2. Epilepsy:
• is a chronic condition defined by
repeated and intermittent
seizures, caused by abnormal
electrical activity within the brain.
• Of all the nervous system
disorders, epilepsy is the largest
cause of hospitalisations
3. What is an epileptic seizure?
• A transient occurrence of signs and/or
symptoms due to abnormal excessive
or synchronous neuronal activity in the
brain.
• Commonly generated in cortex and
hippocampus, may also be subcortical
4. Status epilepticus:
• This is defined as a condition in which epileptic
seizures continue, or are repeated without
recovery, for a period of 30 minutes or more.
5. Provoked seizures
• (acute symptomatic seizures) that have an
obvious and immediate preceding cause (for
instance an acute systemic or metabolic
disturbance or exposure to toxins or drugs), or
which are the direct result of recent acute
cerebral damage (for instance stroke, trauma,
infection).
• often do not recur when the cause is removed.
• The use of the term to include seizures after
acute cerebral damage, however, is rather
unsatisfactory as the damage is not reversible
and the propensity for seizure recurrence is
higher
6. Idiopathic, symptomatic and
cryptogenic epilepsy
• Epilepsy can have many causes. Where the
cause is clearly identified, the epilepsy is
categorized as ‘symptomatic’(i.e. of known
cause).
• Where no cause is known, the epilepsy is known
as ‘cryptogenic’ (i.e. hidden cause).
• Where the epilepsy is part of the genetic
syndrome of ‘idiopathic generalized epilepsy’ it is
known as idiopathic.
7. EPILEPSY IN THE ELDERLY
epidemiology:
• Epileptic seizures are the third most frequently
identified neurological condition identified in the
elderly, with only cerebrovascular disease and
dementias being more common.
• When plotted against age, the incidence of
epilepsy has a distinctly U-shaped distribution,
with children under 5 years and people over 60
years of age having an elevated risk of epilepsy.
8. • in the older age group the incidence of partial
(focal) onset epilepsy outstrips that of generalized
epilepsy.
• Status epilepticus, which may be convulsive or
non-convulsive, accounts for approximately 6% of
all seizures in the aged, which is twice that found
in the general population.
9. Etiology:
• stroke : the most common etiology in elderly
patients
– Approximately 7% of ischaemic and15% of
haemorrhagic cortical strokes are complicated by
– acute or early seizures (within 2 weeks of stroke
onset),and approximately one-third of these patients
develop late epilepsy.
• tumour
• degenerative disorders such as Alzheimer’s
disease, approximately16% of all patients with
Alzheimer’s disease will go on to develop seizures
• head trauma,
• toxic/metabolic factors and drug induced seizures
10. Conditions that provoke seizures
• Metabolic abnormalities
– Hypoglycemia
– Hypo and hypernatremia
– Hypo and hypercalcemia
– Hypomagnesemia
• Uremic encephalopathy
• Hepatic encephalopathy
• Systemic infection
11. • Sleep deprivation
• Drugs
– Intoxication with stimulants
• Amphetamines
• Cocaine
– Withdrawal from sedatives
• Alcohol
• BZD
• Barbiturate
• An unprovoked seizure has no clear underlying
cause, and increases the risk of further seizures
12. Drug induced seizures
• Theophylline is a potent convulsant which can
result in seizures or status epilepticus, possibly
due to the antiadenosine action.
• β-blockers and other antiarrhythmic agents have
been reported to precipitate seizures, particularly
in overdose.
• Cimetidine, levodopa, insulin, thiazide diuretics,
lidocaine, salicylates, chemotherapeutic agents,
L-asparaginase and baclofen have been reported
to cause seizures.
• The non-steroidal analgesics also predispose to
seizures (for example NSAIDs, tramadol
pethidine).
14. DIAGNOSIS OF EPILEPSY IN
ELDERLY IS DIFFICULT:
• Due to:
• great imitators :syncope, episodic vertigo,
hypoglycaemia, metabolic disorders, transient
ischemic attacks, non-specific episodes of dizziness,
confusional states, transient global amnesia or
psychiatric illness.
• On the other hand, focal seizures may remain
ignored and be a cause of underdiagnosis of
epilepsy. Symptoms as confusional states,
hallucinations or automatisms are misleading and
frequently considered as manifestations of
neurodegenerative or psychiatric disorders
15. • There is a different distribution of seizure types and
epilepsy syndromes in the elderly compared to
younger patients.
