A seizure is defined as an occurrence of transient signs and/or symptoms due to abnormal, excessive or synchronous neuronal activity in the brain. It may be defined as epilepsy only after the individual has had two or more such unprovoked seizures.
Absence Epilepsy (AE) is an idiopathic epilepsy that involves brief, sudden lapses of consciousness generally for 5-15 seconds, mainly in children between 4-10 years of age. It encompasses an otherwise structurally normal brain on neuroimaging with epilepsy as the only neurological problem.
Absence seizures in children and teenagers were generally considered relatively benign because of their non-convulsive nature and the large incidence of remittance in early adulthood. However recent studies show that 30% of children with absence seizures are pharmaco-resistant and 60% are affected by severe neuropsychiatric comorbid conditions, including impairments in attention, cognition, memory and mood. Attention deficits can be detected even before the epilepsy diagnosis, and they may persist even when seizures are pharmacologically controlled. Ethosuximide, sodium valproate and lamotrigine are the first line drugs and recent studies indicate that the attention deficits may be aggravated by valproic acid monotherapy. Thus there is a need to emphasize on the importance of a detailed clinical history and examination for the early detection of these non-motor seizures or a very mild motor phenomena which may otherwise go unnoticed or be considered non epileptic.
KEY WORDS: Absence seizures/ Epilepsy, Homoeopathy, pediatrics
INTRODUCTION:
Absence seizures affect around 6-8 per 100,000 in children younger than 15 years. AE constitutes 10% of all patients with pediatric epilepsy.
The first description of absence seizures was made by Poupart in 1705 and Tissot in 1770. In 1824, Calmeil introduced the term, absences, and in 1838, Esquirol for the first time used the term petit mal. Delasiauve introduced the concept of idiopathic epilepsy. The term pyknolepsy belongs to the 20th century. It was definitely recognized as an epileptic entity only in 1945, based on EEG recordings.
AE is more common in females than in males. AE may be typical, atypical, myoclonic or eyelid myoclonias.
A typical AE usually presents with multiple daily blank spells with sudden cessation of activity for a few seconds (5-15s) associated with fluttering or uprolling of eyes or staring
and automatisms, only noticeable by others but the patient himself being unaware of it promptly resumes his activity without a postictal state. Hyperventilation for 3-5 minutes can demonstrate suspected typical AE in a child in the OLD settings. The classic EEG finding is of 3 Hz spike-and-slow-wave discharges.
Eyelid myoclonia (Jeavons syndrome i.e. eye closure) or myoclonic absences (i.e. periorbital, perioral or limb myoclonic jerks) along with typical AE are difficult to treat.
Atypical AE is associated with myoclonia and hypotonia/atonia of the head and the body and is precipitated by drowsiness. These episodes have a slow onset and offset. They are difficult to treat. They display 1-2 Hz spike-and-slow-wave discharges.
Juvenile AEs are similar to typical AEs but they begin later (7-17 yrs) associated with Juvenile myoclonic epilepsy and generalized clonic tonic seizures. ECG shows 4-6 Hz spike-and slow-wave discharges.
PATHOPHYSIOLOGY:
This electro-clinical syndrome may also be described as an age related non motor genetically generalized epilepsy (GGE) whereby the pathophysiology of AE points towards a genetically predetermined lowered threshold for seizures. Early onset AE (<4 yr of age) or drug resistance may be related to an abnormal glucose transporter defect with low CSF glucose levels.
Blood oxygenation level-dependent (BOLD) functional MRI studies help in identifying the key regions involved in human absence seizures. The lack of generalization at the start of an absence seizure and localized changes in precuneus, posterior cingulate cortex, lateral parietal cortex and/ or frontal cortex referred to as the cortical initiation network (CIN) are observed before other brain areas become involved in the paroxysm. Different individuals may display diverse CINS depending on their peculiar genotypes.
The persistent ictal and interictal altered cortical sensorimotor network in people with absence seizure is a major finding to correlate these seizures with their neuropsychiatric comorbidities.
Changes in the firing of cortical, thalamic and basal ganglia neuronal populations just around short wave diathermy (SWD) offset have been proposed as terminators of the seizure.
RISK FACTORS
Recurrent febrile seizures
Febrile seizure plus syndrome
Familial predisposition to epilepsy or neurological illnesses
Genetic disorders associated with epilepsy
Familial discords or psychological problems faced at school by the child contribute to stress.
