The process of preparing a consensus document on the diagnosis and management of WS was initiated by the members of Association of Child Neurology (AOCN). In association with Indian Epilepsy Society (IES), a consensus document was envisaged on the same. The invited experts included pediatricians, pediatric neurologists, neurologists, and epileptologists (Annexure 1), who were categorized into one of five groups: definitions, etiology, early diagnosis and prognosis; diagnostic evaluation; hormonal treatment; vigabatrin and other drugs; and diet, surgery and supportive care. First the evidence was reviewed. For areas where the evidence was not certain, the Delphi consensus method was adopted [6]. The writing group members of each group identified a set of open- ended questions which were discussed in their respective groups. These open-ended questions were administered using Google form to all experts. In this process, the experts gave their opinions to the moderator, who anonymized the responses and sent them back to all experts. A guarantor ensured that responses were blinded and the methodology of Delphi was adopted.

The responses to the open-ended questions obtained were qualitatively analyzed, and similar responses were categorized, clubbed and converted into closed ended responses. Based on these responses, new questions with close-ended responses were framed. These questions were again sent to experts in the second round. Their responses were collated and presented in the meeting of experts. Categorical responses where more than 75% of experts agreed on single response were considered to have reached a consensus. The concerns, discrepancies and responses where consensus was not reached (<75% agreement) were polled again using audience response system. Questions where polling did not reach 75% consensus were re-polled. Any question where second polling also failed to establish a consensus were considered as having failed to reach the same, and the data was presented as a range rather than a definitive response.

A final consensus meeting was held on 1 September, 2019 at Delhi. The coordinator of each group made a presentation of the draft document for consensus. Deliberations were held, and inputs and suggestions by the various participating members were incorporated into the document. The final document was prepared and circulated to all the participating members for inputs and approval.

As per the 2004 International Delphi consensus statement on WS[1], definitions of clinical spasms, epileptic spasms, and WS were framed (Box 1). Spasms may be confused with myoclonic seizures but the longer duration, presence of a tonic phase, occurrence in clusters and the relationship with the sleep wake cycle help to differentiate spasms from myoclonic seizures [1]. Differentiation from paroxysmal non-epileptic pheno-mena in typically developing children such as benign myoclonus, benign myoclonic epilepsy of infancy, Sandifer syndrome, etc may require video telemetry with concurrent surface electromyography. As per the International League Against Epilepsy (ILAE) 2017 seizure and epilepsy classification, epileptic spasms may be of focal, generalized or unknown onset [2].

1. Consensus Statement: Definitions

Most recent studies classify spasms into two broad categories- known and unknown etiology. Known causes can further be classified into pre-natal, perinatal and postnatal, depending on the timing of central nervous system insult. Another classification scheme is as per the new ILAE 2017 classification [2], wherein the etiology is classified into structural-metabolic, genetic, infectious, etc. However, this can be a bit confusing as there may be overlaps; e.g. tuberous sclerosis may be classified as both structural and genetic. For practical purposes, the etiology should be classified as known or unknown. If known, the exact etiology should be mentioned.

The etiological profile of WS in India is different, as compared with the developed world, where genetic and presumed genetic (unknown etiology) is higher. In India, the etiology is known in 80-85% of affected children [3,4]. Perinatal causes, including perinatal hypoxia and neonatal hypoglycemia are the most predominant [3,4].

Clinical suspicion remains the cornerstone of diagnosis of epileptic spasms. An evaluation including a thorough history, examination and EEG are important in the diagnosis of infantile spasms. As etiology is the most important predictor of outcome, efforts should be made to establish the underlying etiology, as this may also affect the treatment decisions and prognosis; e.g. children with tuberous sclerosis complex are more likely to respond to VGB, while most with unidentified etiology may respond better to steroids. The evaluation should follow a step wise process to avoid unnecessary tests, due to the costs involved (Fig. 1).

Fig. 1 Diagnostic algorithm for child with West syndrome.

An EEG (preferably video-EEG) is the most important tool in diagnosis and management of epileptic spasms, and the following protocol may be followed:

Basic level: Recording for sufficient length to capture sleep is strongly recommended and if achieved, further recording for at least 10 minutes after awakening should be attempted, as epileptic spasms occur very often in that period. The EEG should be planned preferentially during spontaneous sleep and after feeding. This may require planning arrangements with parents. In infants whose EEG is abnormal and the epileptic spasms have not been captured during the EEG, a home video is suitable to establish presence of clinical spasms.

