inflammation, hydrocephalus
Functional - idiopathic epilepsy
9
Q
Describe idiopathic epilepsy.
A
Most common cause of seizures
Commonly animals between 6 months and 6 years
Recurrent seizures
Normal inter-ictal exam/metabolic investigation/MRI scan of brain/CSF
10
Q
How can we begin to diagnose the cause of seizures?
A
Detailed history
Blood tests - haem/biochem, fasted blood glucose, pre-and post-prandial bile acids
MRI scan - gadolinium contrast used
CSF analysis
Videos from owner
Monitoring and recording
Retinal exam and BP measurement (if possible)
11
Q
What other disorders can look like seizures?
A
Narcolepsy/cataplexy Fly-catching syndrome Movement disorder Syncope 3rd degree AV block Canine epileptoid cramping syndrome Peripheral vestibular disease
12
Q
What emergency management can we provide for seizure patients?
A
Provide oxygen therapy
Place IV catheter if possible
Admin diazepam IV/rectally/intranasally
Assess circulation and temp.
Intubate if required to maintain patent airway
Active cooling if hyperthermic
Give mannitol slowly IV if seizure activity lasts more than 15 mins/if there is any reason to suspect cerebral oedema
Collecting full bloods - glucose/electrolyte/calcium levels
13
Q
How do we carry out phone triage for seizure patients?
A
Stay calm and reassure owner Any known history of seizures? Any known toxin exposure? Any known head trauma? How long has patient been seizuring for? How many seizures has patient had? Is patient conscious and responsive? Any urination/defecation? Advise to travel when safe to do so (after end of seizure!)
14
Q
What hospitalisation considerations should we have for seizure patients?
A
Area of ward with less noise
Lights dimmed as much as possible
Bottom kennel
Seizure plan on kennel with doses calculated
Seizure pack with medication drawn up
Sign on door to limit staff numbers/traffic
15
Q
What should we do if a patient seizures?
A
Stay calm! Note the time Call the clinician in charge for help Remove any dangers Dim the lights Reduce noise Limit handling Monitor vital signs Follow seizure plan (if one in place) DO NOT put hands in patient's mouth!
16
Q
What should we do when a seizure patient arrives from home?
A
Reassure the owner Triage - airway, breathing, circulation Oxygen therapy IV access Anticonvulsants Check temperature Active cooling (if required) Mannitol? CRI? Intubation?
17
Q
What are our aims for recurrent seizure patients?
A
Improve quality of life for owner and patient Reduce seizure frequency Reduce severity Acceptable side effects Acceptable costs
18
Q
What medications can we use to manage seizure patients?
A
Phenobarbital Potassium bromide Levetiracetam Imepitoin Gabapentin Diazepam Zonisimide
19
Q
What home care considerations should we make the owner aware of?
A
Family situation - work patterns, children, admin of medication
Financial situation - lifelong meds, repeats bloods/visits
Type of property
Communication
20
Q
Describe polyradiculoneuritis.
A
Immune-mediated disease
Affects the myelin and/or axons (axonopathy)
Most common peripheral neuropathy in dogs
21
Q
How do polyradiculoneuritis patients present?
A
Short-strided gait that progresses to tetraparesis
Ambulatory or non-ambulatory
Dysphonia present to varying degrees
Autonomic function remains
Once signs stabilise, recovery within 1-4 months
Clinical signs can vary between patients
22
Q
How do we diagnose polyradiculoneuritis?
A
Accurate patient history
Physical and neurological exam
Electrodiagnostic testing - EMG, NCV
Muscle and nerve biopsies
23
Q
How can we treat polyradiculoneuritis?
A
Intensive nursing care and physiotherapy
Medical treatment with corticosteroids shown to have little/no effect
24
Q
Describe myasthenia gravis.
A
Disease of neuromuscular transmission, affecting the NMJ (junctionopathy)
Congenital or acquired
Autoantibodies act on ACh receptor and alter function
Reduction in number of functional receptors
Muscles are unable to contract normally
25
How do myasthenia gravis patients present?
Muscle weakness and fatigue
Usually more obvious when patient is exercising
Focal / generalised / acute fulminating
Regurgitation commonly seen due to oesophageal dilation/weakness
26
How do we diagnose myasthenia gravis?
