PATIENT HISORY

PATIENT NAME - Mr ananad pal

AGE- 22 year

GENDER- male

M.R.NO- 5001242

WARD- general ward

ADDRESS-

EDUCATION-12 th pass

OCCUPATION- farmar

MARITAL STATUS-unmarried

RELIGION- hindu

DATE OF ADMISSION- 24/8/2023

DIAGNOSIS – epilepsy
CHIFF COMPLAINS-

a person experiences abnormal behavior, involuntary movement of limbs and sensations,

sometimes including loss of consciousness.

PRESENT COMPALAIN-

Abnormal behavior and muscles starching in suddenly.

PAST MEDICAL HISTORY-

Epilepsy since 2 years and visite the mental hospital doctor starts tb. levers 500 mg OD.

PRESENT SURGICAL HISTORY-

No significant history

PAST SURGICAL HISTORY-

No significant history

SOCIO- ECONOMIC HISTORY-

Patient is living in pakka house. Electricity facility available. Source of water is tap

water. He also gave history of good sanitation in his house. There is proper satiation

facility available.

All are using common washroom.

PERSONAL HISTORY-

DIET- veg
SMOKING - no
ALCOHOL-no
BOWEL & BLADDER- normal
FAMILY HISTORY-

Patient belong to middle class family. There are 5 member in her family , patient, his

mother, his father and 2 sister . children are not yet married.

S.NO NAME FO AGE/SEX EDUCATION OCCUPATION HEALTH

THE STATUS
 FAMILY

MEMBERS

1. Suryaprakash 46Y/M 8th pass Farmer Healthy

pal

2. Sunita bai 43Y/F Illiterate House wife Healthy

3. Anand pal 22Y/M 12th pass Farmer Unhealthy

4. Pinki kumara 20Y/F 10 th pass House wife Healthy

5. Rinku 5Y/F First standard student Healthy

FAMILY MEDICAL HISTORY-

There is no significant family medical history of family member

PHYSICAL EXAMINATION
GENERAL APPWARENCE
Look- anxious
Posture- normal
Health- unhealthy
Mourishment- nourished
Consciousness- conscious

Anthropometric measurement
Hight- 150cm
Weight-55kg
BMI- 23.5

Vital sign
Temp- 98*f
Pulse-80 beats/min
Res.-17 breath/min
B.P -120/80 mm of hg
HEAD TO TOE EXAMINATION

Head

Skull- NO nodules or masses

Scalp- Clear

Shape- Normal

Size- normal

Hair- Normally distributed

Eyes

Eyebrows- Evenly distributed

Eyelashes- Equally distributed

Eyelids- Symmetrical
Vision- Normal

Ears

External Ear- Normal

Symmetry- symmetrical

Hearing- Normal

Nose

Symmetry- symmetrical

Discharge-absent

Mouth

Lips -pink

Teeth-no dislocation

Gums-no retraction

Neck

Lymph node- no enlarge

Movement- normal

Chest-

Symmetry-symmetrical

Chest wall-intact

Abdomen

Inspection-no scars

Palpation-no tenderness, no masses

Percussion-normal

Auscultation- mornal
Upper extremities

Symmetry--symmetrical

Movement-normal

Lower extremities

Symmetry--symmetrical

Movement-normal

DISEASE CONDITION

Meaning and Definition

Epilepsy (seizure disorder): When nerve cells in the brain fire electrical impulses at a rate
of up to four times higher than normal, this causes a sort of electrical storm in the brain,
known as a seizure. A pattern of repeated seizures is referred to as epilepsy. Known
causes include head injuries, brain tumors, lead poisoning, and mal development of the
brain, genetic and infectious illnesses. But in fully half of cases, no cause can be found.
Medication controls seizures for the majority of patients.

Classification

Epilepsies are classified in five ways:

1. By their first cause (or etiology).

2. By the observable manifestations of the seizures, known as semiology.
3. By the location in the brain where the seizures originate.
4. As a part of discrete, identifiable medical syndromes.
5. By the event that triggers the seizures, as in primary reading epilepsy or
musicogenic epilepsy.