Advanced level: If there is diagnostic uncertainty e.g. if EEG is not diagnostic or spasms are not observed, a prolonged overnight inpatient video EEG recording for 24 hours with polygraphic (with neck and bilateral deltoid EMG) parameters is desirable as it will capture awake as well as all sleep stages and possibly also capture spasms. However, if inpatient facilities are not available, a prolonged EEG record for 2-4 hours to capture stage 2 of non-REM sleep followed by 30 minutes after awakening should be considered [5]. Long term video EEG may also pick up other coexisting seizure types, as noted in 22% of infants with epileptic spasms in a study; especially in those who had etiology of preterm birth or birth asphyxia [6].

Depending on the clinical and EEG findings, the level of diagnostic certainty can be classified as confirmed, probable and possible WS according to following criteria [1,5]:

Depending on the clinical and EEG findings, the level of diagnostic certainty can be classified as confirmatory, probable and possible WS [1,5]. In probable or possible cases, parents should be encouraged to bring home video of the spasms. Repeat EEG at advanced level can be planned to record hypsarrhythmia or spasms.

Following the initiation of any first line treatment, the efficacy of therapy should be assessed within 2-3 weeks; in terms of cessation of spasms and resolution of hypsarrhythmia on EEG [4]. If no/partial response to treatment is seen, a repeat EEG may be considered to plan the next level of treatment. EEG should also be repeated after 2 weeks if the first EEG is normal or inconclusive, or if there is a suspicion of additional/change in seizure type, which may occur in 12-42.3% of cases [6]. If focal abnormalities are identified in infants with additional focal seizures, further investigations like high resolution multi-modality magnetic resonance imaging (MRI)/ positron emission tomography (PET) can be planned to search for a resectable lesion [6].

2. Consensus statement: EEG for Suspected West Syndrome

EEG background is mostly abnormal during both wakefulness and sleep. The inter-ictal patterns vary according to the underlying pathology, age and stage of sleep.

Ictal EEG pattern (during spasms): The most common pattern seen in 72% of the attacks is a brief duration (1-5 sec) three phased pattern: a) diffuse high amplitude slow wave, b) low amplitude fast activity, and c) short lasting diffuse flattening of ongoing activity (electro-decremental response) [10]. In asymmetric spasms, there may be focal discharges preceding, during or following it; indicating the side with focal cortical lesion.

Evolution of EEG: On effective treatment, rapid improvement in EEG is seen, which may even completely normalize. However, resolution of hypsarrhythmia with persistence of background abnormalities occurs more frequently, as a reflection of underlying abnormalities. In most symptomatic cases, there is return of spike wave discharges with development of other seizure types [11]. The chaotic pattern gradually becomes more organized and disappears by 2-4 years and may evolve into other abnormal patterns [12].

If available and feasible, MRI is preferred over Computed Tomography (CT) scan in view of higher yield of abnormalities. Early MRI (T2, T1, FLAIR) with epilepsy protocol should be considered to reach an etiologic diagnosis. However, treatment should not be delayed if MRI cannot be done immediately due to lack of availability or need of anesthesia.

One third of cases considered idiopathic on clinical assessment enter the symptomatic category of structural-metabolic following the MRI scan. In the National Infantile Spasms Consortium, a causal abnormality was identified in 40.9% of infants who underwent MRI with epilepsy protocol, making it the highest yield test [13]. Common abnormalities picked up in Indian scenario include sequelae of perinatal asphyxia and hypoglycemia.

Timing of MRI: Ideally MRI should be obtained prior to initiation of therapy, as Adrenocorticotropic hormone (ACTH) therapy may cause transient abnormalities that may be falsely misinterpreted as brain atrophy. Also, Vigabatrin (VGB) can induce T2 signal abnormalities [14]. On the other hand, MRI done in early infancy may miss cortical dysplasias in view of immature myelination [15].

Repeat MRI: If initial MRI is normal, and seizures persist, MRI may be repeated after 6 months, and certainly at 24-30 months age when myelination is more mature [11].

Additional neuroimaging studies: Magnetic resonance spectroscopy (MRS) can help to delineate a possible metabolic or mitochondrial cause. Areas of hypo metabolism on a Positron emission tomogram (PET) may indicate a cortical malformation. PET may be important in a child with asymmetric spasms, focal EEG changes and a normal MRI of the brain. Positive PET localization has led to seizure remission following the resection surgery done (based on the PET finding) even with a normal MRI [16]. Ictal and interictal single photon emission computed tomography (SPECT) has been used to aid in the localization of the epileptic focus in children with asymmetric infantile spasms who are being evaluated for surgery.

