Epilepsy Flashcards
Epidemiology of epilepsy
Commonest serious neurological condition - prevalence 0.6% of the population
- annual incidence 0.07%
Higher incidence in developing countries and more common onset in young children and the elderly
Define epilepsy
The tendency to have recurrent, unprovoked seizures
A seizure is an abnormal paroxysmal synchronous discharge of many cortical neurones causing symptoms
Causes of epilepsy
A common symptom of many neurological diseases, 50% of new adult cases are never explained
Common causes - tumours (especially benign)
- brain malformations - cerebrovascular disease
- previous neurological infection. - learning disability and autism
Risk factors for epileptic attack
Known neurological/cerebrovascular disease
Family history, childhood febrile convulsions or abnormal neurological development
Previous head injury
Substance misuse
Taking a history of an epileptic attack
Must take both account from patient and witness account
Circumstances, warning symptoms, detailed chronology, any poetical phenomena and recovery.
Have there been any other attacks, are they all then same, is there any pattern?
Features indicating a loss of consciousness event is epileptic
Abrupt onset and short event ~1min
Confused and drowsy after, often taking several hours to recover
Similar stereotyped attacks
Specific recognisable features of certain seizure types
Features indicating that a loss of consciousness event is non-epileptic
Gradual onset + pre-syncopal symptoms->neurocardiac syncope
Several cardiac risk factors and preceding cardiac symptoms - chest pain, pallor, sweating, link to exercise->cardiac syncope
Prolonged episode with variable, psychogenic and somatic symptoms which vary in severity-> dissociative convulsions
Types of epileptic seizures
Seizures arising from specific foci in the brain –> focal seizures
Seizures arising from bilateral brain networks –> generalised seizures
Time course of epileptic seizures
Most seizures are self limiting but they can continue for hours–> status epilepticus
Types of generalised seizures
Tonic-clonic seizures, with or without tonic features
Absence seizures, typical/atypical, myoclonic, tonic or spasms
Myoclonic seizures, with or without absence
Types of Focal seizures
Focal sensory seizures, elementary (occipital/parietal) or experiential (temporo-parieto-occipital junction)
Focal motor seizures, elementary clonic or asymmetrical tonic
Focal motor seizures with typical (temporal lobe) automatisms
Secondarily generalised seizures
Continuous seizures
Most common generalised tonic-clonic status epilepticus
Can also be - absence SE, tonic or clonic SE, myoclonic SE, focal SE
Principles of epileptic management
Full history of seizures leading to syndrome diagnosis
Involve patient in decisions, giving clear advice
Try drugs singly at therapeutic dose, if they fail change drug
Seek specialist help if - drugs fail to stop seizures, cognitive decline, neurological symptoms, child or psychiatric co-morbidity
Antiepileptic drugs
Are teratogenic and often have complex interactions with other drugs - may require blood monitoring
Frequently have side effects
Should always be started by a specialist
Important points to record about an epileptic attack
Age of onset Diurnal pattern
Seizure type/syndrome Witness account
Cause/trigger of epilepsy Any history of non-epileptic seizures
Complications of epilepsy
Injuries or accidents during seizures
Prolonged or serial seizures/status epilepticus
Cognitive decline
Anxiety or depression
When giving drugs for heart failure consider
Are there any issues with interactions or allergies
Is there an issue with patient compliance/how often do they forget to take them
Will it require blood level monitoring
Treatments for epilepsy
Epilepsy surgery
Vargas nerve stimulator
Anti-epileptic drugs
Treatment of status epilepticus
Medical emergency
At home: Clobazam, rectal diazepam or buccal midazolam
In AnE: IV lorazepam, midazolam, propofol, phenobarbitone, phenytoin
If needed - intubation and ventilation
Epilepsy and psychiatric conditions
Most patients with epilepsy do not suffer from psychiatric conditions
People suffering from severe epilepsy are at an increased risk
Incidence of psychiatric co-morbidity in people with epilepsy
30-50% at GP level and 60% attending specialist services have current or past psychiatric diagnosis
People with severe/poorly controlled epilepsy are at highest risk
Only at increased risk of psychosis compared to other patient groups
Risk factors for psychiatric conditions in epilepsy
Intractable epilepsy Associated brain damage Temporal lobe/early onset epilepsy Perceived seizure severity Social handicap/adverse family background
