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Epilepsy is
defined as a brain disorder involving recurrent seizures and
is the most common chronic neurological disorder in the
adolescents. There are about 40 million people are affected worldwide.
With increasing
surgical advances, the present day Neurosurgeons do not seem to pay much
attention to this common
presenting symptom in Neurology, and leave it to the physicians. Surgeons
should be aware of the basics and something about the recent trends in
epilepsy. With the rebirth of 'Surgery for Epilepsy', it is all the more
important.
SURGICAL NEUROPHYSIOLOGY:
Normal cells
have both inhibitory and excitory influences causing excitory and
inhibitory postsynaptic potentials (EPSPs and IPSPs). Once a critical
membrane depolarisation occurs an action potential is propagated. This leads to firing of
individual neurons in a repetitive fashion.
Focal
discharge:
Neurons in
epileptogenic foci exhibit a different pattern with a parodoxical
depolarisation shift (PDS) which is more prolonged than the EPSP. Such
'group 1' neurons are found at the centre of an epileptic focus and fire
spontaneously, acting as a pace maker. The surrounding 'group 2' neurons
are influenced and recruited, resulting in a focal seizure and
corresponding EEG discharge.
The pathological
changes capable of giving rise to fits are diverse.
There is selective loss of inhibitory interneurons within epileptic foci.
Decreased GABA content may be found in the epileptic foci.
There may be loss of dendritic spines and terminal branches.
A scar in the
brain is NOT a focus. A dead neuron does not cause abnormal discharge.
It is the
partially damaged surrounding neurons that are hyper excitable, and hyper
metabolic during the ictus and hypo metabolic during the interictal
phase.
These give rise
to hyper excitability and paradoxical discharge either due to cortical
deafferentation and resultant receptor super-sensitivity.
Increased
numbers of fibrous or reactive glial cells might impair extra-cellular K+
and excitary neurotransmitters contributing to membrane instability, and
may be an additional cause for focal discharge.
The
spread:
Normal
consciousness is maintained by the interaction of cortical
structures with brainstem reticular formation. The nonspecific
thalamo-cortical pathways synchronize the cortical activity when a
discharge arises primarily at a reticular or thalamic
level or secondarily to a focal cortical discharge.
The bilateral
cortical role is of primary importance in generalized discharges. This
synchrony is disrupted in corpus callosum section.
A focus in one
hemisphere may, after a latent
period, lead to the
development of spike discharges from the contra lateral homologous cortex
(Mirror focus). Eventually the mirror focus may become independent.
Commisurotomy
prevents the development of mirror focus.
CLASSIFICATION
OF SEIZURES :
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InTERNATIONAL
LEAGUE AGAINST EPILEPSY CLASSIFICATION (1989)
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1)
Partial (focal, local) seizures
a) Simple partial seizures (consciousness not impaired )
1) with motor signs
2) with somatosensory or special sensory symptoms
3) with autonomic symptoms
4) compound forms
b) Complex partial seizures (with impairment of consciousness)
1) Simple partial followed by impairment of consciousness
2) Impairment of consciousness at onset
c) Partial seizures with secondary generalization
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2)
Generalized seizures (convulsive or nonconvulsive )
a)
Tonic-Clonic (grand mal)
b)
Petit mal (absence)
c)
Atonic (drop attack)
d)
Tonic
e)
Clonic
f)
Myoclonic
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3) Unclassified epileptic seizures
(with incomplete data)
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1)
Partial (Focal) Seizures:
A partial, or
focal, seizure is the more common type of epilepsy and is caused by a
disorder of a neuron population in a specific site on one side of the
brain. They are further categorized as simple partial, complex partial,
and secondarily generalized seizures.
A person with a
SIMPLE partial seizure (sometimes known as Jacksonian epilepsy) does not
lose consciousness but may experience confusion, jerking movements,
tingling, or odd mental and emotional events, such as deja vu, mild
hallucinations, or extreme responses to smell and taste. After the
seizure, the patient usually has temporary weakness in certain muscles.
Slightly over
half the seizures in adults are COMPLEX partial types, and about
80% of these seizures originate in the temporal lobe of the brain, which
is located close to the ear. Disturbances there can result in loss of
judgment, involuntary or uncontrolled behavior, or even loss of
consciousness. About 20% of these patients have seizures that start in
the frontal lobes of the brain.
Prior to the
actual seizure, people sometimes experience a warning sign, known as an
aura, which can be an odd odour or a visual or auditory hallucination.
