SEIZURES Flashcards
Common causes of blackouts?
Syncope
Panic attacks
Epilepsy
Blank spells/microsleeps
Non-epileptic attack disorder
Narcolepsy
Hyperrekplexia
Idiopathic drop attacks
Migraine without headache
TIAs
Transient global amnesia
Cerebrovascular disorders
POTS
What is syncope?
Loss of conciousness usually from a sudden decrease in cerebral blood flow
Most common cause of syncope?
Vasovagal syncope
Functions of vagus nerve?
Sensory: Innervates the skin of the external acoustic meatus and the internal surfaces of the laryngopharynx and larynx. Provides visceral sensation to the heart and abdominal viscera.
Special Sensory: Provides taste sensation to the epiglottis and root of the tongue.
Motor: Provides motor innervation to the majority of the muscles of the pharynx, soft palate and larynx.
Parasympathetic: Innervates the smooth muscle of the trachea, bronchi and gastro-intestinal tract and regulates heart rhythm. Its cardiac branches act to slow the rate of heartbeat; its bronchial branch acts to constrict the bronchi; and its esophageal branches control involuntary muscles in the esophagus, stomach, gallbladder, pancreas, and small intestine, stimulating peristalsis and gastrointestinal secretions
Pathophysiology of Vasovagal syncope
Overstimulation of the vagus nerve which slows the heart rate down = loose consciousness
May also affect bladder/bowel = incontinence
Typical triggers of Vasovagal syncope?
Prolonged standing
Rising suddenly
Emotional trauma
Pain
Sight of blood/something gory
Symptoms of Vasovagal syncope?
Gradual onset light headedness, nausea, sweating, palpitations, greying of vision, muffled hearing, feeling distant
Rapid recovery with no confusion
They look pale, cold skin, may have uncoordinated jerks
Who does orthostatic syncope occur in?
Olde people on multiple medications or those with autonomic neuropathy e.g. DM
Characteristics of orthostatic syncope?
Occurs with changes in posture, after rising or after a large meal
Characteristics of carotid sinus syncope?
Caused by hypersensitivity of the carotid sinus
Attributable to neck pressure e.g. tight collar, turning neck, shaving etc
What are reflex anoxic attacks?
Occur in children 6 months-3 years in response to increased vagal tone with brief asystole
Often occurs in response to pain or emotional stimuli
The child will go pale, fall to the floor and rapidly recover
Characteristics of cardiac syncope?
No prodrome
Occur in any posture
Can occur when awake or asleep, at rest or during exercise
Causes of cardiac syncope?
Tachycarrhythmias e.g, WPW syndrome, long QT syndrome
Bradyarrhthmias e.g. complete heart block, sick sinus syndrome, swallow syncope
Structural heart disease e.g. aortic stenosis, HOCM, mitral stenosis, atrial myxoma, IHD
Causes of respiratory syncope?
Cough syncope - stimulates Vargas nerve -> bradyarthhymia
Valsalva manoeuvre
Breath holding spells
Hyperventilation - drop in CO2 = vasoconstriction
Primary CNS causes of syncope?
Note these are rare!!
Raised ICP e.g. obstructive hydrocephalus, 3rd ventricular colloid cyst, chiari malformation
Autonomic dysreflexia e.g. intermittent massive hypertension
Diencephalic attacks e.g. post head injury or hypoxia
What are non-epileptic attack disorders?
Aka psychogenic nonepileptic seizures or pseudoseizures
These are dissociative phenomenon that often occur in people with LD, or those with a history of abuse and complex psychosocial problems
Sufferers often have other unexplained medical symptoms e.g. CFS or IBD
Note these are not malingering!!
Think of it like overwhelming stress causes the brain to reboot!
Characteristics of non-epileptic attack disorder?
