Introduction: The Antiepileptic medications are frequently categorized into divisions such as ‘first-generation’ (i.e., carbamazepine, phenobarbital, phenytoin, primidone, and valproate) and ‘second-generation’ (lamotrigine, levetiracetam, felbamate, gabapentin, topiramate, tiagabine, oxycarbazepine, zonisamide, and pregabalin). Chronic phenytoin ingestion leads to its impact in the cerebral cortex, resulting in atrophy of cerebellum, cause ataxia and nystagmus.

Objective: To recapitulate the International league against epilepsy classifications, first treatment for epilepsy based on their classifications, antiepileptic medications adverse drug reaction,

Methodology: The author used 74 distinctive published articles for the accomplishment of this review article. Google search engine was used for accessing published articles from databases like Google Scholar, Research Gate, PubMed, NCBI, NDSS, PMID, PMCID, Cochrane Database and CLINMED international library.

Findings: Tonic-clonic is characterized by stiffness for loss of consciousness occurred by tonic extension and rhythmic clonic contractions of all considerable muscle groups. Antiepileptic drugs are implicitly an effective treatment for patient with epilepsy. Carbamazepine cause serious and sometimes fatal dermatologic reactions, including toxic epidermal necrolysis and stevens-johnson syndrome, aplastic anemia and agranulocytosis, Suicidal Behavior and Ideation, Stevens johnson syndrome, cholestatic jaundice, ataxia, xerostomia, speech disturbances, feeling sleepy

Conclusion: Commonly happening side-effects of AEDs are memory troubles, exhaustion, tremors, gastrointestinal symptoms, osteoporosis, depression, drowsiness, dizziness, weight change, nausea. In generalized seizures, on the other hand, the seizure is generalized from the endeavor (i.e., primary generalized seizures), launching in both hemispheres of the brain contemporaneously.

Keywords: Antiepileptic Medications, Apothegmatic, Clinical Practice, ILAE Classifications, Seizures

Epilepsy is a chronic neurologic disorder characterized by repeated epileptic seizures attacks which result from paroxysmal uncontrolled discharges of neurons within the central nervous system. The definition of epilepsy requires the circumstance of slightlysingle epileptic seizure. Epilepsy is a chronic disorder of the brain and is unique of the most common severe  slightly single epileptic seizure. Epilepsy is a chronic disorderedness of the brain and is unique of the consummate ubiquitous solemn neurological abnormalities leading fifty million people existing in all parts of the world without limit to age, race, social class, nationality, or geographical location.¹ Anti-epileptic medications are implicitly an efficient management for patient with epilepsy. Treatment failure and poorcompliance are, nevertheless, extremely ordinary in patient expertise adverse drug reactions owing to anti-epileptic medications. Comparatively twenty five percent of the patients, anti-epileptic medications influence to management withdrawn and have anoutstanding, antipathetic impress on the marvelous of life.^2-5 The AEDs are frequently categorized into divisions’ such like ‘1^st-generation’ (i.e., carbamazepine, phenobarbital, phenytoin, primidone, and valproate) and ‘2^nd-generation’ (lamotrigine, levetiracetam, felbamate, gabapentin, topiramate, tiagabine, oxycarbazepine, zonisamide, and pregabalin)^6,7 of anti-epileptic medications. Commonly happening adverse drug reactions of anti-epileptic medications are mind troubles, exhaustion, shake, GI problems, bone break easily, state of feeling sad, sleepy, light-headed, weight change, vomiting.⁸ These perhaps necessitate medical management grading from a junior intermediating to intensely priceless specialist care and hospital admission. Besides to those healthcare charges, patient and parents charges (i.e. unconventional care) and charges in distinctive areas (example. unemployment) can be indispensable.^9-15 Categorization of epileptic seizures is depending on electroencephalogram results combining with the clinical results of the seizure concerns. The foremost division in this categorization is into partial seizures and generalized seizures. In the partial seizures the anomalous electrical discharges launch in a localized area of the brain. The clinical manifestations are based on which section of the brain is affected. Those discharges perhaps stay localized, or they perhaps disseminate to distinctive sections of the brain and then the seizures become generalized (2^ndry generalized seizures). In generalized seizures, in the other way, the seizure is generalized from the onset (i.e., 1^ry generalized seizures), launching in both hemispheres of the brain concurrently.¹⁶