People with a
complex partial seizure may lose consciousness briefly and appear to
others as motionless with a vacant stare. Emotions can be exaggerated,
and some sufferers appear to be drunk.
After a few
seconds, some may begin to perform repetitive movements, such as chewing
or smacking of lips.
Episodes usually
last no more than two minutes, and people can have them infrequently or
as often as every day. A throbbing headache may follow this seizure.
Aura alone is a
partial seizure !!
In some cases,
simple or complex partial seizures evolve into generalized seizures,
which are known as secondarily generalized seizures .The progress may be
so rapid that the partial stage is not even noticed.
2)
Generalized Seizures:
Generalized
seizures are caused by disturbances of nerve cells in more diffuse areas
of the brain than with partial seizures and therefore have a more serious
affect on the patient.
The first stage
of a GRAND MAL seizure is called the tonic phase , in which the
muscles suddenly contract, causing the patient to fall and lie rigidly
for about 10 to 30 seconds. Some people experience a premonition or aura
before a grand mal or tonic-clonic seizure; most, however, lose
consciousness without warning.
If the throat or
larynx is affected, there may be a high-pitched musical sound called
strider when the patient inhales.
Spasms occur for
about 30 seconds to a minute as the seizure enters the clonic phase, when
the muscles begin to alternate between relaxation and rigidity. After
this phase, the patient may lose bowel or urinary control.
The seizure
usually lasts a total of two to three minutes, after which the patient
remains unconscious for a while and then awakens to confusion and extreme
fatigue. A severe, throbbing headache, similar to migraine, may also
follow the tonic-clonic phases.
PETIT
MAL or absence seizures are brief (3 to
30 seconds) and may consist of only a short cessation of physical
movement and loss of attention. They may even pass unnoticed by others.
Small children may simply be observed staring or walking distractedly.
Petit mal may be confused with simple or complex partial seizures; in
petit mal, however, a person loses consciousness and may experience
attacks as often as 50
to 100 times a day
About 25% of
patients with petit mal develop grand mal seizures.
A person who has
an ATONIC or akinetic, seizure loses muscle tone. Sometimes it may
affect only one part of the body, so that, for instance, the jaw slackens
and the head drops. At other times, the whole body may lose muscle tone,
and the person suddenly falls. A brief atonic episode is known as a drop
attack.
In TONIC
seizures, the muscles contract and consciousness is altered for
about 10 seconds, but the seizures do not progress to the clonic or
jerking phase.
CLONIC
seizures, which are very rare, occur
primarily in young children, who experience spasms of the muscles but not
the tonic rigidity.
MYOCLONIC
seizures are a series of brief,
jerky, contractions of specific muscles groups ,such as the face or
trunk.
3)
Unclassified seizures:
They include all
seizures that cannot be classified because of inadequate or incomplete
data.
EPILEPSY
SYNDROMES:
Epilepsy is also
classified by syndrome or grouped according to a set of common
characteristic, such as age, type of seizure or seizures, or whether a
cause is known or not (idiopathic).
A few syndromes
and inherited epilepsies are listed below:
They by no means
represent all epilepsies:
West
syndrome (also called
infantile spasms), a disorder that involves spasms and developmental delay in
children within the first year, usually infants between four and eight
months.
Benign
familial neonatal convulsions, a rare inherited form of generalized seizures
that occur in infancy.
Juvenile
myoclonic epilepsy (impulsive petit mal), characterized by generalized
seizures, usually tonic-clonic signalled by myoclonia (jerky movements)
or absences. This accounts for 7% of epilepsies usually occurring in
individuals ages 8 to 20.
Lennox-Gastaut
syndrome, a severe form
of epilepsy in young children that causes multiple seizures and some
developmental retardation. It usually involves absence, tonic, and
partial seizures.
Myoclonic-astatic
epilepsy (MAE), a
combination of myoclonic seizures and atstasia (which involves loss of
muscular coordination).
Progressive
myoclonic epilepsy , an inherited disorder occurring between the ages
six and 15.It usually involves tonic-clonic seizures and marked
sensitivity to light flashes. Although previously the disease was
considered to be progressive throughout life, current therapies have significantly
improved its outlook.
Autosomal
dominant nocturnal frontal lobe epilepsy, a rare inherited epilepsy that usually occurs
during childhood, on average at 11 years (although onset varies widely
within families). Seizures can be dystonic (twisting contractions), tonic
(muscle contractions), or involve thrashing around. They are brief,
frequent, and occur in clusters during the night. The seizures often
subside with age.
