“PREVALENCE OF SEIZURE AND PRESCRIBING PATTERNS OF AED IN

PATIENTS WITH NEURO-PSYCHIATRIC AND THYROID ABNORMALITIES”

Dissertation work submitted to

KERALA UNIVERSITY OF HEALTH AND SCIENCES, THRISSUR-680596

In partial fulfillment for the award of degree of

PHARM D
(DOCTOR OF PHARMACY)
Submitted by
113260067, 113260075, 113260081, 113260083
Under the Guidance of
Dr. Vini Pavithran PHARM D (PB)

DEPARTMENT OF PHARMACY PRACTICE

GRACE COLLEGE OF PHARMACY
PALAKKAD-678004, KERALA
Certificat
Prof. Dr. Y. Haribabu, M. Pharm., Ph.D. Date:
Principal,
E-mail : yellinah@rediffmail.com
Mob : +91 9645527607

CERTIFICATE

This is to certify that the dissertation entitled “PREVALENCE OF SEIZURE AND

PRESCRIBING PATTERNS OF AED IN PATIENTS WITH NEURO-

PSYCHIATRIC AND THYROID ABNORMALITIES” submitted Ms. Ayisha
Jasmine K , Mr. Joji G Ponnachan, Mr. Ridhin Joy, Ms. Sheba Baby John, to Kerala
University of Health Science, Thrissur in partial fulfillment for the award of degree of Pharm D,
is a group Bonified work of the candidates carried out under the guidance of of Dr. Vini
Pavithran PHARM D (PB).,Grace College of Pharmacy, Palakkad during the academic year
2015-2016.

Prof. Dr. Y. Haribabu, M. Pharm., Ph.D.

Principal
 CERTIFICATE

This is to certify that the dissertation entitled “PREVALENCE OF SEIZURE AND

PRESCRIBING PATTERNS OF AED IN PATIENTS WITH NEURO-PSYCHIATRIC AND
THYROID ABNORMALITIES” submitted by Ms. Ayisha Jasmine K , Mr. Joji G
Ponnachan, Mr. Ridhin Joy, Ms. Sheba Baby John ., Kerala University of Health Sciences,
Thrissur in partial fulfillment for the award of degree of Pharm D, is a group Bonafide work of
the candidates carried out in the department of Pharmacy Practice, Grace College of Pharmacy,
Palakkad during the academic year 2015-2016.

Place : Palakkad Prof. Dr. C. I. SAJEETH, M. Pharm., Ph.D.,

Date : Head of the Department
Department of Pharmacy Practice
E-mail : sajeeth3@gmail.com
Mob : +91 9447255002
 CERTIFICATE

This is to certify that the dissertation entitled “PREVALENCE OF SEIZURE AND

PRESCRIBING PATTERNS OF AED IN PATIENTS WITH NEURO-PSYCHIATRIC AND
THYROID ABNORMALITIES” submitted by Ms. Ayisha Jasmine K , Mr. Joji G Ponnachan,
Mr. Ridhin Joy, Ms. Sheba Baby John ., Kerala University of Health Sciences, Thrissur in partial
fulfillment for the award of degree of Pharm D, is a group Bonafide work of the candidates
carried out in the department of Pharmacy Practice, Grace College of Pharmacy, Palakkad
during the academic year 2015-2016 under my guidance and supervision.

Place : Palakkad Dr. Vini Pavithran Pharm D (PB)

Date : Research guide
Asst professor
Department of Pharmacy Practice
 DECLARATION

We hereby declare that this dissertation “PREVALENCE OF SEIZURE AND

PRESCRIBING PATTERNS OF AED IN PATIENTS WITH NEURO-PSYCHIATRIC AND
THYROID ABNORMALITIES” was carried out by us in the Department of Pharmacy Practice,
Grace College of Pharmacy, Palakkad under the guidance of Dr. VINI PAVITHRAN PHARM
D (PB) and submitted to Kerala University of Health Sciences, Thrissur in partial fulfillment for
the award of degree of Pharm D.

Ms. Ayisha Jasmine K

Place: Palakkad Mr. Joji G Ponnachan
Date: Mr. Ridhin Joy

Ms. Sheba Baby John

 EVALUATION CERTIFICATE

This is to certify that the dissertation entitled “PREVALENCE OF SEIZURE AND

PRESCRIBING PATTERNS OF AED IN PATIENTS WITH NEURO-PSYCHIATRIC AND
THYROID ABNORMALITIES” submitted by Ms. Ayisha Jasmine K , Mr. Joji G Ponnachan,
Mr. Ridhin Joy, Ms. Sheba Baby John, to Kerala University of Health Sciences, Thrissur in
partial fulfillment for the award of degree of Pharm D, is a Bonafide work carried out by the
candidates at department of Pharmacy Practice, Grace College of Pharmacy, Palakkad and was
evaluated by us during the academic year 2015-2016.

Signature and Name of the Signature and Name of the

Internal Examiner with date External Examiner with date

Examination Centre: Grace College of Pharmacy

Acknowledg
 ACKNOWLEDGEMENT
The successful completion of our project work is in complete unless we mention the names of the
people, who made it possible, whose constant encouragements, dedication and guidance served us the
constant energy for fulfillment of our project work.

First and foremost we express our bow down towards God for his blessing in completing this project
work.

We are highly indebted to our esteemed guide Dr Vini Pavithran, Pharm D, Assistant professor,
Department of Pharmacy Practice for her creative ideas, constant encouragement and advice,which
motivated for successful completion of our project work. We also convey our hearty gratitude to our
Bincy Mam, who was our previous guide who help with her ideas and prayer for selection of our topic,
and we also thank her for giving us full support and encouragement to complete our study.

We would like to convey our gratitude to our Principal Dr.Y.Haribabu, M.Pharm, Ph.D and our vice
Principal Dr.Sajeeth C.I, M.Pharm, Ph.D Grace College of Pharmacy, Palakkad for giving us an
opportunity to do this project work.

We are really thankful to all the lecturers of Grace College of Pharmacy for their valuable suggestions
and constant encouragement during our project.

We are greatly thankful to our beloved parents and family members who have encouraged and
supported us throughout the work.

We express our heartfelt thanks and respectful regards to Dr. Kumara lingam ,for permitting us to do this
work in this well equipped and managed hospital and for all the facilities which were provided to us at
the institution enabling to do this work, we are also very thankful to all other sta ffs of Karuna
Medical College, Chittur, Palakkad, for their kind co-operation.

We would also like to extend our special thanks to, Sree Medicals Palakkad for providing us all the
necessary materials to carry out our work with great ease.
We are also using this opportunity to express our heartfelt regards to our beloved classmates, friends,
seniors (Shafeer Rahman, Sajad C P) well wishers and supporters who had actively assisted us in
accomplishing our target.
ement
DEDICATED TO
OUR FORMER
GUIDE
BINCY MAM
Abbreviati
Contents
 CONTENTS
SL PARTICULARS PAGE NO.
NO.
1 INTRODUCTION
2 AIM & OBJECTIVES
3 REVIEW OF LITERATURE
4 PLAN OF WORK
5 METHODOLOGY
6 OBSERVATIONS AND
RESULTS
7 DISCUSSION
8 SUMMARY
9 CONCLUSION
10 BIBLIOGRAPHY
11 ANNEXURE
12 PROFORMA
13 COMPLETION LETTER
14 PUBLICATION
INTRODUCTION
Epilepsy is a neurological disorder – a physical condition which causes sudden bursts of
hyperactivity in the brain. This hyperactivity produces “seizures” which vary from one person to
another in frequency and form.
A seizure may appear as
• A brief stare
• A change of awareness
• A convulsion
A seizure may last a few seconds or a few minutes.

CAUSES

In approximately 60-75% of all cases, there is no knownidentified causes.

Identifiable Causes
• Brain injury to the fetus during pregnancy
• Birth trauma (lack of oxygen)
• Aftermath of infection (meningitis)
• Head trauma (car accident, sports injury, shaken baby syndrome)
• Substance abuse
• Alteration in blood sugar (hypoglycemia)
• Hypocalcaemia
• Brain-tumor
• Stroke

TYPES OF SEIZURES

Complex partial seizure: a person loses awareness as the seizure begins and appears dazed and
confused. The person will exhibit meaningless behaviors such as random walking, mumbling,
head turning, or pulling at clothing. These behaviors cannot be recalled by the person after the
seizure.

Generalized seizures occur when the excessive neural activity in the brain encompasses the
entire brain. The 2 most common forms are generalized absence seizures and Tonic- Clonic
Seizures.
a) Absence seizure: during this type of seizure a person may appear to be staring into space
and his/her eyes may roll upwards. This kind of seizure is characterized by 5 to 15 second
lapses of consciousness and, when it has ended, the person will not recall this lapse of
consciousness. Generalized absence seizuremost often occur in childhood and disappear
during adolescence. They are less prevalent in adulthood.
b) Tonic-Clonic seizure: during this seizure a person will usually emit a short cry and fall
to the floor. This cry does not indicate pain. The muscles will stiffen and the body
extremities will jerk and twitch (convulse). Bladder control may be lost. Consciousness is
lost and may be regained slowly.
DIAGNOSIS

CAT Scan
Computerized Axial Tomography, also known as CT (Computed Tomography) imaging, is
safe and non-invasive procedure which uses low radiation X-rays to create a computer-
generated, three-dimensional image of the brain.
It provides detailed information about the structure of the brain by using a series of X-ray beams
to scan the head to create cross-sectional Images of the brain.

MSI
Magnetic Source Imaging, is a non-invasive scanning technique which provides information
about the function of the brain

MSRI
Magnetic Resonance Spectroscopic Imaging is similar to MRI but while MRI looks at the
signals detected from the protons of water in the body, MRSI looks at the signals detected from
other proton-containing metabolites

PET
Positron Emission Tomography is a scanning technique which detects chemical and
physiological changes related to metabolism

MRI
Magnetic Resonance Imaging is a safe and non-invasive scanning technique that uses a
magnetic field, radio waves, and a computer to produce two or three dimensional images of the
brain.

SPECT
Single Photon Emission Computed Tomography is a functional imaging technique which
creates 3-dimensional images of the brain on a computer, allowing physicians to visualize blood
flow through different areas of the brain.

EEG
An electroencephalogram is a noninvasive test which detects and records electrical impulses on
the surface of the brain. These impulses are transmitted from small metal discs, placed on the
person’s scalp, through wires which are connected to an electroencephalograph.

TREATMENT
NON PHARMACOLOGICAL

Vagus Nerve Stimulation

Vagus Nerve Stimulation (VNS) involves periodic mild electrical stimulation of the vagus nerve
in the neck by a surgically implanted device similar to a heart pacemaker. VNS has been
effective in controlling some epilepsies when anti-epileptic drugs have been inadequate or their
side effects intolerable, and neurosurgery has not been an option.

Ketogenic Diet

This strictly supervised diet is prescribed for children. The diet is high in fat and low in
carbohydrates. In many of the children who stick with the diet, seizures are brought under
control and are eliminated - sometimes permanently.

Surgery

Surgery may be an option for the 30% of epilepsy cases that do not respond to medication.
Surgery is used when the injured brain tissue causing the seizures can be identified and safely
removed without damaging psychological or major body functions. This applies only to a small
percentage of persons living with epilepsy

PHARMACOLOGICAL THERAPY

PARTIAL GENERALIZED ABSENCE MYOCLONIC

SEIZURE TONIC CLONIC SEIZURE SEIZURE
SEIZURE

DRUG OF CARBAMAZEPIN VALPROATE ETHOSUXIMID VALPROATE

CHOICE E PHENYTOIN E LAMOTRIGIN
PHENYTOIN LAMOTRIGINE VALPROATE E
LAMOTRIGINE LAMOTRIGINE
TOPIRAMATE
ALTERNATIV GABAPENTIN LEVETRIACETA CLONAZEPAM CLONAZEPA
E LEVETRIACETA M M
M PHENYTOIN TOPIRAMATE
PREGABALIN PHENOBARBITA
VALPROATE L
PRIMIDONE
RELATION BETWEEN NEUROLOGICAL CASES WITH SEIZURE

Stroke is the sudden death of brain cells caused by blockage of blood flow or rupture of an artery
to the brain, lead to lack of oxygen. Sudden slurred speech, weakness, or paralysis of one side of
the body can be symptoms .About 10% of all stroke patients experience seizures as its
complication.

Most early-onset seizures occur within one day after the stroke. A first late-onset epileptic event
occurs between six months and two years after the stroke. Large cortical infarcts located in the
temporal–regions increased risk of developing seizures. Epileptic spells can also triggered by
alcohol or drug abuse. Late seizure can be due to recurrent infarction due to cardio-embolic
origin. Arterial hypertension, coronary and valve disorders, diabetes and hypercholesterolemia
are not risk factors for seizures in stroke patients

An increase in intracellular Ca 2+ and Na+ results lower threshold for depolarization, glutamate
excitotoxicity, hypoxia, metabolic dysfunction, global hypo perfusion, injury have been reported
as the risk factors. Seizures after hemorrhagic strokes are caused due to irritation caused by
products of blood metabolism.

Posttraumatic epilepsy (PTE) is a recurrent seizure disorder that apparently results from the brain
injury. Immediate and early seizures are thought to be a direct reaction to the injury, whereas late
seizures are believed to result from damage to thecerebralcortex by excitotoxicity and iron
present in theblood. Late seizures are thought to be the result of epileptogenesis, in which neural
networks are restructured.

During the early stages of bacterial meningitis, seizures may result from
swelling, pressure and bacterial toxins in the fluid surrounding the brain. As the meningitis
infection progresses, there may be focal seizures, seizures that involve one limb or one part of
the body. Bacterial meningitis may also cause a condition that prevents the body from
eliminating fluids properly, which can cause the hyponatremia this can also trigger seizures.