Partial seizures

When the seizure commences in a localized area of the brain, it is delineated as partial.¹⁷

Simple

The long-suffering will have a perception or unrestrained muscle shifting of a part of their body without are vamp in consciousness. The class of perception or movement is depending on the emplacement of seizure in the brain.^18-20

Complex

Not with standing the seizure is localized in a particular area of the brain, like a simple partial seizure, this seizure cause a changing in the patient degree of consciousness. There is an aura, an extraordinary sensing in the stomach retrograde to the throat and head, or a perception of light, smell, sound or taste. There is a slow rehabilitation later a complex partial seizure, with a period of confused. Later the strike there is comprehensive unable to remember things of it.^21,22

Partial seizures secondarily generalized

Seizures that launch as a simple or complex partial seizure and disseminate to enclose the whole brain. Patient  perhaps chronicle a caution or aura, and those are frankly the resume of the seizure.^23,24

Primary Generalized Seizures

If the whole cerebral cortex is enclosed in the seizure from the onset of the seizure, the seizure is categorized as 1^ry generalized.^25,26

Tonic-clonic: Characterized by stiffness for loss of consciousness attended by tonic extension and rhythmic clonic contractions of all considerable muscle classes. The duration of the seizure is ordinarily one to three minutes. That seizure is frequently defined as “grand mal.^27,28

Absence: Stiffness and brief (i.e., many seconds) loss of consciousness without muscle movements. These seizures are frequently defined as daydreaming or blanking out episodes. A common term for these seizures is “petit mal.” It is unexpectedly over, and the children persists what he was doing prior to the seizure came. The children have not mind of these seizures. They should not be confused with brief complex partial seizures.^29,30

Myoclonic: Single and extremely all considerable muscle classes. Patients with these perhaps not lose consciousness, due to the seizure lasting <three to four seconds. They perhaps single jerks, or jerks repeated over extended periods or Patients perhaps define these seizures as shoulder shrugs or spinal chills.^31,32

Atonic: The patient losses loses consciousness and muscle tone. No muscle movements are commonly signified. They are thereupon also called “drop attacks”. There is loss of consciousness, stiffness for onset and no post-ictal phase. The patient stands up and persists what he was doing. It so appears that loss of tone solely influences a section of the body; particularly the head with a head drop or nod.^33-37

Tonic seizures: is stiffness for sustained muscle contractions, fixing the limbs in certain strained location. There is instantaneous loss of consciousness. Frequently there is a divergence of the eyes and head towards one side, occasionally rotation of the whole body. Tonic seizures are a recognized sign/symptoms of frontal lobe epilepsy particularly commenced in the auxiliary motor cortex.^38-40

Clonic seizures: These seizures are generalized seizures, where the tonic component is not available, only repetitive clonic jerks (clonic jerks are repetitive rhythmic flexing and stretching of limbs). When the prevalence expresses the amplitude of the jerks do not.^41,42

Generalized tonic-clonic seizures (GTCS): The patient loses consciousness, falls down, occasionally with a scream, and advances a generalized stiffness (the tonic phase). Breathing ceases, as all the muscles of the trunk are in spasm, and the patient becomes cyanotic, the head is taken back, the arms flexed and the legs extended. Beyond the muscle stiffening and jerks is loss of consciousness, sphincter control and post ictal confusion.^43-45

Infantile spasms: These are characterized by stiffness for flexion of limb and truncal muscles and ordinarily appear in series or they are flexor spasms of the head, bending of the knees and flexion with abduction of the arms. They appear in the 1^st year of life, and are sophisticated to manage. They are a fingerprint presentation of the west syndrome which presents in infancy unceasing to early childhood.^46-48

Note: Adrenocorticotropic hormone or prednisolone is the drug of choice for infantile spasms.