Landa-Kleffner
syndrome, an epileptic
condition that results in the inability to communicate either with
speech or by writing (aphasia).
CAUSES
OF SEIZURES:
Some of the more
common causes of seizures include:
1) Idiopathic
(no identifiable cause)-
usually begin between ages 5 to 20, can occur at any age,
no other neurological abnormalities present,
often a family history of epilepsy or seizures.
2) Congenital
defects and perinatal (near the time of birth) injuries-
seizures usually begin in infancy or early childhood.
3) Metabolic
abnormalities-
may affect any age,
diabetes mellitus complications, electrolyte imbalances, kidney failure,
uremia
Nutritional deficiencies,
Phenylketonuria (PKU)--can rarely cause seizures in infants,
Intoxication / withdrawal from alcohol or drugs,
4) Degenerative
disorders (senile dementia Alzheimer type, or similar organic
brain syndromes)-
mostly affect older people.
5) Disorders
affecting the blood vessels (stroke, TIA, and so on)-
most common cause of seizures after age 60.
6) Tumors and
brain lesions –
may affect any age, more common after age 30,
partial (focal) seizures most common initially, may progress to
generalized tonic-clonic seizures.
7) Infections –
may affect all ages,
may be a reversible cause of seizures,
brain infections (meningitis, encephalitis), brain abscess,
acute severe infections of any part of the body, due to high fever,
chronic infections (such as neurosyphilis),
complications of AIDS or other immune disorders.
8)
Post-traumatic seizures-
(a) Early
(within the 1st week):
The risk of early seizures after brain injury is 2.5% to 7%.
About 35% of acute SDHs and ICHs, and 10% of EDHs,10% of Depressed
fractures,10% of patients with PTA lasting for more
than a day are at risk. 60% of them
go on for late seizures.
1/3 of all early seizures occur within 1st hour,1/3 within 24hrs and 1/3
between the 2nd and 7th days.
More than half of all seizures are focal.
Studies suggest
that anticonvulsants are administered only after the 1st seizure and that
prophylactic therapy has no role.
(b)
Late (after a week):
The risk is reported to be 5% in a series of unselected patients. 50% of
all SDHs and ICHs, 20% of EDHs and 60% of all with
neurological deficit or those with Depressed fractures with dural tear or
those with PTA lasting for more than a day or the patients
with early seizures run the risk.
They are more likely to have persistent epilepsy.
9) Post operative
seizures-
The risk varies with the condition for which craniotomy was done.
The incidence after tumor surgery is obviously more difficult to
assess, with various surgical techniques and the natural
history of the tumor. Fronto parietal lesions are more prone.
It is suggested that the incidence
is
20% following craniotomy for gliomas.
9% following burr hole/stereotactic biopsy.
22%
following craniotomy for meningiomas
6% following craniotomy for suprasellar lesions.
24%
following shunt procedures (more with revisions).
95% following craniotomy for supratentorial abscesses
20% of the patients undergoing aneurismal surgery will have seizures,
preoperative hematoma and other conditions and surgical techniques do
have a role.
All things being equal, the incidence
is
38% following MCA aneurismal surgery.
21%
following A.COM.A aneurismal surgery.
7.5% following internal carotid aneurismal surgery.
37% of all who
experience postoperative seizures do so within the 1st week and 40% of
this group continue to experience seizures later. Only 5% of those
developing seizures later than one week postoperatively have
a single
seizure.
MANAGEMENT:
Investigations:
Despite numerous
technologic advances in the evaluation of neurological disorders,
diagnosis of the first seizure is still based predominantly on the patient's
medical history.
Many paroxysmal
events may be confused with epileptic seizures, including syncope,
movement disorders, and psychogenic seizures.
Probably the
most common entity that is confused with epileptic seizures is syncope.
Diagnostic
studies must be tailored to individual patients.
1) Basic
laboratory evaluation focuses on detecting systemic
disturbances potentially associated with seizures and
includes a complete blood count and measurements of
electrolytes, calcium, magnesium, phosphorus, blood urea nitrogen,
creatinine and glucose.
2) Consideration
also should be given to obtaining a toxicology screen and evaluating
hepatic function with synthetic and enzyme studies.
3) Lumbar
puncture is essential in patients in whom meningitis or encephalitis is
suspected, as well as in immuno-compromised patients, since occult
meningitis is a common finding in this group.