Often occurs in company
Pt often reluctant to discuss symptoms
Attacks are variable and not stereotyped i.e. seizures are different each time
Might verbalise during attacks and show some awareness
Normal pupil size
Movements are flailing, arched back, pelvic thrusting
Eyeslids are clenched with resistance to eye opening
Rapid recovery
Often cry’s after the seizure
(Seems like a generalised convulsion die to whole body convulsions but there is no loss of consciousness, no post ictal state and pt can remember what happened)
What is transient global amnesia?
A temporary anterograde amnesia with an acute onset
Usually;y occurs in middle-aged or older activities
Often precipitated by strenuous activity, high-stress events or coitus
What is POTS syndrome?
Postural orthostatic tachycardia syndrome
Uncommon but diagnosis is often missed
Characterised by orthostatic tachycardia that can cause LOC - do a standing and sitting HR measurement
This does not cause hypotension!!
Seizure vs syncope features?
Trigger common in syncope e.g. standing, sight of blood
Prodrome in seizure is common with aura, dejavu. Prodrome in syncope is almost always present with nausea, sweating, palpitations, light headedness, visual greying, muffled hearing
Seizures are sudden but syncope is more gradual
Seizures last 1-2 minutes but syncope < 30 seconds
Both can cause convulsive jerks but likely to be very brief in syncope
Both commonly cause incontinence
Seizures often cause tongue biting but this is rare in syncope
Postictal recovery is much slower after a seizure and person will be confused
Seizures can happen at night whereas this is rare for syncope, unless its a cardiac cause
What is epilepsy?
A neurological disorder characterised by recurring seizures
At least 2 unprovoked seizures occurring >24 hours apart
OR
One unprovoked seizure and a probability of further seizures similar to the general recurrence risk after 2 unprovoked seizures over the next 10 years (>60%)
Epidemiology of epilepsy?
3% of general population
Note 8-10% of the genrral population will have one seizure in their lifetime
Incidence is higher in LIC
Highest risk is in childhood and people >50
People with LD have higher rates
About 2/3rds of patients achieve satisfactory seizure control with AEDs
Classification of seizures?
Focal vs generalised vs unknown
If its focal, is it focal aware or focal impaired awareness
Does seizure remain focal or does it evolve into a bilateral seizure?
Focal onset:
Motor onset vs non-motor onset seizures
Generalised onset:
Motor vs non-motor (i.e absence)
Frontal lobe epilepsy symptoms?
Brief
Hand and leg movements
Posturing
Eyes deviate away from side of brain
Jacksonian march
Explosive screams, profanities or laughter
Post-octal weakness
Tend to occur at night
Temporal lobe epilepsy symptoms?
Last about 1 minutes
Rising epigastric sensation or abdominal discomfort
Psychic or experimental phenomen e.g. Deja vu, jamais vu
Hallucinations - auditory, gustatory or olfactory
changes in emotions e.g. feelings of fear
Vertigo
Automatisms e.g. lip smacking, swallowing, grabbing, plucking
Dysphasia if from the language dominant side of the brain
Occipital lobe epilepsy symptoms?
Distortion of vision - floaters and flashers
Parietal lobe epilepsy symptoms?
Alteration of sensual sensation e.g. paraesthesia, pain
Types of motor generalised onset seizures?
Atonic
Tonic
Clonic
Tonic-clonic
Myoclonic
Epileptic spasms
Myoclonic-tonic-clonic
Types of non-motor generalised onset seizures?
Typical
Atypical
Myoclonic
Eyelid myoclonia
(These are all types of absence seizures)
Epilepsy syndromes?
Childhood absence epilepsy
Juvenile absence epilepsy
Juvenile myoclonic epilepsy
Generalised tonic-clonic epilepsy
Genetic generalised epilepsy
West syndrome
Dravet syndrome
Lennox gastaut
Lundborg syndrome
Benign Rolandic epilepsy
Juvenile myoclonic epilepsy?
typical onset is in the teenage years - more common in girls
features: infrequent generalized seizures, often in morning//following sleep deprivation
daytime absences, sudden, shock-like myoclonic seizure (these may develop before seizures)
treatment: usually good response to sodium valproate
Aetiology of epilepsy?
