




































Sikdar et al.                                                 Advances in Epilepsy Research: From Mechanisms to Therapeutics 

Vol 2 | Issue 4 | Oct – Dec 2023                                                                          Indian J Pharm Drug Studies | 148  

Review Article 

Epilepsy Unveiled: Advances in Understanding, Diagnosis, and 

Management 

Shrijita Sikdar1, Udita Dutta2 , Ayan Ghosh3, Suparna Mondal4, Krisnendu Das5 

From, 1PG Student, S.N Pradhan Centre for Neuroscience, Ballygunge Science College, Calcutta University, Kolkata, 2UG 

Student, Eminent College of Pharmaceutical Technology, Moshpukur, Barbaria, Paschim Khilkapur, Barasat, Jagannathpur, 
3UG Student, Department of Pharmacy, Gupta College of Technological Sciences, Asansol, 4Nursing Tutor and Coordinator, 

Department of Nursing, M.R Institute of Nursing, Bira, 5Assistant Professor, School of Pharmaceutical Sciences, The Neotia 

University, Diamond Harbour, West Bengal, India 

ABSTRACT 

In addition to the numerous stress that characterize individuals today's fast-paced lives, the majority of people on the planet 

encounter various neurological problems. Epilepsy, one of the most common neurological disorders of the brain, affects over 

50 million people worldwide. 90% of whom are from developing nations. Genetic factors, brain infections, strokes, tumors, 

and high body temperatures are all contributors to epilepsy. Along with the social stigma that brings discrimination against 

patients and even their families in the community, it also, creates a significant financial burden on the healthcare systems of 

different countries. People with epilepsy frequently experience extreme mental suffering, behavioral problems, and little to no 

social engagement. Numerous seizure types exist, as are numerous mechanisms by which the brain can trigger seizures. 

Neuronal hyperexcitability and neural circuit hypersynchrony are the two fundamental features of seizure genesis. Numerous 

mechanisms may disturb the equilibrium between excitation and inhibition, predisposing a specific or generalized region of the 

brain to hyperexcitability and hypersynchrony. The review will include the classification, background, epidemiology, etiology, 

pathophysiology, symptoms, diagnosis, and management of epilepsy. 

Key words:  Epilepsy, Seizure, Anti-epileptic Drug, Pathophysiology 

pilepsy is a widespread chronic neurological 

illness that affects up to 1% of the population, 

making it the second most prevalent serious 

neurologic disorder after stroke [1]. It affects around 50 

million individuals worldwide, with 90% of those affected 

living in underdeveloped nations [2]. Epilepsy is defined 

by recurrent unprovoked 3-5 seizures, with substantial 

changes in the biology and consequences of seizures 

between the immature and mature brain [3]. It refers to a 

variety of seizures that vary in severity, appearance, cause, 

effect, and management. Epilepsy frequently causes brief 

impairments in consciousness, putting people in danger 

and interfering with schooling and jobs.  

Access this article online 

Received – 30th Oct 2023 

Initial Review – 16th Nov 2023 

Accepted – 07th Dec 2023 
 

Quick Response Code 

It has no age, gender, geographical, social class, or 

racial boundaries. Epilepsy is more common in young 

children and those over the age of 65, but it can develop at 

any age [4]. Seizure onset can be focal, generalized, or 

unknown, and can be classified based on awareness or 

motor or nonmotor aspects. Active epilepsy is defined by 

regular treatment with antiepileptic medications or the 

most recent seizure occurring within the last 5 years [5]. A 

condition known as Status Epilepticus (SE) is a prolonged 

or repeated seizure that can lead to long-term 

consequences, including neuronal injury or death. A new 

diagnostic classification for SE has been proposed [6]. 

Sudden unexpected death in epilepsy (SUDEP) is defined 

as a sudden, unexpected, witnessed or unwitnessed death 

in epileptic patients, with or without seizure evidence, and 

excluding established SE.  