4) All patients
who experience an unprovoked seizure undergo a brain imaging study in an
effort to detect underlying cerebral lesions e.g., tumor,
abscess, vascular malformation, stroke, and traumatic injury.
MRI is the
procedure of choice. In patients presenting with a seizure in whom the
history/examination suggests new focal deficits, persistent altered mental
status, fever, recent trauma, persistent headache, cancer, treatment with
anti-coagulation or immunocompromised state, emergency neuroimaging is
recommended.
5)
Electroencephalography (EEG) is often helpful in the evaluation of
patients presenting with a seizure.
The
utility of EEG includes
- Detection of epileptiform activity, strengthening the diagnosis;
- Identification of focal electro cerebral abnormalities suggesting
a focal structural brain lesion;
- Documentation of specific epileptiform patterns associated with particular
epilepsy syndromes.
for example, generalized spike and-wave
discharges associated with a generalized epilepsy, or focal discharges
associated
with a localization-related
epilepsy).
- While planning surgical treatment for a refractory epilepsy.
- EEG can predict the risk of recurrent seizures.
- EEG findings should be reviewed with other parameters.
People
with epilepsy may have normal EEG and normal EEG alone does
not rule out epilepsy.
Medical
management:
Modern treatment of seizures started in 1850 with the
introduction of bromides, on the basis of the theory that epilepsy was
caused by an excessive sex drive. In 1910, phenobarbital, which then was
used to induce sleep, was found to have antiseizure activity and became
the drug of choice for many years. Since then many drugs are in use.
Some physicians
prefer not to prescribe ongoing antiepileptic therapy or patients with a
single seizure and the decision to treat initial seizures with medication
remains controversial.
Several factors
should be considered when making a decision, including he likelihood of
recurrent seizures, the risk of the treatment itself, he ability of the
treatment to decrease the risk of recurrent seizures and the
consequence of further seizures to the patient.
Since these
factors vary from patient to patient, treatment decisions need to be
individualized.
The goal of
treating patients with epilepsy is to control seizures completely without
causing unacceptable side effects. In the past several years, a number of
new antiepileptic drugs have become available, and more will soon be
released. To achieve optimal treatment results, several strategies should
be used.
The most
important step is to select an antiepileptic drug that is appropriate for
the patient's particular type of epilepsy. Specific epilepsy syndrome
diagnosis is based on the history of the patient’s seizure types,
neurological status and EEG findings.
From the
appropriate medications, choose the agent best suited for he patient
based on patient and medication characteristics.
Initiate and
titrate the medication at appropriate dosages.
Increase the
medication, regardless of serum levels, until complete seizure control is
achieved or until persistent and unacceptable side effects occur.
If satisfactory
seizure control is not achieved, change to another agent appropriate for the epilepsy
syndrome being treated; the goal should be antiepileptic drug monotherapy
in each patient, when possible. Plasma
drug level monitoring is useful when compliance or toxicity is suspected.
Antiepileptics:
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Antiepileptics
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indications
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DOSAGE
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SIDE EFFECTS
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The Barbiturates, Phenytoin,
Valproic acid, and Ethosuximide have been in
use for long and are considered as the first line drugs.
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Phenobarbital
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may be effective, especially in
children, in the treatment of both generalized and simple partial
seizures, including status epilepticus.
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Maintenance doses average 3 to 5
mg/kg/day.
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sedation and ataxia and
hyperactivity is occasionally evident. Risk for idiosyncratic hepato-
toxicity and for rash is probably not dose related.
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Phenytoin
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effective in the treatment of both
generalized and partial seizures may be administered
intravenously as treatment for status epilepticus.
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Maintenance doses average 4 to 7
mg/kg/day. Intravenous infusion of a loading dose (18 mg/kg) should be
performed slowly and cautiously due to risk of hypotension.Oral
absorption is slow.
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sedation and ataxia.
Long-term use may be complicated by gingival hyperplasia,
hirsutism, or lymphadenopathy. Potential idiosyncratic side
effects include rash, hepatotoxicity, or a lupus-like syndrome.
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Valproic acid
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useful in treating a variety of
generalized (tonic-clonic, absence) and partial seizure disorders as
well as some myoclonic epilepsies. It is particularly useful in
treatment of mixed seizure disorders.
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Maintenance doses range from 30 to
60 mg/kg/day PO.
