IC6 Flashcards
what is the definition of epilepsy?
disease of the brain with any of the following
1) ≥2 unprovoked seizures >24h apart.
2) 1 unprovoked seizure with a probability of further seizures being similar to part 1).
3) diagnosis of an epileptic syndrome.
what is the difference between acute and remote seizure?
acute seizures occur immediately after a recognisable stimulus/cause
VS
remote seizures occur >1 week following a disorder known to increase risk
what is an unprovoked seizure
occuring in the absence of a potentially responsible clinical condition OR beyond the interval estimated for occurrence of acute symptomatic seizures.
etiology of acute symptomatic seizures
Metabolic
* Hyponatremia
* Hypocalcemia
* Hypomagnesemia
* Hypoglycaemia
Toxic subst/drugs
* Illicit drugs (e.g. cocaine, amphetamines)
* Drugs (e.g. Tricyclic antidepressants, carbapenems, baclofen)
* ETOH (withdrawal & intoxication)
* Benzodiazepine withdrawal
Structural
* Stroke
* Traumatic Brain Injury
Infection/Inflammation
* CNS Infection
* Febrile illness
wht is your understanding of drug induced seizures
drugs don’t really induce seizures. rather, they lower the seizure threshold.
risk depends on
- effects on neurotransmission
- time course (starting new drug, withdrawal)
- concentration reaching brain
- susceptibility risk factors (PMH seizure, structural or functional brain abnormalities, concurrent drug use).
what are common drugs that lower seizure thresholds?
antimicrobials (high dose beta lactams eg carbapanems)
analgesics (opiods eg pethidine/meperidine, tramadol..)
antipsychotics (clozapine)
antidepressants (bupropion, overdose situations)
immunosuppressants (cyclosporin)
stimulants (eg dextroamphetamine, methylphenidate)
what are non-epileptic events
not related to abnormal epileptiform discharges but manifests like epileptic seizures.
1) psychogenic non-epileptic seizures (PNES)
- caused by stressful psychological experiences/emotional trauma.
- involuntary.
- partial alteration of LOC with partial preservation of awareness.
2) physiological non-epileptic events (PNEE)
- symptoms of paroxysmal systemic disorder.
- convulsive syncope, hypoglycemia, migraine aura, non-ictal dysautonomia, intoxications, transient ischemic attacks, panic attacks
- movement disorders, balance disorder, sleep disorders,
pathophysiology of a seizure
1) short in circuit
- paroxysmal depolarisation shift, where instability = one cell or a group of cells become excited.
2) driving of normal neighbours
(synchronisation OR synchronised paroxysmal discharges)
- repeated paroxysmal depolarisation will increase extracellular K+
- less K+ able to diffuse out during the hyperpolarised state and the cell remains partially depolarised + depolarise other cells.
3) failure of inhibition
- loss of hyperpolarisation
- loss of surround inhibition (neurons that drive inhibitory tone are reduced)
- excess glutamate stimulation/excess excitatory neurotransmitters)
- increase intracellular Ca2+ (and other intracellular and extracellular substance abnormalities)
what part of the brain plays a large role in epilepsy?
hippocampus
plays a role in hyper-synchronisation
- hippocampal sclerosis
- intrinsic reorganisation of local circuits (hippocampus, neocortex, thalamus) = synchronisation and promotes generation of epileptiform activityt.
etiology of epilepsy
- Structural
– E.g. Hippocampal sclerosis, brain tumours, vascular malformations, glial scarring (including stroke and traumatic brain injury) - Genetic/presumed genetic
– E.g. Dravet syndrome with SCN1A mutations - Neurodegenerative
– E.g. Alzheimer’s disease - Metabolic
– E.g. inborn errors of metabolism, mitochondrial disorders - Infectious
– E.g. bacterial meningitis, encephalitis, neurocysticercosis
how does ILAE classify seizures
1) region where seizure begins in the brain
- focal onset (partial) - one hemisphere
- generalised onset - both hemisphere
- secondarily generalised - start from one, then spreads to another.
2) impairment of consciousness
or level of awareness
what are the phases of a seizure?
prodromal
early ictal (aura)
ictal
postictal
clinical presentation of focal onset/simple partial seizure (motor, sensory, autonomic, psychic)
motor:
- clonic movement (repeat jerking)
- speech arrest
sensory
- numbness, tingling
- visual disturbance = flashing lights
- rising epigastric sensation
autonomic
- sweating, saliva, pallor
- BP, HR
psychic
- flashbacks, dé j à vu (memory
- Visual, auditory, auditory, gustatory or olfactory hallucinations
- Affective symptoms include fear (most common), depression, anger and irritability
ILAE classification of partial/focal seizure
simple:
- retained consciousness
- retained msucle tone
- staring spells
complex
- initial aura
- LOC
- ictal automatisms (repeated movement)
- postictal confusion
secondary generalised (starts as focal)
- initial aura
- convulsion W/W/O jacksonian march
- postictal confusion W/W/O todds paralysis
characteristics of tonic-clonic (grand mal) seizure
tonic phase (stiffening limbs) > clonic (jerking limbs/face)
tonic phase
- breathing decrease/cease
- cyanosis of nail beds, lips, face
clonic phase
- 1 min (appx)
- brain then becomes extremely hyperpolarised and insensitive to stimuli.