In 1981, the International League Against Epilepsy (ILAE) proposed a

classification scheme for individual seizures that remains in common use. [8] This
classification is based on observation (clinical and EEG) rather than the underlying
pathophisiology or anatomy and is outlined later on in this article. In 1989, the ILAE
proposed a classification scheme for epilepsies and epileptic syndromes. [9] This can be
broadly described as a two-axis scheme having the cause on one axis and the extent of
localization within the brain on the other. Since 1997, the ILAE have been working on a
new scheme that has five axes:

1. ictal phenomenon, (pertaining to an epileptic seizure)

2. Seizure type,

3. Syndrome,

4. Etiology,

5. Impairment. [10]

Seizure types

Seizure types are organized firstly according to whether the source of the seizure within
the brain is localized (partial or focal onset seizures) or distributed (generalized
seizures). Partial seizures are further divided on the extent to which consciousness is
affected. If it is unaffected, then it is a simple partial seizure; otherwise it is a complex
partial (psychomotor) seizure. A partial seizure may spread within the brain - a process
known as secondary generalization. Generalized seizures are divided according to the
effect on the body but all involve loss of consciousness. These include absence (petit
mal), myoclonic, clonic, tonic, tonic-clonic (grand mal) and atonic seizures.

Children may exhibit behaviors that are easily mistaken for epileptic seizures but
are not caused by epilepsy. These include:

 Inattentive staring
 Benign shudders (among children younger than age 2, usually when they are tired
or excited)
 Self-gratification behaviors (nodding, rocking, head banging)
 Conversion disorder (flailing and jerking of the head, often in response to severe
personal stress such as physical abuse)

Conversion disorder can be distinguished from epilepsy because the episodes

never occur during sleep and do not involve incontinence or self-injury.[11]

Epilepsy syndromes

There are over 40 different types of epilepsy, including: Absence seizures, atonic
seizures, benign Rolandic epilepsy, childhood absence, clonic seizures, complex partial
seizures, frontal lobe epilepsy, Febrile seizures, Infantile spasms, Juvenile Myoclonic
Epilepsy, Juvenile Absence Epilepsy, Hot Water Epilepsy, lennox-gastaut syndrome,
Landau-Kleffner Syndrome , myoclonic seizures, Mitochondrial Disorders, Progressive
Myoclonic Epilepsies, Psychogenic Seizures , Reflex Epilepsy, Rasmussen's Syndrome,
Simple Partial seizures, Secondarily Generalized Seizures, Temporal Lobe Epilepsy,
Toni-clonic seizures, Tonic seizures, Psychomotor Seizures, Limbic Epilepsy,
Partial-Onset Seizures, generalized-onset seizures, Status Epilepticus, Abdominal
Epilepsy, Akinetic Seizures, Auto-nomic seizures, Massive Bilateral Myoclonus,
Catamenial Epilepsy, Drop seizures, Emotional seizures, Focal seizures, Gelastic
seizures, Jacksonian March, Lafora Disease, Motor seizures, Multifocal seizures,
Neonatal seizures, Nocturnal seizures, Photosensitive seizure, Pseudo seizures, Sensory
seizures, Subtle seizures, Sylvan Seizures, Withdrawal seizures, Visual Reflex Seizures
amongst others.[12]

Each type of epilepsy presents with its own unique combination of seizure type, typical
age of onset, EEG findings, treatment, and prognosis. The most widespread classification
of the epilepsies [9] divides epilepsy syndromes by location or distribution of seizures (as
revealed by the appearance of the seizures and by EEG) and by cause. Syndromes are
divided into localization-related epilepsies, generalized epilepsies, or epilepsies of
unknown localization.

Below are some common seizure syndromes:

 Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is an

idiopathic localization-related epilepsy that is an inherited epileptic disorder that
causes seizures during sleep. Onset is usually in childhood. These seizures arise
from the frontal lobes and consist of complex motor movements, such as hand
clenching, arm raising/lowering, and knee bending. Vocalizations such as
shouting, moaning, or crying are also common. ADNFLE is often misdiagnosed
as nightmares. ADNFLE has a genetic basis[13]. These genes encode various
nicotinic acetylcholine receptors.

