3. EPILEPSY
⢠A seizure can be defined as the occurrence of signs and/or symptoms due to
abnormal, excessive or synchronous neuronal activity in the brain
⢠âEpilepsyâ is the tendency to have unprovoked seizures
⢠Lifetime risk: 5%, highest at extremes
⢠Prevalence of active epilepsy in European: 0.5%, higher in developing nation
d/t parasites eg. cysticercosis
4. ⢠Grand mal: Tonicâclonic seizures
⢠Petit mal: Absence seizures
⢠Subsequent revisions, Complex partial and Simple partial
5.
6. Pathophysiology
⢠Normally, balance between excitation and inhibition, in order to remain
responsive
⢠The inhibitory transmitter GABA enhance chloride inflow and reduce action
potential formation
⢠Excitatory amino acids (glutamate and aspartate) allow influx of sodium and
calcium, producing contrary
⢠Seizures result from an imbalance between this excitation and inhibition
⢠Paroxysmal depolarisation shift in neuronal membrane potential, predisposing to
recurrent action potentials
7. ⢠Epileptic cortex shows repetitive discharges involving large groups of
neurons
⢠Related to a localised disturbance: focal seizures ( Focal infection, tumour,
hamartoma or trauma-related scarring)
⢠If remain localised, symptoms depend on which area is affected
⢠Temporal lobes: awareness of the environment impaired but without tonicâ
clonic movements
⢠When both hemispheres involved, either at onset or after spread, the
seizure becomes generalised
8. ⢠In those with generalised at onset, abnormal activity probably originates in
the central mechanisms controlling cortical activation and spreads rapidly
constitute around 30% of all
⢠Seizure activity is usually apparent on EEG as spike and wave discharges
⢠Other generalised seizure activity may involve merely brief loss of
awareness (absence seizures), single jerks (myoclonus) or loss of tone
(atonic seizures), as detailed
9.
10. Clinical features
Seizure type and epilepsy type
⢠To classify ask whether focal onset, and second whether the seizures conform to one of the
recognised patterns
⢠Beyond mid-thirties almost focal cerebral event
⢠Even when generalised tonicâclonic seizures occur, those beginning in one area will cause
positive neurological symptoms and signs corresponding to the normal function of that area
⢠Occipital onset: visual changes (lights and blobs of colour),
⢠Temporal lobe: False recognition (dÊjà vu)
⢠Sensory strip involvement: Sensory alteration (burning, tingling)
⢠Motor strip involvement: Jerking
11. ⢠Patients can have more than one type but important to document each
attack type, age at onset, and frequency, duration and typical features
⢠Triggers should be identified
12.
13. Focal seizures
⢠d/t localised cortical activity with retained awareness
⢠Spreading pattern may occur, the abnormal sensation spreading much faster (in
seconds) than a migrainous focal sensory attack
⢠Awareness may become impaired if spread occurs to the temporal lobes
(previously âcomplex partial seizureâ)
â˘
14. ⢠Patients stop and stare blankly, often blinking repetitively, making
smacking movements of their lips or displaying other automatisms,
such as picking at their clothes
⢠After a few minutes, consciousness returns but the patient may be
muddled and feel drowsy for a period of up to an hour
⢠The age of onset, preceding aura, longer duration and post-ictal
symptoms usually make these easy to differentiate from childhood
absence seizures
15. ⢠Seizures arising from the anterior parts of the frontal lobe produce
bizarre behaviour patterns, including limb posturing, sleep walking, or
even frenetic ill-directed motor activity with incoherent screaming
⢠Video EEG may be necessary to differentiate these from psychogenic
attacks (which are more common), but abruptness of onset, stereotyped
nature, relative brevity and nocturnal preponderance may indicate the
frontal onset
16.
17.
18. Generalised seizures
Tonicâclonic seizures
⢠An initial âauraâ may be experienced by the patient, depending on the cortical area of
origin
⢠The patient then becomes rigid (tonic) and unconscious, falling heavily if standing (âlike a
logâ) and risking facial injury
⢠During this phase, breathing stops and central cyanosis may occur.
⢠As cortical discharges reduce in frequency, the limbs produce jerking (clonic) movements
for a variable time
⢠Afterwards, there is a flaccid state of deep coma, which can persist for some minutes
19. ⢠The patient may be confused, disorientated and/or amnesic after
regaining consciousness
⢠During the attack, urinary incontinence and tongue-biting may occur
⢠A severely bitten, bleeding tongue after an attack of loss of
consciousness is pathognomonic of a generalised seizure
⢠Subsequently, the patient usually feels unwell and sleepy, with headache
and myalgia
⢠In less typical episodes, post-ictal confusion, or sequelae such as
headache or myalgia, may be the main pointers to the diagnosis
20.
21.