RELATION BETWEEN SEIZURE AND THYROID ABNORMALITIES

Thyroid disorder is a general term representing several different diseases involving thyroid
hormones and the thyroid gland. Thyroid disorders are commonly separated into two major
categories, hyperthyroidism and hypothyroidism, depending on whether serum thyroid hormone
levels (T4 and T3) are increased or decreased, respectively. Thyroid disorders are more common
in women than men, and in older adults compared with younger age groups. The prevalence of
unsuspected overt hyperthyroidism and hypothyroidism , are both estimated to be 0.6% or less in
women, based on several epidemiologic studies . A similar pattern is observed for the prevalence
rate of hypothyroidism.
 HYPERTHYROIDISM

Hyperthyroidism represents a myriad of thyroid disorders characterized by elevated levels of

circulating thyroid hormones. The annual incidence of hyperthyroidism is three per 1,000 in the
general population, and the condition is eight times more common in women. Hyperthyroidism
may result from generalized thyroid gland over-activity (“true”hyperthyroidism) or from causes
other than over-activity of the gland. It is important to distinguish between these since the
prognosis and treatment will be different. Once hyperthyroidism is suspected based on clinical
presentation, and confirmed by thyroid hormone and TSH level determination , the general form
of disease can be differentiated by radioactive iodine uptake (RAIU) studies as indicatED The
normal RAIU over a 24 hour period ranges from 10%-35%.

HYPOTHYROIDISM

Decreased thyroid hormone synthesis and low levels of circulating thyroid hormones result in
biochemical and/or clinical hypothyroidism. This condition occurs more frequently in women;
the overall incidence is about 3% of the general population. The clinical presentation,
particularly in elderly patients, may be subtle; therefore, routine screening of thyroid function
tests is generally recommended for women more than 50 years of age. Hypothyroidism is
classified as primary or secondary. Primary hypothyroidism results from ;
 1)Defective hormone biosynthesis resulting from Hashimoto's or autoimmune
thyroiditis (most common), other forms of thyroiditis (acute thyroditis, subacute
thyroiditis), endemic iodine deficiency, or antithyroid drug therapy (goitrous
hypothyroidism).
 2)Congenital defects or loss of functional thyroid tissue due to treatment for
hyperthyroidism including radioactive iodine therapy or surgical resection of the
thyroid gland.
 THYROID HORMONES WITH NORMAL VALUES AND FUNCTION TESTS

PREVALENCE RATE

The prevalence rate of overt hypothyroidism is 2% for women aged 70 to 80, 1.4% for all
women 60 years and older, and 0.5% for women aged 40 to 60. In comparison, the Prevalence
rate of overt hypothyroidism is 0.8% for men 60 years and older. In terms of hypothyroidism, the
estimated incidence is 2.4 per 1,000 women each year. Overt thyroid dysfunction is uncommon
in women Less than 40 years old and in men <60 years of age. Thyroid-stimulating hormone:
assays to measure TSH are conducted using an extremely sensitive radioimmunoassay. The
origin of hypothyroidism-whether at the level of the pituitary gland, hypothalamus, or thyroid
gland-can be determined by using the test for TSH. Levels of TSH are used to diagnose or screen
for hypothyroidism and to evaluate adequacy of replacement therapy.

Age is also a factor; for overt hyperthyroidism. The prevalence rate is 1.4% for women aged 60
or older and 0.45% for women aged 40 to 60. For men more than 60 years of age, the prevalence
rate of hyperthyroidism is estimated to be 0.13%. The estimated annual incidence of
hyperthyroidism for women ranges from 0.36 to 0.47 per 1,000 women, and for men ranges from
0.087 to 0.101 per 1,000 men.

THE ELECTROENCEPHALOGRAM (EEG)

The electroencephalogram (EEG) is readily available, relatively cheap, and the most widely used
technique to detect and monitor electrocerebral activity (Hooshmand and Maloney, 1980). In the
evaluation of the encephalopathic patient, EEG may help in differentiating organic from
psychiatric conditions, and is the only tool that can diagnose nonconvulsive status epilepticus
(NCSE). Furthermore, EEG may help determine the severity of the underlying brain dysfunction,
and may assist in predicting clinical outcome (Kaplan, 2004).

MECHANISM OF THYROID ABNORMALITIES CAUSING SEIZURE

The continuum of central nervous system (CNS) symptoms associated with various degrees of
hyperthyroidism ranges from subtle impairment of cognitive function, insomnia, emotional
liability and anxiety, to severe and potentially life threatening manifestations, such as severe
encephalopathy, seizures and coma. The latter is most frequently encountered during thyroid
storm which has a mortality rate of up to 20%. There is no clear correlation between the degree
of EEG abnormality and serum thyroid hormone level. An increase in frequency of the posterior
dominant rhythm, an increase in fast activity, as well as a higher incidence of theta and delta
activity have been observed in thyrotoxicosis, and in experimental hypermetabolism. High-
voltage and prolonged EEG responses to photic stimulation have also been described. Wilson et
al. noted that these changes were most profound in young women. Rarely, triphasic waves (TWs)
have been reported in patients with acute hyperthyroidism. A case of thyrotoxic stormpresenting
as posterior reversible encephalopathy syndrome (PRES) in a patient with generalized
convulsions and coma, has been described, however, PRES associated with hyperthyroidism is
exceedingly rare. Hyperthyroidism lowers seizure threshold in patients with preexisting epilepsy.
Furthermore, de novo convulsive seizures in the setting of thyrotoxicosis are well recognized.
Thyrotoxicosis presenting as new-onset seizures is often refractory to antiepileptic drugs
(AEDs), and may only be controlled after reaching an euthyroid state. In a case report of a
patient with iatrogenic hyperalimentation with levothyroxine, the EEG revealed NCSE with
almost continuous bisynchronous spike-and-wave discharges with an occipital predominance.

In the adult, symptoms of hypothyroidism range from mild cognitive slowing and memory
impairment to stupor and coma, referred to as myxedema. The EEG in hypothyroid adults may
be entirely normal, but in more severe cases, the EEG may show a slow posterior basic rhythm,
as well as low-voltage activity predominantly in the theta and delta range with poor or absent
EEG background reactivity to noxious. TWs and generalized periodic sharp waves resembling
Creutzfeld-Jacob Disease have been described. Rarely, frontal intermittent rhythmic delta
activity (FIRDA) occur. In infants with congenital hypothyroidism, there is a delay in
development of the EEG phenomena of sleep, particularly sleep spindles.

Some of the studies suggested that the changes of thyroid hormones in epileptics were due to the
effect of some AEDs and not due to the disease itself (2,3). Earlier studies frequently reported
abnormal thyroid hormonal levels with enzyme inducing AEDs [carbamazepine (CBZ),
phenytoin (PHT) and phenobarbital (PB)]. These abnormalities included reduced serum
concentrations of total thyroxine (T4), free T4 (fT4), Tri-iodothyronine (T3), free T3 (fT3), free
T4-index(fT4i), free T3-index (fT3i), thyroxine binding globulin (TBG) and increased
concentrations of thyroid Stimulating hormone (TSH) (2-6). Also earlier studies reported normal
thyroid hormonal levels with non-enzyme inducing AED (valproate or VPA) which included
normal concentrations of T4 (7-9), T3, T3 Uptake (T3u) and thyrotropin (TSH) and thyrotropin
Releasing hormone (TRH) stimulation (4,7,10-16). Further studies reported that non-enzyme
inducing AED (valproate or VPA) is also associated with thyroid hormonal dysfunction (17-25).
Induction of metabolism of thyroid hormones by the hepatic microsomal enzyme system has
been suggested as the main mechanism for decreased serum T4, fT4, T3 and fT3 concentrations
with enzyme Inducing AEDs. The reduction in thyroid hormone concentrations in the periphery
is associated with compensatory increase in the serum TSH enhancement. Some suggested that
interference with hypothalamic regulation of thyroid function by AEDs seems a possible
mechanism for thyroid hormonal Abnormalities with AEDs (30).

TREATMENT PLAN

DISEASE CONSIDERING THYROID ABNORMALITIES

FIRST LINE CARBAMAZEPINE

ALTERNATIVE NIL
RELATION BETWEEN SEIZURE AND PSYCHIATRIC CASES

Psychogenic nonepileptic seizures are episodes of movement, sensation, or behaviors that are
similar to epileptic seizures but do not have a neurologic origin; rather, they are somatic
manifestations of psychological distress. Patients with psychogenic non-epileptic seizures
frequently are misdiagnosed and treated for epilepsy. Video-electroencephalography monitoring
is preferred for diagnosis. From 5 to 10 percent of outpatient epilepsy patients and 20 to 40
percent of inpatient epilepsy patients have psychogenic non-epileptic seizures. These patients
inevitably have comorbid psychiatric illnesses, most commonly depression, posttraumatic stress
disorder, other dissociative and somatoform disorders, and personality pathology, especially
borderline personality type. Many patients have a history of sexual or physical abuse. Between
75 and 85 percent of patients with psychogenic non-epileptic seizures are women. Psychogenic
non-epileptic seizures typically begin in young adulthood. Treatment involves discontinuation of
antiepileptic drugs in patients without concurrent epilepsy and referral for appropriate psychiatric
care. More studies are needed to determine the best treatment modalities.
Non-epileptic seizures are involuntary episodes of movement, sensation, or behaviors (e.g.,
vocalizations, crying, and other expressions of emotion) that do not result from abnormal cortical
discharges. The seizures can mimic any kind of epileptic seizure and thus can be mistaken for
generalized Tonic-Clonic seizure, absence seizure, and simple or complex partial seizures. Early
recognition and appropriate treatment of non-epileptic seizures can prevent significant iatrogenic
harm and may result in a better outcome.

Classification of Non-epileptic Seizures

Psychogenic
1. Misinterpretation of physical symptoms
2. Psychopathologic processes
3. Anxiety disorders, including posttraumatic stress disorder
4. Conversion disorder
5. Dissociative disorders
6. Hypochondriasis
7. Psychoses
8. Somatization disorders
9. Reinforced behavior patterns in cognitively impaired patients
10. Response to acute stress without evidence of psychopathology

Clinical and Historical Features Suggesting a Diagnosis of Psychogenic SeizuresClinical

features
i. Ability of observer to modify the patient’s motor activity
ii. Asynchronous limb movements
 iii. Avoidance behavior during seizures
iv. Change in symptomatology, or nonstereotypical seizure patterns
v. Closed eyes during seizures
vi. Dystonic posturing (including opisthotonos)
vii. Emotional or situational trigger for the seizures
viii. Gradual onset and cessation of seizures
ix. Ictal crying, weeping
x. If tongue biting is present, usually the tip (not the side) of the tongue
xi. Intermittent or waxing and waning motor activity
xii. Nonphysiologic progression
xiii. Pelvic movements (especially forward thrusting)
xiv. Prolonged seizures (duration of 2 to 3 minutes)
xv. Resisted eyelid opening
xvi. Seizures provoked by suggestion
xvii. Side-to-side head movements

Historical features
i. Associated (often multiple) psychiatric disorders
ii. Flurries of seizures or recurrent pseudo–status epilepticus that lead to multiple emergency
department visits or hospitalizations
iii. High seizure frequency
iv. History of sexual or physical abuse
v. Lack of concern or an excessive or exaggerated emotional response
vi. Multiple unexplained physical symptoms
vii. No history of injury from seizures
viii. No response to antiepileptic drugs or a paradoxical increase in seizures
ix. with antiepileptic drug treatment
x. Personal, family, or professional experience with epilepsy
xi. Seizures that occur only in the presence of others or only when the patient is alone

Epidemiology
The prevalence of non-epileptic seizures ranges from two to 33 cases per 100,000persons in the
general population. Hence, these seizures are approximately as common as multiple sclerosis and
trigeminal neuralgia. From 5 to 10 percent of outpatient epilepsy populations have psychogenic
non-epileptic seizures, compared with 20 to 40 percent of inpatient epilepsy populations
(hospitals and specialty epilepsy centers). Between 75 and 85 percent of patients with
psychogenic non-epileptic seizures are womanlike conversion disorder, psychogenic non-
epileptic seizures tend to begin in young adulthood, although the seizures can occur in a wide
range of age. The prevalence of psychogenic non-epileptic seizures is increased in patients with
head injuries, learning disabilities, or isolated neuropsychological deficits.
Etiology
All psychogenic non-epileptic seizures function as a coping mechanism. Patients with these
events are more likely to use maladaptive coping strategies to handle stress. In psychogenic non-
epileptic seizures, psychological conflicts are translated into a physical symptom—the seizure. In
this way, intolerable distress is dissociated from the painful conscious experience of the trauma
or forbidden emotions that are causing the distress. Thus, genuine psychogenic non-epileptic
seizures (as opposed to factitious disorder or malingering) are not intentional: they are created as
a psychological defense mechanism to keep internal stressors out of conscious awareness.
Psychogenic non-epileptic seizures do not have a single etiology; rather, they are the product of
several different causal pathways. The seizures may be the result of psychopathologic processes,
a response to acute stress in patients without evidence of psychopathology, or a reinforced
behavior pattern in cognitively impaired patients. Rarely, malingering or factitious disorder
presents as psychogenic non-epileptic seizures.

SLEEP DEPRIVATION AND SEIZURE

Yes, it can. Seizures are very sensitive to sleep patterns. Some people have their first and only
seizures after an "all-nighter" at college or after not sleeping well for long periods. If you have
epilepsy, lack of ‘good sleep’ makes most people more likely to have seizures. It can even
increase the intensity and length of seizures. Some forms of epilepsy are especially prone to
sleep problems.