_______________________________________________ 

Correspondence to: Krishnenedu Das, 36A, Mahanirban 

Road, Kolkata-700029, West Bengal, India. Email: 

krishnendas96@gmail.com, Tel.: +91 9874377408 

E 

mailto:krishnendas96@gmail.com


Sikdar et al.                                                 Advances in Epilepsy Research: From Mechanisms to Therapeutics 

Vol 2 | Issue 4 | Oct – Dec 2023                                                                          Indian J Pharm Drug Studies | 149  

Seizures cause SUDEP, which may include seizure-

induced cardiorespiratory changes. The frequency of 

epilepsy is determined by its incidence, prevalence, and 

mortality, whereas the burden is determined by disability-

adjusted life-years (DALYs), years of life lost, and years 

of living with disability [7]. Conventional treatment 

generally consists of anticonvulsant drugs, however even 

with the finest current treatments; more than 30% of 

persons with epilepsy do not have seizure control [8]. 

Therapy is symptomatic because existing medications 

reduce seizures, but there is no effective preventive or 

cure. Medication adherence is a big issue due to the long-

term negative effects of many medicines [9]. 

History of Epilepsy: Epilepsy, originating from the Greek 

term "epilepsia," which means "to seize," has long been 

tied with religion and demon possession. Epilepsy was 

once thought to be a sacred sickness, with many believing 

that it affected those who were abducted by demons or that 

their visions were sent by the gods. Epilepsy was 

considered a demonic spirit attack in Hmong generations, 

although affected persons could become honored as 

shamans as a result of their explicit experiences [10].  

Epileptic people were scorned and even imprisoned in 

most societies. Jean-Martin Charcot noted that epileptic 

persons were mentally retarded and criminally insane in 

the Salpetriere, the birthplace of contemporary 

neuroscience. People in Tanzania believed epilepsy was 

caused by bad spirits, witchcraft, poisoning, or was 

communicable. Epilepsy was considered a god-given curse 

in Rome, known as Morbus comitialis [11]. Stigma 

continues to this day, but it is gradually decreasing in 

developed countries. Hippocrates predicted that it would 

not take much time to eradicate epilepsy as it is not divine. 

Epidemiology: Epilepsy is a common neurological illness, 

affecting an estimated 55 lakhs individuals in India, 20 

lakhs in the United States, and three lacks in the United 

Kingdom. In the United States, 120 persons out of every 

100,000 have a seizure each year, with a recurrence rate 

ranging from 23% to 80%. The annual age-adjusted 

incidence of epilepsy is 44 per 100,000 persons. Every 

year, around 125,000 new cases are diagnosed, with 30% 

of those diagnosed being under the age of 18. The elderly 

have a high prevalence of epilepsy, which is now 

acknowledged. At least 10% of patients in long-term care 

facilities are on at least six antiepileptic medications. The 

National Sentinel Audit of Epilepsy-Related fatalities 

highlights the problem, indicating that 1,000 people die in 

the UK each year as a result of epilepsy, with 42% of these 

fatalities being avoidable [12]. 

Causes of Epilepsy: Epilepsy is a disorder in which the 

cause or severity of seizures is not directly connected. 

Some cases are genetic, while others are the result of brain 

traumas, strokes, infections, high fever, or malignancies 

[13]. Many incidences of epilepsy in young children are 

caused by heredity, but it can affect people of any age. 

Specific precipitants or triggers, such as reading, flashing 

lights, mental stress, sleep deprivation, heat stress, alcohol, 

and febrile sickness, are required for reflex epilepsy 

disorders [14]. The impact of these precipitants varies 

depending on the epileptic syndrome. In epileptic women, 

the menstrual cycle can also alter seizure recurrence 

patterns. The most prevalent causes of epilepsy in infants 

and early infancy are hypoxic-ischemic encephalopathy, 

CNS infections, trauma, congenital CNS abnormalities, 

and metabolic problems. CNS infections and trauma can 

cause febrile seizures in late infancy and early childhood. 

Cerebrovascular disease is the most common cause of 

death in the elderly, followed by CNS malignancies, head 

trauma, and degenerative disorders such as dementia [15]. 

Pathophysiology of Epilepsy: Seizures are paroxysmal 

manifestations of the cerebral cortex caused by a transient 

imbalance in excitatory and inhibitory forces in the cortical 

neuron network. The seizure event is recognized in an 

unstable cell membrane or its surrounding cells, arising 

from either cortical or subcortical area's gray matter. A 

small number of neurons fire inappropriately at first, and 

normal membrane conductance and inhibitory synaptic 

current breakdown, as well as excess excitability, spread 

either locally to cause a focal seizure or more broadly to 

produce a generalized seizure. This onset spreads through 

physiologic pathways to include nearby and remote 

locations [16].  