Therapeutic intention in epilepsy treatment is complete seizure control without excessive side effects. AEDs are chemically and pharmacologically distinctive, having in common only their capability to inhibit seizure activity without impairing consciousness.^49,50

All anticonvulsant medications are associated with adverse effects which perhaps importantly jounce on fantabulous of life, kick in to non-compliance and in rare circumstances be implicitly life-threatening.^51-54

Common side effects of some anti-epileptics medications

Diazepam: Cause respiratory depression, hypotension, drowsiness, dizziness, muscle weakness, headache, dry mouth, constipation, ataxia (loss of control of body movement), somnolence, confusion.^55-57

Phenobarbital: Cause behavioral problems, hyperactivity, sedation is major side effect, dementia, loss of appetite, tiredness, dizziness, drowsiness.^58,59

Phenytoin: Cause sedation, psychosis, hyperkinesias, megaloblastic anemia, decreased serum folate degree, gingival hyperplasia (overgrowth of the gums), IGA deficiency, lowered bone mineral composition, liver disease, acne, hirsutism (excessive hair on the face/body/overgrowth of hair ), coarseness of facial features, unsteady or shaky, atrophy of cerebellum, cause ataxia and nystagmus, gingival hypertrophy perhapscharacterized to changed collagen metabolism. Changed metabolism of sex steroid hormones by phenytoin can initiatehyperandrogenic symptoms like hirsutism and nodular skin lesions, diplopia (cerebrovascular dysfunction), exfoliative dermatitis and toxic epidermal necrosis, lupus-like syndrome.^60,61

Valproic acid: Cause severe weight gain, tremors in a part of your body or unusual eye movements, stomach pain, dry or sore mouth, sluggishness, yellowish eyes or skin, low platelet count (clotting abnormalities), hair loss, fatal hepatotoxicity (children under 2years), incidence of neural tube defects in fetus, liver impairment.⁶²

Carbamazepine: Cause severe solemn and occasionally fatal dermatologic reactions, involving toxic epidermal necrolysis and stevens-johnson syndrome, aplastic anemia and agranulocytosis, Suicidal Behavior and Ideation, Stevens johnson syndrome, cholestatic jaundice, ataxia, xerostomia, speech disturbances, feeling sleepy, weight gain, drowsiness is the most common side effect, diplopia, vertigo, hyponatremia.^63,64

Ethosuximide: Cause weight loss, stomach upset, dizziness, drowsiness, loss of coordination, blurred vision.^65-67

Lamotrigine: Cause  double vision, blurred vision, loss of balance or coordination, uncontrollable movements of the eyes, difficulty thinking or concentrating, difficulty speaking, drowsiness, skin rashes and headaches are the most common side effects, dark urine, stomach pain, throat irritation, dry mouth, insomnia, multiorgan failure, hepatic failure.⁶⁸ 

Levetiracetam: Cause feeling sleepy, blocked nose/itchy throat, headache are the most common side effects, drowsiness, dizziness, low energy, decreased appetite, generalized weakness, psychosis, feeling aggressive, infection.^69,70

Topiramate: Cause feeling sleepy, dizziness, diarrhea, feeling are the most common side effects, acute close angle glaucoma, heat stroke, weight loss, coordination problems, numbness/tingly in the hands or feet, drowsiness, tiredness, kidney stones.⁷¹

Oxycarbazepine: Cause  symptomatic hyponatremia, dizziness, drowsiness, abdominal pain, trouble sleeping, headaches, constipation, double vision (Table 1 - 4).^72-74

Epilepsy is a chronic disorder of the brain and is unique of the most common severe neurological abnormalities leading fifty million people existing in all parts of the world without limit to age, race, social class, nationality, or geographical location.Categorization of epileptic seizures is depending on electroencephalogramresults combining with the clinical results of the seizure affairs. The foremost division in this categorization is into partial seizures and generalized seizures.Absence means stiffness and brief (i.e., many seconds) lossof consciousness without muscle movements.Adrenocorticotropic hormone or prednisolone is the drug of choice for infantile spasms. Phenobarbital causesbehavioral problems, hyperactivity; sedation is major side effect, dementia, loss of appetite, tiredness, dizziness, drowsiness.

The authors acknowledged those who support him during this manuscript preparation.

Sources searched include Google Scholar, Research Gate, PubMed, NCBI, NDSS, PMID, PMCID, and Cochrane database. Search terms included: ILAE classifications of seizures and antiepileptic medications.

None.

The author has no financial or proprietary interest in any of material discussed in this article.

