Vigabatrin is an active pharmaceutical ingredient in the Fatty Acid Derivatives group (N03AG). The information below is compiled per regulator from the product labels on record, with direct links to the original documents.
GBOfficial regulatory label· revised May 22, 2026[1]
Treatment in combination with other antiepileptic medicinal products for patients with resistant partial epilepsy with or without secondary generalisation, that is where all other appropriate medicinal product combinations have proved inadequate or have not been tolerated.
Monotherapy in the treatment of infantile spasms (West's syndrome).
How to take
USUnited States· FDA
4 products
Uses
USOfficial regulatory label· revised November 18, 2024[2]
1) ]. VIGADRONE is not indicated as a first line agent for complex partial seizures. 1) ].
How to take
US
CACanada· Health Canada
2 products
Uses
CAOfficial regulatory label· revised January 28, 2026[3]
37 Vigabatrin Product Monograph Page 3 of 44 SABRIL® vigabatrin PART I: HEALTH PROFESSIONAL INFORMATION SUMMARY PRODUCT INFORMATION Route of Administration Dosage Form / Strength Non-medicinal Ingredients Oral tablet / 500 mg Hydroxypropyl methylcellulose, magnesium stearate, microcrystalline cellulose, polyethylene glycol, povidone, sodium starch glycolate, titanium dioxide Oral sachet / 500 mg Povidone INDICATIONS AND CLINICAL USE Sabril (vigabatrin) is indicated for: Treatment of epilepsy only in those patients who respond inadequately to alternative treatment combinations or in whom other drug combinations have not been tolerated and in whom the potential benefits conferred by its use outweigh the risk of ophthalmologic abnormalities (see WARNINGS and PRECAUTIONS, Serious Warnings and Precautions and Ophthalmologic).
Sabril is not indicated as a first line antiepileptic treatment. If these criteria are met and the patient and caregiver have been fully apprised of the risk, Sabril can be considered for the adjunctive management of partial epilepsies, with or without secondary generalization, which are not satisfactorily controlled by other antiepilepsy drug combinations.
EUEuropean Union· EMA
1 product
Uses
EUOfficial regulatory label· revised February 19, 2026[4]
Kigabeq is indicated in infants and children from 1 month to less than 7 years of age for: - Treatment in monotherapy of infantile spasms (West's syndrome). - Treatment in combination with other antiepileptic medicinal products for patients with resistant partial epilepsy (focal onset seizures) with or without secondary generalisation, that is where all other appropriate medicinal product combinations have proved inadequate or have not been tolerated.
How to take
Drug interactions
Known interactions involving Vigabatrin. Select one for details. This list is informational and not a complete interaction checker.
Showing 240 of 246. Type above to find a specific drug.
Interaction data compiled from DDInter (academic, CC-BY). Severity classification only - this is not a complete interaction checker and not medical advice.
Sources & citations
[1]MHRA (UK) · PL508050122 · revised May 22, 2026
[2]FDA DailyMed · 01f7f049-78c2-47… · revised November 18, 2024 [PDF]
[3]Health Canada (DPD) · 02065819 · revised January 28, 2026
[4]European Medicines Agency · EMEA/H/C/004534 · revised February 19, 2026
[5]OpenFDA adverse-event reports (US), 12 months ending June 4, 2026.
Information on this page is compiled from public regulatory records. Drugvu is not affiliated with any regulator or pharmaceutical manufacturer. This is not medical advice. Always consult a qualified healthcare professional.
Vigabatrin MSN treatment may only be initiated by a specialist in epileptology, neurology or paediatric neurology. Follow-up should be arranged under supervision of a specialist in epileptology, neurology or paediatric neurology. Posology Vigabatrin MSN is for oral administration once or twice daily and may be taken before or after meals.
g. water, fruit juice or milk) immediately before oral administration. If the control of epilepsy is not clinically significantly improved after an adequate trial, vigabatrin treatment should be discontinued. Vigabatrin should then be gradually withdrawn under close medical supervision.
A clinically meaningful improvement is usually observed within 2 to 4 weeks in patients with infantile spasms, and within 12 weeks in patients with refractory complex partial seizures. Adults Maximal efficacy is usually seen in the 2-3 g/day range.
A starting dose of 1 g daily should be added to the patient's current antiepileptic medicinal product regimen. 5 g increments at weekly intervals depending on clinical response and tolerability. The highest recommended dose is 3 g/day.
No direct correlation exists between the plasma concentration and the efficacy. 2). Paediatric population Resistant partial epilepsy The recommended starting dose in neonates, children and adolescents is 40 mg/kg/day. 5-3 g/day >50 kg: 2-3 g/day The maximum recommended dose in each of these categories should not be exceeded.
Monotherapy for infantile spasms (West's Syndrome) The recommended starting dose is 50 mg/kg/day. This may be titrated over a period of one week if necessary. Doses of up to 150 mg/kg/day have been used with good tolerability. Older people and patients with renal impairment Since vigabatrin is eliminated via the kidney, caution should be exercised when administering the drug to the older people and more particularly in patients with creatinine clearance less than 60 ml/min.
Adjustment of dose or frequency of administration should be considered. Such patients may respond to a lower maintenance dose. 8).
This is not medical advice. Consult a qualified healthcare professional.
Side effects & warnings
GBOfficial regulatory label· Adverse reactions· revised May 22, 2026[1]
Summary of the safety profile Visual field defects ranging from mild to severe have been reported frequently in patients receiving vigabatrin. Severe cases are potentially disabling. The onset is usually after months to years of vigabatrin therapy.
4). Approximately 50% of patients in controlled clinical studies have experienced undesirable effects during vigabatrin treatment. In adults, these were mostly central nervous system related such as sedation, drowsiness, fatigue and impaired concentration.
However, in children excitation or agitation is frequent. The incidence of these undesirable effects is generally higher at the beginning of treatment and decreases with time. As with other antiepileptic drugs, some patients may experience an increase in seizure frequency, including status epilepticus with vigabatrin.
Patients with myoclonic seizures may be particularly liable to this effect. New onset myoclonus and exacerbation of existing myoclonus may occur in rare cases. Tabulated list of adverse reactions Undesirable effects ranked under headings of frequency are listed below, using the following convention: Very common (≥ 1/10); common (≥ 1/100 to <1/10); uncommon (≥ 1/1,000 to <1/100); rare (≥ 1/10,000 to <1/1,000); very rare (<1/10,000); not known (cannot be estimated from the available data).