 Benign centrotemporal lobe epilepsy of childhood or Benign rolandic epilepsy

is an idiopathic localization-related epilepsy that occurs in children between the
ages of 3 and 13 years with peak onset in prepubertal late childhood. Apart from
their seizure disorder, these patients are otherwise normal. This syndrome features
simple partial seizures that involve facial muscles and frequently cause drooling.
Although most episodes are brief, seizures sometimes spread and generalize.
Seizures are typically nocturnal and confined to sleep. The EEG may demonstrate
spike discharges that occur over the centrotemporal scalp over the central sulcus
of the brain (the Rolandic sulcus) that are predisposed to occur during drowsiness
or light sleep. Seizures cease near puberty.[14] Seizures may require anticonvulsant
treatment, but sometimes are infrequent enough to allow physicians to defer
treatment.
 Benign occipital epilepsy of childhood (BOEC) is an idiopathic localization-
related epilepsy and consists of an evolving group of syndromes. Most authorities
include two subtypes, an early subtype with onset between 3–5 years and a late
onset between 7–10 years. Seizures in BOEC usually feature visual symptoms
such as scotoma or fortifications (brightly colored spots or lines) or amaurosis
(blindness or impairment of vision). Convulsions involving one half the body,
hemiconvulsions, or forced eye deviation or head turning are common. Younger
patients typically experience symptoms similar to migraine with nausea and
headache, and older patients typically complain of more visual symptoms. The
EEG in BOEC shows spikes recorded from the occipital (back of head) regions.
The EEG and genetic pattern suggest an autosomal dominant transmission as
described by Ruben Kuzniecky et al.[15] Lately, a group of epilepsies termed
Panayiotopoulos syndrome[16] that share some clinical features of BOEC but have
a wider variety of EEG findings are classified by some as BOEC.

 Catamenial epilepsy (CE) is when seizures cluster around certain phases of a

woman's menstrual cycle.

 Childhood absence epilepsy (CAE) is an idiopathic generalized epilepsy that

affects children between the ages of 4 and 12 years of age, although peak onset is
around 5–6 years old. These patients have recurrent absence seizures, brief
episodes of unresponsive staring, sometimes with minor motor features such as
eye blinking or subtle chewing. The EEG finding in CAE is generalized 3 Hz
spike and wave discharges. Some go on to develop generalized tonic-clonic
seizures. This condition carries a good prognosis because children do not usually
show cognitive decline or neurological deficits, and the seizures in the majority
cease spontaneously with on ging maturation.

 Dravet's syndrome Severe myoclonic epilepsy of infancy (SMEI). This

generalized epilepsy syndrome is distinguished from benign myoclonic epilepsy
by its severity and must be differentiated from the Lennox-Gastaut syndrome and
Doose’s myoclonic-astatic epilepsy. Onset is in the first year of life and
symptoms peak at about 5 months of age with febrile hemiclonic or generalized
status epilepticus. Boys are twice as often affected as girls. Prognosis is poor.
Most cases are sporadic. Family history of epilepsy and febrile convulsions is
present in around 25 percent of the cases.[17]

 Frontal lobe epilepsy, usually a symptomatic or cryptogenic localization-related

epilepsy, arises from lesions causing seizures that occur in the frontal lobes of the
brain. These epilepsies can be difficult to diagnose because the symptoms of
seizures can easily be confused with non epileptic spells and, because of
limitations of the EEG, be difficult to "see" with standard scalp EEG.

 Juvenile absence epilepsy is an idiopathic generalized epilepsy with later onset

that CAE, typically in pre pubertal adolescence, with the most frequent seizure
type being absence seizures. Generalized tonic-clonic seizures can occur. 3 Hz
 spike-wave or multiple spike discharges can be seen on EEG. Prognosis is mixed,
with some patients going on to a syndrome that is poorly distinguishable from
JME.

 Juvenile myoclonic epilepsy (JME) is an idiopathic generalized epilepsy that

occurs in patients aged 8 to 20 years. Patients have normal cognition and are
otherwise neurologically intact. The most common seizures are myoclonic jerks,
although generalized tonic-clonic seizures and absence seizures may occur as
well. Myoclonic jerks usually cluster in the early morning after awakening. The
EEG reveals generalized 4–6 Hz spike wave discharges or multiple spike
discharges. Interestingly, these patients are often first diagnosed when they have
their first generalized tonic-clonic seizure later in life when they experience sleep
deprivation (e.g., freshman year in college after staying up late to study for
exams). Alcohol withdrawal can also be a major contributing factor in
breakthrough seizures as well. The risk of the tendency to have seizures is
lifelong; however, the majority have well-controlled seizures with anticonvulsant
medication and avoidance of seizure precipitants.