Most often idiopathic - 2/3rds of cases
Structural - stroke, trauma, malformation of cortical development
Genetic
Infectious e.e. TB, cerebral malaria, HIV, congenital infections
Metabolic e.g. porphyria, pyridoxine deficiency
Immune disorders e.g. anti-NMDA receptor encephalitis and anti-LG11 encephalitis
Channelopathies and genetic examples
Tuberous sclerosis
Neurofibromatoiss
Juvenile myoclonus epilepsy
Autosomal dominant nocturnal frontal lobe epilepsy
Dravet syndrome
Investigtaions for epilepsy?
History is most important
ECG
Bloods: full blood count, urea and electrolytes, liver function tests, glucose, and calcium.
Brain imaging - MRI best
EEG
Types of EEGs?
Standard awake and sleep EED
Ambulatory EEG
Video EED telemetry
Cortical mapping
Depth electrode EED
Triggers for seizures?
Lack of sleep
Psychological and emotional stress
Depression
Medications
Metabolic derangements - sodium, K+, Ca2+
Hormonal changes - worst around periods, on contraception, menopause
Alcohol
Recreational drugs
Stimulants e.g. caffeiene
Prn use of benzodiazepines
E.g. using short course around time of period
AED for generalised tonic-clonic seizures?
Males - Sodium valproate
Females - lamotrigine or levetiracetam
AED for absence seizures?
Ethosuximide
AED for focal seizures?
Levetiracetam or lamotrigine
Which AEDs can give rise to an allergic rash and Steven’s Johnson syndrome?
Phenytoin, lamotrigine, carbamazepine
Treatment options for epilepsy?
Drugs
Vagal nerve stimulation
Surgery - lobectomy, lesion surgery, gamma knife surgery, hemispherectomy, corpus callosotomy (very rarely done but can be done in children to prevent the generalisation of seizures??)
Deep brain stimulation
Ketogenic diet may be used in children to reduce the number of seizures
What is SUDEP?
Sudden Unexplained Death in Epilepsy
When a person with epilepsy dies suddenly without an identifiable cause
Most common cause of epilepsy-related death in young adults with uncontrolled epilepsy
Risk is reduced in people with optimised seizure control
What is convulsive status epilepticus?
A prolonged convulsive seizure lasting for 5 minuets or longer, or recurrent seizures 1 after the other without recovery in between
Risk factors for epilepsy?
Premature birth
Cerebral palsy
Complicated febrile seizures
Genetic conditions e.g. tuberous sclerosis or neurofibromatosis or mitochondrial diseases
Brain development malformations
FHx of epilepsy or neurologic illness
Head trauma
Infections e.g. meningitis or encephalitis
Brain tumours
Comorbid conditions e.g. CVD, strokes
Dementia and neurodegenerative disorders
Complications of epilepsy?
SUDEP
Injuries
Depression and anxiety
Absence from school and work
Prognosis of epilepsy?
In children and adults with epilepsy, 70% will be in remission but 30% will have ongoing seizures. Risk of recurrent seizures is highest in the first 12 months
In some people who remain seizure-free for >2 years, medication can be slowly withdrawn
What are predictive factors for epilepsy?
Frequency of seizures in the 6 months after first presentation
Response to AED treatment
The type of epilepsy syndrome - e.g. 80% of children with absence epilepsy will be in remission by adulthood
History for seizures?
Triggers - sleep deprivation, stress, light sensitivity, alcohol use
Aura -
During - muscle stiffening, jerking, urinary incontinence, tongue biting, behavioural arrest, loss of muscle tone, shock-like movements, LOC
Post-octal - drowsiness, headaches, amnesia, confusion
Physical exam for seizures?