Why does sleep deprivation provoke seizures?

Sleep can affect seizures in many different ways. During normal sleep-wake cycles, changes in
the brain’s electrical and hormonal activity occur. These changes can be related to why some
people have more seizures during sleep than others, and why not getting enough sleep can trigger
seizures. Some people’s seizures are tied very closely with their sleep. They may have all of their
seizures while sleeping, when falling asleep or waking up. For others, sleep may not be a
common trigger, or the association is less clear. For example not getting enough sleep may
trigger seizures only when other triggers are going on too.

What causes sleep problems?

Lot of things can affect a person’s sleep and make them more likely to have seizures. Here are a
few factors to consider.

 Not getting enough sleep: 

 Not getting ‘good quality’ sleep:
 Having seizures at night: Seizures at night can wake people up or just disrupt their sleep
so they aren’t getting a good quality of sleep. Their brains may be missing some of the
important sleep cycles. As a result, someone who has lots of seizures at night may have
trouble functioning during the day. They may also be chronically sleep deprived
and have more seizures during the day too!
 Difficulty falling asleep: 
 Poor eating habits:
  Side effects of medications
 Sleep disorders: Sometimes people can’t sleep because they have a sleep disorder, like
sleep apnea, restless legs or other sleep problems. Sleep disorders can leave a person
chronically sleep deprived and tired. It’s not unusual to see people with seizures also have
sleep disorders.
THERAPY CONSIDERATIONS

DISEASE CVA THYROID DEPRESSION, SLEEP

CONSIDERIN ABNORMALITI ANXIETY, DISORDER
G ES PSYCHOSIS
FIRST LINE CARBAMAZEPI CARBAMAZEPI PHENYTOIN, LORAZEPA
THERAPY NE NE CARBAMAZEPI M
LAMOTRIGINE NE CLONAZEPA
TOPIRAMATE VALPROIC M
VALPROIC ACID
ACID
ALTERNATIV PHENYTOIN ALPRAZOLA
E CARBAMAZEPI M
NE
CLONAZEPAM
 Aim and
objectives

AIM

To assess the prevalence of seizure and prescribing pattern of Anti-Epileptic Drugs in patients
with neuropsychiatric and thyroid abnormalities
OBJECTIVES

• To analyses prevalence and prescription pattern of seizure induced by depression, anxiety

and sleep disorder.

• To study the relationship and management between thyroid abnormalities and seizure.

• To understand the occurrence of seizure and prescribing pattern for a patient after CVA
attack.
 Review of

LITERATURE REVIEW
NEUROLOGY DEPARTMENT
1. E. L. So etal, 1996 :
conducted a study on determination of the magnitude of the risk and identified the factors
predictive of developing seizure disorders after cerebral infarction. Thirty-three patients (6%)
developed early seizures (within 1 week), 78% of which occurred within the first 24 hours after
infarction. Twenty-seven patients developed an initial late seizure (past 1 week), whereas 18
developed epilepsy (recurrent late seizures). Independent predictive factors on multivariate
analysis for initial late seizures were early seizure occurrence (hazard ratio of 7.8 [95% CI 2.8 to
21.7]) and stroke recurrence (3.1 [1.2 to 8.3]). Both early seizure occurrence (16.4 [5.5 to 49.2])
and stroke recurrence (3.5 [1.2 to 10.5]) independently predicted the development of epilepsy as
well. We also found that early seizure occurrence predisposed those with initial late seizures to
develop epilepsy.

2. Paolucci etal, 1997 :

Conducted a prospective study of 306 first-time stroke patients assessed at discharge and at 1-
year follow-up and they found that Post-stroke late seizures occurred in 15.03% of patients.
Putaminal and lobar hemorrhages showed a significant positive association with the development
of seizures, whereas high scores on the Canadian Neurological Scale (CNS) and increasing age
were negatively associated.
3. Daniel L. Labovitz etal, 2001
Evaluated that in 904 patients, early seizure (ES) occurred in 37 (4.1%). The frequency of ES by
stroke subtype and location was deep infarct 0.6% (2/356), lobar infarct 5.9% (20/341), deep
intracerebral hemorrhage (ICH) 4.0% (4/101), lobar ICH 14.3% (7/49), and subarachnoid
hemorrhage 8.0% (4/50). SE occurred in 10 patients (1.1%), representing 27.0% of patients with
ES. Diabetes, hypertension, current smoking, alcohol use, age, gender, and race/ethnicity were
not significant determinants of ES. In a subgroup of patients who had an NIH stroke scale
(NIHSS) score recorded, NIHSS score was not an independent predictor of ES in multivariate
analysis.
4. Osyaldo Camilo etal, 2003
Interpreted that estimates of the rate of early postischemic stroke seizures range from 2% to 33%.
The rates of late seizures vary from 3% to 67%. The rate of postischemic stroke epilepsy is ≈2%
to 4% and is higher in those who have a late seizure. Although mortality rates in stroke patients
with status epilepticus can be high, data reflecting the independent affect of postischemic status
epilepticus on outcome is limited because it is confounded by other factors related to the stroke,
particularly stroke severity.
5. S. K. Das etal, 2005
concluded that the crude prevalence rates (per 100,000 population) of major neurological
disorders with 95 per cent confidence intervals (95% CI) and age adjusted rates (AAR) based on
US 2000 population were 557.5 (95% CI 496.17-624.40 and AAR - 516.77) in epilepsy, 486.85
(95% CI 377.0 to 551.11 and AAR-765.68) in stroke, 87.82 (95% CI 64.02-117.50 and AAR-
168.4) in dementia and 45.82 (95% CI 29.64-67.63 and AAR-71.64) in Parkinsonism.
6. Ryvlin P etal, 2006
Concluded that development of poststroke epilepsy occurs in 54–66 % of those who experience
late seizures, and less than 43 % in early-seizure patients. Similarly, the use of prophylactic
AEDs in acute traumatic brain injury without an initial seizure is not recommended because it
has been found to be ineffective in reducing mortality, functional outcome, and eventual
development of epilepsy, even if it potentially reduces the likelihood of early seizures.
7. P K Myint etal, 2006

Found that post‐stroke epilepsy imposes a clinical dilemma in terms of diagnosis and its
management is controversial. Moreover, standard mortality rate, a ratio of the number of deaths
found in the patient population, compared with that expected in age and sex matched population,
for epilepsy related to cerebrovascular disease, was higher than for all other causes (4.3% and
3.0%). Therefore, a secure diagnosis of epilepsy, treatment tailored to the patient, and continuing
integrated care and support are essential.
8. Anupol Panitchot etal, 2010

Reported that, in their study included 372 patients with stroke; of whom 15.6% had the seizures
after the stroke. The length of follow-up was at least 5 years. Generalized tonic-clonic seizures
were the most common type of post-stroke seizures. The time from the onset of stroke to the
seizures was mostly (60.3%) less than 2 weeks (i.e., early post-stroke seizures). The associated
factors of post-stroke seizures were non-dyslipidemia (p = 0.0007), intracerebral hemorrhage (p
= 0.015), and lesions at cortical area (p = 0.05).

9. Ryan C Turner etal, 2015

Concluded that Post-traumatic epilepsy continues to be a major concern for those experiencing
traumatic brain injury. Post-traumatic epilepsy accounts for 10-20% of epilepsy cases in the
general population. While seizure prophylaxis can prevent early onset seizures, no available
treatments effectively prevent late-onset seizure. . In the final section, we highlight current
experimental therapies that may prove promising in preventing and treating post-traumatic
epilepsy. By increasing understanding about post-traumatic epilepsy and injury expansion over
time, it will be possible to design better treatments with specific molecular targets to prevent
late-onset seizure occurrence following traumatic brain injury .
MEDICINE DEPARTMENT

1. Sherifa A hamed , Mostafa A haridi, Mahmoud M hassan etal. (2015)

Thyroid gland volume in adults with epilepsy: relationship to thyroid hormonal function.
Neurology and neuroscience 2015; 1 ( 2). CBZ and VPA as mono- or polytherapies may
cause thyroid hormonal and structural abnormalities.thyroid enlargement is due to
associated subclinical hypothyroidsm. This data have implications suggesting prevention
strategies.

2. Juan Bernal, M.D., Ph.D. (2015)

Thyroid Hormones in Brain Development and Function.Thyroid disease messenger :
2015:2. “ Thyroid hormones are essential for brain developat through specific time
 windows influencing neurogenesis, neuronal migration, neuronal and glial cell
differentiation, myelination, and synaptogenesis. The actions of thyroid hormones are
mostly due to interaction of the active hormone T3 with nuclear receptors and regulation
of gene expression. T4 and T3 also perform non-genomic actions. The genomically active
T3 in brain derives in part from the circulation, and in part is formed locally by 5’-
deiodination of T4, mediated by Dio2 in the astrocytes, in proportions that depend on the
developmental stage. T4 and T3 are degraded by Dio3 present in neurons. Entry of T4
and T3 in brain is facilitated by specific transmembrane transporters, mainly the
monocarboxylate transporter 8 (Mct8) and the organic anion transporter polypeptide 1c1
(Oatp1c1). In rodents Mct8 facilitates the transfer of T4 and T3 through the blood-brain
barrier (BBB).”

3. Ali A. Raouf,, Gianluca tamagno. (2014)

Encephalopathy associated with autoimmune thyroid disease. European medical journal
2014;1:72-77. “EAATD is the most precise denomination of this condition, as it takes
into account the relationship of the encephalopathy with the ATD, regardless of the
nature of the same (either HT or GD, which is not a thyroiditis), and it does not limit the
definition to the patients who respond to corticosteroids.”
4. Trasciatti S, Prete C, Palummeri E . (2014)
Thyroid storm as precipitating factor in onset of coma in an elderly woman: case report
and literature review. Aging Clin Exp Res. 2004;16(6):490-4.

5. D J  Stott, AR Mclellan, J Finlayson. (2012)

Elderly patients with suppressed serum TSH but normal free thyroid hormone levels
usually have mild thyroid over activity and are at increased risk of developing overt
hyperthyroidism. “ The clinical and biochemical characteristics of 15 elderly patients
with low levels of thyrotrophin (TSH) (<0.1 mU/L) but normal free tri-iodothyronine,
(T3) and free thyroxine (T4) (group S) were compared with 10 euthyroid subjects (group
E) and 10 hyperthyroid patients (group T). Free T3 and free T4 were significantly higher
(p<0.05) in group S(6.3±0.5 and 18.6±1.0 pmol/l, respectively) than in group E(4.6±0.3,
12.6+0.6). In common with elderly hyperthyroid patients (group T)patients in group S
had few signs or symptoms of thyrotoxocosis, but the Wayne score (clinical index of
hyperthyroidism) was higher in group S than in euthyroid subjects (p<0.05). Thyroid
microsomal, thyrogolobulin or thyrotrophin receptor antibodies were common in group T
(n=9)but not in groups S(n=2) or E(n=1). This suggests a low prevalence of Graves'
disease in group S compared to group T. Combined thyrotrophin releasing hormone
(TRH; 200 μg i.v.) and gonadotrophin releasing hormone GnRH; 100 μg i.v.) tests were
performed; no cases of low TSH due to hypopituitarism were identified in group S.
During a mean of 7.9 (4–12) months of observation TSH reverted to the normal range
(>0.2mU/L) in 7 of 15 patients in group S; thyroid hormone concentrations rose above
the normal range in four, however, only two patients required treatment for
hyperthyroidism. It is unlikely that the suppressed TSH of patients in group S was due to
mild thyroid hormone excess; although this is often a transitory phenomenon, these
patients are at increased risk of developing overt hyperthyroidism.”

6. Philip S , Kuan C , Hsu M C. (2012)

 Thyroid Hormone-Induced Seizures A Case Report and Review of Literature. Pediat
Therapeut2012; 2 (5 ) 2-5. “ Thyroxine may induce seizures in patients of all ages, and
has been reported in only few cases. Electroencephalogram, computerized tomography
and other imaging techniques may be helpful in early diagnosis. The measurement of
thyroid hormone levels might be justifiable if the cause of convulsion in a patient is not
apparent. We report a case of hyperthyroidism presented with a generalized tonic clonic
seizures in a 14-year-old female patient and also a review of diagnosis, management and
outcomes of the reported series of seizures in Thyrotoxicosis.
7. Lee HS, Hwang JS. (2011)
Seizure and encephalopathy associated with thyroid storm in children. J Child
Neurol. 2011 ;26(4):526-8. “Thyroid storm with seizures is very rare in children. The
authors report 3 children with thyroid storm who had a seizure in the absence of a history
of neurologic disease. Acute medical management with propylthiouracil, Lugol's iodine
solution, hydrocortisone, and propranolol led to a complete resolution of the symptoms.
Patients with thyroid storm may be predisposed to the development of neuropsychiatric
change. Early recognition and treatment of thyroid storm are essential to reduce
morbidity and mortality from this disorder.