 Lennox-Gastaut syndrome (LGS) is a generalized epilepsy that consists of a

triad of developmental delay or childhood dementia, mixed generalized seizures,
and EEG demonstrating a pattern of approximately 2 Hz "slow" spike-wave.
Onset occurs between 2–18 years. As in West syndrome, LGS result from
idiopathic, symptomatic, or cryptogenic causes, and many patients first have West
syndrome. Authorities emphasize different seizure types as important in LGS, but
most have astatic seizures (drop attacks), tonic seizures, tonic-clonic seizures,
atypical absence seizures, and sometimes, complex partial seizures.
Anticonvulsants are usually only partially successful in treatment.

 Ohtahara Syndrome is a rare but severe form of epilepsy syndrome combined

with cerebral palsy and characterized with frequent seizures which typically start
in the first few days of life. Sufferers trend to be severely disabled and their lives
very short (they are unlikely to reach adulthood).

 Primary reading epilepsy is a reflex epilepsy classified as an idiopathic

localization-related epilepsy. Reading in susceptible individuals triggers
characteristic seizures.[18]

 Progressive myoclonic epilepsies define a group of symptomatic generalized

epilepsies characterized by progressive dementia and myoclonic seizures. Tonic-
clonic seizures may occur as well. Diseases usually classified in this group are
Unverricht-Lundborg disease, myoclonus epilepsy with ragged red fibers
(MERRF syndrome), Lafora disease, neuronal ceroid lipofucinosis, and sialdosis.

 Rasmussen's encephalitis is a symptomatic localization-related epilepsy that is a

progressive, inflammatory lesion affecting children with onset before the age of
10. Seizures start as separate simple partial or complex partial seizures and may
 progress to epilepsia partialis continuata (simple partial status epilepticus).
Neuroimaging shows inflammatory encephalitis on one side of the brain that may
spread if not treated. Dementia and hemiparesis are other problems. The cause is
hypothesized to involve an immulogical attack against glutamate receptors, a
common neurotransmitter in the brain.[19]

 Symptomatic localization-related epilepsies Symptomatic localization-related

epilepsies are divided by the location in the brain of the epileptic lesion, since the
symptoms of the seizures are more closely tied to the brain location rather than
the cause of the lesion. Tumors, atriovenous malformations, cavernous
malformations, trauma, and cerebral infarcts can all be causes of epileptic foci in
different brain regions.

 Temporal lobe epilepsy (TLE), a symptomatic localization-related epilepsy, is

the most common epilepsy of adults who experience seizures poorly controlled
with anticonvulsant medications. In most cases, the epileptogenic region is found
in the midline (mesial) temporal structures (e.g., the hippocampus, amygdala, and
parahippocampal gyrus). Seizures begin in late childhood and adolescence. Most
of these patients have complex partial seizures sometimes preceded by an aura,
and some TLE patients also suffer from secondary generalized tonic-clonic
seizures. If the patient does not respond sufficiently to medical treatment, epilepsy
surgery may be considered.

 West syndrome is a triad of developmental delay, seizures termed infantile

spasms, and EEG demonstrating a pattern termed hypsarrhythmia. Onset occurs
between 3 months and 2 years, with peak onset between 8–9 months. West
syndrome may arise from idiopathic, symptomatic, or cryptogenic causes. The
most common cause is tuberous sclerosis. The prognosis varies with the
underlying cause. In general most surviving patients remain with significant
cognitive impairment and continuing seizures and may evolve to another
eponymic syndrome, Lennox-Gastaut syndrome.

Causes

The diagnosis of epilepsy usually requires that the seizures occur spontaneously.
Nevertheless, certain epilepsy syndromes require particular precipitants or triggers for
seizures to occur. These are termed reflex epilepsy. For example, patients with primary
reading epilepsy have seizures triggered by reading. Photosensitive epilepsy can be
limited to seizures triggered by flashing lights. Other precipitants can trigger an epileptic
seizure in patients who otherwise would be susceptible to spontaneous seizures. For
example, children with childhood absence epilepsy may be susceptible to
hyperventilation. In fact, flashing lights and hyperventilation are activating procedures
used in clinical EEG to help trigger seizures to aid diagnosis. Finally, other precipitants
can facilitate, rather than obligately trigger, seizures in susceptible individuals. Emotional
stress, sleep deprivation, sleep itself, heat stress, alcohol and febrile illness are examples
of precipitants cited by patients with epilepsy. Notably, the influence of various
precipitants varies with the epilepsy syndrome. [20]. Likewise, the menstrual cycle in
women with epilepsy can influence patterns of seizure recurrence. Catamenial epilepsy is
the term denoting seizures linked to the menstrual cycle.[21]