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sedation, GI
upset, thrombo cytopenia, and hyperammonemia. Fulminant hepatotoxicity
is the most feared idiosyncratic complication of therapy;
children under 2 years of age and children receiving multiple
anticonvulsants appear to be at greatest risk.
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Ethosuximide
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primarily in the treatment of
absence (petit mal) epilepsy and occasionally as an adjunctive agent in
other generalized seizure disorders
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Maintenance doses average 20 to 30
mg/kg/day.
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sedation, headache, and stomach
upset. Idiosyncratic reactions may include rash or blood dyscrasias.
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carbamazepine,
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effective against both partial and
secondarily generalized seizures
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Maintenance doses average 10 to 20
mg/kg/day PO.
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stomach upset, sedation, and
ataxia. Potential idiosyncratic reactions include leukopenia
,aplastic anemia, rash and Stevens-Johnson syndrome.
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NEWER
DRUGS (recommended as adjunctive therapy)
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Gabapentin(Neurontin)
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Adjunctive therapy for partial
seizures with or without secondary generalization
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Begin with 300 mg daily; increase
to 900 to 1,800 mg daily given every 6-8hrs
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Somnolence,
fatigue, ataxia, dizziness, gastro intestinal upset, dyspnoea.
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Lamotrigine(Lamictal)
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Adjunctive therapy for partial
seizures with or without secondary generalization
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Begin with 50
mg daily; increase to 300 to 500 mg daily given every 12 hours;
for
concomitant use with valproic acid : begin with 25 mg every other day;
increase to 150 mg daily given every 12 hours
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Rash, including life-threatening
rashes, dizziness, ataxia, blurred vision, nausea.
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Felbamate(Felbatol)
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Adjunctive therapy or monotherapy
in adults when seizures are so severe as to warrant use despite risk of
aplastic anemia or hepatic failure; in children with Lennox-Gastaut
syndrome when seizures are not controlled
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Adults: begin
with 1,200 mg daily given every 6 to 8 hours
children:
15 to 45 mg per kg per day given every 6 to 8 hours;
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Anorexia, vomiting, insomnia,
somnolence, aplastic anemia, hepatotoxicity,
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Topiramate(Topamax)
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Adjunctive therapy for partial
onset of seizures
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Begin with 50 mg daily; increase
to 50 to 400 mg daily given every 12 hours
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Dizziness,
somnolence, ataxia, confusion, fatigue, paresthesias, speech
difficulties,
side
effects: diplopia, impaired concentration and nausea
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Fosphenytoin(Cerebyx)
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Status
epilepticus; parenteral maintenance of phenytoin levels;parenteral
treatment and/or prevention of seizures
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For status epilepticus: 22.5 to 30
mg per kg IV
for nonemergent therapy: 15
to 30 mg per kg IV or IM, followed by 6 to 12 mg per kg IV
orIM
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Pruritus, nystagmus, dizziness,
somnolence, ataxia, nausea, tinnitus, hypotension.
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Only phenytoin and phenobarbital can be administered
parenterally; all others must be taken orally, which precludes their use
in acute seizure control.
The complex pharmacokinetic and pharmaceutical properties of
antiepileptic drugs make administration difficult at times. Many of
these drugs are potent enzyme inducers or inhibitors, and significant
drug interactions occur when they are co administered with hormones or
other medications.
AEDs & oral contraceptives:
Carbamazepine, phenytoin, phenobarbital, primidone,
and ethosuximide will reduce estradiol levels by 40% through their
effect on the P450 system, and they may also reduce free progestin levels.
The dosage of the hormonal components need to be increased..
Valproic acid and gabapentin do not induce the P450 system,
and do not affect oral contraceptive levels.
Pregnancy and AEDs:
Most women with epilepsy today can conceive and bear normal,
healthy children, but their pregnancies present an increased risk for
complications. Epileptics who are
on anticonvulsant therapy during pregnancy have a 5% risk of fetal
malformations, which is double the risk seen in the general population. Clinicians
are uncertain how much of the adverse outcome is secondary to AED,
maternal seizures, or simply to the genetics of having epilepsy. The most common birth defects in this
group are cleft lip / cleft palate and congenital heart defects. In
addition, 1% of epileptic women treated with valproic acid during
pregnancy will have a baby with neural tube defects, and 5%-10% of
fetuses exposed to hydantoin will have fetal hydantoin syndrome, which
includes microcephaly growth deficiency developmental delays and mental
retardation, dysmorphic craniofacial features, and hypoplasia of nails
and distal phalanges. Despite this, it is well recognized
that the benefits of anticonvulsant therapy in pregnancy outweigh the
risks as long as the therapy is truly necessary, and women with epilepsy
who are considering pregnancy be reevaluated by a neurologist to confirm
their true need for anticonvulsant therapy. As
the pregnancy progresses, a woman may need more of the drug to remain in
the therapeutic range. Later in pregnancy, when seizures can also be
induced by other causes, such as hypertension, hyponatremia, and
hypoalbuminemia, higher doses may be needed.