3. Consensus Statement: Neuroimaging in WS

More than 25 IEM have been found to be associated with WS, with frequency of metabolic disorders in epileptic spasms estimated to be 4.7% [13]. A wide range of metabolic disorders, including mitochondrial disorders, such as Leigh’s disease, aminoacidopathies, such as non-ketotic hyperglycinemia, can present with infantile spasms. Other metabolic conditions include glucose transporter defects, pyridoxine deficiency, pyridoxal-5-phosphate deficiency, disorders of cerebral folate metabolism, Menkes’ disease, and biotinidase deficiency. At the very least, disorders treatable at low cost-e.g. pyridoxine dependency and biotinidase deficiency should be ruled out, if required, by a therapeutic trial.

Clues to the presence of IEM include a positive family history, consanguinity, previous sibling deaths, failure to thrive, fluctuating course, deterioration after a period of apparent normalcy, tone abnormalities or movement disorders. Ophthalmological examination, unusual odors and visceromegaly may provide other clues. MRI may show non-specific or specific patterns (for few disorders). However, if none of these features are present, the yield of metabolic investigations is very low [17].

4. Consensus Statement: Metabolic Testing

Genetic causes are being increasingly recognized in epileptic encephalopathies of unexplained etiology. A timely genetic diagnosis has potential for precision treatment decisions, which can improve seizure and development outcomes. It also helps to counsel the parents regarding prognosis and recurrence risk in future pregnancies. A combination of genetic tests provided a definitive diagnosis in more than 40% of children presenting with new-onset spasms without an obvious cause after clinical evaluation and MRI [4,13,18].

Copy number variants (CNVs) are deletions and duplications of stretches of DNA ranging from 1 kb to an entire chromosome. These CNVs can be detected by chromosomal microarrays (CMA) which include comparative genomic hybridization (CGH). Pathogenic CNVs were detected in 3.6-11.8% of children with epileptic encephalopathies [17]. The yield is likely to be higher in case of associated dysmorphism, intellectual disability, developmental delay disproportionate to seizure etiology/frequency, and presence of behavioral issues including autism in non-consanguineous families.

The applications of NGS include targeted gene panel, whole exome (WES) and whole genome sequencing (WGS). However, WES has shown to have higher diagnostic yield compared to gene panels, as it sequences the entire coding genome. The current diagnostic yield of genetic tests is below 60%; and a substantial number of patients may still remain undiagnosed.

In one Indian study, in 36 patients with WS with presumed genetic etiology, genetic causes were identified in 17 children [4]. In a multicentric study, out of 100 infants with epileptic spasms of unknown cause undergoing whole exome sequencing, pathogenic mutations were identified in 15 [19]. Etiology was more likely to be identified in those children who had abnormal development (32.5%) vs. those with normal development (8.3%) [19].

5. Consensus Statement: Genetic Testing

The treatment algorithm for WS is shown in Fig. 2.

aVigabatrin dose: Start with 50 mg/kg/d and hike by 50 mg/kg every 3-7 d interval as tolerated to a maximum dose of 150 mg/kg/d; bACTH Dose: 150 IU/m2 or 6 IU/Kg IM daily for 2 wk, Oral Prednisolone dose: 4 mg/kg/d for 2 wk; cIf EEG shows continued presence of epileptiform abnormalities despite the resolution of hypsarrhythmia, consider starting sodium valprote, topiramate or zonisamide for 12-24 mo; dOther AEDs which may be considered include topiramate, zonisamide, benzodiazepines, or sodium valproate. Pyridoxine trial may be considered in cases with unknown etiology. Fig. 2 Treatment algorithm for West syndrome.

High-quality evidence is available for hormonal therapy (adrenocorticotropic hormone or oral steroids), VGB and combination of hormonal therapy with VGB in the treatment of WS. The United Kingdom Infantile Spasms Study compared hormonal treatment with VGB for epilepsy and development outcome at short-term (14 months and four years of age). It was observed that hormonal therapy was superior in terms of an initial cessation of epileptic spasms, but not at 14 months and four years of age [21]. However, successful initial control of epileptic spasms was associated with better long-term developmental outcome [22].