A failure in potassium conductance, a defect in 

voltage-activated ion channels, or a shortage in membrane 

ATPases involved in ion transport can all lead to neuronal 

membrane instability and a seizure. Certain 

neurotransmitters, such as glutamate, aspartate, 

acetylcholine, norepinephrine, histamine, corticotropin-

releasing factor, purines, peptides, cytokines, and steroid 

hormones, increase neuronal excitability and propagation, 

whereas -amino butyric acid (GABA) and dopamine 

decrease neuronal excitability and propagation [18]. 

During a seizure, the demand for blood flow to the brain 

increases in order to remove CO and bring substrate for 

neuronal metabolic activity. Some types of epilepsy may 

be connected to mutations in many genes. 



Sikdar et al.                                                 Advances in Epilepsy Research: From Mechanisms to Therapeutics 

Vol 2 | Issue 4 | Oct – Dec 2023                                                                          Indian J Pharm Drug Studies | 150  

 
Figure 1: Pathophysiology of Epilepsy and Understanding Seizure Mechanisms [17] 

Diagnosis: A number of different tests have been 

developed to determine the epilepsy in an individual and 

its type. This may include a neurological exam that 

examines behavior, emotions, and mental function to 

diagnose and classify epilepsy. Blood tests look for 

evidence of infections, genetic disorders, or other seizure-

related illnesses. Genetic testing, which is commonly 

performed in children but can also benefit some adults 

with epilepsy, can provide more information about the 

condition and therapy [19]. 

Some brain imaging tests and scans that detect changes 

are- 

Electroencephalogram (EEG) Monitoring:  Electron 

encephalograms are extremely helpful in the identification 

of many seizure disorders. Even if the EEG is normal in 

some people, they stillhave the clinical diagnosis of 

epilepsy. Many people who do not have epilepsy have 

atypical brain activity. Video monitoring is frequently used 

in conjunction with EEG to establish the type of seizures a 

person has [20]. 

High-density EEG:. In this test, electrodes are put closer 

together than in a traditional EEG. High-density EEG may 

aid in pinpointing which parts of the brain are affected by 

seizures [21]. 

Computerized tomography (CT) scan: CT scans use X-

rays to create cross-sectional images of the brain, which 

can help detect tumors, bleeding & cysts that cause 

epilepsy [22]. 

Magnetic resonance imaging (MRI): An MRI, like a CT 

scan, employs powerful magnets and radio waves to 

provide a precise image of the brain in order to detect 

future seizures, but it provides a more detailed view than a 

CT scan [23]. 

Functional MRI (FMRI): A functional MRI measures 

blood flow changes in brain parts, aiding in identifying 

critical functions like speech & movement before surgery, 

enabling surgeons to avoid these areas during the 

procedure [24]. 

Positron emission tomography (PET): PET scans use 

low-dose radioactive material injected into veins to 

visualize brain metabolic activity and detect changes, 

potentially identifying low metabolism areas as seizures 

[25]. 

Single-photon emission computerized tomography 

(SPECT): A SPECT test uses low-dose radioactive 

material to create a 3D map of blood flow during seizures, 

indicating seizure locations. SISCOM, or subtraction ictal 

SPECT connected to MRI, overlaps SPECT results with 

brain MRI results for more detailed results [26]. Other 

techniques, such as Statistical Parametric Mapping (SPM), 

Electrical Source Imaging (ESI), and Magneto 

encephalography (MEG), can be used to detect seizures. 

SPM contrasts locations with increased blood flow during 

seizures versus those without seizures. For a more 

thorough picture of seizures, ESI projects EEG data onto 

an MRI. MEG detects magnetic fields generated by brain 

activity, resulting in more accurate results due to reduced 



Sikdar et al.                                                 Advances in Epilepsy Research: From Mechanisms to Therapeutics 

Vol 2 | Issue 4 | Oct – Dec 2023                                                                          Indian J Pharm Drug Studies | 151  

interference from the skull and surrounding tissue. These 

approaches, when combined, provide images of areas 

impacted and not affected by seizures, allowing for a more 

complete knowledge of the brain's origins [27]. 