Cardiac, neurological, mental state, developmental assessment
Assess oral mucosa to identify lateral tongue bites
Identify any injuries sustained
Investigtaions following a seizure?
12-lead ECG
Bloods - FBC, U&Es, LFTs, glucose, Ca2+
Toxicology screen
EEG
Head CT or MRI
What are focal seizures?
Previously termed partial seizures
They start in a specific area on 1 side of the brain and the level of awareness can vary; can be focal awareness, focal impaired awareness and awareness unknown
They are classified as motor, non-motor or having other features e.g. aura
What are generalised seizures?
Seizures that engage both sides of the brain at onset
Consciousness is lost immediately
Can be motor and non-motor
What are focal to bilateral seizures?
Previously termed secondary generalised seizures
When they start on 1 side of the brain in a specific area before spreading to both lobes
What are infantile spasms aka?
When do they begin?
What do they look like?
Aka wests syndrome
Brief spasms that begins in the first few months of life
Salaam attacks which last 1-2 seconds and repeat up to 50 times (flexion of head/trunk/limbs and extension of arms). May also have progressive mental handicap
What usually causes infantile spasms?
usually secondary to serious neurological abnormality (e.g. tuberous sclerosis, encephalitis, birth asphyxia) or may be idiopathic
absence seizures
What age do they usually occur?
What do they look like?
Most commonly 4-8 years
Usually a few-30 seconds with no warning the child will seem spaced out and not responsive. They recover quickly. There are often many in a day
Prognosis of absence seizures?
good prognosis: 90-95% become seizure free in adolescence
What is Lennox-gustaut syndrome?
What age is the usual onset?
How do they present?
May be an extension of infantile spasms
1-5 years
Causes different types of seizures e.g. atypical absences, tonic, Atonic and myoclonic. 90% will have moderate-severe mental handicap
Who does benign Rolandic epilepsy usually occur in?
How does it present?
In children. More common in males
Paraesthesia unilaterally on the face or inside the mouth on waking
Twitching can occur - mostly in the face
Drooling, hypersalivation, speech arrest
When does juvenile myoclonic epilepsy usually occur?
How does it present?
Teenage years, more common in girls
Causes infrequent generalised seizures in the morning or following sleep deprivation. May have daytime absences. May have sudden shock-like myoclonic seizures
Who do febrile convulsions typically occur in?
How common are they?
What causes them?
Children 6 months - 5 years
Around 3% of children will have at least 1 febrile convulsions in their lifetime
Usually they occur early in a viral infection as the temperature rises rapidly
When do alcohol withdrawal seizures tend to occur?
In pt with a history of alcohol excess who suddenly stop drinking -> 36 hours later
Pathophysiology of alcohol withdrawal seizures?
Chronic alcohol consumption enhances GAB-mediated inhibition in the CNS and inhibits NMDA-type glutamate receptors
Alcohol withdrawal is the opposite which means the enhanced GABAergic inhibition is suddenly decreased leading to a relative state of hyper excitability. On top of this the inhibition of NMDA receptors is stopped causes increased glutamate activity, an excitatory neurotransmitter
This leads to hyperexcitability
AED choice for myoclonic seizures?
Males - sodium valproate
Females - levetiracetam
AED choice for tonic or Atonic seizures?
Males - sodium valproate
Females - lamotrigine
Which AED can exacerbate absence seizures?
Carabamazapine
What should you do to protect a person from injury during a seizure?
Cushioning their head, for example with a pillow.
Removing glasses if they are wearing them.
Removing harmful objects from nearby, or if this is not possible, moving the person away from immediate danger.
Do not restrain them or put anything in their mouth
When the seizure stops check their airway and place them in the recovery position
Observe them until they have recovered
Arrange emergency admission if first seizure
How do you treat tonic-clonic seizures lasting >5 minutes or those who have had >3 seizures in an hour?
Buccal midazolam as first-line treatment in the community.
Rectal diazepam can be used
IV lorazepam if they have IV access already
Moa of sodium valproate?
