Epilepsy and Blackouts Flashcards
What is a seizure?
Sudden Synchronous Discharge of Cerebral Neurones that is apparent either to the patient
only (e.g. Simple Partial Seizure) or to an observer (e.g. Generalised Seizure); Definition
excludes Migraine Aura (more gradual onset, more prolonged, on EEG correlation)
What is epilepsy?
Ongoing liability to recurrent epileptic seizures; Common (0.7-0.8%, more common
in developed countries); Highest incidence at young/elderly; Often goes into remission
Generalised onset
Discharge arises from both hemispheres
o Includes Absence, Myoclonic, Tonic, Tonic-Clonic, Atonic; Combination or Sequential
Focal Onset
Arises from one or part of one hemisphere; LOC may be retained, lost or evolve
into secondary GTCS
Frontal Lobe Seizures
Motor or Premotor Cortex; Clonic movements which may travel proximally (Jacksonian march) or Tonic seizure (e.g. both upper limbs raised high for several seconds)
Temporal Lobe Seizures
Strange warning feelings, or Aura with Smell/Taste
abnormalities, Distortion of Sound and Shape etc
▪ Automatisms – Lip-smacking, Plucking, Walking in Non-purposeful manner;
due to spread to Pre-motor Cortex
▪ Consciousness can be impaired, usually longer than absence seizures
Occipital Lobe Seizures
Stereotyped Visual Hallucinations
Parietal Lobe Seizures
Contralateral dysaesthesia or distorted body image
ILAE 2017
– Focal (Awareness/Impaired, Motor/Non-motor, Focal to Bilateral Tonic-
Clonic), Generalised (Motor or Non-motor), or Unknown (Motor or Non-motor)
Epilepsy syndromes by age groups
In Adolescents, Genetic, Perinatal and Congenital Disorders predominate; In Younger Adults, Trauma, Drugs, Alcohol are common while in the Elderly, Cerebrovascular Disease and Mass Lesions (e.g. Brain Tumours) are commoner
Primary Generalised Epilepsies
Presents in Childhood and Early Adult life; Accounts for up to 20% of all patients with
Epilepsy; Polygenic with complex inheritance
Structurally normal brain but abnormal Ion Channels which lead to abnormal Neuronal,
Neurotransmitter and Synaptic Functioning
Juvenile Myoclonic Epilepsy
10% of all Epilepsy patients; Myoclonic Seizures start in teenage years; Followed by GTCS; 1/3 of patients also have Absence Seizures
o Often occur in the morning after waking; Lack of sleep, Alcohol, Strobe lighting are
triggers; Responds well to treatment
o Usually associated with EEG abnormalities and requires life-long therapy
Hippocampal Sclerosis
Major cause of Epilepsy; Damage leading to
Scarring and Atrophy of the Hippocampus (usually
visible on MRI) leading to Temporal Lobe Epilepsy,
leading cause of LRE
• Childhood Febrile Convulsions are the main Risk Factor; One of the commoner causes of Refractory Epilepsy; Surgical Resection of damaged Temporal Lobe might be useful
Causes of Epilepsy: TBI
Might cause Epilepsy, even years after; Risk is not increased for minor injury (LOC/Amnesia <30 mins); Depressed Skull Fracture, Penetrating Injury and ICH increases risk significantly
Causes of Epilepsy: Perinatal Brain Injury and Cerebral Palsy
Periventricular Leukomalacia and ICH associated
with Prematurity and Foetal Hypoxia can cause Early Onset Epilepsy; 1/3 of Cerebral Palsy patients have Epilepsy
Causes of Epilepsy: Brain neurosurgery
Seizures in up to 17% of cases; Prophylactic Anticonvulsant use
Postoperatively is not recommended (Risk of Altered Mental Consciousness>Benefits)
Causes of Epilepsy: Genetic Disorders
Genetic Disorders (>200 types) can cause Epilepsy; Only counts for 2% of Epilepsy causes;
Developmental Disorders E.g. Neuronal Migration detects during Brain development,
Dysplastic Cerebral Cortex and Hamartomas also contribute to Seizures
Causes of Epilepsy: Vascular Disorders