• 1- Primary generalised epilepsy rarely occur
• 2- The majority of seizures are partial, either simple,
complex or secondarily generalised.
• 3-Status epilepticus, both convulsive and non-
convulsive, is relatively common in the aged,
16. • the diagnosis becomes challenging because the
symptomatology of simple and complex partial
seizures can be subtle. elderly patients do not
exhibit automatisms; consequently, a disturbance
of consciousness with a blank stare or brief gaps
in conversation or periods of confusion may be
the only manifestation of a complex partial
seizure.
• One of the most striking differences between
older and younger adults is the length of the
postictal confusional state, which may last for
hours, days, or even l to 2 weeks in older patients
compared with minutes in younger adults.
17. • Electroencephalograms (EEGs) often are
nonspecific, showing focal or generalized slowing
in this population, or are even normal (31%).
• Interictal epileptiform activity is present in only
26% to 38% of initial EEGs of patients ultimately
diagnosed with seizures
• Few seizures after stroke (only 10% to 20%) and
few cerebral tumors (10% to 20%) have interictal
epileptiform activity on EEG
19. Common differential diagnoses of
seizures
• Neurological
– TIA
– Migraine
• Cardiac
– Vasovagal syncope
– Arrhythmias
• Metabolic
– Hypoglycemia
• Psychiatric
– Non-epileptic seizures
20. Diagnostic evaluation
• A thorough history, examination, neuroimaging,
and EEG are indicated in the diagnostic
evaluation. If collectively the results are
inconclusive, then prolonged inpatient EEG video
monitoring is recommended.
21. History:
• from the patient and observers
• Seizures are, paroxysmal, unpredictable, and
usually stereotyped from patient to patient.
• Focal paroxysmal transient deficits in language,
memory,motor, or sensory testing can occur not
only with TIAs and such syndromes as transient
global amnesia but also as the first manifestation
of partial seizures (aura) or more commonly after
a seizure (postictal Todd paralysis).
• By history, the description can help with seizure
recognition and localizationof the potential focus,
which may be further supported by examination
andimaging findings.
22. • Before the event
– Provoking factors
– Preceding symptoms (aura)
– Duration of symptoms
• During the event
– Motor symptoms
– Level of consciousness
– Injury
– Incontinence
– Duration
• After the event
– Confusion
– Focal neurologic signs
– Duration
23. Physical examination
• General examination
– Injury or Signs of infection
• Neurological examination
– Assess mental status
• Post-ictal state
– Look for focality, may be indicative of an underlying
lesion or a Todd’s paralysis
• Cardiological examination (to exclude)
– arrhythmia or orthostatic hypotension
– A tilt table test can be helpful diagnostically in this population,
particularly if it reproduces exactly the reported stereotyped
symptoms
24. Neuroimaging:
• Neuroimaging is essential in the evaluation,
particularly in older patients whose seizures are
often attributable to structural abnormalities.
• Magnetic resonance imaging (MRI) is the imaging
of choice in patients with epilepsy and is
particularly useful in those:
who have suggestions of a focal seizure onset
from history, examination or EEG.
in whom seizures continue in spite of first line
medication
• Computed tomography (CT) scan has a role in
the urgent assessment of seizures or when MRI
is contraindicated
25. EEG
• Routine recording is 30 minutes
• Looking for:
– Background rhythm. May be generally slow in
dementia. Focally slow with tumor or stroke
– “Epileptogenic” features, like sharp waves or spikes
• May be normal or non-specific in ~50% of seizure
patients, Rare to capture a seizure, normal EEG doesn’t
exclude epilepsy
• interictal epileptiform activities were recorded less often
(26-37%)
• specific indication for EEG recording in elderly patients,
even in emergency conditions, is the suspicion of non
convulsive status epilepticus when the patient is
confused without known aetiology as metabolic disorder.
26. Inpatient electroencephalogram video
monitoring
• Long-term video or ambulatory EEG may be used
in the assessment of individuals who present
diagnostic difficulties after clinical assessment
and standard EEG
27. Other required investigations
• Routine blood studies are indicated to identify
common metabolic causes of seizure such as
abnormalities in electrolytes, glucose, calcium,
magnesium, hepatic and renal diseases.