Recently, the effectiveness of the combination of hormonal therapy with VGB was studied in comparison with hormonal therapy alone [23,24]. Initial results demonstrated that the combination therapy was significantly superior to the hormonal therapy for the cessation of epileptic spasms as a short-term response. However, the combination therapy did not significantly improve epilepsy or neurodevelopmental outcome at 18 months of age. Pyridoxine, as an adjunct with steroid therapy was not been found superior to steroid therapy alone [25].

6. Consensus Statement: First-line treatment for WS

The first-line treatment options are hormonal therapy (adrenocorticotropic hormone or oral steroids) and VGB. Hormonal therapy should be preferred for cases other than tuberous sclerosis complex and VGB should be the first choice for tuberous sclerosis complex. Regarding combination treatment, in view of limited literature, the group suggested the need for more data, before recommending as it as routine first line treatment.

Hormonal therapy in the form of ACTH and oral steroids has been widely used. ACTH has disadvantages of parenteral route and cost. Oral steroids have advantages of ease in administration due to oral route and low-cost. It is difficult to summarize evidence comparing these two modalities of treatment, as different preparations (synthetic and natural ACTH), different doses of ACTH and prednisolone, and different regimens have been used in various studies. Also, many of the studies were underpowered or used varying outcomes. The most important outcomes would be electroclinical resolution and neurodevelopmental outcomes. However, many studies have only used clinical spasm cessation, or surrogate markers such as EEG improvement.

In the 2004 United Kingdom Infantile Spasms study, spasm freedom was achieved in 70% of children taking high dose oral prednisolone (40-60 mg/day) and 76% of children taking ACTH (40 IU/alternate day) [21]. A few recent studies [26,27]used high-dose oral steroids as initial management of WS, and subsequent treated failed cases with ACTH and demonstrated a response rate of 40% and 33% respectively, with high-dose ACTH therapy among non-responders with high-dose oral steroids [26,27]. Two recent systematic reviews have suggested equivalent efficacy of high dose prednisolone as ACTH [28,29].

There is no published evidence on what treatment the child should be started after there is clinical cessation of spasms and EEG resolution of hypsarrhythmia or its variants. There is no evidence that anti-epileptic drug treatment will prevent relapses or further development of epilepsy.

8. Consensus Statement: Further Treatment After Electroclinical Resolution

After clinical cessation of spasms, if the EEG shows resolution of hypsarrhythmia, the following actions are recommended:

Relapse of epileptic spasms is frequent and constitute major challenge as it is an adverse prognostic variable for long-term epilepsy and neurological outcome [32]. There is a paucity of evidence on how to manage these patients. Options include a second trial of hormonal therapy or starting VGB.

9. Consensus Statement: Treatment of Relapses

The treatment of children who have initially responded with hormonal therapy should be individualized. Options include a repeat trial of hormonal therapy or vigabatrin.

There are no published guidelines or recommendations on the plan of investigations before and during steroid or ACTH therapy in children with WS. The dwelling environment and socioeconomic strata would determine the risk of exposure to pathogens and subsequent infection.

Both ACTH and oral steroid treatment are commonly associated with adverse effects such as irritability, increased appetite, hypertension, weight gain, hyper-pigmentation and risk of infections. Adverse effects are associated with high dose and longer duration of therapy. It is routine to monitor blood pressure, blood sugar and urine sugar. There is variability in frequency of monitoring for these adverse effects.

10. Consensus Statement: Pre-Hormonal Therapy Investigations, Monitoring and Precautions on Hormonal Therapy

Vigabatrin (VGB) is a GABA agonist that acts by inhibiting 4-aminobutyrate transaminase, the enzyme for catabolism of GABA. VGB is the drug of choice for epileptic spasms in tuberous sclerosis [18]. VGB is less effective that hormonal therapy as first line drug in treatment of infantile spasm. In terms of short term efficacy, cessation of spasm ranges from 27.3-55.3% with the use of VGB [21]. However, there is a considerable variation in the definition of spasm cessation among various studies. Apart from TSC, there are few etiological predictors of favorable response to VGB. Data from the International Collaborative Infantile Spasms Study (ICISS) [23] study revealed that children with stroke and infarcts responded well to combination of VGB and steroids when compared to those with other etiology. However, there is limited data on predictors of clinical response to VGB among non-TSC patients with epileptic spasms.

There is limited number of studies on long term efficacy of VGB in infantile spasms. The United Kingdom Infantile Spasms Study (UKISS) included non-tuberous sclerosis infants aged 2–12 months who were followed up to determine the long term developmental outcome at 12-14 months of age. It was observed that mean Vineland adaptive behaviour scales (VABS) score were comparable between the high dose steroid group and VGB group [22].