Pathophysiology

Mutations in several genes have been linked to some types of epilepsy. Several genes that
code for protein subunits of voltage-gated and ligand-gated ion channels have been
associated with forms of generalized epilepsy and infantile seizure syndromes. [22] Several
ligand-gated ion channels have been linked to some types of frontal and generalized
epilepsies. One speculated mechanism for some forms of inherited epilepsy are mutations
of the genes which code for sodium channel proteins; these defective sodium channels
stay open for too long thus making the neuron hyper-excitable. Glutamate, an excitatory
neurotransmitter, may thereby be released from these neurons in large amounts which—
by binding with nearby glutamatergic neurons—triggers excessive calcium (Ca 2+) release
in these post-synaptic cells. Such excessive calcium release can be neurotoxic to the
affected cell. The hippocampus, which contains a large volume of just such
glutamanergic neurons (and NMDA receptors, which are permeable to Ca 2+ entry after
binding of both sodium and glutamate), is especially vulnerable to epileptic seizure,
subsequent spread of excitation, and possible neuronal death. Another possible
mechanism involves mutations leading to ineffective GABA (the brain's most common
inhibitory neurotransmitter) action. Epilepsy-related mutations in some non-ion channel
genes have also been identified.

Epileptogenesis is the process by which a normal brain develops epilepsy after an insult.
One interesting finding in animals is that repeated low-level electrical stimulation to
some brain sites can lead to permanent increases in seizure susceptibility: in other words,
a permanent decrease in seizure "threshold." This phenomenon, known as kindling (by
analogy with the use of burning twigs to start a larger fire) was discovered by Dr.
Graham Goddard in 1967. Chemical stimulation can also induce seizures; repeated
exposures to some pesticides have been shown to induce seizures in both humans and
animals. One mechanism proposed for this is called excitotoxicity. The roles of kindling
and excitotoxicity, if any, in human epilepsy are currently hotly debated.

Other causes of epilepsy are brain lesions, where there is scar tissue or another abnormal
mass of tissue in an area of the brain.

The complexity of understanding what seizures are have led to considerable efforts to use
computational models of epilepsy to both interpret experimental and clinical data, as well
as guide strategies for therapy.

Management

Epilepsy is usually treated with medication prescribed by a physician; primary caregivers,

neurologists, and neurosurgeons all frequently care for people with epilepsy. However, it
has been stressed that accurate differentiation between generalized and partial seizures is
especially important in determining the appropriate treatment. [23] In some cases the
implantation of a stimulator of the vagus nerve, or a special diet can be helpful.
Neurosurgical operations for epilepsy can be palliative, reducing the frequency or
severity of seizures; or, in some patients, an operation can be curative.

relayed to a neurologist, may be of help in diagnosing the type of seizure which occurred.

Pharmacologic treatment

The mainstay of treatment of epilepsy is anticonvulsant medications. Often,

anticonvulsant medication treatment will be lifelong and can have major effects on
quality of life. The choice among anticonvulsants and their effectiveness differs by
epilepsy syndrome. Mechanisms, effectiveness for particular epilepsy syndromes, and
side effects, of course, differ among the individual anticonvulsant medications. Some
general findings about the use of anticonvulsants are outlined below.

History and Availability- The first anticonvulsant was bromide, suggested in 1857 by
Charles Locock who used it to treat women with "hysterical epilepsy" (probably
catamenial epilepsy). Potassium bromide was also noted to cause impotence in men.
Authorities concluded that potassium bromide would dampen sexual excitement thought
to cause the seizures. In fact, bromides were effective against epilepsy, and also caused
impotence; it is now known that impotence is a side effect of bromide treatment, which is
not related to its anti-epileptic effects. It also suffered from the way it affected behaviour,
introducing the idea of the 'epileptic personality' which was actually a result of the
medication. Phenobarbital was first used in 1912 for both its sedative and antiepileptic
properties. By the 1930s, the development of animal models in epilepsy research lead to
the development of phenytoin by Tracy Putnam and H. Houston Merritt, which had the
distinct advantage of treating epileptic seizures with less sedation [24]. By the 1970s, an
National Institutes of Health initiative, the Anticonvulsant Screening Program, headed by
J. Kiffin Penry, served as a mechanism for drawing the interest and abilities of
pharmaceutical companies in the development of new anticonvulsant medications.