 
Figure 2: A) Types of Seizure B) Symptoms of Seizure [28]. 

Table 1: Classification of Drugs use in therapy of epilepsy [29] 

AED Class of 

Drug 

Mechanism of Action Uses Advantages Disadvantages 

Pregabalin Anticonv

ulsants 

inhibiting calcium influx 

and subsequent release 

of excitatory 

neurotransmitters. 

Treat epilepsy, 

anxiety and 

neuropathic 

pain. 

Add on efficacy: partial 

onset seizures, no drug 

interactions. 

No hypersensitivity skin 

reactions. 

Work also in neuropathic 

pain and generalized 

anxiety disorders. 

Weight gain. 

Increased side effect risk in patients 

with low glomerular filtration rate 

requires a lower dose. 

Seizure aggravation in idiopathic 

generalized epilepsy (absence or 

myoclonic seizures). 

Pheno-

barbital/ 

primidone 

Barbiturat

e 

Prolonged and frequency 

of GABA mediated 

chloride channel 

opening. 

Blockade of AMPA 

receptors. 

Anti-seizure, 

Anti-epileptic, 

treat insomnia, 

treat anxiety. 

Efficacy: partial-onset 

seizures and generalized 

myoclonic seizures. 

Rash is uncommon. 

Phenobarbital is widely 

available and 

inexpensive parenteral 

formulation. 

Drug interactions(may lower the 

efficacy of concomitant medications 

metabolized by the P450 hepatic 

enzyme system). 

Sedation, cognitive slowing, 

arthralgia 

Phenytoin Anticonv

ulsants 

Voltage gated sodium 

channel blocker, keep 

maintain the sodium 

channel’s inactive 

condition and extending 

the neuronal refractory 

period. 

Anti-epileptic. Efficacy: partial-onset 

seizures. 

Long accumulated 

experience. 

Can be loaded orally or 

intravenously 

(intravenous phenytoin 

or the prodrug 

fosphenytion). 

Drug interaction (through P450 

enzyme induction and extensive 

protein binding). 

Nonlinear pharmacokinetics (small 

changes in dose or bioavailability 

may produce large fluctuations in 

level). 

Ataxia, rash. 

Seizures aggravation in idiopathic 

generalized epilepsy (absence or 

myoclonic seizures). 



Sikdar et al.                                                 Advances in Epilepsy Research: From Mechanisms to Therapeutics 

Vol 2 | Issue 4 | Oct – Dec 2023                                                                          Indian J Pharm Drug Studies | 152  

Rufinamide Anticonv

ulsants 

It is a triazole derivative 

antiepileptic which 

prolong the inactive state 

of voltage gated sodium 

channel. 

Control 

Seizure. 

Efficacy: Lennox-

Gastaut syndrome. 

Drug interactions (clearance 

decreased by valproate and increased 

by enzyme inducers, may reduce 

efficacy of oral contraceptives). 

Tiagabine Anticonv

ulsants 

Inhibit the reuptake of 

GABA into presynaptic 

neurons and increase the 

amount of GABA to 

postsynaptic neurons. 

Treat partial 

seizure in 

epilepsy. 

Efficacy: partial-onset 

seizures. 

Does not affect other 

AEDs. 

Relatively favorable 

cognitive profile 

Only indicated as adjunctive therapy. 

Requires a show titration, given three 

or four times daily. 

Can cause nonconvulsive status 

epilepticus or encephalopathy that 

resembles nonconvulsive status 

epilepticus, even in the absence of 

prior epilepsy. 

Topiramate Second 

generatio

n 

antiepilep

tic drug. 

It blocks voltage gated 

sodium channels. 

Increasing GABA 

activity and inhibit 

glutamate activity. 

Inhibition of kinate-

evoked currents. 

Manage and 

treat epilepsy 

and migraine. 

Efficacy: partial-onset 

seizures and generalized 

seizures. 

Rash is uncommon. 

Efficacy against 

migraine. 

Weight loss. 

Weight loss: aphasia and cognitive 

impairement, nephrolithiasis, 

metabolic acidosis, hypohidrosis. 

Requires slow titration rate 

because of adverse cognitive 

effects 

Valproate Anticonv

ulsants 

Blocks voltage gated ion 

channel and increase the 

inhibitory 

neurotransmission. 