Although it hasn't been proven to reduce the risk of neural
tube defects in exposed babies, many would agree that women on valproic
acid or carbamazepine should take 4 mg of folic acid a day rather than
0.4 mg before conception and during the first trimester.
Breastfeeding and AEDs:
Carbamazepine, valproic acid, and phenytoin are compatible
with breastfeeding; a very small amount of these drugs is excreted into
breast milk and has no apparent effect on the baby.Phenobarbital,
however, is excreted in large amounts into breast milk and is not
compatible with breast-feeding, because it may cause sedation and CNS
depression in the baby.
STATUS
EPILEPTICUS:
Definition:
According to the
International Classification of Seizures, it is ''a condition
characterized by an Epileptic seizure that is so frequent or so
prolonged as to create a fixed and lasting condition".
It is an
emergency.
Diagnostic
evaluation:
Immediately
arrange for complete blood count, a serum chemistry profile, and drug
screen.
Assess for
possible drug intoxication or drug withdrawal.
Keep in mind
that anticonvulsant drug withdrawal is a common cause of status
epilepticus.
Obtain an
arterial blood gas if there is evidence of respiratory compromise.
Management:
It is important
to establish that there is no respiratory compromise and no evidence of
cardiovascular collapse. Preparation for possible intubation should be
made. Correction for metabolic disturbance, if present, is clearly
indicated. Low serum Na+, glucose, Ca++, or Mg++ can result in recurrent
seizure activity. Drug or alcohol withdrawal, or certain drug
intoxication, can be precipitating factors.
It is important
to recognize that withdrawal from phenobarbital generally requires
resumption of phenobarbital with a loading dose, which will necessitate
intubation with respiratory support.
An intravenous
line is mandatory.
One of the drug
regimes, suggested, is given below.
Initial, i.e.,
short-term, control of generalized seizure activity can often be obtained
with either intravenous lorazepam, at a dose of 0.1 mg/kg, or diazepam at
0.2 mg/kg. Either agent is infused over two minutes.
It is important
to recognize that these agents can promote respiratory depression at
relatively small doses in certain individuals.
Lorazepam's effect is longer lasting (hrs) and diazepam (hrs). If either of these agents is used,
it is with the understanding that longer term, i.e., maintenance, therapy must also
be initiated unless there is recognized metabolic derangement that can be
rapidly corrected.
The phenytoin
loading dose in status epilepticus is 15 to 20 mg /kg at maximum
intravenous infusion rate of 50mg /min over 10 minutes. Fosphenytoin, if
available is ideal alternative for phenytoin and has no risk of cardiac
events.
If the patient
continues to have seizure activity despite adequate intravenous loading
with phenytoin, then phenobarbital loading is indicated. Phenobarbital is
given at an intravenous dose of approximately 20 mg/kg at an infusion
rate of no more than 1.5 mg/kg/min.
If this is
unsuccessful, then intravenous pentothal is given at a loading dose of 3
to 4 mg/kg over two minutes followed by a continuous infusion at a rate
of 0.2 mg/kg/min. The dose is then adjusted upward, every 3 to 5
minutes by 0.1 mg/kg/min, until the EEG, if available bed side, becomes
isoelectric.
SURGERY for intractable Epilepsy:
(A detailed
account is beyond the scope of this article.)
Surgery can be
considered in certain patients with surgically remediable syndromes.
Candidates typically have seizures that impair consciousness, that cause
falling with injury, that have adverse psychosocial or social effects,
and that persist after trials of three appropriate medications. A
multidisciplinary evaluation should take place at a surgery centre with
experience and documented success.
Favorable
results from surgery can be expected in a large proportion of patients.
CONCLUSION:
Patients with
epilepsy now have available to them more therapeutic options than ever
before. In order for patients to benefit from these advances, physicians
must make an accurate diagnosis of epilepsy syndrome, selecting and using
medications properly, and promptly referring patients who do not
completely respond to treatment to a comprehensive epilepsy centre.
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