Currently there are 20 medications approved by the Food and Drug Administration for
the use of treatment of epileptic seizures in the US: carbamazepine (common US brand
name Tegretol), clorazepate (Tranxene), clonazepam (Klonopin), ethosuximide
(Zarontin), felbamate (Felbatol), fosphenytoin (Cerebyx), gabapentin (Neurontin),
lacosamide (Vimpat), lamotrigine (Lamictal), levetiracetam (Keppra), oxcarbazepine
(Trileptal), phenobarbital (Luminal), phenytoin (Dilantin), pregabalin (Lyrica), primidone
(Mysoline), tiagabine (Gabitril), topiramate (Topamax), valproate semisodium
(Depakote), valproic acid (Depakene), and zonisamide (Zonegran). Most of these
appeared after 1990.

Medications commonly available outside the US but still labelled as "investigational"

within the US are clobazam (Frisium) and vigabatrin (Sabril). Medications currently
under clinical trial under the supervision of the FDA include retigabine, brivaracetam, an
seletracetam.
Other drugs are commonly used to abort an active seizure or interrupt a seizure flurry;
these include diazepam (Valium, Diastat) and lorazepam (Ativan). Drugs used only in the
treatment of refractory status epilepticus include paraldehyde (Paral), midazolam
(Versed), and pentobarbital (Nembutal).

Some anticonvulsant medications do not have primary FDA-approved uses in epilepsy

but are used in limited trials, remain in rare use in difficult cases, have limited
"grandfather" status, are bound to particular severe epilepsies, or are under current
investigation. These include acetazolamide (Diamox), progesterone, adrenocorticotropic
hormone (ACTH, Acthar), various corticotropic steroid hormones (prednisone), or
bromide.

Other treatment

Ketogenic diet- a high fat, low carbohydrate diet developed in the 1920s, largely
forgotten with the advent of effective anticonvulsants, and resurrected in the 1990s. The
mechanism of action is unknown. It is used mainly in the treatment of children with
severe, medically-intractable epilepsies.

Electrical stimulation [33]- methods of anticonvulsant treatment with both currently

approved and investigational uses. A currently approved device is vagus nerve
stimulation (VNS). Investigational devices include the responsive neurostimulation
system and deep brain stimulation.

Vagus nerve stimulation (VNS)- The VNS (US manufacturer = Cyberonics) consists of
a computerized electrical device similar in size, shape and implant location to a heart
pacemaker that connects to the vagus nerve in the neck. The device stimulates the vagus
nerve at pre-set intervals and intensities of current. Efficacy has been tested in patients
with localization-related epilepsies demonstrating that 50% of patients experience a 50%
improvement in seizure rate. Case series have demonstrated similar efficacies in certain
generalized epilepsies such as Lennox-Gastaut syndrome. Although success rates are not
usually equal to that of epilepsy surgery, it is a reasonable alternative when the patient is
reluctant to proceed with any required invasive monitoring, when appropriate presurgical
evaluation fails to uncover the location of epileptic foci, or when there are multiple
epileptic foci.

Responsive Neurostimulator System (RNS) (US manufacturer Neuropace) consists of

an computerized electrical device implanted in the skull with electrodes implanted in
presumed epileptic foci within the brain. The brain electrodes send EEG signal to the
device which contains seizure-detection software. When certain EEG seizure criteria are
met, the device delivers a small electrical charge to other electrodes near the epileptic
focus and disrupt the seizure. The efficacy of the RNS is under current investigation with
the goal of FDA approval.

Deep brain stimulation (DBS) (US manufacturer Medtronic) consists of computerized

electrical device implanted in the chest in a manner similar to the VNS, but electrical
stimulation is delivered to deep brain structures through depth electrodes implanted
through the skull. In epilepsy, the electrode target is the anterior nucleus of the thalamus.
The efficacy of the DBS in localization-related epilepsies is currently under investigation.