Causes of psychiatric disease in epileptic patients
Same pathology underlying epilepsy/psychiatric disorder
Seizure induced damage/change
Effects of treatment
Psychosocial correlates of epilepsy
Possible features during seizures (Ictal)
Experiential aura - affect, perceptual, aberrations of thinking, dymnesic
Frontal seizures - posturing or hypermotor seizures
Automatism - semi-purposeful activity with impaired consciousness - may last several minutes
Possible features before seizures (prodromal)
Non-specific unwell/dysphoria
Hours to days
Occurs in 30% of patients, more common in focal than generalised
Mechanism unknown
Possible features after seizures (post-Ictal)
Delirium - may be prolonged especially in the elderly/patients with underlying brain disease
Psychosis - brief, dramatic and self limiting (1-18 days), can have a lucid interval, occurs in 6-7% of patients with severe epilepsy, associated with bilateral pathology
Common co-morbid (interictal) psychiatric disorders
Depression Anxiety disorders Non-affective psychosis Personality disorders Cognitive impairment
InterIctal depression
Common, worst with FH, frequency of seizures and certain drugs
Up to 50% ‘atypical’ –>interictal dysphoric disorder
3-5x higher risk of suicide in epilepsy
InterIctal anxiety
Similar prevalence and risk factors to depression Can occur as 'Seizure phobia' - fear of having attack in public - agoraphobic avoidance - can be worse than seizures
InterIctal non-affective psychosis
2-3x increased risk
Similar presentation to schiz but with negative family history and lack of premorbid personality disturbance
Usually in severe, bilateral epilepsy and is associated to some drugs
InterIctal personality disorders
18-22% of intractable TLE are DSM dependent/avoidant
Juvenile myoclonic epilepsy may also be associated with unstable personality traits
Geschwind syndrome now discredited
Epilepsy and cognitive impairment
Most patients with epilepsy have normal IQ
TLE often have memory impairments - dominant side: verbal
- non-dominant side: non-verbal progressive dementia due to - SE, serial head injury, medication, underlying condition or the cumulative effect of seizures
Epilepsy and violence
Epilepsy is 4x more common in prison - due to social factors not violence
Criminal life may predispose to epilepsy
Ictal aggression is rare - usually resistive aggression provoked by attempts to contain patient during automatism
Dissociative seizures
Also know as psychogenic/non-epileptic/pseudoseizures/NEAD/ hysterical/functional seizures
Occur in 20% of patients with intractable seizures, 15% overlap with epilepsy
75% female, usually starts early 20s and lasts for 3 years
Features of dissociative seizures
Long (>2mins) and atypical sequence,tend to be–> conscious but unresponsive, eyes closed, violent movements
On examination –> out of phase clonic movement, avoidance/resistance, ‘Henry & woodruff’ sign, ‘prof binnie mirror sign’
Diagnosing dissociative seizures
Clinical suspicion - gradual onset, eyes closed, long duration etc
InterIctal EEG excludes epilepsy
Telemetry
Post-Ictal serum prolactin is negative (not raised)
Clinical suspicion and excluding epilepsy
Electroencephalogram (EEG)
Spatio-temporal average of the synchronous post-synaptic potentials of the cells aligned perpendicular (tangential) beneath the electrode. Thalamocortical loop generates oscillations in EEG waves. Reach electrodes by volume conduction and neuronal propagation
The difference between volume conduction and neuronal propagation
Volume conduction –> preserves the morphology or the wave without delays but with amplitude decrement
Neuronal propagation –> Morphology changes and time delays but amplitude may increased due to recruitment
EEG are always a combination of the two
Role of the thalamus in the EEG
α waves –> represent synchrony generated by the thalamus
θ waves–>limbic or slowing of α waves by hyperpolar thalamus
δ waves –> suppression of the brainstem+Thalamocortical loop
Indirectly by modifying excitability of cortical neurons
Location of EEG electrodes
Scalp or intra-cranially by placing through the foremen ovale (intracranial epileptiform)
Differences in scalp and intracranial epileptiform (ECoG) EEG readings
ECoG –> Greater sharpness and amplitude
Less spatial distribution
Reduced latency
Discharges from deep structures don’t reach the scalp
EEG –> dominated by discharge from nearby neocortex
Simple vs complex
Simple - no loss of memory or consciousness
Complex - loss of consciousness and/or memory
Targets for anti-epileptic drugs
Inhibits sodium channels