Presumptive based on history and presentation
Thoracic radiographs - megaoesophagus
Electrodiagnostics not usually specific
Edrophonium/tensilon test (patient injected with drug IV, able to walk normally within seconds)
27
How do we treat myasthenia gravis patients?
Anticholinesterase therapy e.g. pyridostigmine/neostigmine bromide
Side effects = GI signs, excessive salivation, lacrimation
Corticosteroids at immunosuppressive doses can be used alongside
BUT care taken as increase in weakness increases risk of aspiration pneumonia
Intensive nursing care and support
28
Describe polymyositis.
Immune-mediated inflammatory myopathy
Infiltration of inflammatory cells into the skeletal muscle
Idiopathic but can be associated with systemic disease
Focal / diffuse
29
How do polymyositis patients present?
Most common is exercise intolerance and stiffened gait
Other signs = muscle weakness, muscle atrophy, dysphonia, dysphagia and regurgitation
Signs often wax and wane in initial period
30
How do we diagnose polymyositis?
```
Criteria not well defined - diagnosis of exclusion
Clinical history
Biochemistry
Electrodiagnostic testing
Muscle biopsy
```
31
How can we treat polymyositis?
Corticosteroids at immunosuppressive doses
Intensive nursing care and support very important
Azathioprine can be used alongside steroids if patients cannot tolerate their side effects
32
What are the clinical signs of aspiration pneumonia?
Coughing
Tachypnoea
Harsh lung sounds/crackles on auscultation
33
How can we treat aspiration pneumonia?
```
Careful and close monitoring of patients
Early admin of antibiotics
IV fluids
Oxygen therapy
Supportive care - respiratory physiotherapy?
Walking/turning patients very important
Feeding balls of food from height
Severe cases may need mechanical ventilation
```
34
What are the 4 stages of pressure sores?
Stage 1 = lightly pigmented skin
Stage 2 = broken skin
Stage 3 = deeper wound through fat layer
Stage 4 = can be deep to the bone, necrotic
35
How can we prevent pressure sores?
```
Thick padded bedding
Turning every 2-4hrs
Donut bandage
Porous bedding
Incontinence pads
Non-slippery floors
Physiotherapy
Monitoring patients closely
Checklists
Expressing/catheterising bladder
```
36
How can we treat pressure sores?
Patients with myasthenia prone to developing sores
Bandages and commercial boots useful
Debride if necessary and use antibiotics if suspected infection
Prevention is better than cure!
37
What is muscle contracture?
Recumbency and immobilisation leads to: adaptive shortening of muscle / soft tissues, inelasticity of soft tissues
38
How can we treat muscle contracture?
Intensive physiotherapy - massage, passive range of motion, proprioceptive exercises, neuromuscular stimulator
39
What considerations should we have for any treatments?
```
Temperament
Client expectations
Client limits
Disease process
Previous injuries/surgeries
Other medical conditions
```
40
When and why should we carry out a neurological exam?
```
When = seizures, behaviour changes, gait abnormalities, change in posture/positioning
Why = identify if nervous system involvement, identify specific location/localisation, aid diagnosis and prognosis, continuous assessment of condition
```
41
What does upper motor neuron damage look like?
Loss of motor function, paresis/paralysis, normal/increased reflexes, increased extensor muscle tone, chronic muscle atrophy
42
What does lower motor neuron damage look like?
Flaccid paresis/paralysis, reduced/absent reflexes, reduced/absent muscle tone, muscle atrophy
43
What do we check in a neurological examination?
```
Mentation
Gait and posture
Cranial nerves
Postural reactions
Spinal reflexes
Sensory evaluation
Palpation
```
44
List some definitions relating to gait abnormalities.
```
Ataxia = uncoordinated gait
Paresis/paretic = weakness, decreased voluntary movement
Paralysis/plegic = no voluntary movement
```
```
Mono = one limb affected
Hemi = both limbs on one side affected
Para = both pelvic limbs affected
Quadra/tetra = all four limbs affected
```
45
List some abnormal postures and define them.
Head tilt = one ear is below the other
Head turn = nose is turned towards the body
Ventroflexion of the neck = low head carriage
Decerebrate rigidity = extension of all limbs, head and neck
Decerebellate rigidity = extension of the thoracic limbs, head and neck
Wide-based stance
46
In what three ways can the spine curve?