Stroke and Small Vessel Cerebrovascular Disease is the commonest cause of Epilepsy after 60yrs; AVMs including Cavernous Haemangiomas
Causes of Epilepsy: Neurodegenerative Disorders
Involvement of the Cerebral Cortex e.g. Alzheimer’s Disease is associated with increased risk for Epilepsy
Causes of Epilepsy: Inflammatory Conditions
Encephalitis, Cerebral Abscess, Tuberculomas; Also occurs in Chronic TB Meningitis and rarely Acute Bacterial Meningitis; Parasitic infections commoner in
less developed countries
Causes of Epilepsy: Chronic Alcohol Use
Common cause; Occur while heavy drinking or during withdrawal; Induced Hypoglycaemia and Head Injury also can cause seizures
Causes of Epilepsy: Drugs
Antipsychotics, TCAs, SSRIs, Lithium, Class Ib Anti-Arrhythmics (Lidocaine), Ciclosporin and Mefloquine; Stimulants e.g. Cocaine
Causes of Epilepsy: Metabolic
Hypocalcaemia, Hypoglycaemia, Hyponatraemia, Acute Hypoxia, Uraemia
and Hepatic Encephalopathy, Porphyria
Management of First Fit
Clinical diagnosis based on History taking; Majority of patients referred to First Fit
clinic have not had a seizure; Most commonly misdiagnosed Syncope
If not doubt, do not diagnose Epilepsy
• Bloods (FBC, U/Es, Serum Calcium), ECG
• EEG – Most useful to categorise Epilepsy rather than confirm diagnosis; High False Negative Rate and low False Positive Rate
o Focal Cortical Spikes (e.g. Temporal Lobe Epilepsy) or Generalised Spike-and-Wave Activity (e.g. in PGE); Continuous in Status
Epilepticus
• MRI Brain indicated in most patients after
first Seizure; Especially for Partial Onset or
Elderly (Greater risk of Focal Brain Lesions);
Not essential if <30yrs with definite EEG/Clinical Diagnosis of PGE
Distinguishing Syncope from Seizure
Distinguishing from Syncope – Seizures
have prolonged recovery period, tongue
may be bitten, colour change (Cyanosis
occurs in Seizure, Pallor in Syncope)
Advice for First Seizure
Avoid precipitants, Advice on safety, stop driving and ask patients to inform DVLA
• Recurrence after first fit in 70-80% of people; Risk highest 6 months after initial seizure; Risk is significantly increased by features of PGE on EEG, Partial Seizures and Structural Brain Lesion
Management of Continuous Seizure
Seizure >5mins or repeated Seizure treated with Rectal Diazepam, IV Lorazepam or Buccal Midazolam; O2 and monitor Airway
Status Epilepticus
Continuous Seizures for >30mins; Mortality 10-15%;
Longer duration of status increases risk of Permanent
Cerebral Damage; Rhabdomyolysis leads to AKI in convulsive Status Epilepticus
What kind of form can SE take
Status can be Convulsive, Absence or Focal; Epilepsia Partialis Continua is continuous Seizure
activity in one part of the limb without loss of Consciousness; Often due to Cortical Neoplasm
or Cortical Infarct (especially in the Elderly)
How are antiepileptic drugs given?
Indicated if firm clinical diagnosis of Epilepsy and Substantial Risk of Recurrent Seizures;
Introduced at low dose and titrated upwards until Seizures controlled or SE intolerable
• 70% of patients only require monotherapy
• If seizures not controlled with first drug, introduce second agent and withdraw first drug; if not seizure free, combination therapy required
• Non-Generic prescribing to ensure consistent drug levels
• Routine monitoring not required; For assessing compliance and toxicity
SE of AEDs?
Unsteadiness, Nystagmus, Drowsiness; Skin rashes in Lamotrigine, Carbamazepine
and Phenytoin; Variety of Idiosyncratic drug reactions
AEDs and pregnancy?
Increased risk of Birth Defects; Recommend switching to Monotherapy at low-dose; Folate
and Vitamin K supplementation; Risk of Birth Defect < Risk of Seizures to Foetus
AEDs and oral contraception?