4). Eye disorders visual field defect vision blurred, diplopia, retinal disorder (mainly optic atrophy Reduced visual acuity nystagmus peripheral) Gastrointe stinal disorders nausea, vomiting, abdominal pain Hepato- biliary disorders hepatitis Skin and subcutane ous tissue disorders alopecia rash angioedema, urticaria Musculosk eletal and connective tissue disorders arthralgia General disorders and administrat ion site conditions fatigue oedema, irritability Investigatio ns*** weight increased *Psychiatric reactions have been reported during vigabatrin therapy.
4). Depression was a common psychiatric reaction in clinical trials but seldom required discontinuation of vigabatrin. **Rare reports of encephalopathic symptoms such as marked sedation, stupor and confusion in association with non- specific slow wave activity on electroencephalogram have been described soon after the initiation of vigabatrin treatment.
4). ***Laboratory data indicate that vigabatrin treatment does not lead to renal toxicity. Decreases in ALT and AST, which are considered to be a result of inhibition of these aminotransferases by vigabatrin, have been observed. Chronic treatment with vigabatrin may be associated with a slight decrease in haemoglobin which rarely attains clinical significance.
Paediatric population Psychiatric disorders Very common: excitation, agitation Reporting of suspected adverse reactions Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product.
uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.
GBOfficial regulatory label· Warnings and precautions· revised May 22, 2026[1]
Except for the treatment of infantile spasms, Vigabatrin MSN should not be initiated as monotherapy. Visual field defects (VFD) have been reported in patients receiving vigabatrin with a high prevalence (about 1/3 of patients). 1. The onset is usually after months to years of vigabatrin therapy.
The degree of visual field restriction may be severe. Most of the patients with perimetry-confirmed defects have been asymptomatic. Hence, this undesirable effect can only be reliably detected by systematic perimetry which is usually possible only in patients with a developmental age of more than 9 years.
For infants, children and those not able to perform perimetry, electroretinography (ERG), optical coherence tomography (OCT) and/or other methods appropriate for the patient can be considered. Patients should undergo systematic screening examination when starting vigabatrin and at regular intervals for detection of visual field defects and reduced visual acuity (see Visual Field Defects and Visual Acuity).
Vision assessment is recommended at baseline (no later than 4 weeks after starting vigabatrin), every 3 to 6 months during therapy, and about 3 to 6 months after the discontinuation of therapy. Available data suggests that visual field defects are irreversible even after discontinuation of vigabatrin.
A deterioration of VFD after the treatment is discontinued cannot be excluded. Therefore, vigabatrin should only be used after a careful assessment of the balance of benefits and risk compared with alternatives. Because of the risk of visual loss, a gradual withdrawal should start immediately if no meaningful improvement is observed following an adequate treatment attempt.
Patient response to and continued need for vigabatrin should be periodically reassessed. Vigabatrin is not recommended for use in patients with any pre-existing clinically significant visual field defect. Visual Field Defects (VFD) Based on available data, the usual pattern is a concentric constriction of the visual field of both eyes, which is generally more marked nasally than temporally.
In the central visual field (within 30 degree of eccentricity), frequently an annular nasal defect is seen. However, the VFDs reported in patients receiving vigabatrin have ranged from mild to severe. Severe cases may be characterized by tunnel vision.
This is not medical advice. Consult a qualified healthcare professional.
Who should not take it
GBOfficial regulatory label· Contraindications· revised May 22, 2026[1]
1.
This is not medical advice. Consult a qualified healthcare professional.
1) ]. 3) ]. 4) ]. Monitoring of VIGADRONE plasma concentrations to optimize therapy is not helpful. Administration VIGADRONE tablets are given orally with or without food. 6) ]. 2 Refractory Complex Partial Seizures Adults (Patients 17 Years of Age and Older) Treatment should be initiated at 1,000 mg/day (500 mg twice daily).
Total daily dose may be increased in 500 mg increments at weekly intervals, depending on response. The recommended dose of VIGADRONE in adults is 3,000 mg/day (1,500 mg twice daily). A 6,000 mg/day dose has not been shown to confer additional benefit compared to the 3,000 mg/day dose and is associated with an increased incidence of adverse events.
6) ]. Pediatric (Patients 2 to 16 Years of Age) The recommended dosage is based on body weight and administered as two divided doses, as shown in Table 1. The dosage may be increased in weekly intervals to the total daily maintenance dosage, depending on response.
Pediatric patients weighing more than 60 kg should be dosed according to adult recommendations. Table 1. CPS Dosing Recommendations for Pediatric Patients Weighing 10 kg up to 60 kg Patients weighing more than 60 kg should be dosed according to adult recommendations Body Weight [kg] Total Daily Administered in two divided doses.
Starting Dose [mg/day] Total Daily Maintenance Dose Maintenance dose is based on 3,000 mg/day adult-equivalent dose [mg/day] 10 kg to 15 kg 350 mg 1,050 mg Greater than 15 kg to 20 kg 450 mg 1,300 mg Greater than 20 kg to 25 kg 500 mg 1,500 mg Greater than 25 kg to 60 kg 500 mg 2,000 mg In patients with refractory complex partial seizures, VIGADRONE should be withdrawn if a substantial clinical benefit is not observed within 3 months of initiating treatment.
1) ]. 6) ]. 4) ]. Table 2 provides the volume of the 50 mg/mL dosing solution of vigabatrin for oral solution that should be administered as individual doses in infants of various weights. Table 2. 5 mL twice daily 16 8 mL twice daily 24 mL twice daily In patients with infantile spasms, VIGADRONE should be withdrawn if a substantial clinical benefit is not observed within 2 to 4 weeks.
1) ]. 6) ]. 4 Patients with Renal Impairment VIGADRONE is primarily eliminated through the kidney. Infants Information about how to adjust the dose in infants with renal impairment is unavailable. 6) ].
This is not medical advice. Consult a qualified healthcare professional.