Treat epilepsy 

and bipolar 

disorder. 

Wide spectrum of 

efficacy against partial-

onset seizures and 

generalized seizures. 

No hypersensitivity skin 

reactions. 

Work for bipolar 

disorder and migraine. 

Intravenous preparation. 

Weight gain: encephalopathy, 

tremor, Parkinsonian syndrome. 

Teratogenicity and permanent 

adverse cognitive outcomes in 

fetus. 

Drug interaction (due to inhibition 

of P450 enzymes and extensive 

protein binding). 

Vigabatrin Anti-

epileptic/ 

Anticonv

ulsants 

Inhibit GABA degraded 

enzyme GABA-

Transaminase, increase 

GABA concentration in 

the brain 

Treat refractory 

complex partial 

seizure. 

Add-on efficacy for 

partial-onset seizures and 

West syndrome. 

No interactions. 

Concentric visual field defects, 

irreversible. 

Zonisamide Sulfonam

ide anti-

epileptic 

drug/ 

Anticonv

ulsants 

Block voltage sensitive 

Sodium channel and T-

type Calcium channel. 

Enhancement of 

GABAergic transmission 

and inhibition of 

glutamatergic transmiss. 

Treat partial 

onset seizure in 

the treatment of 

epilepsy. 

Efficacy: partial-onset 

seizures; generalized- 

onset seizures(evidence 

not rigorous). 

Long half-life (allows 

once daily dosing). 

Weight loss 

Weight loss, aphasia and cognitive 

impairement, nephrolithiasis, 

metabolic acidosis; anhidrosis in 

children (fever). 

 

Blood Biomarkers in Epilepsy: Biochemical marker 

advancements can identify brain pathology, increasing 

hope in epilepsy. Although connectivity/resting state 

imaging and gadgets such as smartwatches and 

implantable EEG can detect epilepsy, their cost and 

impracticality limit their usage in larger patient 

populations. Blood testing may be a more scalable method 

of diagnosing epilepsy and seizure burden. Pilot studies 

have shown feasibility, and trials with acute brain illnesses 

with a high risk of epileptogenesis could be used as well. 

Biomarkers of disease activity, such as NT-proBNP or 

HBA1c, may help in illness management and intervention [30]. 

Neuronal/brain biomarkers: Neuronal/brain biomarkers 

like S100B, NSE, GFAP, NfL, Tau, UCHL-1, and MMP-9 

are crucial for identifying epileptic pathophysiological 

changes. S100B, primarily expressed in astrocytes, is 

linked to poststroke epilepsy. GFAP, NSE, NfL, and 

UCHL-1 are linked to neurodegenerative illnesses. 

Elevated serum concentrations in epilepsy patients are 

detected in plasma. Further research is needed to 

determine their clinical use and role in epilepsy [31]. 

Neuroinflammatory biomarkers: Neuroinflammatory 

indicators, such as cytokines like IL-1, IL-2, and IL-4, are 

potential biomarkers for epilepsy. Elevated interleukins 

(IL) and plasma IL-6 levels are associated with long-term 

seizures. Individuals with epilepsy have higher levels of 

IFNs, TNFs, CCL17, and other neuroinflammatory 

mediators. These factors contribute to inflammation and 

seizure development [32]. 



Sikdar et al.                                                 Advances in Epilepsy Research: From Mechanisms to Therapeutics 

Vol 2 | Issue 4 | Oct – Dec 2023                                                                          Indian J Pharm Drug Studies | 153  

Epilepsy and Oral Contraceptives: Antiepileptic 

medications such as carbamazepine, phenytoin, 

barbiturates, topiramate, and Oxcarbazepine can result in 

hormonal contraception failure, requiring patients to use a 

higher estrogen-containing oral contraceptive (50 

mg/mg/day) [33]. 

Pregnancy and Epilepsy: Pregnancy epilepsy can lead to 

difficulties for both the mother and the fetus, increasing 

the chance of spontaneous abortion and stillbirth. To avoid 

anoxiosis and metabolic abnormalities, it is critical to 

manage the illness effectively and cure it before 

pregnancy. Minor seizures should not be eliminated, and 

patients should take folic acid and vitamin K supplements 

orally. Some antiepileptic medicines can interfere with 

folic acid metabolism, resulting in neural tube 

abnormalities. Hepatic enzyme-inducing medications can 

also cause postpartum bleeding by lowering the mother's 

vitamin K levels [34]. 