8. Alberto verrotti, Melissa laus, Alessandra scardapane et al, (2009)

Thyroid hormones in children with epilepsy during long-term administration of
carbamazepine and valproate . European journal of endocrinology 2009: 160 ;81–86.
“Data suggest that VPA monotherapy does not alter thyroid hormones. On the contrary,
alterations of thyroid hormones occur in CBZ -treated children. However, the patients are
euthyroid and thyroid hormone alterations are not associated with clinical or subclinical
hypothyroidism.”
9. Gerhard Luef , Markus Rauchenzauner. (2009)
Epilepsy and hormones: A critical review. Epilepsy & Behavior 2009; 15(1): 73-77.
“Especially during growth, puberty, and menopause, profound changes including
maturation of the growth hormone, sex steroid, and thyroid axes, as well as alterations in
lipid homeostasis, cardiac integrity, and other enzyme systems, occur physiologically.
With epilepsy, however, things are often changing, and there may be a complicated
interplay between hormones, epilepsy, and antiepileptic drugs (AEDs). On the one hand,
epilepsy itself possibly elicits diverse effects on different enzyme systems including sex
steroids, the neuro-cardio-endocrine axis, and bone health. On the other hand, different
AEDs are known to induce neuroendocrine changes (e.g., lipid metabolism) that may
have deleterious consequences on health and well-being later in life. It is important for
physicians and epileptologists to have in mind and to consider the endocrine effects
induced by epilepsy itself or by a certain AED when starting antiepileptic therapy,
especially when it is expected that long-term treatment will be necessary.”
10. Page B. Pennell.. (2009)
Neurol Clin 27 (2009) 941–965. Several alterations in different hormonal profiles have
been described for patients with epilepsy. The brain directly regulates hormonal status
through hypothalamus-pituitary- endocrine gland feedback loops. Epilepsy itself, with
both interictal and ictal effects, and the medications used to treat epilepsy can have direct
effects on the regulation of these hormone systems. Epilepsy and antiepileptic drugs
 (AEDs) can target a number of substrates to affect hormone levels, including the limbic
system, hypothalamus, pituitary, peripheral endocrine glands, liver, and adipose tissue.
Abnormalities of the sex steroid hormones have been described most frequently, but have
also been reported for thyroid hormone levels, prolactin, and vitamin D.

11. M  Strolin Benedetti , R  Whomsley, E  Baltes. (2005)

Alteration of thyroid hormone homeostasis by antiepileptic drugs in humans:
involvement of glucuronosyltransferase induction. European Journal of Clinical
Pharmacology 2005; 61(12) : 863-872 “Concerning the antiepileptic drugs which alter
thyroid hormone homeostasis, it is highly probable that the mechanism of induction of
uridine diphosphate glucuronosyltransferases (UGT) is involved, at least partially, in such
an alteration. However, it is not possible to estimate the relative contribution of the UGT
induction by these drugs on the total alteration observed in thyroid hormone levels, as
other mechanisms not investigated, or not examined in the present article, could
contribute”
12. Sherifa A Hamed, Enas A Hamed, Mahmoud R Kandil. (2005)
Serum thyroid hormone balance and lipid profile in patients with epilepsy. Epilepsy
Research 2005;66(1-3): 173–183 “The serum levels of FT3 was elevated in 10.2% of
patients, FT4 was low in 28.4%, TSH was high in 4.6% and low in 2.3%. 13.6% of
patients had high TC, 17.1% had high LDL-c, 60.2% had marked reduction of HDL-c
levels (P < 0.0001) and only 2.3% had high TG levels. Abnormalities were predominated
in CBZ-treated patients. 27.3% patients with abnormal hormones had abnormal lipid
profile. Significant association was identified between the serum TC, LDL-c, TG, GGT
and EIAEDs and between the duration of illness and TG (r = −0.411; P = 0.017), and
FT4 (r = −0.412; P = 0.018). HDL was higher in women than men (r = 0.416; P < 0.002).
However, changes in HDL-c levels associated neither with duration of illness, type or
serum levels of AEDs nor with age or degree of control on AEDs.”

13. Jack deruiter.(2002)

Thyroid hormone tutorial: thyroid pathology. Endocrine Module (PYPP 5260), Thyroid
Section, Spring 2002. “ The prevalence and incidence of thyroid disorders is influenced
primarily by sex and age. Thyroid disorders are more common in women than men, and
in older adults compared with younger age groups. The prevalence of unsuspected overt
hyperthyroidism and hypothyroidism are both estimated to be 0.6% or less in women,
based on several epidemiologic studies. Age is also a factor; for overt hyperthyroidism,
the prevalence rate is 1.4% for women aged 60 or older and 0.45% for women aged 40 to
60. For men more than 60 years of age, the prevalence rate of hyperthyroidism is
estimated to be 0.13%. A similar pattern is observed for the prevalence rate of
hypothyroidism. The prevalence rate of overt hypothyroidism is 2% for women aged 70
to 80, 1.4% for all women 60 years and older, and 0.5% for women aged 40 to 60.”

14. Jouko I. T. Isojärvi, Jukka Turkka, Arto J. Pakarinen,Et al (2001)

Thyroid Function in Men Taking Carbamazepine,Oxcarbazepine, or Valproate for
epilepsy. Epilepsia,2001 ; 42(7):930–934. “Serum thyroid hormone concentrations are
low in CBZ- or OCBZ-treated men. However, these low levels do not seem to be due to
liver enzyme induction or activation of immunologic mechanisms. Therefore,
 interference with hypothalamic regulation of thyroid function by CBZ and OCBZ seems
possible. VPA does not have any significant effects on thyroid function”

15. Ra CS, Lui CC, Liang CL. (2001)

Superior sagittal sinus thrombosis induced by thyrotoxicosis. Case report. J
Neurosurg. 2001;94(1):130-2. “There is a wide variety of disorders associated with
thrombosis of the superior sagittal sinus (SSS), including infectious disease.
noninfectious conditions such as vasculitis and hypercoagulable states, and complications
arising from pregnancy or use of oral contraceptive medications. Despite these well-
defined associations, approximately 25% of the cases remain idiopathic. In this article the
authors describe a patient who was found to have SSS thrombosis while experiencing a
thyrotoxic phase of Graves disease. The patient presented with intracerebral hemorrhage,
subarachnoid hemorrhage, seizure, coma, a raised fibrinogen concentration, low protein
C activity, and atrial fibrillations. Thrombolysis was successfully performed despite the
coexistence of thrombosis and intracranial hemorrhage. Patients with thyrotoxicosis and a
diffuse goiter may be predisposed to the development of SSS thrombosis, as a result of
hypercoagulation and stasis of local venous blood flow. In the present case, a patient in
whom thrombosis coexisted with intracranial hemorrhage was successfully treated using
thrombolytic therapy.”
16. Li Voon Chong JS, Lecky BR, Macfarlane IA . (2000)
Recurrent encephalopathy and generalised seizures associated with relapses of
thyrotoxicosis. Int J Clin Pract. 2000 ;54(9):621-2. “Seizures or encephalopathy
associated with thyrotoxicosis are very rare. A 30-year-old man with thyrotoxicosis and
strongly positive thyroid antibodies presented with generalised seizures preceded by an
encephalopathic illness of a few days duration. CSF protein was raised and EEG showed
bilateral slowing of activity. Antithyroid drug treatment rendered him biochemically
euthyroid, his cognitive state returned to normal and his seizures stopped. Subsequently
he had a recurrence of both encephalopathy and seizures on two occasions, coinciding
with relapses of the thyrotoxicosis. This supports the view that the hyperthyroid state
caused this serious neurological condition. Treatment with 131I caused hypothyroidism
and he has remained seizure free and well for six years on thyroxine replacement.
Corticosteroids may have been helpful in the management of his encephalopathy.”
17. Lin CS, Yiin KT, Lin WH . (1992)
Thyrotoxicosis accompanied with periodic seizure attacks a case report and review of
literature. Chinese medical journal 1992 ;50(4):335-7. “A 58-year-old female was
admitted and discovered to be a victim of thyrotoxicosis. She had experience periodic
seizure attacks for 14 months. These seizures disappeared when function of the thyroid
returned to normal. We performed many studies to search for the cause of the seizures.
No epileptic focus could be detected from an EEG or a MRI of the brain. There was no
abnormal laboratory data such as: hypoglycemia, hypoxemia, serum electrolyte
imbalance, or an acid-base imbalance. No evidence of CNS infection was noted. She had
good response to antithyroid treatment. We therefore suggest, that the seizure attacks may
be related to thyrotoxicosis. In reviewing the literature, we found that only 13 cases of
thyrotoxicosis with seizures have been reported since 1956.”
18. Safe AF, Griffiths KD, Maxwell RT. (1990)
Thyrotoxic crisis presenting as status epilepticus. Postgrad Med J. 1990 ;66(772):150-2.
“A 30 year old male patient with thyrotoxic crisis presenting as status epilepticus is
reported. The aetiology, manifestations and management of this medical emergency are
discussed. The importance of prompt, vigorous and comprehensive treatment of
thyrotoxic crisis is emphasized. Rapid control of hyperthyroidism as well as other
supportive measures are essential if the high fatality rate is to be reduced. Comprehensive
management reduces mortality from 90% to 20%.

19. Primavera A, Brusa G, Novello P.(1990)

Thyrotoxic encephalopathy and recurrent seizures. Eur Neurol. 1990;30(4):186-8.
“Epilepsy is a rare but possible manifestation of thyrotoxicosis. The patient reported here
developed recurrent, generalized and focal seizures, as presenting symptoms of a
thyrotoxic encephalopathy. Intercritic EEG records showed triphasic waves. Seizures and
signs of encephalopathy disappeared and the EEG reverted to normal only after treatment
of the thyroid hyperfunction. It is concluded that thyroid function should be evaluated in
cases of otherwise unexplained encephalopathy with untreatable seizures and triphasic
waves.
20. Roland Faigle, MD, PhD, Raoul Sutter MD, Peter W. Kaplan. (1990)
The electroencephalography of encephalopathy in patients with endocrine and metabolic
disorders . “The continuum of central nervous system (CNS) symptoms associated with
various degrees of hyperthyroidism ranges from subtle impairment of cognitive function,
insomnia, emotional liability and anxiety, to severe and potentially life threatening
manifestations, such as severe encephalopathy, seizures and coma . The latter is most
frequently encountered during thyroid storm which has a mortality rate of up to
20% .There is no clear correlation between the degree of EEG abnormality and serum
thyroid hormone level . An increase in frequency of the posterior dominant rhythm, an
increase in fast activity, as well as a higher incidence of theta and delta activity have been
observed in thyrotoxicosis, and in experimental hypermetabolism .High-voltage and
prolonged EEG responses to photic stimulation have also been described .Wilson et al.
noted that these changes were most profound in young women .Rarely, triphasic waves
(TWs) have been reported in patients with acute hyperthyroidism .A case of thyrotoxic
stormpresenting as posterior reversible encephalopathy syndrome (PRES) in a patient
with generalized convulsions and coma, has been described, however, PRES associated
with hyperthyroidism is exceedingly rare .Hyperthyroidism lowers seizure threshold in
patients with preexisting epilepsy . Furthermore, de novo convulsive seizures in the
setting of thyrotoxicosis are well recognized. Thyrotoxicosis presenting as new-onset
seizures is often refractory to antiepileptic drugs (AEDs), and may only be controlled
after reaching an euthyroid state . In a case report of a patient with iatrogenic
hyperalimentation with levothyroxine, the EEG revealed NCSE with almost continuous
bisynchronous spike-and-wave discharges with an occipital predominance .

21. Aiello DP, DuPlessis AJ, Pattishall EG . (1989)

Thyroid storm. Presenting with coma and seizures. In a 3-year-old girl. Clin Pediatr
(Phila). 1989 ;28(12):571-4. “ Thyroid storm is a rare occurrence in the adult population
and is even more unusual in children. The current report is of a 3.5-year-old girl who had
thyroid storm with unique neurologic manifestations, namely seizure and coma. Acute
medical management with propylthiouracil, saturated solution of potassium iodide,
hydrocortisone, and propranolol brought about complete resolution of symptoms”
22. Sundaram MB, Hill A, Lowry N.(1985)
Thyroxine-induced petit mal status epilepticus. Neurology. 1985 ;35(12):1792-3. “Petit
mal status epilepticus was induced by high doses of thyroxine, confirming experimental
evidence that thyroxine may lower the seizure threshold. This is another hazard of rapidly
correcting the hypothyroid state.”
23. Jabbari B, Huott AD. (1980)
 Seizures in thyrotoxicosis. Epilepsia. 1980 ;21(1):91-6. “ Over a period of 2 years we
have observed 3 thyrotoxic patients who presented with a convulsive encephalopathy.
These patients had no history of seizures before and experienced no further seizures after
subsidence of the thyroid dysfunction. During the convulsive period,
electroencephalograms of 2 patients showed evidence of cerebral hyperexcitability, but in
both cases it returned to normal once the thyroid disorder was corrected. We believe that
thyrotoxic seizures are not rare. These seizures can be focal as well as generalized and
can constitute the presenting symptoms of the disease. Absence of other laboratory
abnormalities such as serum electrolytes, or osmolality changes, or hypoglycemia in all
patients who reportedly suffered from thyrotoxic seizures, and the data obtained from
animal studies, suggest that human thyrotoxic seizures result mainly from the direct
effect of thyroid hormones over the cerebral tissue.”
24. Jabbari B, Huott AD. (1980)
Seizures in thyrotoxicosis. Epilepsia. 1980 ;21(1):91-6. “Over a period of 2 years we
have observed 3 thyrotoxic patients who presented with a convulsive encephalopathy.
These patients had no history of seizures before and experienced no further seizures after
subsidence of the thyroid dysfunction. During the convulsive period,
electroencephalograms of 2 patients showed evidence of cerebral hyperexcitability, but in
both cases it returned to normal once the thyroid disorder was corrected. We believe that
thyrotoxic seizures are not rare. These seizures can be focal as well as generalized and
can constitute the presenting symptoms of the disease. Absence of other laboratory
abnormalities such as serum electrolytes, or osmolality changes, or hypoglycemia in all
patients who reportedly suffered from thyrotoxic seizures, and the data obtained from
animal studies, suggest that human thyrotoxic seizures result mainly from the direct
effect of thyroid hormones over the cerebral tissue.”
25. Korczyn AD, Bechar M. (1976)
Convulsive fits in thyrotoxicosis. Epilepsia. 1976 ;17(1):33-4. “A patient with
hyperthyroidism is described who developed grand mal seizures when anth-thyroid
medication was withdrawn. Pyramidal signs were also present. The EEG reverted to
normal and the clinical signs and symptoms disappeared when his thyroid status was
again controlled.

