Вы находитесь на странице: 1из 5

Risk factors

A risk factor is something that makes a person more likely to


develop seizures and epilepsy. Sometimes a risk factor can
cause scarring of the brain or lead to areas of the brain not
developing or working right. Risk factors include:
Babies who are born small for their age
Babies who have seizures in the first month of life
Babies who are born with abnormal areas in the brain
Bleeding into the brain
Abnormal blood vessels in the brain
Serious brain injury or lack of oxygen to the brain
Brain tumors
Infections of the brain: abscess, meningitis, or encephalitis
Stroke resulting from blockage of arteries
Cerebral palsy
Conditions with intellectual and developmental disabilities
Seizures occurring within days after head injury ("early
posttraumatic seizures")
Family history of epilepsy or fever-related seizures
Alzheimer's disease (late in the illness)
Autism spectrum disorder
Fever-related (febrile) seizures that are unusually long
Long episodes of seizures or repeated seizures called status
epilepticus
Use of illegal drugs such as cocaine

Mild head injuries, such as a concussion with just a very brief


loss of consciousness, do not cause epilepsy. Yet the effects
of repeated mild head injuries and epilepsy is unknown.
Although the disorders and injuries on these lists help to explain
many cases of epilepsy, more people with epilepsy don't have any
of these. Often we just don't know how or why epilepsy gets
started.
http://www.epilepsy.com/learn/epilepsy-101/what-are-risk-factors
Authored by: Steven C. Schachter, MD | Patricia O. Shafer,
RN, MN | Joseph I. Sirven, MD on 7/2013
Reviewed by: Joseph I. Sirven, MD | Patricia O. Shafer, RN,
MN on 3/2014

Pathophysiology
Seizures are defined as paroxysmal events of transitory alteration
in consciousness or other signs or symptoms that can be due to
brain dysfunction. Epileptic seizures are seizure events that are
caused by excessive, abnormally synchronized, localized or widely
distributed neuronal electrical discharges3. The paroxysmal
depolarization shift (PDS) is the pathophysiological cellular
phenomenon that underlies all types of epileptic seizures. PDSs
are cellular events in which rapidly repetitive action potentials are
not followed by the usual refractory period, thereby generating a
prolonged membrane depolarization .When a PDS occurs as an
abnormally prolonged run of action potentials during sustained
membrane depolarization in a single neuron, it will increased
glutamate (Na+) concentration which is associated with influx of

cations initially, and it followed by increased GABA concentration


with efflux of potassium (K+). Paroxysmal depolarization shifts
(PDS) by altering the usual balance of Na+ and K+ ion
conductance across neuronal membranes. Increased Na+
conductance creates a situation in which a single action potential
initiates sustained depolarization as a PDS. Decreased K+
conductance also can predispose to PDS. The tendency of
individual neurons to enter pathological states in which PDSs are
generated can be based on intrinsic neuronal properties, such as
dysfunctional ionophores in the genetically determined
channelopathies, or on extrinsic mechanisms such as inadequate
inhibitory neurotransmitter concentrations or exposure to
excessive concentrations of excitatory amino acids or exogenous
excitotoxins. However, large groups of neurons must generate
PDSs simultaneously to account for the episodic nature of
seizures. When PDSs in a large number of neurons are
synchronized for less than 200 ms, these electrical potentials may
summate as a spike-wave complex. When sustained repetitive
firing of PDSs in a large number of neurons becomes synchronized
for many seconds or longer, an electrographic seizure occurs.
(Adapted with permission from Holmes GL, Ben-Ari Y. Seizing hold
of seizures. Nature Med 2003;9:9946.)
There is evidence that in certain epilepsies specific
channelopathies operate to initiate PDSs in individual neurons and
produce seizures through normal mechanisms of interneuronal
synchronization, while other epilepsies appear to require
abnormal interneuronal pathways to generate pathological
synchronization.
3. Fisher RS, Boas WVE, Blume W, et al. Epileptic seizures and
epilepsy: definitions proposed by the International League Against
Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE).
Epilepsia 2005;46:4702.
7. Bragin A, Engel J Jr, Wilson CL, et al. Hippocampal and
entorhinal cortex high-frequency oscillations (100--500 Hz) in

human epileptic brain and in kainic acid--treated rats with chronic


seizures. Epilepsia 1999;40:12737.
8. Chang BS, Lowenstein
2003;349:125766.

DH.

Epilepsy.

Engl

Med

Pathogenesis of partial seizures caused by abnormal electrical


discharges from certain areas of the cortex. In experimental it has
been confirmed that the onset of focal epilepsy is caused by the
"kindling" that is a result of the subconvulsive stimulus in several
brain
structures
and
caused
the
structure
becomes
electroencephalography seizure which means the neurons that
had to be normal become epileptic. If the stimulus continuously
repeated, it can cause seizures.
In partial seizure which become secondary generalized seizures,
focal seizures arising from the electric spark which comes from an
area of the cortex and then spread throughout the cerebral cortex
that produce tonic-clonic seizure.

The phenomenon that occurs in complex partial seizures depends


on the location of epileptogenic lesions, the symptoms are clearly
visible when the lesion is impaired presentral gyrus. If the
disorders occur in the epileptogenic lesion of the presentral gyrus
the symptoms may be a focal motor seizures which occur on the
face and the contralateral limb of the lesions ,and sensory focal
seizures in the form of unpleasant feelings, mild pain samapai
burning sensation on the face and contralateral extremity of the
lesion.
On the epileptogenic lesions occur in the frontal lobe can cause
spasms in the eyes, head and neck as well as the contralateral
flexion and extension movements of the shoulder. Epiletogenik
lesions occurring in the temporal regions may cause interference
in the temporal lobe functions such as memory, power of smell
and taste.
Misbach J. Patofisiologi epilepsi. Dalam: Simposium updates in
epilepsy. 14 Desember 2002. Jakarta.