Breastfeeding: Antiepileptics are normally present in low 

amounts in breast milk, making breastfeeding safe when 

administered in standard doses. However, benzodiazepines 

and barbiturates, which are found in high concentrations in 

breast milk, might cause newborn drowsiness, posing a 

risk to breastfeeding [35]. 

Epilepsy in Children: Children with epilepsy who have 

fits are treated similarly to adults, but they may react 

differently and be unpleasant. If febrile convulsions occur, 

a significant epilepsy medicine may be administered 

consistently until the kid reaches the age of five. Because 

prolonged therapy may interfere with cognitive 

development, the medicine is discontinued [36]. 

Future Directions in Research and Treatment: Epilepsy 

research is evolving towards preventive and curative 

strategies, emphasizing a shift from symptom control. 

Recent breakthroughs involve identifying mutated genes in 

inherited epilepsy, characterizing brain networks at the 

molecular level, enhancing seizure origin imaging, and 

advancing quantitative EEG analysis for seizure 

prediction. Therapeutic advancements focus on new 

molecular targets, EEG-tailored drug delivery, gene/cell 

therapy, and innovative surgical/non-ablative approaches 

[37]. 

Integrated methods, like combining imaging with 

electrophysiology, play a central role in localizing epilepsy 

development and improving prediction and treatment. 

Speculative approaches explore preventing epileptogenesis 

through cellular phenotype modulation, investigating 

protective factors, and understanding the fate of 

endogenous neural stem cells in the mature CNS. Novel 

pharmacotherapies, biosensor-coupled delivery systems, 

gene/cell therapy, and progressive surgical methods 

represent emerging directions for epilepsy therapy. These 

advancements collectively contribute to a comprehensive 

understanding and treatment of epilepsy, providing a 

foundation for further research and breakthroughs [38]. 

Challenges in new drug development: Epilepsy research 

and treatment encounter multifaceted challenges, including 

the diverse origins of the condition, hindrances in 

identifying reliable biomarkers for early diagnosis, and the 

emergence of drug resistance in some patients. The 

complex interplay of epilepsy with comorbidities 

necessitates a holistic patient care approach, while the 

incomplete understanding of underlying mechanisms 

impedes the development of targeted therapies [39]. 

Societal stigma surrounding epilepsy and its impact on 

individuals' quality of life constitute significant hurdles. 

Furthermore, global discrepancies in accessibility to 

specialized epilepsy care underscore the need for more 

equitable healthcare distribution. Emerging research 

pointing to neuroinflammation and immune system 

involvement adds another layer of complexity, calling for 

further exploration and potential anti-inflammatory 

strategies [40]. 

Addressing these challenges requires collaborative 

efforts involving diverse stakeholders, an increase in 

funding to support comprehensive research endeavors, and 

a multidisciplinary approach to advance both the 

understanding and treatment of epilepsy. The integration 

of knowledge from various fields, coupled with innovative 

strategies, is pivotal for overcoming these challenges and 

improving outcomes for individuals affected by epilepsy. 

CONCLUSION 

Epilepsy is a complex condition that affects people of all 

ages, with a special preference for children and the elderly. 

Its causes range from monogenic to cortical acquired 

diseases and its severity varies from patient to patient. 

Despite different treatments, public health surveys reveal 

that many people have a low quality of life as a result of 

the impact of recurring seizures on everyday activities. 

Thus, the selection of an anticonvulsant medication is 

mostly based on its efficacy for specific types of seizures 

and epilepsy. Despite adequate seizure control, a 

considerable proportion of epilepsy patients have 

intractable or drug-resistant epilepsy, necessitating the 

development of novel medications with better side effects 

and tolerance profiles, even at the expense of efficacy, 

when compared to existing antiepileptic therapies. 



Sikdar et al.                                                 Advances in Epilepsy Research: From Mechanisms to Therapeutics 

Vol 2 | Issue 4 | Oct – Dec 2023                                                                          Indian J Pharm Drug Studies | 154  

REFERENCE  

1. Joshi R, Tripathi M, Gupta P, et al. Prescription pattern of 

antiepileptic drugs in a tertiary care center of India. Indian 

journal of pharmacology. 2020; 52(4): 283–289.  