26. P.Zander Olsen, M Støier, K Siersbaek-Nielsen Etal. (1972)

Electroencephalographic findings in hyperthyroidism Electroencephalography
and Clinical Neurophysiology, 1972 ; 32 (2) : 171-177. “ Twenty-six of thirty-
two patients with untreated thyrotoxicosis had an abnormal EEG. The severity of
the hyperthyroidism evaluated by several thyroid function tests was correlated
with the degree of diffuse paroxysmal activity and fast activity above 15 μV, but
no correlation was found with the alpha frequency. After 2–6 weeks of treatment
the EEGs showed a decrease in the alpha frequency parallel to the normalization
of the thyroid function tests. The paroxysmal and fast activities subsided
gradually and incompletely but significantly, while the slow activity did not show
any significant decrease after 2–3 years. At the end of the observation period
more than half of the patients still had EEGs which were abnormal, although less
pronounced. Six patients with relapses of hyperthyroidism had aggravation of the
 EEG abnormalities, which again subsided after treatment was reinstituted. It is
concluded that hyperthyroidism causes a characteristic pattern of severe EEG
changes which may only subside gradually and incompletely, indicating
persisting cerebral dysfunction in spite of an otherwise successful treatment of
the hyperthyroidism.”

PSYCHIATRY DEPARTMENT
1. Verrotti A, D’alonzo R And Rinaldi Ve (2014)

Sleep Disorders in Epileptic Patients: The Role of Epilepsy and the Role of AEDs
The effects of AEDs on sleep have been studied independent of seizures showing both
detrimental and beneficial effects. AEDs affect sleep architecture by inducing sedation or
insomnia. In addition some AEDs can be weight inducing, therefore fragmenting sleep.
Virtually all AEDs have effects on sleep architecture and many studies have analyzed
these effects. In particular Class 1 studies in healthy adults suggest that Phenobarbital and
levetiracetam reduce REM sleep whereas it is enhanced by gabapentin. Other studies
demonstrated that clobazam decreases slow wave sleep in the same type of population
while it is increased by levetiracetam, pregabalin and tiagabine. Clobazam also reduces
sleep latency and arousals/wake time also reduced by levetiracetam, Phenobarbital,
tiagabine and pregabalin. Class 3 evidence based studies show that carbamazepine
favours sleep efficiency and extends total sleep time increasing slow wave sleep in
healthy subjects and diminishes sleep latency, arousals REM sleep and wake time. On the
other hand class 1 evidence based studies in epileptic adult patients showed that
pregabalin increases slow wave sleep that is instead reduced by levetiracetam [16].
Moreover, Phenobarbital and gabapentin reduce sleep latency and arousals. Regarding
slow wave sleep it has been seen that carbamazepine and gabapentin have an enhancing
effect contrarily to ethosuximide. Conflicting results were seen with lamotrigine on REM
sleep and slow wave sleep. Phenobarbital and phenytoin cause a reduction in patients
REM sleep that was not demonstrated with the administration of ethosuximide or
gabapentin. Finally class 3 evidence based studies show that Phenobarbital increases
daytime sleepiness, an effect that was not seen when topiramate, lamotrigine, zonisamide
or vigabatrin were administered to epileptic patients.

2. Vladimir Shvarts And Steve Chung(2013)

A reciprocal relationship exists between sleep and epilepsy. The quality of sleep is affected by
the presence and frequency of seizures, type of antiepileptic therapy utilized, and coexisting
primary sleep disorders. Daytime somnolence is one of the most common adverse effects of
antiepileptic therapy, with specific pharmacologic agents exhibiting a unique influence on
components of sleep architecture. The newer generation of antiseizure drugs demonstrates
improved sleep efficiency, greater stabilization of sleep architecture, prolongation of REM sleep
duration, and increased quality of life measures. The emerging field of chronoepileptology
explores the relationship between seizures and circadian rhythms, aiming for targeted use of
antiseizure therapies to maximize therapeutic effects and minimize the adverse events
experienced by the patients.

3. Sherifa Ahmad Hamed, Nabil Abdel-Hakim Metwaly, Mahmoud Mohamad Hassan

(2012)

The study was to characterize the relationship between depression and epilepsy-related
seizures, treatment, hormonal and biological variables. Depressive or depressive/anxiety
manifestations associated with epilepsy appear to be more closely related to seizure type,
focus, side, severity and intractability to medications as well as epilepsy-related
neurotransmitter changes rather than the effect of treatment-related adverse effects. However,
it is possible that the overall function and well-being of the patient, the presence of negative,
depressed or irritable mood, periods of anxiety and stress in combination with negative life
events, may increase the frequency of seizures. Attention should be paid to optimizing
seizure control and the early recognition of depression and its correlates. Regular psychiatric
consultation, psychotherapy and medical treatment are sometimes needed. It is also
imperative to properly understand the pathophysiologic mechanisms of co morbid depression
with epilepsy. This should move the treatment of patients toward a comprehensive
biopsychosocial model that focuses on the whole person rather than on the disease process.

4. Raffaele Manni, , Michele Terzaghi (2010)

Despite being relatively common and potentially able to have clinical and pathophysiological
consequences, the co morbidity between epilepsy and sleep disorders is poorly investigated in
the literature and rarely taken into consideration by clinicians in general practice. There is
increasing evidence that obstructive sleep apnoea (OSA) coexists in epilepsy (in 10% of
unselected adult epilepsy patients, 20% of children with epilepsy and up to 30% of drug-resistant
epilepsy patients). A few lines of evidence suggest that continuous positive airway pressure
treatment of OSA in epilepsy patients improves seizure control, cognitive performance and
quality of life. Parasomnias and epileptic seizures can coexist in the same subject making the
differential diagnosis of these conditions particularly challenging. In childhood, a frequent
association between epilepsy and NREM arousal parasomnias, enuresis and rhythmic movement
disorder has been documented. A particular pattern of association has been found between
nocturnal frontal lobe epilepsy (NFLE) and NREM arousal parasomnias, the latter being found in
the personal or family history of up to one third of NFLE patients. As far as REM parasomnias
are concerned, REM sleep behaviour disorder, unrecognised or misdiagnosed, has been found to
co-occur in 12% of elderly epilepsy patients. Patients with epilepsy often complain of poor, non-
restorative sleep; however, insomnia in epilepsy is poorly investigated, with the literature giving
conflicting prevalence data and no information on the impact of this disorder on seizure control,
or on the best therapeutic approach to insomnia in this particular group of patients. A greater
awareness, among clinicians, of the co morbidities between sleep disorders and epilepsy may
help to prevent misdiagnosis and mistreatment. Sleep hygiene measures in epilepsy need to be
more comprehensive, taking into account the various pathologies that may underlie disordered
sleep in epilepsy patients.
 5. Sanjeev V Kothare, Joseph Kaleyias (2010)

Sleep and epilepsy in children and adolescents Epilepsy and sleep disorders are considered by
many to be common bedfellows. Several sleep phenomena may occur during nighttime taking a
wide variety of forms and which can mimic seizures. Although most seizure sub-types have the
potential to occur during sleep or wakefulness, sleep has a well-documented and strong
association with specific epilepsy syndromes. Seizures in sleep also tend to occur during lighter
stages of non-REM (NREM) sleep. The neurophysiologic process involved in the deepening of
NREM sleep may also facilitate both seizures and IEDs. Epilepsy per se and/or seizures
themselves promotes sleep disruption and significantly affects the quality, quantity, and
architecture of sleep. There are many causes of sleep disruption in patients with epilepsy,
including inadequate sleep hygiene, coexisting sleep disorders, and circadian rhythm
disturbances. Seizures themselves can disrupt sleep, even when they occur during wakefulness.
Anti-epileptic drugs (AEDs) can also alter sleep in positive and negative ways, and these effects
are independent of anticonvulsant actions. The end result of sleep disruption is excessive daytime
sleepiness, worsening seizures, and poor quality of life. Screening for sleep disorders in the
epilepsy population and appropriate intervention strategies will lead to overall improved quality
of life and seizure control.

6. P. Montagna, F. Bisulli, I. Naldi, L. Vignatelli,F. Provini, G. Plazzi, R. Vetrugno

And P. Tinuper (2006)

In NFLE, attacks (paroxysmal arousals, nocturnal paroxysmal dystonia, and epileptic

wanderings) occur during NREM sleep with features comparable to arousal disorders such as
pavor nocturnus and somnambulism. Moreover NFLE attacks may recur quasi-periodically
during light sleep, associated with EEG arousals and cyclic alternating patterns. NFLE may be
inherited as an autosomal dominant trait related to mutations in neuronal acetylcholine receptors
subunit genes. NFLE and arousal disorders are universally considered clearly distinct diseases,
and the presence of parasomnias in NFLE families has been considered a mistake due to
misdiagnosis. To verify whether NFLE patients and their relatives have a higher frequency of
parasomnias, and to clarify the still unknown physiopathological mechanisms underlying NFLE,
we performed a familial aggregation study of probands with documented hyper motor seizures
polygraphically recorded, utilizing a standardized interview applying the ICSD-R minimal
criteria to diagnose the main parasomnias (lifetime risk). For each proband, 7 relatives were also
interviewed, and a control subject, matched for sex, age, education and place of residence. For
each control again seven relatives were recruited. Overall, 395 subjects were enrolled, 31
probands, 25 control subjects, and their relatives. Arousal parasomnias and nightmares were
significantly increased in probands_ relatives, while no difference was found for other
parasomnias such as sleep paralysis and the wake-sleep transition disorders. Our findings are still
preliminary and need careful analysis. However they might suggest common (genetic?)
mechanisms underlying the arousal parasomnias and NFLE, possibly undergoing developmental
modulation.

7. L. Nobili1, I. Sartori1, S. Francione1, R. Mai1, L. Tassi1, M. Cossu1, M. Terzaghi2

And G. Lo Russoirccs (2006)
Patients affected by Nocturnal Frontal Lobe Epilepsy (NFLE), often report a poor quality of
sleep and excessive daytime sleepiness. This has been ascribed to the presence of recurrent
motor episodes fragmenting sleep. Indeed, apart from major seizures, NFLE patients frequently
present a high number of minor motor events (MMEs) lasting 2–4 s recurring periodically during
NREM sleep. The epileptic origin of MMEs has not been definitively proven as they generally
lackscalp EEG epileptic correlates. Studies with intracerebral electrodes in patients with drug
resistant NFLE (21 patients; 11 males and 10 females) have shown that periodic epileptic
discharges (EDs), not detectable on scalp EEG, play the main role in the mechanism inducing
arousal instability. EDs may act as a non-specific internal trigger able to operate directly on the
sleep regulatory arousal mechanisms. Periodically recurrent EDs may increase arousal
fluctuations, expressed by an augment of CAP rate, and in turn enhance and modulate the
occurrence of different kind of motor events: brief ictal epileptic events (these occur when
epileptic discharges arise from a
Motor cerebral area), physiological movements, non-epileptic pathological events such as
periodic leg movements, bruxism, sleep talking etc. In several of these instances the severity of a
co-morbid sleep disorder is enhanced by the periodic occurrence of arousals induced by Beds.
One can look at this mechanism as a sort of feedback network in which sleep disturbances are
involved in the maintenance of arousal instability which represents the permissive background
for the manifestation of EDs and MMEs during sleep. Thus MMEs seem not to be induced only
by the direct effect of EDs, but, more likely, seem to be related to the loss of cortical inhibition
secondary to arousal, which is triggered by internal epileptiform stimuli. In this framework, the
production of MMEs may be regarded as the result of aspecific disinhibition of innate motor
patterns.