Increases the activity of GABA which increases the inhibitory activity
Notable side effects of sodium valproate?
Teratogenic - neural tube defects and developmental delay
Liver damage and hepatitis
Hair loss
Tremor
Stomach pain, n&v, diarrhoea
Reduce fertility
Tremor
Hyponatraemia
Rare but serious:
Suicidal ideation
Acute pancreatitis
Hepatotoxic
Thrombocytopenia
Hyperammonemic encephalopathy
Risk of congenital defects if a woman doesnt and does take AEDs?
1-2% of newborns born to non-epileptic mothers have congenital defects
This rises to 3-4% if the mother takes AEDs
Best AEDs for pregnancy?
Lamotrigine
Leveteracetam
DVLA rules for driving after first unprovoked seizure?
6 months off if there is no relevant structural abnormalities on brain imaging and no definite epileptiform activity on the EEG
12 months if these conditions are not met
DVLA rules for driving for patients with established epilepsy or multiple unprovoked seizures?
12 months off driving
After vbeing seizure free for 5 years a ‘til 70 licence is usually restored
DVLA rules on driving during withdrawal of epilepsy medication?
Should not drive whilst AEDs are being withdrawn and must wait until 6 months after the last dose
AED in breast feeding?
All AEDs are generally considered safe for breast feeding except for barbiturates
Drugs that lower the seizure threshold?
Beta lactam antibiotics
Isoniazid
Antimalarials
Opioid analgesics
NSAIDs
Methylxantines e.g. theophylline
Antipsychotics e.g. clozapine
Antidepressants - SSRIs, TCAs, MAOIs
Bupropion
Anaesthetics
Management of status epilepticus?
ABC
PR diazepam or buccal midazolam if in community
IV lorazepam if in hopsital
Repeat IV lorazepam if after 5-10 mins
If ongoing then start levetiracetam, phenytoin or sodium valproate
If refractory status i..e 45 mins from onset, then induce GA or phenobarbital
What is Todd’s paresis?
Weakness or paralysis in part of or all of the body after a seizure
Common syndrome
Psychosocial impact of epilepsy?
Stigma -> social isolation and discrimination
Emotional impact e.g. distress, anxiety, concerns about safety
educational and occupation challenges e.g. driving restrictions, job restrictions
Impacts with ADLs which may impact QoL
Family dynamics may change e.g. parents worrying about child’s safety
May affect self-esteem and self image
MOA of carbamazepine?
Inhibits voltage-sensitive sodium channels, stabilising neuronal membranes and modulating the release of presynaptic excitatory neurotransmitters
MOA of phenytoin?
Inhibits voltage-sensitive sodium channels, stabilising neuronal membranes and modulating the release of presynaptic excitatory neurotransmitters
MOA of lamotrigine?
Inhibits voltage-sensitive sodium channels, stabilising neuronal membranes and modulating the release of presynaptic excitatory neurotransmitters
MOA of Ethosuximide?
Inhibits voltage-sensitive calcium channels, stabilising neuronal membranes and modulating the release of presynaptic excitatory neurotransmitters
MOA of benzodiazepines?
Bind to benzodiazepine receptors in post-synaptic GABA chloride channels = increases GABA inhibitory effects = increased flow of Cl- into the cell = hyper polarisation and stabilisation of plasma membrane
What blood test can distinguish between seizures and pseudo seizures?
Prolactin - raised after a true seizure
Common adverse effects of phenytoin?
Acute:
Dizziness, diplopia, nystagmus, slurred speech, ataxia
Later - confusion and seizures
Chronic:
Gingival hyperplasia, coarsening of facial features, drowsiness, Megaloblastic anaemia, peripheral neuropathy, osteomalacia, lymphadenopathy, dyskinesia
DVLA rules for bus/coach/lorry drivers after a seizure?
5 years off driving if it was only 1 seizure
10 years off driving if multiple seizures