Most-reported reactions to the US regulator (12 mo to June 4, 2026): 711 reports total. [5]
Seizure 107
Drug Ineffective 57
Somnolence 49
Death 48
Hospitalisation 46
Vomiting 36
Off Label Use 35
Product Dose Omission Issue 31
Infantile Spasms 27
Respiratory Disorder 27
Pneumonia 26
Hypotonia 20
Side effects & warnings
USOfficial regulatory label· Adverse reactions· revised November 18, 2024[2]
gov/medwatch. 1 Clinical Trial Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
S. S. clinical studies of 4,079 vigabatrin-treated patients, the most common (≥5%) adverse reactions associated with the use of vigabatrin in combination with other AEDs were headache, somnolence, fatigue, dizziness, convulsion, nasopharyngitis, weight gain, upper respiratory tract infection, visual field defect, depression, tremor, nystagmus, nausea, diarrhea, memory impairment, insomnia, irritability, abnormal coordination, blurred vision, diplopia, vomiting, influenza, pyrexia, and rash.
The adverse reactions most commonly associated with vigabatrin treatment discontinuation in ≥1% of patients were convulsion and depression. In patients with infantile spasms, the adverse reactions most commonly associated with vigabatrin treatment discontinuation in ≥1% of patients were infections, status epilepticus, developmental coordination disorder, dystonia, hypotonia, hypertonia, weight gain, and insomnia.
Adverse reactions that are listed occurred in at least 2% of vigabatrin-treated patients and more frequently than placebo. 9 mg/kg). Table 6. Adverse Reactions in Pooled, Adjunctive Trials in Pediatric Patients 3 to 16 Years of Age with Refractory Complex Partial Seizures Body System Adverse Reaction All Vigabatrin [N=165] % Placebo [N=104] % Eye Disorders Diplopia 3 2 Blurred vision 2 0 Gastrointestinal Disorders Upper abdominal pain 4 3 Constipation 2 1 General Disorders Fatigue 10 7 Infections and Infestations Upper respiratory tract infection 15 11 Influenza 7 3 Otitis media 6 4 Streptococcal pharyngitis 4 3 Viral gastroenteritis 2 0 Investigations Weight gain 15 2 Nervous System Disorders Somnolence 6 5 Nystagmus 4 3 Tremor 4 2 Status epilepticus 2 1 Psychiatric Disorders Abnormal behavior 7 6 Aggression 6 2 Disorientation 3 0 Safety of vigabatrin for the treatment of refractory CPS in patients 2 years of age is expected to be similar to pediatric patients 3 to 16 years of age.
Infantile Spasms In a randomized, placebo-controlled IS study with a 5 day double-blind treatment phase (n=40), the adverse reactions that occurred in >5% of patients receiving vigabatrin and that occurred more frequently than in placebo patients were somnolence (vigabatrin 45%, placebo 30%), bronchitis (vigabatrin 30%, placebo 15%), ear infection (vigabatrin 10%, placebo 5%), and acute otitis media (vigabatrin 10%, placebo 0%).
In a dose response study of low-dose (18 to 36 mg/kg/day) versus high-dose (100 to 148 mg/kg/day) vigabatrin, no clear correlation between dose and incidence of adverse reactions was observed. The adverse reactions (≥5% in either dose group) are summarized in Table 7.
Table 7. 2 Post Marketing Experience The following adverse reactions have been identified during post approval use of vigabatrin. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Adverse reactions are categorized by system organ class.
USOfficial regulatory label· Warnings and precautions· revised November 18, 2024[2]
1 Permanent Vision Loss VIGADRONE can cause permanent vision loss. Because of this risk and because, when it is effective, VIGADRONE provides an observable symptomatic benefit; patient response and continued need for treatment should be periodically assessed.
Based upon adult studies, 30 percent or more of patients can be affected with bilateral concentric visual field constriction ranging in severity from mild to severe. Severe cases may be characterized by tunnel vision to within 10 degrees of visual fixation, which can result in disability.
In some cases, VIGADRONE also can damage the central retina and may decrease visual acuity. Symptoms of vision loss from VIGADRONE are unlikely to be recognized by patients or caregivers before vision loss is severe. Vision loss of milder severity, while often unrecognized by the patient or caregiver, can still adversely affect function.
Because assessing vision may be difficult in infants and children, the frequency and extent of vision loss is poorly characterized in these patients. For this reason, the understanding of the risk is primarily based on the adult experience.
The possibility that vision loss from vigabatrin may be more common, more severe, or have more severe functional consequences in infants and children than in adults cannot be excluded. The onset of vision loss from VIGADRONE is unpredictable and can occur within weeks of starting treatment or sooner, or at any time after starting treatment, even after months or years.
The risk of vision loss increases with increasing dose and cumulative exposure, but there is no dose or exposure known to be free of risk of vision loss. In patients with refractory complex partial seizures, VIGADRONE should be withdrawn if a substantial clinical benefit is not observed within 3 months of initiating treatment.
6) ]. In patients with infantile spasms, VIGADRONE should be withdrawn if a substantial clinical benefit is not observed within 2 to 4 weeks. 6) ]. VIGADRONE should not be used in patients with, or at high risk of, other types of irreversible vision loss unless the benefits of treatment clearly outweigh the risks.
The interaction of other types of irreversible vision damage with vision damage from VIGADRONE has not been well-characterized but is likely adverse. VIGADRONE should not be used with other drugs associated with serious adverse ophthalmic effects such as retinopathy or glaucoma unless the benefits clearly outweigh the risks.
This is not medical advice. Consult a qualified healthcare professional.
Who should not take it
USOfficial regulatory label· Contraindications· revised November 18, 2024[2]
4 CONTRAINDICATIONS None. None ( 4 )
This is not medical advice. Consult a qualified healthcare professional.
Management of infantile spasms (IS or West syndrome), as monotherapy, although the benefits of its use and the risks of ophthalmologic abnormalities must be taken into account. While Sabril may be effective initially as monotherapy, clinical experience indicates that at least 50% of patients may require the addition of other antiepileptic drugs owing to relapse or emergence of other seizure types following an initial response to the treatment of infantile spasms with Sabril.
Vigabatrin Product Monograph Page 4 of 44 Sabril should be used under close monitoring by a neurologist and an ophthalmologist.
Geriatrics (≥65 years of age):
Evidence from clinical studies and experience suggests that use in the geriatric population is associated with differences in safety or effectiveness (see WARNINGS AND PRECAUTIONS, Geriatrics). Caution should be exercised in elderly patients, particularly those with known decreased renal function.
Elderly patients should be monitored closely for adverse events such as sedation and confusion.