8. K. Sonka And M. Jakoubkova (2006)

The relationship between sleep disordered breathing (SDB) and epilepsy is interesting from
different points of view: epileptic seizures promotion by SDB, probable SDB induction by
epilepsy, SDB worsening by vagal nerve stimulation, and possible indirect SDB worsening by
antiepileptic drugs through the weight gain. Differential diagnosis of SDB and seizures is also
important and according to some reports, SDB may well be one of the reasons of unexpected
death in epilepsy. Epileptic seizures promotion by SDB is theoretically supported by the
assumption that some SDB features facilitate epileptic paroxysms (sleep deprivation, REM sleep
and SWS reduction, sleep fragmentation, daytime sleep and drowsiness, hyperventilation,
oxygen saturation drops, brain perfusion changes). Some case reports and small sample studies
show frequent seizures in patients suffering from SDB, and even some relief after CPAP therapy.
In our retrospective survey of 480 adults without any other neurological and neurosurgical
diseases suffering from SDB, 19 subjects (=4%) experienced at least two seizures in adult age.
More importantly, 79% of them had seizures exclusively during sleep, and their average age at
the first seizure was 48 years. We were not able to confirm CPAP treatment as lowering the rate
of seizures in these patients. In a prospective PSG study of 17 patients with sleep apnea and
epilepsy we found epileptic interictaldischarges (IEDs) in seven patients. In this IEDs+ patient’s
subgroup 87% of respiratory events were accompanied by IEDs and only 13% of them occurred
without IEDs. The rate of IEDs in 30 s epochs without respiratory events (12.8 } 9.4) was
significantly lower (P < 0.003) than that of epochs with respiratory events (21.4 } 16.3).
Literary data and our own experience suggest that the relationship between SDB and epilepsy is
underestimated and requires a closer study

9. R. Manni And M. Terzaghi (2006)

The relationship between REM sleep and epilepsy are complex. Generally speaking REM sleep
inhibits epileptic phenomena. However focal epileptic seizures have been documented to occur
during REM sleep. Dream content has been reportedly altered (_dreaming seizure_ experience)
in temporal lobe epilepsy patients. Little is known about the co-existence of REM sleep
behaviour and epileptic seizures in spite of potential clinical and neurophysiopathological
implications of such association, which is expected to be high in elderly people. A systematic
investigation about RBD co-existence in 74 (44 men;30 women),over-sixty epilepsy patients
referring to a tertiary epilepsy centre was done, with a definite clinical and polysomnographic
documentation of RBD episodes , generally preceding by years the seizures onset, in 10 subjects
(13.5%). At a preliminary univariate analysis the frequency of RBD was higher in patients with
seizures onset after sixty years of age (6 out of 35 cases: 17.1%) than in those with earlier seizure
onset (4 out of 39 subjects: 10.2%), in patients with only during sleep seizures (4 out of 18
subjects: 22%) than in those with wakefulness or random seizures (6 out of 56 subjects: 10.7%)
and in cryptogenic ( 9 out of 45 subjects:20.0%) than in symptomatic forms of epilepsy (1 out of
22 subjects: 4.5%). The co-existence of RBD episodes and epileptic seizures increases the risk of
misdiagnosis and mistreatment. Yet potential physiopathological implications of RBD in human
epilepsy are discussed also in light of data about facilitation of seizures occurrence during sleep
in animal models of epilepsy after inducing _REM sleep without EEG desynchrony_ and _REM
without atonia_ by pontine dissociation techniques.

10. JACQUELINE FOONG (2005)

Studies have estimated that up to 50% of patients with epilepsy develop psychiatric
disorders, the most common being depression, anxiety and psychotic disturbances1. These
psychiatric disturbances can be classified according to how they relate in time to seizure
occurrence, i.e. ictal, peri-ictal (pre-ictal/prodromal, post-ictal) or inter-ictal. Multiple risk
factors are associated with the increased risk of psychiatric problems in epilepsy which can
be broadly divided into biological (e.g. type and severity of epilepsy), psychosocial and
iatrogenic (antiepileptic drugs, surgery).

11. LESLIE E. PERRY1 AND JENNIFER L. DEWOLFE (2002)

They conducted a study on Epilepsy and Sleep: Sleep Hygiene and Obstructive Sleep Apnea,
Sleep Deprivation, Circadian Patterns and Epilepsy Surgery and found that the relationship
between epilepsy and sleep is complex and dynamic. Sleep complaints and concomitant sleep
disorders are common in people with epilepsy. Seizures and antiepileptic drugs can alter sleep
architecture. There have been conflicting findings on the impact of sleep deprivation on seizures;
however there is evidence to support the improved specificity of epilepsy diagnosis when a
negative routine EEG is followed with a sleep-deprived study. The timing of seizure occurrence
may be influenced by seizure onset localization; however much remains to be investigated
regarding the impact of circadian rhythms and sleep patterns on seizure control. Lastly, epilepsy
surgery has been shown to improve sleep quality in patients who remain seizure free. There have
been advances in epilepsy and sleep research in light of newer investigational techniques,
improved awareness of co morbid sleep disorders and the increasing prevalence of surgically-
cured epilepsy patients. This article reviews the impact of sleep hygiene and obstructive sleep
apnea on seizures, sleep deprivation on seizures, the circadian pattern on seizures, and finally the
impact of epilepsy surgery on sleep.

12. M.N Shouse , P.R Farber,  R.J Staba (2000)

Physiological basis: how NREM sleep components can promote and REM sleep components can
suppress seizure discharge propagation and they found that to describe how the neural generators
of different sleep components can provoke seizure discharge propagation during NREM sleep
and can suppress it during REM sleep. (1) Neural generators of synchronous EEG oscillations,
including tonic background slow waves and phasic ‘arousal’ events (sleep EEG transients such
as sleep spindles, k-complexes), can combine to promote electrographic seizure propagation
during NREM and drowsiness; anti-gravity muscle tone permits seizure-related movement. (2)
Neural generators of asynchronous neuronal discharge patterns can reduce electrographic
seizures during alert waking and REM sleep; skeletal motor paralysis blocks seizure-related
movement during REM. (3) Etiology of the seizure disorder can interact with sleep and arousal
mechanisms to determine sleep-waking state distribution of interictal and ictal events. :
Differential effects of NREM versus REM sleep components on seizure discharge propagation
are to some extent non-specific and in other ways specific to seizure etiology.
Plan of
 PLAN OFSTUDY

Thestudywasplannedtoconductinfourdifferentphases:

PhaseI

Identificationoftargetareasforpossiblestudy.

Designingofdataentryform

Literaturesurvey

PhaseII

Data collection

PhaseIII

Analysisofdata

PhaseIV

Publication and Project Book submission

Methodology
 METHODOLOY

Studysite:

Thestudywasconductedatthedepartmentof Neurology, Medicine and Psychiatric

department in Karuna Medical College, Chittur, Palakkad

ConsentfromtheHospitalAuthorities:

Theauthorizationforconductingthisstudyinthehospitalwasobtainedfromthe Principal Maj.

Gen (Retd) Dr. M. N Sreeram ,MD

Studyperiod:

ThestudywasconductedoveraperiodofsixmonthsfromNovember 2015toApril 2013.

StudyDesign:

The study was designed as a prospective observational study to assess the prevalence
of seizure and prescribing pattern of Anti-Epileptic Drugs in patients with neuropsychiatric and
thyroid abnormalities

Studypopulation:

A total of 655 subjectswereincludedinthestudy.

Studycriteria:

Inclusioncriteria:

a) Neurology Department

All OP cases in neurology department presented with CVA, head ache, head
injury and meningitis.

All IP cases in neurology department presented with CVA, head ache, head injury
and meningitis.

b) Medicine Department
All hypothyroidism cases presented in the IP and OP department

All hyperthyroidism cases presented in the IP and OP departments

c) Psychiatric Department

All cases present in psychiatric department such as BPAD, sleep disorder and anxiety

Exclusion Criteria

a) Neurology Department

All cases of CVA, head ache, head injury and meningitis who having history of
psychiatry disease.

All cases of CVA, head ache, head injury and meningitis who having medical history of
thyroid abnormalities.

b) Medicine Department

All cases of hyperthyroidism and hypothyroidism with other neurologic and diseases as
co-morbidities

All cases of hyperthyroidism and hypothyroidism with other psychiatric illness.

All cases of hyperthyroidism and hypothyroidism presented with seizure before the
diagnosis of thyroid abnormalities

All cases without checking TFT.

c) Psychiatric Department

All cases presented with other thyroid abnormalities

All cases of psychiatry with other neurologic diseases as co-morbidities

All cases presented as a complication of seizure

STUDY PROTOCOL

Literature Survey

Literature survey was carried out regarding the prevalence of seizure in Thyroid
disease, Neurological disease as well as in Psychiatric disease. The various literature
included are Journal of Neurology, British Journal of Psychiatry, British Medical Journal,
New England Journal of Medicine etc.

Data Entry Form

A well designed Data Entry Form was used for this study (Annexure). Data collected
from case files are included.

STATISTICAL ANALYSIS

The statistical analysis was performed by 2- Tailed Fischer Exact Test and the Odd
Ratio was analyzed by Medcal Software
Observations and
Results
Table1.1 cases collected from each department

DEPARTMENT SAMPLE SIZE

MEDICINE 122

NEUROLOGY 217

PSYCHIATRY 316

TOTAL 655

TABLE 1.2: GENERAL AGE DISTRIBUTION

 AGE (YEARS) NO. OF SUBJECTS
<10 3
10 – 20 35
20 – 30 48
30 – 40 101
40 – 50 144
50 – 60 107
60 – 70 105
70 – 80 73
>80 35
TOTAL 655

FIGURE 1.3: GENERAL AGE DISTRIBUTION

TABLE 1.3: GENERAL GENDER DISTRIBUTION

GENDER NO. OF SUBJECTS
MALE 314
FEMALE 341
TOTAL 655

FIGURE 1. 3: GENERAL GENDER DISTRIBUTION

NEUROLOGY DEPARTMENT
TABLE 2.1: DISEASE WISE DISTRIBUTION IN NEUROLOGY
DEPARTMENT
DISEASE NO. OF SUBJECTS
CVA 199
HEAD ACHE 9
HEAD INJURY 5
MENINGITIS 4

FIGURE 2.1: DISEASE WISE DISTRIBUTION IN NEUROLOGY

DEPARTMENT
TABLE 2.2: GENERAL AGE DISTRIBUTION IN NEUROLOGY
DEPARTMENT
AGE (YEARS) NO. OF CASES
<10 1
10 – 20 1
20 – 30 1
30 – 40 13
40 – 50 33
50 – 60 36
60 – 70 61
70 – 80 51
>80 20
TOTAL 217
FIGURE 2.2: GENERAL AGE DISTRIBUTION IN NEUROLOGY
DEPARTMENT

70
60
50
NO. OF SUBJECTS

40
30
20
10
0
<10 10-- 20- 30- 40- 50- 60- 70- >80
20 30 40 50 60 70 80
AGE (YEARS)

TABLE 2.3: GENERAL GENDER DISTRIBUTION IN NEUROLOGY

DEPARTMENT
GENDER NO. OF CASES
MALE 120
FEMALE 97
TOTAL 217

FIGURE 2.3: GENERAL GENDER DISTRIBUTION IN NEUROLOGY

DEPARTMENT
TA
TATA
TABLE 2.4: TOTAL PREVALENCE OF IN NEUROLOGY
DEPARTMENT
NO. OF SUBJECTS
SAMPLE SIZE 217
PREVALENCE OF SEIZURE 49
 FIGURE 2.4: TOTAL PREVALENCE OF IN NEUROLOGY DEPARTMENT

TABLE 2.5: DISTRIBUTION OF SEIZURE IN DIFFERENT NEUROLOGICAL

CASES
DISEASE NO. OF CASES NO. OF CASES WITH
SEIZURE
CVA 199 36
HEAD ACHE 9 6
HEAD INJURY 5 3
MENINGITIS 4 4
TOTAL 217 49
FIGURE 2.5: DISTRIBUTION OF SEIZURE IN DIFFERENT NEUROLOGICAL
CASES

250
NO. OF SUBJECTS

200

150

100

50

0
CVA HEAD ACHE HEAD INJURY MENINGITIS

DISEASES

NO. OF CASES NO. OF CASES WITH SEIZURE

TABLE 2.6: AGE DISTRIBUTION OF PREVALENCE SEIZURE IN
NEUROLOGY DEPARTMENT
AGE (YAERS) NO. OF SUBJECTS
<10 1
10 – 20 3
20 – 30 1
30 – 40 5
40 – 50 10
50 – 60 7
60 – 70 8
70 – 80 11
>80 3
TOTAL 49

FIGURE 2.6: AGE DISTRIBUTION OF PREVALENCE SEIZURE IN

NEUROLOGY DEPARTMENT
12
10
NO. OF SUBJECTS

8
6
4
2
0
<10 10 20- 30- 40- 50- 60- 70- >80
— 30 40 50 60 70 80
20

AGE (YEARS)
TABLE 2.7: GENDER DISTRIBUTION OF PREVALENCE OF SEIZURE
GENDER NO. OF SUBJECTS
MALE 11
FEMALE 38
TOTAL 49

FIGURE 2.7: GENDER DISTRIBUTION OF PREVALENCE OF SEIZURE

ABLE
TABLE 2.8: DISEASE BASED PREVALENCE OF SEIZURE IN
NEUROLOGY DEPARTMENT
DISEASE NO. OF PATIENTS PERCENTAGE (%)
CVA 36 73. 46
HEAD INJURY 3 6. 122
HEAD ACHE 5 10. 20
MENINGITIS 4 8. 163

FIGURE 2.8: DISEASE BASED PREVALENCE OF SEIZURE IN

NEUROLOGY DEPARTMENT
TABLE 2.9: PREVALENCE OF EARLY AND LATE POSTSTOKE
SEIZURE
TYPE OF SEIZURE PERCENTAGE (%)
EARLY SEIZURE 31. 5
LATE SEIZURE 68. 5

FIGURE 2.9: PREVALENCE OF EARLY AND LATE POSTSTOKE

SEIZURE
TABLE 2.10: AED PRESCRIBING PATTERN IN NEUROLOGY
DEPARTMENT
DRUGS PERCENTAGE (%)
SODIUM VALPROATE 16. 6
CLOBAZAM 5. 5
LEVETIRACETAM 38. 8
PHENYTOIN 38. 8

FIGURE 2.10: AED PRESCRIBING PATTERN IN NEUROLOGY

DEPARTMENT

40
30
20
PERCENTAGE (%)

10
0
T E M M IN
A A A O
RO B AZ C E T
NY
T
P O IA E
V AL CL T R PH
E
IUM LE
V
D
SO
DRUGS

TABLE 2.11: DISTRIBUTION OF MONO-THERAPY AND DUAL

THERAPY IN NEUROLOGY DEPARTMENT
TYPE OF THERAPY NO. OF SUBJECTS PERCENTAGE (%)
MONO THERAPY 39 80
DUAL THERAPY 10 20

FIGURE 2.11: DISTRIBUTION OF MONO-THERAPY AND DUAL

THERAPY IN NEUROLOGY DEPARTMENT

TABLE 2.12: DISTRIBUTION OF DUALTHERAPY IN NEUROLOGY

DEPARTMENT
 DUAL THERAPY NO. OF SUBJECTS
PHENYTOIN + LEVETIRACETAM 2
PHENYTOIN+ VALPROIC ACID 2
VALPROIC ACID+ CLOBAZAM 2
LORAZEPAM+ VALPROIC ACID 1
LEVETIRACETAM+ VALPROIC ACID 1
LEVETIRACETAM+ DIAZEPAM 1
PHENYTOIN+ PHENOBARBITONE 1