There is a considerable variation in the dose and regimen for treatment of children with epileptic spasms. Doses from 18 mg/kg/day to 150 mg/kg/day have been used by many authors for infantile spasm. The dose is increased by 50 mg/kg/day every 3-7 days, to a maximum of 150 mg/kg/day [33].

Visual field defects have been reported with use of VGB [34]. Other side effects reported with use of VGB include sedation, irritability, and hypotonia. There are no standard methods to detect visual field loss among young children. A 30 HZ flicker electroretinography (ERG) has been used to monitor ocular toxicity. The proportion of patients with visual field defects in adults (52%) was noted to be higher than children (34%) in a systematic review of 1678 exposed patients to VGB [34].

11. Consensus Statement: Vigabatrin in WS

Other antiepileptic drugs which may be tried in children with epileptic spasms who have failed hormonal therapy and VGB include topiramate, sodium valproate, zonisamide, levetiracetam, and benzodiazepines such as nitrazepam, clobazam and clonazepam. Nitrazepam has been approved by Central Drugs standard Organization (India) for its use in epilepsy. There have also been small studies on the use of pyridoxine (other than when treating pyridoxine-dependent seizures), thyrotropin releasing hormone (TRH), hydrocortisone, sulthiame, and magnesium sulphate. However, considering limited literature with insufficient evidence, none of these drugs are deemed effective in treatment of infantile spasms [35].

12. Consensus Statement: Treatment After Failure of Hormonal Therapy and Vigabatrin

The ketogenic diet (KD) is a high-fat, low-carbohydrate, and restricted protein diet that has been found useful in the management of WS [36]. KD administration in infants needs hospitalization, monitoring and availability of a trained dietician as the diet must be carefully titrated to achieve seizure reduction and provide calories and proteins for growth [37]. This may be difficult to achieve in a low resource setting. Also, ketogenic formula, which makes KD administration easier for infants, is not easily available in India, and is costly. The modified Atkins diet, which is a simpler and easier to administer version of the KD, has also been found to be effective and well-tolerated in children with infantile spasms [38].

13. Consensus Statement: Dietary therapies for WS

In the recent years, there have been studies on epilepsy surgery in refractory epileptic spasms [25]. The various surgeries reported include total hemispherectomy, subtotal hemispherectomy, multilobar resection, lobectomy and tuberectomy. Curative epilepsy surgery has the best outcomes with EEG-concordant lesional abnormalities on MRI [25]. The advances in neuroimaging and invasive monitoring have facilitated patient selection, presurgical evaluation, and ultimately, resection planning [39].

14. Consensus Statement: Epilepsy Surgery in WS

Children should be evaluated for epilepsy surgery after failure of the first line treatments (hormonal treatment and/or vigabatrin), if there is presence of surgically resectable lesions e.g., cortical dysplasias, hemimegalen-cephaly, Sturge Weber syndrome, tuberous sclerosis, and if there is presence of focal features on clinical semiology of spasms and EEG.

As mentioned earlier, the diagnosis of WS is significantly delayed in India, adversely impacting the treatment response and neurodevelopmental outcome [3,4]. In one study, the mean age at diagnosis was 13.1 months and the mean lead time to treatment was 7.9 months [3].

Certain populations are at high risk of developing WS, such as infants with perinatal brain injury and tuberous sclerosis. There is evidence that asymptomatic infants with tuberous sclerosis complex at high risk of developing spasms and epilepsy can be identified in the pre-symptomatic stage using serial surveillance EEGs. All pre-symptomatic patients with tuberous sclerosis showing epileptiform abnormalities detected on serial surveillance EEGs went on to develop epilepsy [40]. Presence of epilepsy in tuberous sclerosis is an important association for mental retardation/intellectual disability. Antiepileptic treatment with VGB in this high-risk group, identified on serial EEGs, can significantly reduce the rates of evolution of asymptomatic EEG abnormalities to epilepsy and give a much better neuro-developmental outcome (nearly 80% normal development vs 20%, with standard treatment) Furthermore, the rates of drug resistant epilepsy were 7 % vs 42 % in the preventive vs standard groups [40].

There are also a few retrospective studies with small numbers of patients on the EEG findings preceding the onset of epileptic spasms and hypsarrhythmia in infants with perinatal asphyxia and periventricular leukomalacia. More evidence is needed before routine serial surveillance EEGs are recommended for presymptomatic diagnosis of WS in at-risk infants with perinatal brain injury.