• Screening for toxins is sometimes done.
• Lumbar puncture is necessary when meningitis or
encephalitis is suspected
• Electrocardiogram (ECG) should be performed in
the assessment of all elderly patients with altered
consciousness, when cardiac arrhythmias can
simulate epilepsy
28. When to start treatment
• After one unprovoked seizure?
– Recurrence in elderly: 34% in 5 years
– Higher risk of recurrence if:
• Underlying structural brain lesion
• Abnormal EEG
• in patients with Todd’s paralysis
• After more than one?
– The risk of seizure recurrence after 2 unprovoked
seizures is 73%.Antiepileptic drugs therefore should
be offered to the patient after explaining the risks and
benefits and after assessing his/her preferences
32. Special considerations in the elderly
• Decreasing renal and hepatic function
• Decreased ratio of muscle to fat
• Decreased binding of drugs to albumin
• Higher susceptibility to toxicity
• Polypharmacy
34. • Consider side effects profile, cost of the drug
• Start with low dose of 1st line antiepileptic drugs (AEDs) is
often necessary due to age-related changes in renal and
hepatic function (monotherapy)
• Increase dosage gradually till least effective dose to
minimize side effects.
• Monitor drug response by:
– Reduction in seizure frequency
– Reduction in seizure severity
– Onset of side effects
– Not by drug therapeutic level
35. • When initiating therapy, increase doses slowly,
until seizure control is achieved or side effects
occur. If seizures are controlled, obtain a serum
concentration at that time. This will identify the
patient’s ‘therapeutic optimal level’.
• Routine checking of antiepileptic drug levels
without a clear clinical indication is not required,
and is not cost-effective
36. Pt not controlled:
Change to another drug (1st line therapy) with tapering
the 1st drug gradually after 2nd drug become
therapeutic. (add on therapy)
• In patients resistant to monotherapy:
1- review diagnosis of epilepsy, adherence to
medication.
2-Combination of 2 of 1st line drugs the first is the drug
produced well tolerated improvement in seizures
control but fail to produce seizure freedom at
maximal dose
3- the 2 drugs better to have different mechanisms of
action, but both matches epilepsy type. Maximal 3
drugs.
37. Monitor antiepileptic drug
• Antiepileptic drug levels may help clinical
management under the following clinical
indications:
• (1) Baseline therapeutic optimal level ?!
• (2)assessment of compliance to drug treatment
for patients with refractory epilepsy compared to
• (3)assessment of symptoms due to possible
antiepileptic drug toxicity
• (4) titration of phenytoin dose.
40. Monitor side effects
• According to antiepileptic drug :
• Types of adverse effect
• Idiosyncracy
• Dose dependent: mostly appear within 6 months
of treatment (not followed after 6 m)
44. Decision to Stop Treatment
• If the patient has been seizure free for at least
three years(3-5), particularly if epileptiform activity
has disappeared from the EEG risk factors for
recurrence include slowing or spikes (maximum
risk with both present) on EEG (not mandatory),
the possibility of ceasing antiepileptic drug
therapy could be considered.
• If the patient has had multiple seizures prior to
commencing treatment, or the epilepsy has been
difficult to control, a more conservative approach
is recommended, and medication should be
continued longer term.
45. • If medication is to be withdrawn, this should
be done gradually over (6 weeks ) several
months and even more slowly for
barbiturates.
• Recurrence of seizures with medication
withdrawal, prior medication should be
reinstituted at the previously effective levels.
48. Other treatment options:
• Vagus nerve stimulation is indicated for
adjunctive therapy and has been shown to reduce
frequency of seizures in patients refractory to
antiepileptic medication who are not suitable for
epilepsy surgery. This includes adults whose
epileptic disorder is dominated by partial seizures
(with or without secondary generalisation) or
generalised seizures
49. Resective Surgery for Epilepsy in
Older Adults
• In younger adults, temporal lobectomy, the most
common surgical procedure for epilepsy, is readily
performed in most settings and its efficacy and
safety have been well documented.