FIGURE 2.12: DISTRIBUTION OF POLY-THERAPY IN NEUROLOGY

DEPARTMENT

TABLE 2.13: STATISTICAL ANALYSIS IN NEUROLOGY

DEPARTMEN
TABLE 2.13: STATISTICAL ANALYSIS
DISEASE P VALUE ODD RATIO
CVA 0.0407 1.696
HEAD ACHE 0.1356 0.4031
HEAD INJURY 0.1326 2.3191
MENINGITIS 0.1676 2.29

Table 3.1 GENERAL GENDER DISTRIBUTION IN MEDICINE DEPARTMENT

GENDER NO. OF SUBJECTS (N=122)

MALE 36
FEMALE 86

Figure 3.1 GENERAL GENDER DISTRIBUTION IN MEDICINE DEPARTMENT

 MALE FEMALE

30%

70%

Table 3.2 GENERAL AGE DISTRIBUTION IN MEDICINE DEPARTMENT

AGE (yrs) NO. OF SUBJECTS (n=122)

< 10 2
10-20 8
20-30 12
30-40 16
40-50 24
50-60 26
60-70 22
70-80 10
>80 2

Figure 3.2 GENERAL AGE DISTRIBUTION IN MEDICINE DEPARTMENT

 30

25

20
NO.OF SUBJECTS

15

10

0
< 10 20-Oct 20-30 30-40 40-50 50-60 60-70 70-80 >80
AGE (yrs)

Table 3.3 DISTRIBUTIONS OF THYROID ABNORMALITY CASES IN MEDICINE

DEPARTMENT

NO.OF SUBJECTS (N=122) PERCENTAGE %

HYPOTHYROIDISM 104 85.25
HYPERTHYROIDISM 18 14.75

Figure 3.3 DISTRIBUTIONS OF THYROID ABNORMALITY CASES IN MEDICINE

DEPARTMENT
 HYPOTHYROIDISM HYPERTHYROIDISM

15%

85%

Table 3.4 PREVALENCE OF SEIZURE IN HYPOTHYROIDISM

HYPOTHYROIDISM
TOTAL NUMBER 104
PATIENTS WITH SEIZURE 22
PERCENTAGE % 21.15

Figure 3.4 PREVALENCE OF SEIZURE IN HYPOTHYROIDISM

 120

100

80
NO. OF SUBJECTS

60

40

20

0
TOTAL NUMBER PATIENTS WITH SEIZURE

Table 3.5 PREVALENCE OF SEIZURE IN HYPERTHYROIDISM

HYPERTHYROIDISM
TOTAL NUMBER 18
PATIENTS WITH SEIZURE 4
PERCENTAGE % 22.22

Figure 3.5 PREVALENCE OF SEIZURE IN HYPERTHYROIDISM

 20

18

16

14
NO. OF SUBJECTS

12

10

0
TOTAL NUMBER PATIENTS WITH SEIZURE

Table 3.6 AGE DISTRIBUTION OF HYPO AND HYPERTHYROIDISM IN MEDICINE

DEPARTMENT

AGE (yrs) HYPER THYROIDISM HYPOTHYROIDISM

(n=18) (n=104)
<10 0 2
10-20 0 8
20-30 2 10
30-40 4 12
40-50 5 19
 50-60 4 22
60-70 2 20
70-80 1 9
>80 0 2

Figure 3.6 AGE DISTRIBUTION OF HYPO AND HYPERTHYROIDISM IN MEDICINE

DEPARTMENT

25

20
NO.OF SUBJECTS

15

HYPER THYROIDISM
10 HYPOTHYROIDISM

0
<10 20-Oct 20-30 30-40 40-50 50-60 60-70 70-80 >80
AGE (yrs)

Table 3.7 GENERAL GENDER DISTRIBUTION IN HYPO AND HYPERTHYROIDISM IN

MEDICINE DEPARTMENT

DISEASES MALE FEMALE NO.OF SUBJECTS

HYPOTHYROIDISM 30 74 104
HYPERTHYROIDISM 6 12 18

Figure 3.7 GENERAL GENDER DISTRIBUTION IN HYPO AND HYPERTHYROIDISM IN

MEDICINE DEPARTMENT
 80

70

60

50
NO.OF SUBJECTS

40
MALE
30 FEMALE

20

10

0
HYPOTHYROIDISM HYPERTHYROIDISM
DISEASES

Table 3.8 AGE DISTRIBUTION OF SEIZURE IN HYPO AND HYPERTHYROIDISM IN

MEDICINE DEPARTMENT

AGE (yrs) HYPERTHYROIDISM HYPOTHYROIDISM

(N=4) (N=22)
<10 0 1
10-20 0 2
20-30 0 2
30-40 2 2
40-50 1 3
50-60 0 1
60-70 0 9
70-80 1 2
 >80 0 0

Figure 3.8 AGE DISTRIBUTION OF SEIZURE IN HYPO AND HYPERTHYROIDISM IN

MEDICINE DEPARTMENT

10
9
8
7
NO. OF SUBJECTS

6
5
4 HYPERTHYROIDISM (N=4)
HYPOTHYROIDISM (N=22)
3
2
1
0
<10 20- 20-30 30-40 40-50 50-60 60-70 70-80 >80
Oct
AGE (yrs)

Table 3.9 GENDER DISTRIBUTION OF SEIZURE IN HYPO AND HYPERTHYROIDISM

HYPOTHYROIDISM HYPERTHYROIDISM
(N=22) (N=4)
MALE 11 1
FEMALE 11 3

Figure 3.9 GENDER DISTRIBUTION OF SEIZURE IN HYPO AND HYPERTHYROIDISM

 12

10

8
NO. OF SUBJECTS

6
HYPOTHYROIDISM (N=22)
HYPERTHYROIDISM (N=4)
4

0
MALE FEMALE
GENDER

Table 3.10 DURATION OF HYPO AND HYPERTHYROIDISM TO DEVELOP SEIZURE

DURATION (yrs) HYPERTHYROIDISM HYPOTHYROIDISM

<5 1 2
5-10 0 3
10-15 2 13
15-20 1 3
>20 0 1
Figure 3.10 DURATION OF HYPO AND HYPERTHYROIDISM TO DEVELOP SEIZURE

14

12

10
NO. OF SUBJECTS

6 HYPERTHYROIDISM
HYPOTHYROIDISM
4

0
<5 10-May 15-Oct 15-20 >20
DURATION (yrs)

Table 3.11 PRESCRIPTION PATTERN OF AEDs

DRUGS PERCENTAGE % (N=26)

POLYTHERAPY 19.2
MONOTHERAPY 80.7
Figure 3.11 PRESCRIPTION PATTERN OF AEDs

90

80

70

60
NO. OF SUBJECTS

50

40

30

20

10

0
POLYTHERAPY MONOTHERAPY
TREATMENT

Table 3.12 COMMONLY USED AEDs

DRUGS PERCENTAGE %(N=26)

CLOBAZAM 11.5
LEVITRIACETAM 34.6
PHENYTOIN 50
LAMOTRIGEN 3.8
LORAZEPAM 11.5
Figure 3.12

60

50

40
NO. OF SUBJECTS

30

20

10

0
CLOBAZAM LEVITRIACETAM PHENYTOIN LAMOTRIGEN LORAZEPAM
DRUGS

Table 3.13 AEDs USED IN HYPOTHYROIDISM

DRUGS PERCENTAGE % (N=22)

LORAZEPAM +MIDAZOLAM + 4.5
CLOBAZAM
LEVITRIACETAM + PHENYTOIN 9.0
LORAZEPAM + PHENYTOIN 9.0
LEVITRIACETAM 22
PHENYTOIN 31.8
CLOBAZAM 4.5
 LAMOTRIGEN 4.5

Figure 3.13 AEDs USED IN HYPOTHYROIDISM

35

30

25
NO.OF SUBJECTS

20

15

10

0 LORAZEPAM LEVITRIACETAM + LORAZEPAM + LEVITRIACETAM PHENYTOIN CLOBAZAM LAMOTRIGEN

+MIDAZOLAM + PHENYTOIN PHENYTOIN
CLOBAZAM

DRUGS

Table 3.14 AEDs USED IN HYPERTHYROIDISM

DRUGS PERCENTAGE % (N=4)

PHENYTOIN 50
CLOBAZAM 50

Figure 3.14 AEDs USED IN HYPERTHYROIDISM

 60

50

40
NO. OF SUBJECTS

30

20

10

0
PHENYTOIN CLOBAZAM
DRUGS

Table 3.15 RELATIONSHIP BETWEEN OCCURRENCE OF SEIZURE IN HYPO AND

HYPERTHYROIDISM

DISEASE NO.OF SUBJECTS NO.OF SUBJECTS ODD RATIO

WITH SEIZURE
HYPOTHYROIDISM 104 22 1.65
HYPER 18 4 1.63
THYROIDISM
TABLE 3.1: DISTRIBUTION OF DISEASE IN PSYCHIATRY DEPARTMENT

DISEASE NO. OF SUBJECTS

BPAD 74
SLEEP DISORDER 65
ANXIETY 14
OTHERS 163
TOTAL 316

FIGURE 3.1: DISTRIBUTION OF DISEASE IN PSYCHIATRY DEPARTMENT

TABLE 3.2: GENERAL AGE WISE DISTRIBUTION IN PSYCHIATRY DEPARTMENT

AGE NO. OF SUBJECTS (N= 316)

<10 0
10 – 20 23
20 – 30 33
30 – 40 67
40 - 50 79
50 - 60 88
60 – 70 12
70 – 80 8
>80 6
TOTAL 316

FIGURE 3.2: GENERAL AGE WISE DISTRIBUTION IN PSYCHIATRY

DEPARTMENT
TABLE 3.3: GENDER DISTRIBUTION IN PSYCHIATRY DEPARTMENT

GENDER NO. OF SUBJECTS (N=316)

MALE 157
FEMALE 159
TOTAL 316

FIGURE 3.3: GENDER DISTRIBUTION IN PSYCHIATRY DEPARTMENT

TABLE 3.4: PREVALENCE OF SEIZURE IN PSYCHIATRY DEPARTMENT

PARAMETER NO. OF SUBJECTS
SAMPLE SIZE 316
PREVALENCE OF SEIZURE 24

FIGURE 3.4: PREVALENCE OF SEIZURE IN PSYCHIATRY DEPARTMENT

TABLE 3.5: AGE DISTRIBUTION OF SEIZURE IN PSYCHIATRY
DEPARTMENT

AGE (YEARS) BPAD SLEEP DISORDER ANXIETY

<10 0 0 0
10 – 20 0 0 0
20 – 30 1 0 0
30 – 40 4 2 0
40 – 50 5 3 3
50 – 60 3 0 1
60 – 70 1 0 0
70 – 80 0 0 0
>80 0 0 0

FIGURE 3.5: AGE DISTRIBUTION OF SEIZURE IN PSYCHIATRY

DEPARTMENT
TABLE 3.6: GENDER DISTRIBUTION OF SEIZURE SUBJECTS IN
PSYCHIATRY DEPARTMENT

GENDER NO. OF SUBJECTS

MALE 10
FEMALE 14
TOTAL 24

FIGURE 3.6: GENDER DISTRIBUTION OF SEIZURE SUBJECTS IN

PSYCHIATRY DEPARTMENT
TABLE 3.7: PREVALENCE OF SEIZURE FOR EACH DISEASE IN PSYCHIATRY
DEPARTMENT

DISEASE NO. OF NO. OF PREVALENCE (%)

SUBJECTS SUBJECTS WITH
(N=316) SEIZURE (N=24)
BPAD 74 14 18. 81
SLEEP DISORDER 65 5 7. 69
ANXIETY 14 4 28. 57

FIGURE 3.8: PREVALENCE OF SEIZURE FOR EACH DISEASE IN

PSYCHIATRY DEPARTMENT
TABLE 3.9: PREVALENCE OF SEIZURE IN ALL PSYCHATRIC DISEASES

DISEASE PREVALENCE OF SEIZURE (%)

BPAD 4. 43
SLEEP DISORDER 1. 58
ANXIETY 1. 26
WITHOUT SEIZURE 92. 73

FIGURE 3.9: PREVALENCE OF SEIZURE IN ALL PSYCHATRIC DISEASES

TABLE 3.10: DISTRIBUTION OF SEIZURE IN PSYCHIATRY DEPARTMENT

DISEASE WITH SEIZURE (N=99) PERCENTAGE (%)

BPAD 14. 14
SLEEP DISORDER 5. 05
ANXIETY 4. 04

FIGURE 3.10: DISTRIBUTION OF SEIZURE IN PSYCHIATRY DEPARTMENT

TABLE 3.11: STATISTICAL ANALYSIS

DISEASE NO. OF NO. OF ODD RATIO

SUBJECTS SUBJECTS WITH
(N=316) SEIZURE (N=24)
BPAD 74 14 1.36
SLEEP DISORDER 65 5 0.44
ANXIETY 14 4 2. 32
OTHER DISEASE 163 0 0

TABLE 3.12: AED PRESCRIBING PATTERN IN PSYCHIATRY DEPARTMENT

DRUGS NO. OF PATIENTS PERCENTAGE (%)

VALPROIC ACID 7 33. 33
CLOBAZAM 5 20
LEVETIRACETAM 4 13. 3
PHENYTOIN 2 6. 6
CARBAMAZAPINE 6 26. 66
FIGURE 3.12: AED PRESCRIBING PATTERN IN PSYCHIATRY DEPARTMENT
Discussio
 DISCUSSION
The study was conducted in 3 departments including Neurology, Medicine, and Psychiatry
department . A total of 655 cases were collected during this time period. Table1.1shows the
general categorization of patents details collected, from neurology department 217 cases
collected and from medicine and psychiatry department 122 and 316 cases collected
respectively. Table1.2 and figure 1.2 shows general age distribution. The common age was found
to be 40 – 50 years. Table 1.3 and figure 1.3 shows general gender distribution and most of them
are females.