Pediatrics (2 months - 2 years of age):
Sabril has been studied in pediatric patients with Infantile Spasms (aged 2 months – 2 years; see CLINICAL TRIALS). In clinical trials, infection-related events were reported at higher frequencies when compared to adult studies (see ADVERSE REACTIONS).
In a retrospective epidemiologic study, abnormal MRI signal changes were observed in some infants receiving vigabatrin. The specific pattern of signal changes was not observed in older children and adult patients (see WARNINGS AND PRECAUTIONS, Magnetic Resonance Imaging (MRI) Abnormalities).
CONTRAINDICATIONS Patients who are hypersensitive to this drug or to any ingredient in the formulation or component of the container. For a complete listing, see DOSAGE FORMS, COMPOSITION AND PACKAGING. Sabril is contraindicated in pregnancy and lactation.
Vigabatrin Product Monograph Page 5 of 44 WARNINGS AND PRECAUTIONS General Information for Patients: Patients receiving Sabril should be given the following instructions by the physician: 1. Patients should be warned that Sabril treatment can damage the vision.
Sabril can result in a loss of peripheral vision (narrowing of the field of vision) which may lead to permanent impairment of eyesight. About 1/3 of patients who take Sabril are affected. 2. Symptoms of vision loss from Sabril are unlikely to be recognized by patients or caregivers before vision loss is severe.
Patients should have their eyes examined before Serious Warnings and Precautions:
VISION LOSS A number of ophthalmological abnormalities, including visual field defects, rare cases of bilateral optic disc pallor, subtle peripheral retinal atrophy, optic atrophy, and rare cases of optic neuritis have been reported in patients receiving […]
Side effects & warnings
CAOfficial regulatory label· Warnings and precautions· revised January 28, 2026[3]
General Information for Patients:
Patients receiving Sabril should be given the following instructions by the physician: 1. Patients should be warned that Sabril treatment can damage the vision. Sabril can result in a loss of peripheral vision (narrowing of the field of vision) which may lead to permanent impairment of eyesight.
About 1/3 of patients who take Sabril are affected. 2. Symptoms of vision loss from Sabril are unlikely to be recognized by patients or caregivers before vision loss is severe.
Patients should have their eyes examined before Serious Warnings and Precautions:
VISION LOSS A number of ophthalmological abnormalities, including visual field defects, rare cases of bilateral optic disc pallor, subtle peripheral retinal atrophy, optic atrophy, and rare cases of optic neuritis have been reported in patients receiving Sabril (see WARNINGS AND PRECAUTIONS, Ophthalmologic).
Visual field defects have been reported in about 1/3 of patients receiving Sabril, although the actual prevalence may be higher. Based on available data, the usual pattern is a concentric constriction of the visual field of both eyes, which is generally more marked nasally than temporally.
In the central visual field (within 30 degrees of eccentricity), a nasal annular defect is frequently seen. To detect visual field defects, appropriate visual field testing (perimetry) by a standardized static perimetry (such as Humphrey or Octopus) or kinetic perimetry (such as Goldmann) must be performed before treatment initiation and at three month intervals.
Available data suggests that visual field defects may be permanent even after discontinuation of vigabatrin treatment. It is possible that vision loss can worsen despite discontinuation of Sabril therapy. Symptoms of vision loss from Sabril are unlikely to be recognized by patients or caregivers before vision loss is severe.
In patients who have any pre-existing visual field defects, either detected on perimetry or through clinical symptoms, vigabatrin use should be considered only if the benefits outweigh the risks. If visual field defects are exhibited in any patients using Sabril, consideration should be given to the gradual discontinuation of Sabril.
Sabril should only be used when the potential benefits outweigh the risk for developing a visual field defect. If clinically meaningful seizure improvement is not observed within 3 months of therapy initiation in adults, and 4 weeks in infants, Sabril therapy should be discontinued.
Sabril should not be used concomitantly with other retinotoxic drugs. Vigabatrin Product Monograph Page 6 of 44 beginning Sabril treatment and at regular intervals (approximately every 3 months) thereafter. 3. Patients should be advised to tell their doctor immediately of any change in their eyesight such as narrowing of the field of vision, blurred vision or any other visual symptoms, if they start to trip, bump into things, or are more clumsy than usual; are surprised by people or things coming in front of them that seem to come out of nowhere.
4. Women of childbearing potential should be advised to inform their doctor if they are pregnant or intend to become pregnant while on Sabril therapy. Sabril is contraindicated in pregnancy and lactation. 5. Mothers should discuss with their doctor whether to take Sabril or breastfeed their baby, they should not do both.
6. Patients should be advised not to drive a car or operate other complex machinery, and refrain from other activities requiring mental alertness or physical coordination until they are familiar with the effects of Sabril on their ability to perform such activities.
Withdrawal of Antiepileptic Drugs (AEDs):
As with other antiepileptic drugs, abrupt discontinuation may lead to rebound seizures. If a patient is to be withdrawn from Sabril treatment, it is recommended that this be done gradually by reducing dose over a 2-4 week period if possible.
In controlled clinical studies in adults with complex partial seizures (CPS) and pediatric patients with IS, Sabril was discontinued by gradual reduction of the daily dose of 1 g/day once a week in adults, and of 25-50 mg/kg/day every 3-4 days in infants.
Somnolence and Fatigue:
Sabril causes somnolence and fatigue. Patients should be advised not to drive a car or operate other complex machinery, and refrain from other activities requiring mental alertness or physical coordination until they are familiar with the effects of Sabril on their ability to perform such activities.
Pooled data from two Sabril controlled trials demonstrated that 24% (54/222) of Sabril patients experienced somnolence compared to 10% (14/135) of placebo patients. In those same studies, 28% of Sabril patients experienced fatigue compared to 15% (20/135) of placebo patients.
Almost 1% of Sabril patients discontinued from clinical trials for somnolence and almost 1% discontinued for fatigue.
Edema:
Sabril causes edema. Pooled data from controlled trials demonstrated increased risk among Sabril patients compared to placebo patients for peripheral edema (Sabril 2%, placebo 1%), and edema (Sabril 1%, placebo 0%). In these studies, one Sabril and no placebo patients discontinued for an edema related AE.
There was no apparent association between edema and cardiovascular adverse events such as hypertension or congestive heart failure. Dependence/Tolerance The abuse and dependence potential of Sabril has not been evaluated in human studies.