Noninvasive surgery- The use of the Gamma Knife or other devices used in
radiosurgery are currently being investigated as alternatives to traditional open surgery in
patients who would otherwise qualify for anterior temporal lobectomy.[34]

Avoidance therapy- Avoidance therapy consists of minimizing or eliminating triggers in

patients whose seizures are particularly susceptible to seizure precipitants (see above).
For example, sunglasses that counter exposure to particular light wavelengths can
improve seizure control in certain photosensitive epilepsies.[35]

Warning systems- A seizure response dog is a form of service dog that is trained to
summon help or ensure personal safety when a seizure occurs. These are not suitable for
everybody and not all dogs can be so trained. Rarely, a dog may develop the ability to
sense a seizure before it occurs.[36] Development of electronic forms of seizure detection
systems are currently under investigation.

Alternative or complementary medicine- A number of systematic reviews by the

Cochrane Collaboration into treatments for epilepsy looked at acupuncture,[37]
psychological interventions,[38] vitamins[39] and yoga[40] and found there is no reliable
evidence to support the use of these as treatments for epilepsy.

Nursing Care

Epilepsy is the most common serious neurological condition after stroke, with a 0.5 per
cent prevalence, and a two to three per cent life time risk of being given a diagnosis of
epilepsy in the developed world. As a result of the perceived deficiencies and suggestions
to improve the quality of care offered to people with epilepsy, two models of service
provision have been suggested by researchers: specialist epilepsy out-patient clinics (as
opposed to the management of patients in general neurology clinics or general medical
clinics) and nurse-based liaison services between primary (GP) and secondary/tertiary
(hospital based) care.

NURSING DIAGNOSIS

 Risk For Injury Related to Loss of muscle control As evidenced by

Increase in seizures .
 Deficient Knowledge related to Poor understanding of seizure

triggers As evidenced by diseae condition.

Conclusion

Epilepsy is a brain disorder that causes people to have recurring seizures. The seizures
happen when clusters of nerve cells, or neurons, in the brain send out the wrong signals.
People may have strange sensations and emotions or behave strangely. They may have
violent muscle spasms or lose consciousness.

Epilepsy has many possible causes, including illness, brain injury and abnormal brain
development. In many cases, the cause is unknown.

Doctors use brain scans and other tests to diagnose epilepsy. It is important to start
treatment right away. There is no cure for epilepsy, but medicines can control seizures for
most people. When medicines are not working well, surgery or implanted devices such as
vagus nerve stimulators may help. Special diets can help some children with epilepsy.

Bibliography

1. Commission on Epidemiology and Prognosis, International League Against

Epilepsy (1993). "Guidelines for epidemiologic studies on epilepsy. Commission
on Epidemiology and Prognosis, International League Against Epilepsy".
Epilepsia 34 (4): 592–6. doi:10.1111/j.1528-1157.1993.tb00433.x.
PMID 8330566. http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1528-
1157.1993.tb00433.x.
2. Blume W, Lüders H, Mizrahi E, Tassinari C, van Emde Boas W, Engel J (2001).
"Glossary of descriptive terminology for ictal semiology: report of the ILAE task
force on classification and terminology". Epilepsia 42 (9): 1212–8.
doi:10.1046/j.1528-1157.2001.22001.x. PMID 11580774. http://www.blackwell-
synergy.com/doi/full/10.1046/j.1528-1157.2001.22001.x.
3. Fisher R, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, Engel J
(2005). "Epileptic seizures and epilepsy: definitions proposed by the International
League Against Epilepsy (ILAE) and the International Bureau for Epilepsy
(IBE)". Epilepsia 46 (4): 470–2. doi:10.1111/j.0013-9580.2005.66104.x.
PMID 15816939. http://www.blackwell-synergy.com/doi/full/10.1111/j.0013-
9580.2005.66104.x.
4. "Epilepsy: aetiogy [sic], epidemiology and prognosis". World Health
Organization. February 2001.
http://www.who.int/mediacentre/factsheets/fs165/en/. Retrieved 2007-06-14.
5. The National Society for Epilepsy (2009), What is Epilepsy?. Available from
http://www.epilepsynse.org.uk/AboutEpilepsy/Whatisepilepsy (Accessed on 15
February 2009).