NEUROLOGY DEPARTMENT

The study was carried out of at neurology department of Karuna Medical College Hospital over a
period of six months. Table1 and graph 1 shows the details of the patient were admitted in the
neurology department during the entire period, a total of 217 patients were included the study in
this, 199 were admitted with CVA, 9 with head ache, 5 with head injury and 4 with meningitis.

Table 2 and graph 2 shows the age distribution of the patients. Highest number of patient was
admitted in the age group of 50-60 (n=36), followed by 40-50 (n=33) and 1 patients were
admitted at the age group of <10. 20 patients were admitted in the category of >80

Table 3 and graph 3 shows the gender distribution of the patients. Total 217 patients were
included of these, 55.29% (n=120) were male and 44.70% (n=97) were female.

Table 4 and graph 4 shows the prevalence of seizure in all cases of Neurology was 22.58% that
is 49 out of all 217 neurologic patients had seizure during the study. Which means about 18% of
all neurological cases had seizure during the study

Table 5 and graph 5 shows the prevalence of seizure in different neurological case. Seizure
attack occurs more in the patient having the CVA ie about 36 out of 199 cases and the prevalence
was found to be 18.09%.In our study all the meningitis patient having the seizure attack. In case
of head ache 6 out of 9 patient having the seizure attack and the prevalence is 66.66%

Table 6 and graph 6 shows the age distribution of seizure in neurology department, most no. of
seizure distribution was found to be in the age group of 70-80 (n=11), and followed by in the age
group of 40-50 (n=10),the least no. of cases was found to be in the age group of 20-30 and less
the 10 (n=1)

Table 7 and graph 7 indicate the gender wise distribution of seizure in neurology department,
about 39 male patient having the seizure (80%) and10 female patients having the episodes of
seizure as the complication of neurological disease

Table 8 and graph 8shows the distribution of seizure in various case of neurological department,
about 36 patients having the seizure as a complication of CVA (73.46%) then the occurance of
seizure was found in 5 patient out of 49 patients (10.20%), 3 patients out of 49 patients of head
injury (6.122%) and in case of meningitis 4 patient out of 49 patient (8.163%) having the
prevalence of seizure

Table 9 and graph 9 prevalence of early and late post stroke seizure, the occurrence of late post
stroke seizure was found to be (68.5%) and the occurrence of early seizure was found to be only
31.5%

Table 10 figure 10 shows AED prescribing pattern in neurology department, the most commonly
prescribed drug was found to be Levetriacetam and Phenytoin 38.8% each, the followed by
Sodium Valproic acid of 16.6% and the least prescribed drug was Clobazam, 5.5%

Table 11 and graph 11 shows the distribution of mono-therapy and poly–therapy in neurology
department, most common prescribing pattern is mono-therapy 80%(n=39) and the mono-
therapy is about 20% only (n=10)

Table 12 and graph 12 shows the distribution of drugs in poly-therapy, phenytoin +

Levetriacetam, Phenytoin + Valproic acid and Valproic acid + Clobazam (n=2) and combination
such as theLorazepam+ Valproic acid, Levetriacetam+ Valproic acid, Levetriacetam + Diazepam
and Phenytoin + Phenobarbitone (n=1) is prescribed least.

Table 13 shows the statistical analysis of different Neurological disease, in case of CVA 36 out
of 199 patients had seizure with odd ratio 1.696 were as in Head ache about 6 out of 9 patient
had seizure with odd ratio 0.4031, 3 out of 5 Head injury patient also had seizure with odd ratio
of 2.3191 and 4 out of 4 meningitis patient had seizure with odd ratio 2.29.There is positive
relationship between CVA, Head injury, Meningitis and seizure by showing an odd ratio more
than one (1.696, 2.3191, and 2.29 respectively). But Head ache is not prove to have a positive
relationship with occurrence of seizure because the odd ratio was less than one (0.4031).

MEDICINE DEPARTMENT

The study was carried out at Karuna Medical College Hospital, chittur over a period of six
months from November 2015 to April 2016. During the period a total of 122 patients were
included , of these 29.5%(n=36)were male and70.5% (n=86)were female. Table 3.1, figure 3.1

The patients were categorized according to their age group. Maximum number of patients with
thyroid abnormalities were in age group of 50-60 i.e. 21.3% (n=26), followed by40-50 19.6%
(n=24) age group and 1.6% (n=2) were more than 80 years age group. Table 3.2, figure 3.2

During the study period , 85.2 %(n=104) cases were hypothyroidism and 14.7%(n=18) were
hyperthyroidism. Table 3.3, figure 3.3

The study revealed the prevalence of seizure among 104 hypothyroidism cases was 21.15%%
(n=22 ) and from 18 hyperthyroidism cases 22.22% (n=4). Table 3.4, 3.5; figure 3.4,3.5

General age distribution in hypothyroidism was maximum with 50-60yrs 21.15 %(n=22) and
hyperthyroidism was 40-50 , 27%(n=5)table 3.6, figure 3.6

General gender distribution in hypothyroidism were 28.8%(n=30) male and 71.11% (n=74) were
female and also 33.33%(n=6) were male and 66.6%(n=12) were female in hyperthyroidism table
3.7, figure 3.7

Age distribution of seizure in hypothyroidism was with maximum age group of 60-70 ie.,14.9%
(n=9), followed by 40-50 ie., 13.6%(n=3). The maximum age distribution of seizure in
hyperthyroidism was 30-40, 50%(n=2), followed by 40-50, 25%(n=1). Table 3.8, figure 3.8

The gender distribution of seizure in hypothyroidism from the total of 22 patients, 50%(n=11)
were male and 50%(n=11) were female. And from hyperthyroidism, among 4 patients, 25%(n=1)
were male and 75%(n=3) were female. Table 3.9, figure 3.9
The duration of hypothyroidism to develop seizure was found to be 10-15 years 59.0%(n=13) of
maximum and the minimum of less than 5years 9.09% (n=2). Table 3.10, figure 3.10

The duration of hyperthyroidism to develop seizure was found to be 10-15 years 50%(n=2) and
with minimum of less than 5 years 25% (n=1). Table 3.10, figure 3.10

For the purpose of analysing the prescription pattern of AED agents in the treatment of seizure,
the pharmacologically categorized into mono therapy and poly therapy. The present study
revealed that the majority of the patients under went monotherapy with ie., 80.7% (n=21)
followed by poly therapy 19.2% (n=5). Table 3.11, figure 3.11

During the entire study period, the usage of various AEDs among the patients showed that
most of the patients under went phenytoin which was accounted by 50% (n=13) cases followed
by levitriacetam with 34.6%(n=9). Table 3.12, figure 3.12

AEDs used in hypothyroidism was phenytoin 31% (n=11) and followed by levitriacetam 22%
(n=5)table 3.13, figure 3.13

AEDs used in hyperthyroidism was phenytoin 50%(n=2) and clobazam 50%(n=2). Table 3.14,
figure 3.14

The relationship between occurrence of seizure in hypothyroidism in terms of odd ratio was
1.65. and in hyperthyroidism was 1.63. table 3.15

PSYCHIATRY DEPARTMENT

The study was carried out of at psychiatry department of karuna medical college hospital over a
period of six months. Table1 and graph 1 shows the details of the patient were admitted in the
psychiatry department During the entire period, a total of 316 patients were included the study
in this 316, 74 were admitted with BPAD, 65 with sleep disorder 14 with anxiety and 163 with
other psychiatric illness.

Table 2 and graph 2 shows the age distribution of the patients. Highest number of patient was
admitted in the age group of 50- 60 (n=88), followed by 40-50 (n=79) and no patients were
admitted at the age group of <10. 6 patients were admitted in the category of >80
Table 3 and graph 3 shows the gender distribution of the patients. Total 316 patients were
included of these, 50% (n=157) were male and 50% (n=159) were female. Approximately same
number of female and male subjects was included in the study.

Table 4 and graph 4 shows the prevalence of seizure in all cases of psychiatry was 18% that is 24
out of all 316 psychiatric patients had seizure during the study. Which means about 18% of all
psychiatric cases had seizure during the study

Table 5 and graph 5 shows the age distribution of the patient who had seizure during the study in
psychiatry department. The age group 40-50 shows the highest number of seizure in BPAD
(n=5), sleep disorder (n=3), and anxiety (n=3).no patient in age group greater than 70 years had
seizure. Age group 30-40 have also increased number of seizure cases, that is BPAD (n=4) and
sleep disorder (n=2).

Table 6 and graph 6 shows the gender distribution of patients in psychiatry department seizure.
The seizure attack was more for female 58% (n=14) than in male 42% (n=10). We observed the
same result in the previous study done by Lesser RP in Psychogenic seizures published in
Neurology 1996.

Table 7 and graph 7 indicate the prevalence of seizure in the disease in the psychiatry
department. 14 out of 74 patients who admitted with BPAD had seizure. That is 18.8% of all
BPAD patient had seizure as its complication. In case of sleep disorder 5 out of 65 patients had
seizure that is 7.69% sleep disorder patients also had seizure during this period. In case of
anxiety14 patients were admitted in that 4 patient had seizure, that is about 28.57% patients had
seizure. So the chance of occurring seizure in psychiatry department is with anxiety patients.

Table 8 and graph 8 shows the prevalence of seizure in whole cases collected in the psychiatry
department. 4.43% of the all patients admitted in psychiatry department had seizure due to
BPAD. And in case of sleep disorder about 1.58% patients had seizure and in case of anxiety
about 1.26% patient had seizure.

Table 9 and graph 9 shows the distribution of seizure in the psychiatry department. In the total of
24 seizure cases in the department 14.14% was due to BPAD disease (n=14). And 5.05% was
due to sleep disorder (n=5). In case of anxiety about 4.04% of total seizure in the psychiatry
department is due to anxiety.

Table 10 shows the odds ratio analysis. In case of BPAD 14 out of 74 patients had seizure with
odd ratio 1.36 were as in sleep disorder about 5 out of 65 patient had seizure with odd ratio 0.44
and 4 out of 14 anxiety patient also had seizure with odd ratio of 2.32. From the analysis
psychiatric disease also associated with occurrence of seizure. There is positive relationship
between BPAD and Anxiety and seizure by showing an odd ratio more than one (1.36 and 2.32
respectively). But sleep disorder is not prove to have a positive relationship with occurrence of
seizure because the odd ratio was less than one (0.44)
 Table 11 and graph 11 shows the prescribing patter of anti epileptic drug in psychiatry
department. The common drug used were Valproic acid (33.33%).followed by carbamazepine
(26.66). the least used drug was phenytoin (6.6%)

Table 5.1 and figure 5.1 shows departmental wise prevalence of seizure. in 217 neurological
cases, prevalence of seizure is 49, in 122 thyroid cases 26 having prevalence of seizure and 316
psychiatry cases, the prevalence of seizure is 24.
Summary
Conclusion
 NEUROLOGY DEPARTMENT

 From the study we concluded that neurological disease also associated with occurrence
of seizure.

 There is a significant relationship between CVA, Head injury, Meningitis and seizure by
showing an odd ratio more than one (1.696, 2.3191, and 2.29 respectively).

 Head ache is not prove to have a significant relationship with occurrence of seizure
because the odd ratio was less than one (0.4031)

MEDICINE DEPARTMENT

 From the study we concluded that thyroid abnormalities also associated with occurrence
of seizure.

 There is significant relationship between hyperthyroidism and seizure by showing an odd

ratio more than one (1.63).

 Hypothyroidism also have a significant relationship with occurrence of seizure because

the odd ratio was more than one (1.65)

PSYCHIATRY DEPARTMENT

 From the analysis psychiatric disease also associated with occurrence of seizure.

 There is significant relationship between BPAD and Anxiety and seizure by showing an
odd ratio more than one (1.36 and 2.32 respectively).

 sleep disorder is not prove to have a significant relationship with occurrence of seizure
because the odd ratio was less than one (0.44)
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Annexure
Proforma
 DATA ENTRY FORM
DEPT.OF PHARMACY PRACTICE
GRACE COLLEGE OF PHARMACY, PALAKKAD,KERALA
TOPIC: PREVALENCE OF SEIZURE AND PRESCRIBING PATTERN OF
AED IN PATIENTS WITH NEURO-PSYCHATRIC AND THYROID
ABNORMALITIES

SL No……..

PATIENT NAME

DATE OF ADMISSION / /

DATE OF DISCHARGE / /

I.P NUMBER

AGE

SEX

WIEGHT

WARD

SPECIALITY

PAST MEDICAL HISTORY:

PAST MEDICATION HISTORY:

ALLERGIES:

REASON FOR ADMISSION:

LABORATORY INVESTIGATIONS:
DIAGNOSIS:

DRUGS PRESCRIBED

BRAND GENERIC STRENGTH FREQUENCY DURATION

NAME NAME OF THERAPY

MISCELLAENEUS INFORMATIONS
Completion
Letter
Publication