2. Tchalla, AchilleEdem, et al. Newly diagnosed epileptic 

seizures: focus on an elderly population on the French island 

of Reunion in the Southern Indian Ocean. Epilepsia. 

2011;52(12):2203-2208. 

3. Heger, Katrine, et al. Changes in the use of antiseizure 

medications in children and adolescents in Norway, 2009–

2018. Epilepsy Res. 2022;181:106872. 

4. Bhui U, Sarkar S, Das J, et al. Unraveling the Enigma of 

Anti-Tubercular Drug-Induced Vitamin B6 Deficiency and 

its Role in Provoking Convulsive Seizures: A Revelatory 

Case Report. Indian J of Pharm Drug Studies. 2023;Jul 

1:125-7. 

5. Vitaliti, Giovanna, et al. Molecular mechanism involved in 

the pathogenesis of early-onset epileptic encephalopathy. 

Frontiers in Molecular Neuroscience. 2019;12:118. 

6. Hsieh Liang-Po, Chin-Yin Huang. Prevalence of treated 

epilepsy in western medicine among the adult population in 

Taiwan: a study conducted using antiepileptic drug 

prescription data. Epilepsy Res. 2008;80.2-3:114-118. 

7. Shanmugapriya S, et al. Drug prescription pattern of 

outpatients in a tertiary care teaching hospital in Tamil Nadu. 

Perspectives Clini Res. 2018;9(3):133. 

8. Patterson Victor. The development of a smartphone 

application to help manage epilepsy in resource-limited 

settings. Seizure. 2020;79:69-74. 

9. Liang Chun-Yu, et al. Prescription patterns and dosages of 

antiepileptic drugs in prevalent patients with epilepsy in 

Taiwan: A nationwide retrospective cross-sectional study. 

Epilepsy Behavior. 2022;126:108450. 

10. Religioni, Urszula, Teresa Pakulska. Rational drug use in 

hospital settings–areas that can be changed. J Med 

Economics. 2020;23(10):1205-1208. 

11. Angalakuditi, Mallik, NupurAngalakuditi. A comprehensive 

review of the literature on epilepsy in selected countries in 

emerging markets. Neuropsy. Dis and Treat. 2011;7:585. 

12. Carl E S. Epilepsy: A review of selected clinical syndromes 

and advances in basic science. J Cerebral Blood Flow 

Metabolism. 2006;26:983-04. 

13. Cruz ME, Schantz PM, Cruz I, et al. Epilepsy and 

neurocysticercosis in an Andean community. Inter J 

epidemiology. 1999;28(4):799-803. 

14. Blume W, Luders H, Mizrahi E, et al. Glossary of descriptive 

terminology for ictal semiology; report of the ILAE taskforce 

on classification and terminology. Epilepsia. 2001;42(9): 

1212-18. 

15. Gregory L H, Yehezkiel Ben-A. The Neurobiology and 

Consequences of Epilepsy in the Developing Brain. Ped Res. 

2001;49(3):320-25. 

16. Gidal BE, Garnett WR. Epilepsy. In: Dipiro J T, Talbert RL, 

Yee GC, et al. Pharmacotherapy: A pathophysiologic 

approach. USA: McGraw-Hill Companies Inc. 6th ed. 

2005:1023-46. 

17. Fisher RS, Van Emde B, Blume W et al. Epileptic seizures & 

epilepsy: definition proposed by the International League 

Against Epilepsy, and Inte Bureau Epilepsy. Epilepsia. 

2005;46(4):470-72 

18. Engel J. Jr. Surgery for seizures. New England J Med. 

1996;334(10):647-652. 

19. McNamara J O. Drugs effective in the therapy of the 

epilepsies. In : Hardman JG, Limbird LE, Goodman Gilman 

A, 10th ed. Goodman and Gilman's the pharmacological basis 

of therapeutics. New York: McGraw-Hill Companies Inc. 

2001:521-48. 

20. Jilek-Aall L. Morbus Sacer in Africa; some religious aspects 

of epilepsy in traditional cultures. Epilepsia. 1999;40(3):382-

86. 

21. Sterman MB, Egner T. Foundation and practice of 

neurofeedback for the treatment of epilepsy. Applied 

psychophysiology and biofeedback. 2006;31(3):21-35. 