It is not possible to predict the extent to which a CNS active drug will be misused, diverted, and/or abused once marketed. , incrementation of dose, drug-seeking behaviour). Sabril did not produce adverse Vigabatrin Product Monograph Page 7 of 44 events or overt behaviours associated with abuse when administered to humans or animals.
[…]
This is not medical advice. Consult a qualified healthcare professional.
EUOfficial regulatory label· revised February 19, 2026[4]
Vigabatrin treatment may only be initiated by a specialist in epileptology, neurology or paediatric neurology. Follow-up should be arranged under supervision of a specialist in epileptology, neurology or paediatric neurology. Posology Monotherapy for infantile spasms (West’s Syndrome) The recommended starting dose is 50 mg/kg/day.
Subsequent dosing can be titrated by 25 mg/kg/day increments every 3 days up to the maximum recommended dose of 150 mg/kg/day. Doses of vigabatrin should be given twice daily according to the table below. 5 x 500 mg tablet evening 16 4 x 100 mg tablet morning 4 x 100 mg tablet evening 1 x 500 mg and 1 x 100 mg tablet morning 1 x 500 mg and 1 x 100 mg tablet evening 1 x 500 mg and 3 x 100 mg tablet morning 1 x 500 mg and 3 x 100 mg tablet evening Resistant partial epilepsy (focal onset seizures) The recommended starting dose is 40 mg/kg/day.
5 g/day Doses of vigabatrin should be given twice daily according to the table below. 5 x 100 mg tablet evening 25 1 x 500 mg tablet morning 1 x 500 mg tablet evening 28 1 x 500 mg tablet morning 1 x 500 mg and 1 x 100 mg tablet evening 30 1 x 500 mg and 1 x 100 mg tablet morning 1 x 500 mg and 1 x 100 mg tablet evening Kigabeq is for oral or gastric administration twice daily and may be taken before or after meals.
The maximum recommended dose should not be exceeded. If control of epilepsy is not clinically significantly improved after an adequate treatment course, vigabatrin treatment should be discontinued. Vigabatrin should be gradually withdrawn under close medical supervision.
Special populations Renal impairment Since vigabatrin is eliminated via the kidneys, caution should be exercised when administering the medicinal product to patients with creatinine clearance less than 60 ml/min. Adjustment of dose should be considered.
Such patients may respond to a lower maintenance dose. 8). Hepatic impairment 5 Vigabatrin is not metabolised by hepatic enzymes, hence there is no need of adjustment of dose or frequency of administration. 4). Paediatric population There is no relevant use of Kigabeq in neonates (below 27 days of age) in the indication “infantile spasms” and in children and adolescents above 7 years of age in the indication “resistant partial epilepsy” (focal onset seizures).
Other […]
This is not medical advice. Consult a qualified healthcare professional.
Side effects & warnings
EUOfficial regulatory label· Adverse reactions· revised February 19, 2026[4]
8. The onset is usually after months to years of vigabatrin therapy. The degree of visual field constriction may be severe and this may have practical consequences for the patient. Vigabatrin can cause permanent vision loss. Most of the patients with perimetry-confirmed defects have been asymptomatic.
Hence, this undesirable effect can only be reliably detected by systematic perimetry which is usually possible only in patients with a developmental age of more than 9 years. For younger patients electroretinography should be used (see visual field defects).
Available data suggests that visual field defects are irreversible even after discontinuation of vigabatrin. A deterioration of VFD after the treatment is discontinued cannot be excluded. 6 Therefore, vigabatrin should only be used after careful benefit/ risk assessment compared with alternatives.
Vigabatrin is not recommended for use in patients with any pre-existing clinically significant visual field defect. Patients should undergo systematic screening examination when starting vigabatrin and at regular intervals for detection of visual field defects.
Visual field testing should continue at 6-month intervals for the whole duration of treatment. The assessment must be continued 6 to 12 months after the discontinuation of therapy (see visual field defects). Visual field defects (VFD) Based on available data, the usual pattern is a concentric constriction of the visual field of both eyes, which is generally more marked nasally than temporally.
In the central visual field (within 30 degree of eccentricity), frequently an annular nasal defect is seen. However, the VFDs reported in patients receiving vigabatrin have ranged from mild to severe. Severe cases are potentially disabling and may be characterized by tunnel vision.
Blindness was also reported in severe cases. Most patients with perimetry-confirmed defects had not previously spontaneously noticed any symptoms, even in cases where a severe defect was observed in perimetry. Available evidence suggests that the VFD is irreversible even after discontinuation of vigabatrin.
A deterioration of VFD after the treatment is discontinued cannot be excluded. Pooled data from prevalence surveys suggest that as many as 1/3 of patients receiving vigabatrin therapy have VFDs. Males may be at greater risk than females.
8. A possible association between the risk of visual field defects and the extent of vigabatrin exposure, both in terms of daily dose (from 1 gram to more than 3 grams) and in terms of duration of treatment (maximum during the first three years) has been shown in this study.
All patients should have ophthalmological consultation before or shortly after the initiation of vigabatrin treatment. Perimetry is seldom possible in children less than 9 years of developmental age. The risks of treatment must be very carefully weighed against possible benefit in children.
Currently, there is no established method to diagnose or exclude visual field defects in children in whom a standardised perimetry cannot be performed. Frequency and severity have only been indirectly characterised in this population on the presence of electroretinogram or visual evoked potential anomalies.
Electroretinography is recommended in infants and children who are unable to cooperate with perimetry. Based on the available data the first oscillatory potential and 30 Hz flicker responses of the electroretinogram appear to be correlated with a vigabatrin associated VFD.
These responses are delayed and reduced beyond the normal limits. Such changes have not been seen in vigabatrin treated patients without a VFD. The parents and/or caregivers must be given a thorough description of the frequency and Implications of the development of VFD during vigabatrin treatment.
VFD may not be detected until it is severe and undetected moderate defects may affect child integrity. Therefore, vision assessment is required at baseline (no later than 4 weeks after starting treatment) and at least every 6 months while on therapy.
The assessment must be continued 6 to 12 months after the discontinuation of therapy. Available data suggests that visual field defects are irreversible. If a visual field constriction is observed during follow-up, consideration should be given to gradual discontinuation of vigabatrin.
If the decision to continue treatment is made, consideration should be 7 given to more frequent follow-up (perimetry) in order to detect progression or sight threatening defects. Vigabatrin should not be used concomitantly with other retinotoxic medicinal products.