1. Bereda G. Determination of the Factors Leading To Non Adherence with Anti–Epileptic Medication in Psychiatric Ambulatory Follow up Patients of Mettu Karl Referral Hospital, South Western, Ethiopia: A Prospective Cross Sectional Study. J Basic Clin Pharma. 2021;12(4):51–56.
2. Perucca P, Carter J, Vahle V, Gilliam FG. Adverse antiepileptic drug effects: toward a clinically and neurobiologically relevant taxonomy. Neurology. 2009;72(14):1223–1229.
3. Uijl SG, Uiterwaal CS, Aldenkamp AP, Carpay JA, Doelman JC, Keizer K, et al. Adjustment of treatment increases quality of life in patients with epilepsy: a randomized controlled pragmatic trial. Eur J Neurol. 2009;16(11):1173–1177.
4. Luoni C, Bisulli F, Canevini MP, De Sarro G, Fattore C, et al. Determinants of health–related quality of life in pharmacoresistant epilepsy: results from a large multicenter study of consecutively enrolled patients using validated quantitative assessments. Epilepsia. 2011;52(12):2181–91.
5. Carpay JA, Aldenkamp AP, van Donselaar CA. Complaints associated with the use of antiepileptic drugs: results from a community–based study. Seizure. 2005;14(3):198–206.
6. Cramer JA, Fisher R, Ben–Menachem E, French J, Mattson RH. New antiepileptic drugs: comparison of key clinical trials. Epilepsia. 1999;40:590–600.
7.  Cramer JA, Ben Menachem E, French J. Review of treatment options for refractory epilepsy: new medications and vagal nerve stimulation. Epilepsy Res. 2001;47:17–25.
8. Begley CE, Annegers JF, Lairson DR, Reynolds TF, Hauser WA. Cost of epilepsy in the United States: a model based on incidence and prognosis. Epilepsia. 1994;35(6):1230–1243.
9. Beran RG. The burden of epilepsy for the patient: the intangible costs. Epilepsia. 1999;40(Suppl. 8):40–43.
10. Griffiths RI, Schrammel PN, Morris GL, Wills SH, Labiner DM, et al. Payer costs of patients diagnosed with epilepsy. Epilepsia. 1999;40(3):351–358.
11. Heaney DC, Sander JW, Shorvon SD. Comparing the cost of epilepsy across eight European countries. Epilepsy Res. 2001;43(2):89–95.
12. Kotsopoulos IA, Evers SM, Ament AJ, de Krom MC. Estimating the costs of epilepsy: an international comparison of epilepsy cost studies. Epilepsia. 2001;42(5):634–640.
13. Nsengiyumva G, Druet–Cabanac M, Nzisabira L, Preux PM, Vergnenegre A. Economic evaluation of epilepsy in Kiremba (Burundi): a case–control study. Epilepsia. 2004;45(6):673–677.
14. Thomas SV, Sarma PS, Alexander M, Pandit L, Shekhar L, et al. Economic burden of epilepsy in India. Epilepsia. 2001;42(8):1052–1060.
15. Schmidt D. Drug Treatment of epilepsy: Options and limitations. Epilepsy Behav. 2009;15:56–65.
16. Stein MA, Kanner AM. Management of newly diagnosed epilepsy. A practical guide to monotherapy. Drugs. 2009;69(2):199–222.
17. Stead M, Bower M, Brinkmann BH, Lee K, Marsh WR, et al. Microseizures and the spatiotemporal scales of human partial epilepsy. Brain. 2010;133(9):2789–2797.
18. Lawal M, Omobayo H, Lawal K. Epilepsy: pathophysiology, clinical manifestations and treatment options. British Journal of Neuroscience Nursing. 2018;14(2):58–72.
19. MostafaSaleh EA. Determination of Some CNS Depressant Drugs. CU Theses. 2018.
20. Fisher RS, Cross JH, D'souza C, French JA, Haut SRet al. Instruction manual for the ILAE 2017 operational classification of seizure types. Epilepsia. 2017;58(4):531–42.
21. Tolaymat A, Nayak A, Geyer JD, Geyer SK, Carney PR. Diagnosis and management of childhood epilepsy. Current problems in pediatric and adolescent health care. 2015;45(1):3–17.
22. Perrotta G. Epilepsy: from pediatric to adulthood. Definition, classifications, neurobiological profiles and clinical treatments. Journal of Neurology, Neurological Science and Disorders. 2020;6(1):014–29.