22. Epilepsy A. Proposal for revised classification of epilepsies 

and epileptic syndromes. The treatment of epilepsy: 

Principles & Practice. 2006;354. 

23. Hirtz D, Thurman DJ, Gwinn-Hardy K, et al. How common 

are the 'Common' neurologic disorders? Neurology. 2007;68 

(5):326-37. 

24. Porter RJ, Meldrum BS. Antiseizure drugs. In: Katzung BG, 

ed. Basic Clini pharmacology. New York: Mc Graw-Hill 

Companies Inc. 10th edition. 2006:378. 

25. Rang HP, Dale MM, Ritter JM, et al. Pharmacology. New 

Delhi: Churchill Livingstone Reed Elsevier India (P) Ltd. 5th 

ed. 2006:550-60. 

26. Rüber T, David B, Elger CE. MRI in epilepsy: Clinical 

standard and evolution. Current Opinion in Neurology. 2018; 

31(2):223-31. 

27. Tripathi KD. Essential of medical pharmacology. New Delhi: 

Jaypee Brothers Medical publishers (P) Ltd. 5th ed. 

2003:369-80. 

28. Herzog AG, Harden CL, Liporace J, et al. Frequency of 

catamenial seizure exacerbation in women with localization-

related epilepsy. Annals Neurology. 2004;56(3):431-34. 

29. Bhui U, Mondal S, Sarkar S, et al. Trend Analysis of 

Antiepileptic Prescriptions In Tertiary Care Hospital of 

Asansol Sub-Division. Wjpmr. 2022;8(7):132-150 

30. Lowenstein DH. Seizures and epilepsy. In: Kasper DL, 

Braunwald E, Fauci AS, et al. 16th ed Vol 2. Harrison's 

Princi Internal Med. USA: McGraw-Hill Companies Inc. 

2005:2357-72. 

31. Meisler MH, Kearney JA. Sodium channel mutations in 

epilepsy and other neurological disorders. J of Clini Inves. 

2005;115(8):2010-17 

32. Angeles D K. Proposal for revised clinical and 

electroencephalographic classification of epileptic 

seizures. Epilepsia. 1981;22(4):489-501. 

33. Wolf P. Of cabbages and kings: Some considerations on 

classifications, diagnostic schemes, semiology, and 

concepts. Epilepsia. 2003:44(1), 1-3. 

34. Block JH, Beale JM. Wilson and Gisvold's text book of 

organic medicinal and pharmacyeutical chemistry. 11th ed. 

Lippincott Williams and Wilkins. 2010:503. 

35. Bennett PN, Brown MJ. Clinical pharmacology. New Delhi: 

Elsevier a division of Read Elsevier India (P) Ltd. 9th ed. 

2006:413-22. 

36. Temmerman W, Dhondt A, Vandewoude K. Acute isoniazid 

intoxication: seizures, acidosis and coma. Acta Clinica 

Belgica. 1999;54(4):211-6. 



Sikdar et al.                                                 Advances in Epilepsy Research: From Mechanisms to Therapeutics 

Vol 2 | Issue 4 | Oct – Dec 2023                                                                          Indian J Pharm Drug Studies | 155  

37. Jacobs MP, Fischbach GD, Davis MR, et al. Future directions 

for epilepsy research. Neurology. 2001;57(9):1536-42. 

38. Linehan C, Tellez-Zenteno JF, Burneo JG, et al. Future 

directions for epidemiology in epilepsy. Epilepsy & 

Behavior. 2011;22(1):112-7. 

39. Wahab A. Difficulties in treatment and management of 

epilepsy and challenges in new drug development. 

Pharmaceuticals. 2010;3(7):2090-110. 

40. Holmes GL, Noebels JL. The epilepsy spectrum: targeting 

future research challenges. Cold Spring Harbor perspectives 

in medicine. 2016;6(7).  

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

How to cite this article: Shrijita Sikdar, Udita Dutta, 

Ayan Ghosh, Suparna Mondal, Krisnendu Das. 

Epilepsy Unveiled: Advances in Understanding, 

Diagnosis, and Management. Indian J Pharm Drug 

Studies. 2023; 2(4):148-155. 

Funding: None             Conflict of Interest: None Stated 

 

 

 