3) it is recommended that patients treated with vigabatrin are closely observed for adverse reactions on neurological function. Rare reports of encephalopathic symptoms such as marked sedation, stupor and confusion in association with non-specific slow wave activity on electroencephalogram have been described soon after the initiation of vigabatrin treatment.
Risk factors for the development of these reactions include higher than recommended starting dose, faster dose escalation at higher steps than recommended and renal failure. 8). Abnormal magnetic resonance imaging signals Abnormal magnetic resonance imaging (MRI) signal changes characterised by increased T2 signal and restricted diffusion in a symmetric pattern involving the thalamus, basal ganglia, brain stem, and cerebellum have been observed in some infants treated with vigabatrin for infantile spasms.
In a retrospective epidemiologic study in infants with infantile spasms (N = 205), the prevalence of these changes was 22 % in vigabatrin treated patients versus 4 % in patients treated with other therapies. In the study above, in […]
EUOfficial regulatory label· Warnings and precautions· revised February 19, 2026[4]
Visual field defects (VFD) have been reported in patients receiving vigabatrin with a high prevalence (about 1/3 of patients). 8. The onset is usually after months to years of vigabatrin therapy. The degree of visual field constriction may be severe and this may have practical consequences for the patient.
Vigabatrin can cause permanent vision loss. Most of the patients with perimetry-confirmed defects have been asymptomatic. Hence, this undesirable effect can only be reliably detected by systematic perimetry which is usually possible only in patients with a developmental age of more than 9 years.
For younger patients electroretinography should be used (see visual field defects). Available data suggests that visual field defects are irreversible even after discontinuation of vigabatrin. A deterioration of VFD after the treatment is discontinued cannot be excluded.
6 Therefore, vigabatrin should only be used after careful benefit/ risk assessment compared with alternatives. Vigabatrin is not recommended for use in patients with any pre-existing clinically significant visual field defect. Patients should undergo systematic screening examination when starting vigabatrin and at regular intervals for detection of visual field defects.
Visual field testing should continue at 6-month intervals for the whole duration of treatment. The assessment must be continued 6 to 12 months after the discontinuation of therapy (see visual field defects). Visual field defects (VFD) Based on available data, the usual pattern is a concentric constriction of the visual field of both eyes, which is generally more marked nasally than temporally.
In the central visual field (within 30 degree of eccentricity), frequently an annular nasal defect is seen. However, the VFDs reported in patients receiving vigabatrin have ranged from mild to severe. Severe cases are potentially disabling and may be characterized by tunnel vision.
Blindness was also reported in severe cases. Most patients with perimetry-confirmed defects had not previously spontaneously noticed any symptoms, even in cases where a severe defect was observed in perimetry. Available evidence suggests that the VFD is irreversible even after discontinuation of vigabatrin.
This is not medical advice. Consult a qualified healthcare professional.
Who should not take it
EUOfficial regulatory label· Contraindications· revised February 19, 2026[4]
1.
This is not medical advice. Consult a qualified healthcare professional.
Blindness was also reported in severe cases. Most patients with perimetry-confirmed defects had not previously spontaneously noticed any symptoms, even in cases where a severe defect was observed in perimetry. Available evidence suggests that the VFD is irreversible even after discontinuation of vigabatrin.
A deterioration of VFD after the treatment is discontinued cannot be excluded. Pooled data from prevalence surveys suggest that as many as 1/3 of patients receiving vigabatrin therapy have VFDs. Males may be at greater risk than females.
1. A possible association between the risk of visual field defects and the extent of vigabatrin exposure, both in terms of daily dose (from 1 gram to more than 3 grams) and in terms of duration of treatment (maximum during the first three years) has been shown in this study.
All patients should have ophthalmological consultation with visual field examination before the initiation of vigabatrin treatment. Monitoring of vision by an ophthalmic professional with expertise in visual field interpretation and the ability to perform dilated indirect ophthalmoscopy of the retina is recommended.
Because vision testing in infants is difficult, vision loss may not be detected until it is severe. For patients receiving vigabatrin, visual field and/or retinal assessment is recommended at baseline (no later than 4 weeks after starting vigabatrin), every 3 to 6 months while on therapy, and about 3-6 months after the discontinuation of therapy.
The diagnostic approach should be individualized for the patient and clinical situation. In adults and cooperative pediatric patients, perimetry is recommended, preferably by automated threshold visual field testing. , optical coherence tomography [OCT]), and/or other methods appropriate for the patient.
In patients who cannot be tested, treatment may continue according to clinical judgment, with appropriate patient counseling. Because of variability, results from ophthalmic monitoring must be interpreted with caution, and repeat assessment is recommended if results are abnormal or uninterpretable.
Repeat assessment in the first few weeks of treatment is recommended to establish if, and to what degree, reproducible results can be obtained, and to guide selection of appropriate ongoing monitoring for the patient. The patient and/or caregiver must be given a thorough description of the frequency and implications of the development of VFD during vigabatrin treatment.
Patients should be instructed to report any new visual problems and symptoms which may be associated with visual field constriction. If visual symptoms develop, the patient should be referred to an ophthalmologist. If a visual field constriction is observed during follow-up, consideration should be given to gradual discontinuation of vigabatrin.
If the decision to continue treatment is made, consideration should be given to more frequent follow-up (perimetry) in order to detect progression or sight threatening defects. Vigabatrin should not be used concomitantly with other retinotoxic drugs.
Visual acuity The prevalence of reduced visual acuity in vigabatrin treated patients is unknown. 8). Visual acuity should be assessed during ophthalmological consultations, before initiation of vigabatrin treatment and […]
2) ]. Because vision testing in infants is difficult, vision loss may not be detected until it is severe. For patients receiving VIGADRONE, vision assessment is recommended at baseline (no later than 4 weeks after starting VIGADRONE), at least every 3 months while on therapy, and about 3 to 6 months after the discontinuation of therapy.
The diagnostic approach should be individualized for the patient and clinical situation. In adults and cooperative pediatric patients, perimetry is recommended, preferably by automated threshold visual field testing. , optical coherence tomography [OCT]), and/or other methods appropriate for the patient.
In patients who cannot be tested, treatment may continue according to clinical judgment, with appropriate patient counseling. Because of variability, results from ophthalmic monitoring must be interpreted with caution, and repeat assessment is recommended if results are abnormal or uninterpretable.