Inhibits T/l calcium channels
Increase GABA transmission
Drugs which inhibit sodium channels
Use dependant block of Na channels, so don’t block normal brain activity, just the rapid firing during a seizure. Prevents seizures happening
Valproate - causes birth defects
Carbamazepine, Phenytoin
Precipitating factors for seizures
Acidosis Ethanol withdrawal
Hypoglycaemic Strobe lights
Stress/fatigue Phenothazines ( found in neuroleptics and anti-histamine drugs)
Drugs are effective in
70% of cases
Absence seizures
3hz oscillation on EEG
Activation of T-type Ca channels in the thalamus causing GABA release from the RTN speeding up the refresh rate of Ca channels so that they can response to the returning impulse from the cortex, repeating the loop. Cause temporo cessation of activity
Drugs blocking Ca channels
Block T type channels, important in absence seizures
Ethosuximide and trimethadione - prevent absence seizures
Gabapentin - relieves epilepsy by acting on L type Ca channels
Prevent seizuresu
Drugs which enhance GABA transmission
Used for stopping seizures
Benzodiazepines or barbiturates both enhance GABAa action
Vigabatrin - inhibits GABA breakdown (valproate does this a little)
Tiagabine - inhibits GABA uptake
Why shouldn’t you use GABA enhancing drugs to treat absence seizures
Absence seizures are GABA dependant, so they exacerbate them
Use Ca blockers, Phenytoin is ineffective but valproate is ok
Can use GABAb antagonists such as saclofen or phaclofen as GABAb is excitatory in this circuitry
Is previous surgery important when reading an EEG?
Yes, scalp EEG readings will be distorted by any coverings of the scalp or holes in the skull, such as after surgery
Clinical uses of EEG
Diagnose and classify seizures
Localising epileptogenic foci, especially in pre-surgical candidates
Judging the effectiveness of treatment, and if AEDs should be stopped
Must be considered in light of patient’s history
Types of EEG
Routine - 20mins, sometimes with sleep recording
- 10-20 discs system in maudsley or standard system of electrode placement
- can be visualised using various ‘montages’
Long term is used in certain circumstances
Causes of EEG activations/abnormalities
Routine - opening and closing eyes, changes in light
- hyperventilation
Interesting - sleep deprivation, sedation, and sedated sleep
- seizure precipitation (video games, visual patterns)
- AED withdrawal
Types of brain waves
Alpha - 8-14Hz Beta - 14Hz Theta - 4-8Hz Delta - <4Hz In deep sleep you can get sleep spindles and k complexes
Inter-Ictal EEG patterns in symptomatic generalised seizures
Hypsarrhythmia (big irregular waves on a chotic background)
Slow spike-and-wave (regular, symmetrical pattern of large waves and spike bursts seen in absence seizures)
Inter-Ictal EEG patterns in symptomatic partial seizures
Vary greatly
Generally show similar waveforms to generalised but limited to a specific area of the brain
Inter-Ictal spikes or sharp waves
May occur alone or with slow waves
Last a few seconds
Can be focal or general
No clinical manifestation
Advantages of the EEG
Cheap and easy
Not invasive or dangerous
Gives a direct measure of brain activity with some spatial and temporal information
Often only exam which shows abnormalities in epileptic patients
Limitations of EEG
Pretty low sensitivity and specificity, giving no clue as to aetiology
Vulnerable to physiological or environmental artefacts
Small or deep lesions may not come up on EEG
May falsely localise an epileptic foci
Uses of prolonged EEG sampling
Measure regular or frequent seizures and correlate with symptoms and precipitating factors
Useful when foci must be localised
Can be combined with video recording for best investigating of seizures
Temporal lobe epilepsy (TLE)
Syndrome of partial and possible secondary generalised focal epilepsy due to temporal lobe damage or dysfunction
Can either be medial or lateral TLE
Can be simple (just sensations) or complex (reduced consciousness)
What can cause TLE?
Multiple or complex febrile convulsions as a child can damage the temporal lobes
Most cases show some mesial temporal sclerosis (MTS) in the temporal lobes on MRI
Treatments of TLE
AEDs can be used, but 1/3 of patients are refractory to AEDs
Surgical temporal lobe resection is very effective at preventing seizures but a Wada test should be performed to identify if speech areas could be effected
Wada test
Injecting amobarbital into one carotid to shut down half the brain, The patient is then tested to identify how speech is lateralised.
Performed before temporal lobectomies to decide the safe extent of surgery and if the patient is appropriate