22. Absence seizures
⢠Absence seizures (previously âpetit malâ) always start in childhood
⢠Rarely mistaken for focal seizures because of their brevity
⢠They can occur so frequently (20â30 times a day) that they are
mistaken for daydreaming or poor concentration in school
23. Myoclonic seizures
⢠These are typically brief, jerking movements, predominating in the
arms
⢠In epilepsy, more in morning or on awakening from sleep, and tend to
be provoked by fatigue, alcohol or sleep deprivation
24. Atonic seizures
⢠Brief loss of muscle tone, usually resulting in heavy falls with or
without loss of consciousness
⢠They only occur in the context of epilepsy syndromes that involve
other forms of seizure
25. Tonic seizures
⢠Generalised increase in tone and an associated loss of awareness
⢠Seen as part of an epilepsy syndrome
26. Clonic seizures
⢠Clonic seizures are similar to tonicâ clonic seizures but without
preceding tonic phase
27. Seizures of uncertain generalised or focal
nature
Epileptic spasms
⢠Occur mainly in infancy
⢠Signify widespread cortical disturbance and take the form of marked
contractions of the axial musculature, lasting a fraction of a second but
recurring in clusters of 5â50, often on awakening photic stimulation
⢠If not fit into any categories
Presence or absence of a known structural or metabolic cause
Primary mode of seizure onset (generalized versus focal)
28. Epilepsy syndromes
⢠Many patients will fall into specific patterns depending on seizure
type(s), age of onset and treatment responsiveness: the so-called
electroclinical syndromes
⢠Genetic testing demonstrate similarities in molecular pathophysiology
29.
30.
31.
32. Investigations
Single
⢠12-lead ECG
⢠Where seizure is suspected or definite, imaging with either CT or MRI,
although the yield is low unless focal signs
⢠EEG may help to assess prognosis once a firm diagnosis has been made
⢠Recurrence after first seizure is approximately 40%, and most recurrent
attacks occur within a month or two of the first
33. ⢠EEG performed immediately after a seizure may be more helpful in
showing focal features than if performed after a delay
34.
35. ⢠Inter-ictal EEG is abnormal in about 50% of patients with recurrent
seizures, so it cannot be used to exclude epilepsy
⢠Sensitivity can be increased to 85% by prolonging recording time and
including a period of natural or drug-induced sleep, but not replace a well-
taken history
⢠Ambulatory EEG recording or video EEG monitoring may help with
differentiation of epilepsy from other attack disorders if these are
sufficiently frequent
36. ⢠Imaging cannot establish a diagnosis but identifies any structural cause
⢠It is not required if a confident diagnosis of a recognised epilepsy
syndrome (e.g. juvenile myoclonic epilepsy) can be made
⢠CT excludes major structural cause
⢠MRI is required to demonstrate subtle changes such as hippocampal
sclerosis, which may direct or inform surgical intervention
37.
38. Management
Explain the nature and cause to
patients and their relatives, and to
instruct relatives in first aid
Emphasised that epilepsy is a
common disorder that affects 0.5â
1% of the population, and that full
control of seizures can be expected
in approximately 70% of patients
39.
40.
41. Lifestyle
advice
AVOID ACTIVITIES WHERE THEY MIGHT
PLACE THEMSELVES OR OTHERS AT RISK
IF SEIZURE; APPLIES AT WORK, AT HOME
AND AT LEISURE
ONLY SHALLOW BATHS (OR
SHOWERS)
PROLONGED CYCLE
DISCOURAGED UNTIL
REASONABLE FREEDOM FROM
SEIZURES
PROLONGED PROXIMITY TO
WATER (SWIMMING, FISHING
OR BOATING) SHOULD
ALWAYS BE CARRIED OUT IN
THE COMPANY OF SOMEONE
AWARE OF THE RISKS AND
THE POTENTIAL NEED FOR
RESCUE MEASURES
DRIVING REGULATIONS VARY
BETWEEN COUNTRIES, AND
SHOULD BE AWARE
CERTAIN OCCUPATIONS, SUCH
AS FIREFIGHTER OR AIRLINE
PILOT
42. ⢠The recognised mortality of epilepsy should be discussed at around the
time of diagnosis
⢠Done with care and sensitivity, and with the aim to motivate patient to
adapt habits and lifestyle to optimize epilepsy control
43.