```
Laterally = scoliosis
Ventrally = lordosis
Dorsally = kyphosis
```
47
What postural reactions tests can we perform?
```
Proprioceptive positioning (paw placement)
Hopping
Visual placing
Tactile placement
Hemi-walking
Wheelbarrowing
```
48
What spinal reflexes can we test in the thoracic limbs?
Withdrawal reflex
Extensor carpi radialis reflex
Biceps brachii and triceps reflex
49
What spinal reflexes can we test in the pelvic limbs?
Withdrawal reflex
Patella reflex
Cranial tibial and gastrocnemius
50
What other spinal reflexes can we test?
```
Perineal reflex
Panniculus reflex (pinching back muscles)
```
51
What are the causes of acute spinal injury?
Intervertebral Disc Disease (IVDD)
Trauma - fracture/luxation
Infarction (fibrocartilaginous embolism FCE)
52
What are the causes of chronic spinal injury?
Degenerative disc disease
Degenerative myelopathy
Cervical Stenotic Myelopathy (Wobblers)
53
What are the other causes of spinal injury?
```
Atlanto-axial subluxation
Vertebral abnormalities
Neoplasia
Inflammatory disease
Discospondylitis
```
54
What diagnostics can we run for spinal injury?
Radiographs / CT / MRI (gold standard)
| Possibly CSF tap (cisternal/lumbar)
55
How can we treat spinal injury patients?
```
6 weeks of strict cage rest
Physiotherapy
Anti-inflammatory drugs
Analgesia
Steroid therapy
```
56
What surgical procedures can we carry out on spinal injury patients?
Hemilaminectomy
Ventral slot
Dorsal laminectomy
Spinal stabilisation/fixation
57
How does the bladder function with upper motor neuron damage?
```
Increased urethral resistance
Detrusor and urethral sphincter can contract at the same time
Not able to control bladder function
Urinary retention
Kidney damage possible
Difficult to manually express
Requires catheterisation
Intermittent 'squirting'
```
58
How does the bladder function with lower motor neuron damage?
```
Flaccid bladder
Does not contract spontaneously
Continues to fill
Resulting in 'overflow' - leaking of urine
Bladder muscle is overstretched
Easy to manually express
```
59
What nursing considerations should we have for spinal injury patients?
```
Long-term patients
Holistic care
Enrichment
Nutrition
Turning / physiotherapy
Temp. control
Padded bedding
Excretion management
Grooming
Hygiene
```
60
Define intracranial pressure (ICP).
Exerted between skull and intracranial tissues
| Normal = 5-10 mmHg
61
What are the consequences of intracranial hypertension (ICH)?
Reduced cerebral perfusion pressure (CPP)
| Reduced blood flow and secondary changes
62
What is the Cushing's reflex?
Triggered by severe, acute increase in ICP
Rise in MAP and reflex bradycardia
Sign of potentially life-threatening increase in ICP and should be treated immediately
63
What are the possible causes of intracranial disease?
Trauma e.g. RTA, horse kick
Inflammatory (meningoencephalitis of unknown origin MUO)
Infectious e.g. viral, protozoal, fungal, bacterial
Neoplastic e.g. meningioma, glioma, choroid plexus tumour
Toxins e.g. lead, ivermectin
Seizures
Anomalous e.g. hydrocephalus
64
What are the four types of mentation assessed for in intracranial disease patients?
```
Alert = normal response to surroundings
Obtunded = awake but less responsive, will sleep if left
Stuporous = only responds to noxious/painful stimuli
Coma = unconscious, unresponsive to any stimuli
```
65
What mentation signs might an intracranial disease patient show?
```
Circling
Head pressing
Pacing
Head tilt
Head turn
```
66
What cranial nerve reflexes can we assess in intracranial disease patients?
```
Menace response
Palpebral reflex
Puppilar light reflex
Gag reflex
Oculocephalic reflex
Nystagmus
```
67
What are some definitions relating to pupil size?
```
Miosis/miotic = constricted
Mydriasis/mydriatic = dilated
Anisocoria = asymmetric
```
68
What are some clinical signs of intracranial disease?