• the risk of complications is somewhat higher
compared with that in a younger control group. The
finding of lower post-operative neuropsychological
performance is a cause for concern. The debate will
probably continue as to whether epilepsy surgery
should be performed in older adults. Clearly, more
care must be taken with epilepsy surgery
evaluations before any decision is made to proceed
with a resective procedure. Nevertheless, some
individuals can benefit from surgery.
50. Status epilepticus
• Status epilepticus is defined as a condition in
which epileptic activity persists for 30 minutes or
more. The seizures can take the form of
prolonged seizures or repetitive attacks without
recovery in between.
• Non conulsive status epilepticus: NCSE
• The diagnosis of NCSE is critically dependent on
EEG. In patients with a previous diagnosis of
epilepsy, any prolonged change in personality,
prolonged postictal confusion (greater than 30
min) or recent-onset psychosis should be
investigated with EEG as these can all be
presentations of NCSE
52. Causes of Status epilepticus
• Anticonvulsant non compliance
• Infection
• Pre-existing epilepsy
• Metabolic
• Acute stroke
• Tumor related
• Alcohol or other drug withdrawal
• Drug intoxication
• Acute hypoxic–ischemic encephalopathy
• Acute trauma
• Miscellaneous or undetermined
53. Treatment of Status Epilepticus in Older
People
• Status epilepticus is treated in a manner similar to
younger patients.
• Initial management:
• Assessment and control of airways and ventilation
• Arterial blood gas monitoring
• Electrocardiogram (ECG)
• Blood pressure monitoring
• Intravenous (i.v.) glucose and thiamine
• Emergency measurement of antiepileptic drug levels
• Emergency measurement of electrolytes and magnesium
• Full haematological screen
• Measurement of hepatic and renal function
57. • For adult patients with severe traumatic brain injury
(TBI) (typically with prolonged loss of
consciousness or amnesia, intracranial hematoma
or brain contusion on computed tomography [CT]
scan, and/or depressed skull fracture):
• Prophylactic treatment with phenytoin, beginning
with an intravenous (IV) loading dose, should be
initiated as soon as possible after injury to decrease
the risk of post-traumatic seizures occurring within
the first 7 days (Level A).
• Prophylactic treatment with phenytoin,
carbamazepine, or valproate should not routinely be
used beyond the first 7 days after injury to decrease
the risk of post-traumatic seizures occurring beyond
that time (Level B).
59. • The 30-day risk of seizures after ICH is about 8%.
Seizures most commonly occur at the onset of
hemorrhage and may even be the presenting symptom.
Lobar location is an independent predictor of early
seizures.
• Although, no randomised trial has addressed the
efficacy of prophylactic antiepileptic in ICH patients, the
Stroke Council of the American Heart Association
suggest prophylactic antiepileptic treatment may be
considered for 1 month in patients with intracerebral
hemorrhage and discontinued if no seizures are noted.
• Acute management of seizures entail administering
intravenous lorazepam (0.05–0.10 mg/kg) followed by an
intravenous loading dose of phenytoin or fosphenytoin
(15–20 mg/kg), valproic acid (15–45 mg/kg), or
phenobarbital (15–20 mg/kg).
61. • Patients who develop recurrent early or late
postischemic stroke seizures generally require
pharmacological treatment.
• An observational hospital-based study and a
prospective cohort study showed that 54% and 67% of
patients with cerebral infarction and epilepsy were
seizure-free for at least 1 year with the majority of
patients being treated with a single drug
• phenytoin benzodiazepines lamotrigine, topiramate,
levetiracetam and zonisamide have neuroprotective
properties and might, therefore, have beneficial effects
when used to treat seizures in the setting of hyperacute
stroke
62. • However, there remain no clinical data that
administration of anticonvulsant drugs after stroke, or
other acute brain injuries, prevents the later
development of epilepsy
• Based on experimental studies, there is some concern
that the use of phenytoin, phenobarbital, and
benzodiazepines may impair poststroke recovery
64. • In patients with newly diagnosed brain tumors,
anticonvulsant medications are not effective in
preventing first seizures. Because of their lack of
efficacy and their potential side effects, prophylactic
anticonvulsants should not be used routinely in
patients with newly diagnosed brain tumors
• in patients with brain tumors who have not had a
seizure, tapering and discontinuing anticonvulsants
after the first postoperative week is appropriate,
particularly in those patients who are medically
stable and who are experiencing anticonvulsant-
related side effects