Neurology Flashcards
How can we classify seizures depending on their length?
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
What are the two types of seizure?
Partial/focal - simple/complex
Generalised (tonic/clonic)
Describe partial/focal seizures.
Asymmetric, one part of brain affected Facial twitching Hypersalivation Behavioural changes Consciousness maintained Simple = no change in mentation / complex = change in mentation seen
Describe generalised (tonic/clonic) seizures.
Bilateral cerebral hemisphere involvement
Autonomic signs
Loss of consciousness
Pre-ictal, ictal and post-ictal phases
Describe the three phases of a seizure.
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
What are the extracranial causes of a seizure?
Toxins
Metabolic - portosystemic shunt, hypoglycaemia, hypocalcaemia
Give some examples of toxins that may cause a seizure.
Methaldehyde (slug bait) Ethylene glycol (antifreeze) Permethrin in cats Organophosphates/carbamates (pesticides) Ivermectins in collie breeds Human drugs
What are the intracranial causes of a seizure?
Structural - brain tumour, inflammation, hydrocephalus
Functional - idiopathic epilepsy
Describe idiopathic epilepsy.
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
How can we begin to diagnose the cause of seizures?
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)
What other disorders can look like seizures?
Narcolepsy/cataplexy Fly-catching syndrome Movement disorder Syncope 3rd degree AV block Canine epileptoid cramping syndrome Peripheral vestibular disease
What emergency management can we provide for seizure patients?
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
How do we carry out phone triage for seizure patients?
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!)
What hospitalisation considerations should we have for seizure patients?
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
What should we do if a patient seizures?
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!
What should we do when a seizure patient arrives from home?
Reassure the owner Triage - airway, breathing, circulation Oxygen therapy IV access Anticonvulsants Check temperature Active cooling (if required) Mannitol? CRI? Intubation?
What are our aims for recurrent seizure patients?
Improve quality of life for owner and patient Reduce seizure frequency Reduce severity Acceptable side effects Acceptable costs
What medications can we use to manage seizure patients?
Phenobarbital Potassium bromide Levetiracetam Imepitoin Gabapentin Diazepam Zonisimide
What home care considerations should we make the owner aware of?
Family situation - work patterns, children, admin of medication
Financial situation - lifelong meds, repeats bloods/visits
Type of property
Communication
Describe polyradiculoneuritis.
Immune-mediated disease
Affects the myelin and/or axons (axonopathy)
Most common peripheral neuropathy in dogs
How do polyradiculoneuritis patients present?
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
How do we diagnose polyradiculoneuritis?
Accurate patient history
Physical and neurological exam
Electrodiagnostic testing - EMG, NCV
Muscle and nerve biopsies
How can we treat polyradiculoneuritis?
Intensive nursing care and physiotherapy
Medical treatment with corticosteroids shown to have little/no effect
Describe myasthenia gravis.
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
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
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)
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
Describe polymyositis.
Immune-mediated inflammatory myopathy
Infiltration of inflammatory cells into the skeletal muscle
Idiopathic but can be associated with systemic disease
Focal / diffuse
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
How do we diagnose polymyositis?
Criteria not well defined - diagnosis of exclusion Clinical history Biochemistry Electrodiagnostic testing Muscle biopsy
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
What are the clinical signs of aspiration pneumonia?
Coughing
Tachypnoea
Harsh lung sounds/crackles on auscultation
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
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
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
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!
What is muscle contracture?
Recumbency and immobilisation leads to: adaptive shortening of muscle / soft tissues, inelasticity of soft tissues
How can we treat muscle contracture?
Intensive physiotherapy - massage, passive range of motion, proprioceptive exercises, neuromuscular stimulator
What considerations should we have for any treatments?
Temperament Client expectations Client limits Disease process Previous injuries/surgeries Other medical conditions
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
What does upper motor neuron damage look like?
Loss of motor function, paresis/paralysis, normal/increased reflexes, increased extensor muscle tone, chronic muscle atrophy
What does lower motor neuron damage look like?
Flaccid paresis/paralysis, reduced/absent reflexes, reduced/absent muscle tone, muscle atrophy
What do we check in a neurological examination?
Mentation Gait and posture Cranial nerves Postural reactions Spinal reflexes Sensory evaluation Palpation