23. Lüders H, Amina S, Bailey C, Baumgartner C, Benbadis S, et al. Proposal: different types of alteration and loss of consciousness in epilepsy. Epilepsia. 2014;55(8):1140–1144.
24. Engel J. Seizures and epilepsy. Oxford University Press; 2013.
25. Kramer MA, Cash SS. Epilepsy as a disorder of cortical network organization. The Neuroscientist. 2012;18(4):360–372.
26. Lacombe VA, Mayes M, Mosseri S, Reed SM, Ou TH. Distribution and predictive factors of seizure types in 104 cases. Equine veterinary journal. 2014;46(4):441–445.
27. Elmali AD, Auvin S, Bast T, Rubboli G, Koutroumanidis M. How to diagnose and classify idiopathic (genetic) generalized epilepsies. Epileptic Disorders. 2020;22(4):399–420.
28. Fisher RS, Cross JH, D'souza C, French JA, Haut SR, et al. Instruction manual for the ILAE 2017 operational classification of seizure types. Epilepsia. 2017;58(4):531–542.
29. Valeta T. The Epilepsy Book: A Companion for Patients: Optimizing Diagnosis and Treatment. Springer. 2017.
30. Ganeshkumar J. Evaluation of Anti–Epileptic activity of Ethanolic Extract of Leaves of Cassia Alata Linn. Maximal Elecroshock (MES) and Isoniazid Induced Convulsions on Mice (Doctoral dissertation, CL BaidMetha College of Pharmacy, Chennai). 2016.
31. Sanger TD, Chen D, Fehlings DL, Hallett M, et al. Definition and classification of hyperkinetic movements in childhood. Movement Disorders. 2010;25(11):1538–1549.
32. Fisher RS, Cross JH, D'souza C, et al. Instruction manual for the ILAE 2017 operational classification of seizure types. Epilepsia. 2017;58(4):531–542.
33. Leibetseder A, Eisermann M, LaFrance Jr WC, Nobili L, von Oertzen TJ. How to distinguish seizures from non‐epileptic manifestations. Epileptic Disorders. 2020;22(6):716–738.
34. Graham DW. Corpus callosotomy outcomes in paediatric patients. Master's thesis, University of Sydney.
35. Sheldon RS, Raj SR. Seizures vs Syncope: Distinguishing Features for the Clinic. In Syncope. 2020;69–81.
36. Andrade A, Prasad AN. Update in Pediatric Neurology. In Update in Pediatrics. 2018;439–460.
37. Sheldon RS, Raj SR. Seizures vs Syncope: Distinguishing Features for the Clinic. In Syncope. 2020;69–81.
38. Buttaravoli P, Leffler SM. Minor Emergencies E–Book. Elsevier Health Sciences. 2012.
39. Buttaravoli P. Minor Emergencies E–Book. Elsevier Health Sciences; 2018.
40. Bhidayasiri R, Tarsy D. Movement disorders: a video atlas. Springer Science & Business Media; 2012.
41. Piña–Garza JE. Fenichel's Clinical Pediatric Neurology: A Signs and Symptoms Approach (Expert Consult–Online and Print). Elsevier Health Sciences. 2013.
42. Olson DM. Neonatal seizures. Neoreviews. 2012;13(4):e213–e223.
43. Awaad YM. Epilepsy 2. In Absolute Pediatric Neurology. 2018;237–332.
44. Howlett WP. Neurology in Africa. Cambridge University Press; 2015.
45. Kalam MA. Evaluation of Anticonvulsant Activity of Aqer Qerha (Anacyclus pyrethrum DC) root in Experimental Animals (Doctoral dissertation, Rajiv Gandhi University of Health Sciences).
46. Jankovic J, Lang AE. Diagnosis and assessment of Parkinson disease and other movement disorders. Bradley's Neurology in Clinical Practice E–Book. 2021:310.
47. Dobkin BH. Paraplegia and spinal cord syndromes. Bradley's Neurology in Clinical Practice E–Book. 2021:356.
48. Byrne SK, Dunphy LM, Winland–Brown JE. Musculoskeletal Problems. Family Practice and Adult–Gerontology Primary Care Nurse Practitioner Certification Examination Review Questions and Strategies. 2017:407.
49. Löscher W, Klein P. The Pharmacology and Clinical Efficacy of Antiseizure Medications: From Bromide Salts to Cenobamate and Beyond. CNS drugs. 2021:1–29.