Repeat assessment in the first few weeks of treatment is recommended to establish if, and to what degree, reproducible results can be obtained, and to guide selection of appropriate ongoing monitoring for the patient. The onset and progression of vision loss from VIGADRONE is unpredictable, and it may occur or worsen precipitously between assessments.
Once detected, vision loss due to VIGADRONE is not reversible. It is expected that even with frequent monitoring, some VIGADRONE patients will develop severe vision loss. Consider drug discontinuation, balancing benefit and risk, if vision loss is documented.
It is possible that vision loss can worsen despite discontinuation of VIGADRONE. 2 Vigabatrin REMS Program VIGADRONE is available only through a restricted distribution program called the Vigabatrin REMS Program, because of the risk of permanent vision loss.
com Patients must enroll in the program. Pharmacies must be certified and must only dispense to patients authorized to receive VIGADRONE. com or call 1-866-244-8175. 3 Magnetic Resonance Imaging (MRI) Abnormalities in Infants Abnormal MRI signal changes characterized by increased T2 signal and restricted diffusion in a symmetric pattern involving the thalamus, basal ganglia, brain stem, and cerebellum have been observed in some infants treated with vigabatrin.
In a retrospective epidemiologic study in infants with infantile spasms (N=205), the prevalence of MRI changes was 22% in vigabatrin-treated patients versus 4% in patients treated with other therapies. In this study, in post marketing experience, and in published literature reports, these changes generally resolved with discontinuation of treatment.
In a few patients, the lesion resolved despite continued use. It has been reported that some infants exhibited coincident motor abnormalities, but no causal relationship has been established and the potential for long-term clinical sequelae has not been adequately studied.
Neurotoxicity (brain histopathology and neurobehavioral abnormalities) was observed in rats exposed to vigabatrin during late gestation and the neonatal and juvenile periods of development, and brain histopathological changes were observed in dogs exposed to vigabatrin during the juvenile period of development.
1) ]. The specific pattern of signal changes observed in patients 6 years and younger was not observed in older pediatric and adult patients treated with vigabatrin. In a blinded review of MRI images obtained in prospective clinical trials in patients with refractory complex partial seizures (CPS) 3 years and older (N=656), no difference was observed in anatomic distribution or prevalence of MRI signal changes between vigabatrin treated and placebo treated patients.
In the post-marketing setting, MRI changes have also been reported in patients 6 years of age and younger being treated for refractory CPS. For adults treated with VIGADRONE, routine MRI surveillance is unnecessary as there is no evidence that vigabatrin causes MRI changes in this population.
4 Neurotoxicity Intramyelinic Edema (IME) has been reported in postmortem examination of infants being treated for infantile spasms (IS) with vigabatrin. Abnormal MRI signal changes characterized by increased T2 signal and restricted diffusion in a symmetric pattern involving the thalamus, basal ganglia, brain stem, and cerebellum have also been observed in some infants treated for IS with vigabatrin.
3) ]. Vacuolation, characterized by fluid accumulation and separation of the outer layers of myelin, has been observed in brain white matter tracts in adult and juvenile rats and adult mice, dogs, and possibly monkeys following administration of vigabatrin.
This lesion, referred to as intramyelinic edema (IME), was seen in animals at doses within the human therapeutic range. A no-effect dose was not established in rodents or dogs. In the rat and dog, vacuolation was reversible following discontinuation of vigabatrin treatment, but, in the rat, pathologic changes consisting of swollen or degenerating axons, mineralization, and gliosis were seen in brain areas in which vacuolation had been previously observed.
Vacuolation in adult animals was correlated with alterations in MRI and changes in visual and somatosensory EP. Administration of vigabatrin to rats during the neonatal and juvenile periods of development produced vacuolar changes in the brain gray matter (including the thalamus, midbrain, deep cerebellar nuclei, substantia nigra, hippocampus, and forebrain) which are considered distinct from the IME observed in vigabatrin-treated adult animals.
Decreased myelination and evidence of oligodendrocyte injury were additional findings in the brains of vigabatrin-treated rats. An increase in apoptosis was seen in some brain regions following vigabatrin exposure during the early postnatal period.
Long-term neurobehavioral abnormalities (convulsions, neuromotor impairment, learning deficits) were also observed following vigabatrin treatment of young rats. Administration of vigabatrin to juvenile dogs produced vacuolar changes in the brain gray matter (including the septal nuclei, hippocampus, hypothalamus, thalamus, cerebellum, and globus pallidus).
Neurobehavioral effects of vigabatrin were not assessed in the juvenile dog. 4) ]. In a published study, vigabatrin (200, 400 mg/kg/day) induced apoptotic neurodegeneration in the brain of young rats when administered by intraperitoneal injection on postnatal days 5 to 7.
Administration of vigabatrin to female rats during pregnancy and lactation at doses below those used clinically resulted in hippocampal vacuolation and convulsions in the mature offspring. 5 Suicidal Behavior and Ideation Antiepileptic drugs (AEDs), including VIGADRONE, increase the risk of suicidal thoughts or behavior in patients taking these drugs for any indication.
Patients treated with any AED for any indication should be monitored for the emergence or worsening of depression, suicidal thoughts or behavior, and/or any unusual changes in mood or behavior. 7) of suicidal thinking or behavior compared to patients randomized to placebo.
24% among 16,029 placebo treated patients, representing an increase of approximately one case of suicidal thinking or behavior for every 530 patients treated. There were four suicides in drug treated patients in the trials and none in placebo treated patients, but the number is too small to allow any conclusion about drug effect on suicide.
The increased risk of suicidal thoughts or behavior with AEDs was observed as early as one week after starting drug treatment with AEDs and persisted for the duration of treatment assessed. Because most trials included in the analysis did not extend beyond 24 weeks, the risk of suicidal thoughts or behavior beyond 24 weeks could not be assessed.
The risk of suicidal thoughts or behavior was generally consistent among drugs in the data analyzed. The finding of increased risk with AEDs of varying mechanisms of action and across a range of indications suggests that the risk applies to all AEDs used for any indication.
The risk did not vary substantially by age (5 to 100 years) in the clinical trials analyzed. Table 4 shows absolute and relative risk by indication for all evaluated AEDs. Table 4. 9 The relative risk for suicidal thoughts or behavior was higher in clinical trials for epilepsy than in clinical trials for psychiatric or other conditions, but the absolute risk differences were similar for the epilepsy and psychiatric indications.