Phenytoin, Carbamazepine, Phenobarbital are liver inducers; Oral contraception affected
AED withdrawal
Withdrawal after at least 2-3yrs seizure free; 50% Recurrence Rate after withdrawal
Management of GTCS
1st Line: Valporate, Carbamazepine, Lamotrigine 2nd Line Clobazam, Levetiracetam, Topiramate
Management of Generalised Absence
1st Line Valporate, Ethosuximide, Lamotrigine 2nd Line Clobazam, Levetiracetam, Topiramate
Management of Generalised Myoclonic
1st Line Valporate, Levetiracetam, Topiramate 2nd Line Clobazam, Piracetam
Management of Focal Seizures
1st Line Carbamazepine, Valporate, Levetiracetam, Lamotrigine 2nd Line Clobazam, Topiramate, Gabapentin, Tiagabine
Which drugs should be avoided in absence, myoclonic and JME
Avoid Carbamazepine, Gabapentin and Tiagabine
SE Valproate
Weight gain, Hair loss, Teratogenic, Rare Idiosyncratic Liver Failure
SE Carbamazepine
Rash, Hyponatraemia, Ataxia, Liver Enzyme Induction, Interference with other medications including Oral Contraception
Management of Refractory Epilepsy
- Re-evaluate Diagnosis, Consider drug concordance, Combination therapy to maximum tolerable dose, Referral for Epileptic Surgery (e.g. Temporal Lobectomy, Cure in 50-70%)
- Vagal Nerve Stimulation, Ketogenic Low Carbohydrate Diet might be useful
Vasovagal syncope
Simple faint due to sudden reflex tachycardia with vasodilation of peripheral and splanchnic vasculature
Precipitated by Prolonged Standing,Fear, Venesection or Pain
o Brief Prodrome of Dizziness, Nausea,
Sweating, Heart and Visual Grey-out
o Blackout may be accompanied with
jerking/twitching movements; Pallor
o Rapid recovery (usually seconds) by followed by a feeling of general fatigue
Cardiac Syncope (Stokes-Adams Attacks)
Cardiac Arrhythmias E.g. Heart Block, LVOT
Obstruction; Syncope during exercise is cardiac in origin
Micturition Syncope
More common in men, particularly at night
Cough Syncope
Venous Return to the heart obstructed by coughing; Also, laughter
Postural Hypotension
Occurs in the Elderly, patients with Autonomic Neuropathy, or drugs
e.g. Antihypertensives especially β-Blockers
Carotid Sinus Syncope
Vagal response to pressure on Carotid Sinus Baroreceptors
Convulsive Syncope
Collapsing in a propped-up position results in delayed restoration of
Cerebral Blood Flow; Secondary Anoxic Seizure following Syncope
Management of Syncope
• 12-lead ECG – Identify Heart Block, Pre-Excitation, Long QT syndrome
• Cardiac ECG Holter Monitoring and Echo if Cardiac Syncope suspected; alternatively,
Implantable Loop Recorder for infrequent events
• Tilt table testing sometimes diagnostic but low sensitivity
Non-Epileptic Attack Disorder (Pseudoseizures)
Presents similarly to Grand Mal Seizures;
Bizarre thrashing, non-synchronous Limb Movements; No rise in Prolactin (No rise also seen
in Partial Seizures) and no EEG changes even during attack
Panic Attacks
Sudden Sympathetic Activation; Often Hyperventilation leading to Respiratory Alkalosis; Dizziness, Chest Pain/Tightness, Feeling or Choking, SOB, Facial Tingling and Extremities, Trembling, Feeling of dissociation
o Consciousness is usually preserved, attacks easily recognised
Hypoglycaemia
Confusion followed by LOC, Convulsion, Dysphasia, Hemiparesis; Often
warning with Hunger, Malaise, Shaking and Sweating; Prompt recovery with IV/PO Glucose
o Prolonged Hypoglycaemia can cause widespread Cerebral Damage; Usually related to underlying Diabetes
Vertigo
Acute Vertigo might be severe enough to cause prostration
Migraine
Severe Basilar Migraine and Familial Hemiplegic Migraine may cause LOC
Drop Attacks
Instant, Unexpected episodes of LL Weakness with Falling; Due to sudden drop
in LL Tone? Brainstem origin; More common in 60+ Women; Also occurs in Hydrocephalus
Narcolepsy
Abnormalities of orexin, unusually low, autoimmune hypothalamic damage
Tetrad of excessive daytime sleepiness, cataplexy (sudden loss of tone), dream like hallucinations peri sleep often frightening and sleep paralysis
Management of Narcolepsy
• Multiple Sleep Latency Testing – Demonstrate rapid transition from Wakefulness to Sleep,
Short time to onset from REM sleep
• HLA testing for HLA-DR2 and HLA-DQBI*0602 Antigens (Strong Association)
• Good sleep hygiene advice; CNS Stimulants like Modafinil (? Dopamine Reuptake Inhibitor)
and Methylphenidate (Dopamine-Noradrenaline Reuptake Inhibitor) for treatment although
often only partial response
• TCAs (especially Clomipramine) or SSRIs to improve Cataplexy; Sodium Oxybate also used
Parasomnias
Disruptive Motor/Verbal Behaviours – REM and non-REM parasomnia depending on what
stage of sleep it occurs in
• Includes Sleepwalking, Night Terrors, Confusional Arousals and REM Sleep Behaviour Disorder
o REM Sleep Behaviour Disorder might be early feature of Parkinson’s Disease