Post traumatic brain injury
Cerebrovascular infections
Neuronal damage and nerve conduction defect.
TRIGGERS:
Photic stimulation i.e. strobe lights, flipping through TV channels, viewing video games, prolonged screen time on any digital media
Hyperventilation
sleep deprivation
Alcohol withdrawal
Recreational drug misuse
Physical and mental exhaustion
loud noises, music, reading, hot baths, cold weather.
ROLE OF HOMOEOPATHY IN ABSENCE SEIZURES:
AE is a typical example of a “one sided disease” as described by our master Dr Samuel Hahnemann in aphorism 173 and they belong chiefly to the class of chronic diseases. The treatment of AE can follow Constitutional, Anti Miasmatic or pathological approaches depending on the individuality of each case.
Inputs from Materia medica:
Artemisia vulgaris: epileptic diseases, convulsive diseases of childhood and girls at puberty. petit mal epilepsy without aura after fright, violent emotions, masturbation, several convulsions close together.
Stramonium: convulsions with consciousness renewed by sight of bright light, of mirror, of water. pupils dilate when the child is reprimanded
Nux vomica: Convulsions with consciousness agg anger, emotions, touch, light, moving
Bufo rana: Epileptic syndromes in feeble minded children. Epilepsy at the time of menses, sexual excitement, at the change of moon.
Inputs from Repertory:
Pocket Manual of Homoeopathic Materia Medica by William Boericke Nervous system, Brain, Epilepsy – Petit mal
The Guiding Symptoms Of Our Materia Medica by C Hering:
NERVES, Convulsions, Epileptiform (petit mal)
Synthesis Repertory
Generals-Petit Mal Mind Absences cross referred to: Mind- Unconsciousness frequent spells of unconsciousness
Other rubrics from ‘Generals’ chapter for AE:
Under the Rubric: ‘Convulsions’
SUB RUBRICS:
Children in
Brain complaints of- accompanied by
Exertion after
Mental exertion after
contradiction from
scolded after being
bright light from
Noise
sleep loss of from
Cold and Cold agg becoming
Various repertories have elaborated absence seizures using different rubrics. However when referred back to many materia medicas, it is found that these rubrics may not always correspond to the symptoms of ‘absence’ type of seizures.
Dr JH Clarke quotes in “The Prescriber’ that epilepsy will often be removed by medicines homeopathic to the general conditions when medicines chosen according to the characteristics of the epilepsy alone would have no influence.
This is accurate in the case of absence seizures. Every homeopath must therefore strive to investigate and understand the dynamics that take place in the lives of patients i.e. the most significant points in the whole history of the chronic disease to discover the fundamental cause to prescribe a well suited remedy that brings about a holistic cure.
CONCLUSION:
Creating awareness regarding the recognition and the seriousness of this kind of epilepsy by the parents or bystanders is key for it’s early detection and treatment.
There is a need to explore the scope of lesser known and partially proved homeopathic medicines particularly for “absences” in greater detail. Evidence based studies related to the treatment of children presenting with co-morbidities of AE must be performed. Homoeopathy
has proven to be effective in the treatment and reduction of recurrence of absence seizures however further research studies are needed to show conclusive results.
REFERENCES:
1. Brigo F, Igwe SC. Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents. Cochrane Database Syst Rev. 2017 Feb 14;2(2):CD003032.
2. Crunelli V et. all Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures. Brain. 2020 Aug 1;143(8):2341-2368. doi: 10.1093/brain/awaa072. PMID: 32437558; PMCID: PMC7447525.
3. Tangwiriyasakul C et. al Dynamic brain network states in human generalized spike wave discharges. Brain. 2018 Oct 1;141(10):2981-2994. doi: 10.1093/brain/awy223. PMID: 30169608; PMCID: PMC6158757.
4. Nelson’s Textbook of Paediatrics 21st Edition
5. Piyush Gupta PG Textbook of Paediatrics 3rd Edition
6. The Guiding Symptoms Of Our Materia Medica by Dr C. Hering
7. Pocket manual of Homoeopathic Materia Medica by Dr William Boreicke 8. Synthesis Repertory
9. The Prescriber by Dr JH Clarke