44. Anticonvulsant therapy
⢠Anticonvulsant drug treatment should be considered after more than one unprovoked
seizure
⢠The decision to start treatment should be shared with the patient, to enhance compliance
⢠A wide range of drugs is available
⢠These agents either increase inhibitory neurotransmission in the brain or alter neuronal
sodium channels to prevent abnormally rapid transmission of impulses
⢠In the majority of patients, full control is achieved with a single drug
⢠Dose regimens should be kept as simple as possible
45. ⢠For focal seizures, one large study suggests that lamotrigine is best-tolerated
monotherapy d/t favourable side effect profile, relative lack of pharmacokinetic
interactions
⢠Unclassified or specific syndromes respond best to valproate
⢠Problems in pregnancy mean that sodium valproate should not be used in women
of reproductive age unless the benefits outweigh the risks
⢠The first choice should be an established first-line drug with more recently
introduced drugs as second choice
46.
47.
48. Monitoring therapy
⢠Only indication for measuring serum levels is if there is doubt that the patient
is taking the medication
⢠Blood levels need to be interpreted carefully, and dose changes made to treat
the patient rather than to bring a serum level into the âtherapeutic rangeâ
⢠Some centres advocate serum level monitoring during pregnancy (notably
with lamotrigine) but the evidence of benefit for this is not strong
49. Epilepsy surgery
⢠Some patients with drug-resistant epilepsy benefit from surgical resection of
epileptogenic brain tissue
⢠Less invasive treatments, including vagal nerve stimulation or deep brain stimulation,
may also be helpful in some patients
⢠All those who continue to experience seizures despite appropriate drug treatment
should be considered for surgical treatment
⢠Planning such interventions will require intensive specialist assessment and
investigation to identify the site of seizure onset and the dispensability of any targets
for resection, i.e. whether the area of brain involved is necessary for a critical
function such as vision or motor function
50. Withdrawing anticonvulsant therapy
⢠Considered after seizure-free period for more than 2 years
⢠Childhood-onset epilepsy, particularly classical absence seizures,
carries the best prognosis for successful drug withdrawal
⢠Other epilepsy syndromes, such as juvenile myoclonic epilepsy, have a
marked tendency to recur after drug withdrawal
51. ⢠Seizures that begin in adult life, particularly those with partial features,
are also likely to recur, especially if there is an identified structural lesion
⢠Recurrence rate after drug withdrawal depends on the individualâs
epilepsy history
⢠Patients should be advised of the risks of recurrence, to allow them to
decide whether or not they wish to withdraw
⢠If undertaken, withdrawal should be done slowly, reducing the drug dose
gradually over weeks or months
⢠Withdrawal may necessitate precautions around driving or occupation
52. Contraception
⢠Decreased effect with carbamazepine, phenytoin and barbiturates, but
clinically significant with lamotrigine and topiramate
⢠If the AED cannot be changed, higher-dose preparations of the oral
contraceptive
⢠Sodium valproate and levetiracetam have no interaction with hormonal
contraception
53.
54. Prognosis
⢠The outcome of newly diagnosed epilepsy is generally good
⢠Overall, generalised seizures are more readily controlled than focal
seizures
⢠The presence of a structural lesion reduces the chances of freedom
from seizures
55. Non-epileptic attack disorder
⢠Present with attacks that resemble epileptic seizures but which are
caused by psychological phenomena and have no abnormal epileptic
discharges
⢠Very prolonged, sometimes mimicking status epilepticus
⢠Epileptic and non-epileptic attacks may coexist, and time and effort
are needed to clarify the relative contribution of each, allowing more
accurate and comprehensive treatment
56. ⢠May be accompanied by dramatic flailing of the limbs and arching of the
back, with side-to-side head movements and vocalizing
⢠Cyanosis and severe biting of the tongue are rare, but urinary incontinence
can occur
⢠Distress and crying following non-epileptic attacks
⢠Distinction between epileptic attacks originating in the frontal lobes and
non-epileptic attacks may be especially difficult, and may require
videotelemetry with prolonged EEG recordings
57. ⢠Non-epileptic attacks are three times more common in women than in men
and have been linked with a history of past or ongoing life trauma
⢠Not necessarily associated with formal psychiatric illness
⢠Patients and carers may need reassurance that hospital admission is not
required for every attack
⢠Prevention requires psychotherapeutic interventions rather than drug
therapy
58.
59.
60. Status Epilepticus
⢠Status epilepticus is seizure activity not resolving spontaneously, or recurrent
seizure with no recovery of consciousness in between
⢠Recognised mortality and is a medical emergency
⢠Diagnosis clinical and made on the basis of the description of prolonged rigidity
and/or clonic movements with loss of awareness
61. ⢠As seizure prolonged, movements more subtle
⢠Cyanosis, pyrexia, acidosis and sweating may occur, and complications
include aspiration, hypotension, cardiac arrhythmias and renal or
hepatic failure
⢠In pre-existing epilepsy, the most likely cause is a fall in anti-epileptic
drug levels whereas in de novo essential to exclude precipitants such as
infection (meningitis, encephalitis), neoplasia and metabolic
derangement (hypoglycaemia, hyponatraemia, hypocalcaemia)