- incontinence
- biting tongue
post ictal
- headache, lethargy, confused, sleepy
- minutes to hours to recover
characteristics of clonic seizure
asymmetrical jerking
more common in neonates, infants, young children
characteristics of myoclonic seizure
rapid, brief contraction of both sides of body muscles (CONCURRENT)
- sometimes one arm or one foot
characteristics of tonic seizure
sudden LOC
rigid posture
10-20s
all ages (associated with diffuse cerebral damage, learning disability)
characteristic of lennox-gastaut syndrome
characteristics of absence (petit mal) seizure
abrupt and basic lapse in awareness similar to persistent staring
few seconds (no warning, after-effects)
more common in children
difference vs complex partial:
- no aura
- seconds vs minutes
- frequently and abrupt
- produce characteristic EEG 3hz spike wave pattern.
what is one pertinent characteristic of petit mal seizures
produce characteristic EEG 3hz spike wave pattern.
characteristics of atonic seizure
may result in complete loss of postural tone - static seizure - collapse on ground like rag doll
short episode
immediate recovery
any age (associated with diffuse cerebral damage, learning disability)
common in Lennox-gastaut syndrome, myoclonic astatic epilepsy.
what investigation to use for seizure and wat is the sensitivity/specificity
EEG, or electroencepholography
is the main tool for diagnosis and classification
however, normal EEG =/= no epilepsy, especially if the EEG captured after the seizure occurred.
also, not all epileptic patients will have abnormal EEG
EEG can also be abnormal in norma persons (chance of false positive)
what investigations after seizure diagnosis
MRI with gadolinium
- adult patients with first seizure, patients with focal neurologic deficits, suggestion of focal onset seizure
- Identify focal lesions:
o Mesial temporal sclerosis
o Focal cortical dysplasia
o Remote injury (old stroke etc)
o Tumor
o Vascular malformation
biochemical/toxicology
- rule out electrolyte abnormalities
- CK raised after GTC
what lab is raised after GTC
creatinine kinase
what is the approach to a patient with seizure
was it a seizure (any differential diagnosis)
- obtain history from observers
was it a first seizure?
was it provoked? acute symptomatic? if not, establish likely cause and risk of recurrence. may need to diagnose as epilepsy? or consult for further management
does the patient need antiseizure medication?
- risk of recurrence, patient factors,
what increases risk of seizure recurrence?
increased if
- epileptiform abnormalities on EEG
- prior brain insult (stroke, brain trauma)
- structural abnormality in brain imaging
- nocturnal seizure
what are the list of non-phx treatment modalities?
ketogenic diet
vagus nerve stimulation (VNS)
responsive neurostimular system (RNS)
surgery (if possible to define location of seizure)
ketogenic diet indication and explanation
induction of ketosis (ketones may have antiepileptic effect on brain)
for patients who cannot tolerate or have not responded well to ASM treatment
challenging to adhere to long term
vaugs nerve stimulation indication and explanation
only for (hard to control)
intractable focal seizures
electrodes attach on left branch of vagus nerve and programmable stimulator = deliver cyclical stimulation
responsive neurostimulator system (RNS) indication and explanation
stimulator implanted in skull under scalp. leads implanted in the brain.
continuously monitor electrical activity in brain, detects patient specific patterns and delivers brief pulses of stimulation when it detects activity that could lead to a seizure.
adjunctive tool to reduce freq of partial onset seizure in patients with
- diagnostic testing that localized ≤ 2
epileptogenic foci (a discrete area of the brain in which originate the electrical discharges that give rise to seizure activity.)
– Are refractory to ≥ 2 antiepileptic medications
– Have frequent and disabling symptoms
epilepsy surgey indication
early therapy for specifc epileptic syndromes
1) Temporal lobe epilepsy with vs without mesial temporal sclerosis (70% vs 50%)
2) Frontal lobe epilepsy with vs without identifiable lesion on MRI scan (50% vs 25%)
3) Also considered as a last option (vs continued drug therapy) for certain refractory cases
patient counselling for seizure
identify and avoid triggers that are preventable
note side effects and drug interactions of antiseizure meds
avoid certain activities eg driving, firearms, swimming…
consider a seizure diary to record frequency, type, duration of seizures, triggers, ADR, changes to ASM.
appropriate first aid for seizures
ease person to floor > gently turn to one side to allow breathing (prevent choking) > put something soft/flat under head. remove glasses if any. loosen ties or anything around neck.
clear area around person
time seizure, call 911.
DO NOT HOLD PERSON DOWN, PUT ANYTHING IN MOUTH, GIVE CPR, offer water.