```
Circling
Ataxia
Blindness
Altered mentation
Loss of consciousness, coma
Seizures
Head tilt/turn
Cheyne-Stokes/apneustic/ataxic respiration
Loss of gag reflex
Strabismus/nystagmus/lack of physiological nystagmus
Non-responsive pupils
Decerebrate/decerebellate posture
```
69
Describe the Glasgow coma score.
Three domains = motor activity, brainstem reflexes, level of consciousness
Each domain has a score 1-6
Final score ranges from 3-18
Lower score = more severe neurological deficits = graver prognosis
70
How can we treat raised intracranial pressure?
```
Mannitol infusion - reduces cerebral oedema, increases CPP and CBF
Hypertonic saline therapy
Sedatives/analgesia
Anaesthesia
Mechanical ventilation
Constant rate infusion
```
71
What nursing care can we provide for raised intracranial pressure patients?
Recumbency - turning/padding/physiotherapy/excretions
Elevate cranial part of body 30-40 degrees, no jugular sampling
Ocular care
Mouth checks - 4-6hrs, saliva/excretion build-up, monitor coughing
Nutritional support - if conscious feed in sternal every 4-6hrs, feeding tube
Anaesthetic monitoring
72
What causes hydrocephalus?
Excessive accumulation of CSF within the ventricular system
| Caused by: obstruction to CSF outflow / decreased absorption of CSF / increased production of CSF
73
Describe the difference between congenital and acquired hydrocephalus.
```
Congenital = usually present at birth, specific breed dispositions (e.g. chihuahuas)
Acquired = tumour, inflammation, haemorrhage
```
74
What are the clinical signs of hydrocephalus?
```
Behavioural changes
Slowness in learning
Loss of coordination
Visual deficits
Seizures
Circling
Depressed/obtunded mentation
Enlarged and dome-shaped skull
```
75
How can we medically manage hydrocephalus?
Aim to reduce production of CSF
| E.g. prednisolone, frusemide, omeprazole
76
How can we surgically manage hydrocephalus?
Divert CSF to another location
Ventriculoperitoneal (VP) shunt
Tubing placed from ventricle to peritoneal cavity
Can get complications
77
What is the prognosis for hydrocephalus patients?
Depended on cause and severity of signs
Infectious cause = good prognosis with treatment for underlying infection and removal of CSF build-up
Obstructive cause (from tumour) = guarded prognosis
Treatment with VP shunt can provide a good prognosis
78
Describe meningoencephalitis of unknown origin (MUO).
Inflammatory disorder of CNS, non-infectious
Three types, only distinct at cellular level - granulomatous (GME), necrotising (NME), necrotising leukoencephalitis (NLE)
All termed MUO as not possible to determine which in a live patient
Brain and spinal cord changes
Autoimmune disease
79
What are the clinical signs of MUO?
More commonly small dogs, females, >6 months of age
| Neurological signs e.g. seizures, muscle tremors, blindness, head tilt, altered balance/posture, circling
80
How can we diagnose MUO?
Clinical examination
Blood tests
MRI of brain
CSF analysis (inflammatory signs)
81
How can we manage MUO?
Immunosuppressive drugs e.g. steroids, cyclosporine, azathioprine, cytarabine
Antiepileptics
Nursing care
82
What is the prognosis for an MUO patient?
Variable
Seizures = poorer prognosis
Focal lesions better prognosis than multifocal lesions
If patients show improvement within 3 months, good prognosis
Patients can relapse and present with clinical signs again
83
How should we set up a kennel for a neurological patient?
Thick bedding e.g. duvet/mattress
Layer bedding with incontinence pads
Vet bed as top layer to wick away urine
Pad out sides of kennel with pillows
84
In what three ways can we manage urinary incontinence?
Manual expression
Intermittent catheterisation
Indwelling catheterisation
85
What are the concerns with overflow incontinence?
Urine leaking onto skin causes urine scalding
| Continuously full bladder risks urinary tract infections
86
How do we use our techniques to manage urinary incontinence?
Manually express every q6-8hrs
Pass urinary catheter BID initially as has risk of iatrogenic trauma
Empty indwelling catheter 3-4 times daily
87
What signs of urinary tract infection can we monitor urine for?
Smell, colour and turbidity
88
How can we manage faecally incontinent patients?
