Seizures Flashcards
What is syncope?
Loss of consciousness due to a sudden decrease in cerebral blood flow
- Majority of patient seen in first seizure clinics are there due to hypoxic seizure
- Syncope is often followed by syncopal/ hypoxic seizure
Types of syncope
1. Reflex/ vasovagal syncope: most common form in the young, occurs in response to overstimulation of vagus nerve which slows down the heart
Triggers: prolonges standing, rising, emotional trauma, pain
Features: gradual onset, light-headedness, nausea, sweating, palpitations, greying of vision, feeling distant, cold skin, pallor, rapid recovery with no confusion
2. Orthostatic syncope: common in older age, medications, autonomic neuropathy, autonomic failure
Features: occurs upon standing or changing posture, rising, after meals
3. Carotid sinus syncope: hypersensitivity of the carotid sinus, attributable to pressure on the neck
4. Reflex anoxic attacks: occurs in children, excessive activity of the vagus nerve briefly stops the heart, triggered by pain, fear, anxiety
5. Cardiac syncope: often occurs with no prodrome and in any posture
Tachyarrhythmia: ineffective CO leading to syncope
Bradyarrhythmia: heart block, sick sinus syndrome
Structural heart disease: aortic stenosis, HOCM, mitral stenosis, atrial myxoma, ischaemic heart disease
6. Respiratory syncope: cough syncope, valsalva manoeuvre, breath holding spells, hyperventilation
7. CNS syncope: rare, raised ICP, autonomic dysreflexia
Behavioural causes of syncope
Hyperventilation
Psychogenic, non-epileptic attacks
Seizure vs syncope
What is juvenile myoclonic epilepsy?
Usually begins between 12-16yrs
Slightly more common in girls
Seizures often occur when patient is tired, as they wake up or when having breakfast
Key: patients with JME are more likely to have seizures when they don’t get enough sleep or when they drink excessive amounts of alcohol
What is West syndrome?
AKA infantile spasms
Affects 350-400 children in the UK per year
In 90% the spasms occur in the first year of life
Episodes last 1-2 seconds - looks like body is seizing, can occur in clusters
EEG shows hypsarrhythmia (chaotic, disorganised electrical activity with no pattern)
Can cause developmental delay
Patient: 7 months old, showeing abnormal spasms in clusters, EEG shows totally chaotic pattern (hypsarrhythmia), following spasms baby is off food and irritable
Diagnosis?
West syndrome
Treatment for West syndrome?
Steroids and AEDs (specifically vigabatrin which prevents GABA breakdown)
What is Dravet syndrome?
Rare form of epilepsy that beings within 1st year of life
Causes developmental delays and learning difficulties along with behavioural challenges
Seizures most often associated with high temperature and involve one side of the body
Seizure occur for a prolonged period of time
80% have a mutation in SCN1A
Dravet is drug resistant, some commonly used medications e.g. lamotrigene can cause an increase in seizure frequency
Dravet is the only form of epilepsy in which to use of 3 medications is beneficial
Prognosis is poor and children usually need supportive care throughout life
Epileptic seizure + learning difficulties + developmental delay
Diagnosis?
Dravet syndrome
What is Lennox Gastaut syndrome?
Childhood epilepsy syndrome
Usually begins between 3-5yrs
Causes ‘drop attacks’: atonic or tonic seizures where patient falls to floor suddenly (compared to puppet strings being cut in atonic and tree falling down in tonic)
Can also cause absence seizures
Causes learning difficulties
Treatment resistant - ketogenic diet may help
How can the age of onset give an idea of the cause of a seizure?
- 0-2yrs: birth trauma, congenital defects, familial epileptic syndrome/ channelopathy
- 2-12yrs: idiopathic generalised epilepsy, trauma, infections, accidental poisoning
- 12-30yrs: trauma, alcohol, toxins
- 50+yrs: trauma, alcohol, toxins, tumours
- 70yrs+: dementia
What is status epilepticus?
State of prolonged, uncontrolled seizures
A single seizure that lasts >5mins or multiple seizures without a full neurological recovery between seizures
Aetiology of status epilepticus
1/3 of patients will have an underlying background of chronic epilepsy and SE occurs most commonly due to treatment non-compliance
1/3 patients: SE wwill represent the onset of epilepsy
1.3 patients: episode occurs in isolation with no prior or future seizures
Investigations in status epilepticus
All patients presenting to ED should have an IV cannula inserted and blood sent for U&E, magnesium, calcium and a FBC
Blood gas for determining metabolic status
Further investigations will then depend on individual circumstances e.g. CT brain, blood cultures, serum anticonvulsant levels, lumbar puncture etc
Management of status epilepticus overview
Medical emergency, requires urgent aggressive therapy to limit long term damage
Early initiation of anti-convulsants - the longer time spent in SE the worse the outcome
CHECK BLOOD GLUCOSE
Pre hospital: benzos
Hospital: benzons, phenytoin (has a delayed onset so use alongside benzo), IV sodium bicarbonate for patients in SE with a profound metabolic acidosis
Investigations following a seizure
- History is important because you wont see the person having a seizure
- Bloods: metabolic derangements
- EEG: often only as good as the timing of the test, frequent false negatives. Different types, standard awake and asleep EEG, ambulatory EEG (monitored for 1-3 days), video EEG telemetry, cortical mapping (for when surgery is planned to treat focal epilepsy)
- ECG: to rule out arrhythmia which can trigger syncope and trigger epilepsy
- Brain imaging: always required in focal onset epilepsy. CT/ MRI - MRI more sensitive than CT
Drug treatment in epilepsy overview
Key questions to ask when considering starting a patient on medication for epilepsy: was the definitely an epileptic seizure? Is there an underlying structural cause e.g. stroke or tumour, is there focal active epileptiform activity on EEG, what is the patients choice?
Often a process of trial and error
Options:
- Na+ channel blockers e.g. phenytoin and carbamazepine
- K+ channel blockers retigabine
- Calcium channel blokcers
- GABA receptor agonists e.g. benzos
- Glutamate receptor antagonists e.g. perampanel
*Monotherapy is ideal, never use polytherapy at onset*
Seizure triggers
Lack of sleep, psychological and emotional distress, other medications, metabolic derangement, hormonal changes, alcohol and drugs
What is a vagal nerve stimulator?
Like a pace maker near the vagus nerve, sends regular impulses to the brain in an effort to calm down the irregular electrical brain activity
Unlikely to stop seizures but can reduce frequency and duration
Addressing seizures in known epileptics
- Any change in normal seizure pattern?
- Any cause of poor seizure control e.g. non-compliance, ilness, infection, alcohol, drugs
- Examine to look for injuries associated with seizure
Check obs, blood glucose and anti-convulsant levels if suspecting toxicity or non compliance
Refer patient to medical team if the patient has had a significant change in seizure pattern
Mortality in status epilepticus?
10%
Treatment steps for status epilepticus
- A-E (NP airway may help)
- Monitor obs
- Obtain IV access and assess blood glucose
- Give IV lorazepam into large vein OR buccal midazolam/ rectal diazepam if no IV access
- If suspecting alcohol use or malnutrition give pabrinex (IV thiamine)
- Search for injuries
If seizures continue despite therapy, call ICU and consider using phenytoin (rember to monitor ECG because it can cause widened WRS and dysrhythmias)
RSI after 30mins + tracheal intubation whilst continuing anticonvulsants