50. Alachkar A, Ojha SK, Sadeq A, Adem A, et al. Experimental models for the discovery of novel anticonvulsant drugs: focus on pentylenetetrazole–induced seizures and associated memory deficits. Current pharmaceutical design. 2020;26(15):1693–711.
51. Pellock JM, Arzimanoglou A, D’Cruz O, et al. Extrapolating evidence of antiepileptic drug efficacy in adults to children ≥2 years of age with focal seizures: the case for disease similarity. Epilepsia. 2017;58:1686–1696.
52. Yozawitz E, Stacey A, Pressler RM. Pharmacotherapy for seizures in neonates with hypoxic ischemic encephalopathy. Paediatr Drugs. 2017;19:553–567.
53. Linder C, Wide K, Walander M, et al. Comparison between dried blood spot and plasma sampling for therapeutic drug monitoring of antiepileptic drugs in children with epilepsy: a step towards home sampling. Clin Biochem. 2017;50:418–424.
54. Landmark CJ, Johannessen SI, Tomson T. Dosing strategies for antiepileptic drugs: from a standard dose for all to individualised treatment by implementation of therapeutic drug monitoring. Epileptic Disord. 2016;18:367–383.
55. Jafferany M, Stamu‐O'Brien C, Mkhoyan R, Patel A. Psychotropic drugs in dermatology: A dermatologist's approach and choice of medications. Dermatologic therapy. 2020;33(3):e13385.
56. Munisi KM, Rammutla TR, Vagiri RV. Interventions to improve pharmacist counselling of mental healthcare patients at Weskoppies Hospital. SA Pharmaceutical Journal. 2020;87(4):45–48.
57. Huang–Lionnet JH, Hameed H, Cohen SP. Pharmacologic Management of Myofascial Pain. In Essentials of Pain Medicine. 2018;475–484.
58. McCallum RS. Ryan E. McCallum and R. Steve McCallum. Handbook of Nonverbal Assessment. 2017;21:77.
59. McCallum RE, McCallum RS. Psychological and Physiological Influences on Multicultural and Nonverbal Assessment. In Handbook of Nonverbal Assessment. 2017;77–102.
60. Tsvetanov T. Dental Management of the Medically Compromised Patients. LAP LAMBERT Academic Publishing; 2016.
61. Arndt KA, Hsu JT, Alam M, Bhatia AC, Chilukuri S. Manual of Dermatologic Therapeutics (Lippincott Manual Series). Lippincott Williams & Wilkins; 2014.
62. Behere PB, Das A, Behere AP. Mood Stabilizers. In Clinical Psychopharmacology. 2019;99–116.
63. Khandelwal A, Mahajan C, Prabhakar H. Anti–epileptic Drugs (AEDs). In Pharmacology in Clinical Neurosciences. 2020;173–256.
64. Rogers JP, Leung CC, Nicholson TR. Pocket Prescriber Psychiatry. CRC Press. 2019.
65. Mahmud S, Mattson RH. Antiseizure 21. Understanding Epilepsy: A Study Guide for the Boards. 2019;386.
66. Tharun G, Samala S, Dathar V. Epilepsy and adverse effects of anti–epileptic drugs recent trends in pharmaceutical sciences. 2019:14.
67. Lawal M, Omobayo H, Lawal K. Epilepsy: pathophysiology, clinical manifestations and treatment options. British Journal of Neuroscience Nursing. 2018;14(2):58–72.
68. Costello K, Thrower BW, Giesser BS. Navigating life with multiple sclerosis. Neurology Now Books; 2015.
69. DiVall MV, Woolley AB. CHAPTER Pharmacologic Agents. Acute Care Handbook for Physical Therapists E–Book. 2019;12:431.
70. McCallum RE, McCallum RS. Psychological and Physiological Influences on Multicultural and Nonverbal Assessment. In Handbook of Nonverbal Assessment. 2017;77–102.
71. Vega D, Maalouf NM, Sakhaee K. Increased propensity for calcium phosphate kidney stones with to piramate use. Expert opinion on drug safety. 2007;6(5):547–557.
72. Liu G, Slater N, Perkins A. Epilepsy: treatment options. American family physician. 2017;96(2):87–96.
73. Singhi S, Gupta A. A Review of the Selected and Newer Antiseizure Medications Used in Childhood Epilepsies. Indian Journal of Pediatrics. 2021;1–7.
74. Moavero R, Pisani LR, Pisani F, Curatolo P. Safety and tolerability profile of new antiepileptic drug treatment in children with epilepsy. Expert opinion on drug safety. 2018;17(10):1015–28.