Check beds regularly
Keep patient clean/dry at all times
Regular bathing but pat skin dry to reduce trauma
Check skin daily and apply topicals if necessary (under direction of VS)
89
How can we prevent decubital ulcers forming on recumbent patients?
Turn every 4hrs minimum, more often for bony breeds
Deep, padded bedding - checked regularly
Keep patient clean and dry, reduce trauma from regular bathing
Donut bandages on elbows/hocks
Prop up with pillows
90
How can we exercise a paretic/plegic patient?
Walk using sling/harness
Cover hind paws to prevent trauma to toes/claws
Keep patient's back in a natural position when walking
Allow normal behaviour e.g. sniffing, urinating/defecating
91
How can we exercise tetraparetic/plegic patients?
Walk using secure and supportive chest harness/sling/rear harness
May need a hoist or multiple people for larger dogs
Allow normal behaviour - likely to be continent
92
What wounds will spinal surgery patients have?
Ventral slot = under neck (less complications)
| Hemilaminectomy = on back (risk of seroma due to skin movement, separation of layers of tissue and over midline)
93
How and why do we use cold therapy post-surgery?
Provides analgesia, decreases inflammation
15mins 4x daily for 48-72hrs
ALWAYS wrap in a towel, do not put directly on skin
94
Why might a patient self-mutilate?
Deep pain negative - paraesthesia, boredom, stress
95
What are the benefits of physiotherapy?
```
Pain management
Improve range of motion
Reduce muscle contraction and tension
Stimulate the nervous system
Improve blood perfusion
Improve cardiorespiratory capacity
Encourage relearning of motor patterns
Weight management
```
96
How can nurses help in physiotherapy?
Full workup with VS
Discussion and plan made with VS
Recording changes - positive/negative
97
How and when can we carry out physiotherapy?
Encourage natural movement
Short regular sessions, take it slow
Keep spine in line
Opportunities e.g. grooming, bathing, massage, when turning/feeding, going outside
98
What considerations should we have before beginning physiotherapy?
Patient previous and current ailments
Normal activities
Owner's desired and anticipated expectations
Owner's ability to provide time and expertise
99
What physiotherapy can we do?
```
Massage
Passive range of motion (PROM)
Assisted exercises
Active exercises
Proprioceptive exercises
Neuromuscular electrical stimulation
```
100
Describe the four massage techniques.
```
Effleurage = gentle contact with palm of hand, stroke towards heart, can be used all over body
Petrissage = therapist rolls/squeezes/compresses/kneads skin and muscles to increase circulation
Percussion = gentle tapping of skin with palm/side of hand, increases blood supply and aids relaxation of muscle
Vibration = limbs gently shaken to stimulate whole limb, good for relaxation at end of massage session
```
101
What is coupage?
Respiratory physiotherapy
| Loosens secretions and assists in airway clearance by coughing
102
How do we carry out passive range of motion exercises?
External forces applied to limbs/axial skeleton - flexion and extension
Monitor for pain
3-4 times daily for 10mins
103
What assisted exercises can we do?
Assisted standing/walking
Assisted sit-stand
Three-legged standing
Weight-shifting
104
What proprioceptive exercises can we do?
```
Standing
Wobble board
Uneven surfaces
Over poles
Weaving
Different surfaces
```
105
What active exercises can we do?
```
Figure of 8, circles
Encourage sitting and then standing
Pole walking, weight shifting
Move head/neck with treats
Add in steps, stairs, ramps
Hydrotherapy - underwater treadmill/pool
```
106
Describe E-stim.
Neuromuscular electrical nerve stimulation (NMES)
Applied to skeletal muscle
Stimulates muscle contraction
Delivered percutaneously
Increases tissue perfusion and can help to slow neurogenic muscle atrophy
107
What are the benefits of E-stim?
```
Increased muscle strength / ROM
Improved muscle tone
Enhanced function
Pain control
Oedema reduction
Reduced muscle spasm
```
108
How do we carry out E-stim?
Clip hair, clean with alcohol, apply conducting gel
1 electrode placed near motor point of muscle
Other electrode placed along muscle body
Check for muscle contraction
Contraction/rest cycles, 1:2 or 1:5
10-20 mins daily