15. Consensus Statement: Early Diagnosis

Key facets of supportive care in WS include issues pertaining to nutrition, sleep, dental care, behavior, cognition and schooling.

16. Consensus Statement: Supportive care in WS

Anticipatory evaluation and appropriate management of co-morbidities (specifically related to feeding, oral hygiene, neuromotor delays, constipation, sleep, and growth retardation) should be ensured. Schooling, as per cognitive abilities, should be ensured. Disability certification, if eligible as per government guidelines, should be proactively arranged, so as to facilitate financial and other support.

In this article, the guidelines for the diagnosis and management of West syndrome are provided. These are based on the current evidence and where-in the evidence is insufficient, expert opinion. The neurodevelopmental outcomes of children with West syndrome are likely to improve with timely diagnosis and early appropriate management. As there is on-going research on the many facets of treatment, and there are still many unanswered questions, an update of these guidelines will be provided when new evidence emerges.

Acknowledgment: Dr Sushma Goyal and Dr Chaitanya Datar for helpful inputs in the EEG and genetic testing sections, respectively.

Contributors: SS and RM: conceptualized the idea; SS, JSK, KS, JS, JNG, RM, KPV: constituted the writing committee and drafted the manuscript; JSK devised and conducted Delphi process. All the authors approved the final version of the manuscript.

Funding: The logistics of faculty travel for the West syndrome Delphi Consensus meeting was funded by Intas Pharmaceutical Ltd. and Ferring Pharmaceuticals. The venue support was provided by Army Hospital, Research and Referral, Dhaula Kuan, New Delhi. None of the funding sources had any role in content of the discussion during meeting, or in report or manuscript preparation. They did not have access to any version of the manuscript.

Competing interests: None stated.

Association of Child Neurology – Indian Epilepsy Society Expert Committee (alphabetically arranged)

Razia Adam (Hyderabad, Telengana); Satinder Aneja (Noida, Uttar Pradesh); Biswaroop Chakrabarty (Delhi); Arijit Chattopadhyay (Kolkata); Saurabh Chopra (Delhi), Rajni Farmania (Delhi); Pradnya Gadgil (Mumbai, Maharashtra); Divyani Garg (Delhi); Jatinder Singh Goraya (Ludhiana, Punjab); Sheffali Gulati (Delhi); Aparajita Gupta (Kolkata, West Bengal); Rachana Dubey Gupta (Indore, Madhya Pradesh); Vineet Bhushan Gupta (Delhi); Anaita Udwadia Hedge (Mumbai, Maharashtra); Mary Iype (Trivandrum, Kerala); Vivek Jain (Jaipur, Rajasthan); Prashant Jauhari (Delhi); Veena Kalra (Delhi); Mahesh Kamate (Belgavi, Karnataka); Lakshminarayanan Kannan (Chennai, Tamil Nadu); Anupriya Kaur (Chandigarh); Gurpreet Kochar (Ludhiana, Punjab); Ramesh Konanki (Hyderabad, Telangana); Ajay Kumar (Patna, Bihar); PAM Kunju (Trivandrum, Kerala); Lokesh Lingappa (Hyderabad, Telengana); Priyanka Madaan (Chandigarh); Ranjith Kumar Manokaran (Chennai, Tamil Nadu); MM Mehendiratta (Delhi); Ramshekhar Menon (Trivandrum, Kerala); Devendra Mishra (Delhi); Debasis Panigrahi (Bhubneshwar, Orissa); Harsh Patel (Ahmedabad, Gujarat); Sandeep Patil (Pune, Maharashtra); Bijoy Patra (Delhi); Leema Pauline (Chennai, Tamil Nadu); KVN Raju (Bangalore, Karnataka); Arushi Gehlot Saini (Chandigarh); Lokesh Saini (Chandigarh); Naveen Sankhyan (Chandigarh); Rachna Sehgal (Delhi); Anita Sharma (Delhi); Pratibha Singhi (Gurgaon, Haryana); Vishal Sondhi (Pune, Maharasthra); Renu Suthar (Chandigarh); Sanjeev V Thomas (Trivandrum, Kerala); Manjari Tripathi (Delhi); Vrajesh Udani (Mumbai, Maharasthra); Prashant Utage (Hyderabad, Telengana); Nitish Vora (Ahmedabad, Gujarat); Sangeeta Yoganathan (Vellore, Tamil Nadu).

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