Anyone considering prescribing VIGADRONE, or any other AED must balance the risk of suicidal thoughts or behavior with the risk of untreated illness. Epilepsy and many other illnesses for which AEDs are prescribed are themselves associated with morbidity and mortality and an increased risk of suicidal thoughts and behavior.
Should suicidal thoughts and behavior emerge during treatment, the prescriber needs to consider whether the emergence of these symptoms in any given patient may be related to the illness being treated. Patients, their caregivers, and families should be informed that AEDs increase the risk of suicidal thoughts and behavior and should be advised of the need to be alert for the emergence or worsening of the signs and symptoms of depression, any unusual changes in mood or behavior, or the emergence of suicidal thoughts, behavior, or thoughts about self-harm.
Behaviors of concern should be reported immediately to healthcare providers. 6 Withdrawal of Antiepileptic Drugs (AEDs) As with all AEDs, VIGADRONE should be withdrawn gradually. However, if withdrawal is needed because of a serious adverse event, rapid discontinuation can be considered.
Patients and caregivers should be told not to suddenly discontinue VIGADRONE therapy. In controlled clinical studies in adults with complex partial seizures, vigabatrin was tapered by decreasing the daily dose 1,000 mg/day on a weekly basis until discontinued.
In a controlled study in pediatric patients with complex partial seizures, vigabatrin was tapered by decreasing the daily dose by one third every week for three weeks. In a controlled clinical study in patients with infantile spasms, vigabatrin was tapered by decreasing the daily dose at a rate of 25 to 50 mg/kg every 3 to 4 days .
7 Anemia In North American controlled trials in adults, 6% of patients (16/280) receiving vigabatrin and 2% of patients (3/188) receiving placebo had adverse events of anemia and/or met criteria for potentially clinically important hematology changes involving hemoglobin, hematocrit, and/or RBC indices.
S. controlled trials, there were mean decreases in hemoglobin of about 3% and 0% in vigabatrin and placebo treated patients, respectively, and a mean decrease in hematocrit of about 1% in vigabatrin treated patients compared to a mean gain of about 1% in patients treated with placebo.
06%, 3/4,855) discontinued for anemia and 2 vigabatrin patients experienced unexplained declines in hemoglobin to below 8 g/dL and/or hematocrit below 24%. 8 Somnolence and Fatigue VIGADRONE causes somnolence and fatigue. Patients should be advised not to drive a car or operate other complex machinery until they are familiar with the effects of VIGADRONE on their ability to perform such activities.
Pooled data from two vigabatrin controlled trials in adults demonstrated that 24% (54/222) of vigabatrin patients experienced somnolence compared to 10% (14/135) of placebo patients. In those same studies, 28% of vigabatrin patients experienced fatigue compared to 15% (20/135) of placebo patients.
Almost 1% of vigabatrin patients discontinued from clinical trials for somnolence and almost 1% discontinued for fatigue. Pooled data from three vigabatrin controlled trials in pediatric patients demonstrated that 6% (10/165) of vigabatrin patients experienced somnolence compared to 5% (5/104) of placebo patients.
In those same studies, 10% (17/165) of vigabatrin patients experienced fatigue compared to 7% (7/104) of placebo patients. No vigabatrin patients discontinued from clinical trials due to somnolence or fatigue. 9 Peripheral Neuropathy Vigabatrin causes symptoms of peripheral neuropathy in adults.
Pediatric clinical trials were not designed to assess symptoms of peripheral neuropathy but observed incidence of symptoms based on pooled data from controlled pediatric studies appeared similar for pediatric patients on vigabatrin and placebo.
2% (19/457) of vigabatrin patients developed signs and/or symptoms of peripheral neuropathy. 4% (4/280) of vigabatrin treated patients and no (0/188) placebo patients developed signs and/or symptoms of peripheral neuropathy. Initial manifestations of peripheral neuropathy in these trials included, in some combination, symptoms of numbness or tingling in the toes or feet, signs of reduced distal lower limb vibration or position sensation, or progressive loss of reflexes, starting at the ankles.
Clinical studies in the development program were not designed to investigate peripheral neuropathy systematically and did not include nerve conduction studies, quantitative sensory testing, or skin or nerve biopsy. There is insufficient evidence to determine if development of these signs and symptoms was related to duration of vigabatrin treatment, cumulative dose, or if the findings of peripheral neuropathy were completely reversible upon discontinuation of vigabatrin.
10 Weight Gain VIGADRONE causes weight gain in adult and pediatric patients. Data pooled from randomized controlled trials in adults found that 17% (77/443) of vigabatrin patients versus 8% (22/275) of placebo patients gained ≥7% of baseline body weight.
6 kg for placebo patients. Data pooled from randomized controlled trials in pediatric patients with refractory complex partial seizures found that 47% (77/163) of vigabatrin patients versus 19% (19/102) of placebo patients gained ≥7% of baseline body weight.
6% (31/4,855) of vigabatrin patients discontinued for weight gain. The long-term effects of vigabatrin related weight gain are not known. Weight gain was not related to the occurrence of edema. 11 Edema VIGADRONE causes edema in adults.
Pediatric clinical trials were not designed to assess edema but observed incidence of edema based pooled data from controlled pediatric studies appeared similar for pediatric patients on vigabatrin and placebo. Pooled data from controlled trials demonstrated increased risk among vigabatrin patients compared to placebo patients for peripheral edema (vigabatrin 2%, placebo 1%), and edema (vigabatrin 1%, placebo 0%).
In these studies, one vigabatrin and no placebo patients discontinued for an edema related AE. In adults, there was no apparent association between edema and cardiovascular adverse events such as hypertension or congestive heart failure.
Edema was not associated with laboratory changes suggestive of deterioration in renal or hepatic function.
A deterioration of VFD after the treatment is discontinued cannot be excluded. Pooled data from prevalence surveys suggest that as many as 1/3 of patients receiving vigabatrin therapy have VFDs. Males may be at greater risk than females.
8. A possible association between the risk of visual field defects and the extent of vigabatrin exposure, both in terms of daily dose (from 1 gram to more than 3 grams) and in terms of duration of treatment (maximum during the first three years) has been shown in this study.
All patients should have ophthalmological consultation before or shortly after the initiation of vigabatrin treatment. Perimetry is seldom possible in children less than 9 years of developmental age. The risks of treatment must be very carefully weighed against possible benefit in children.
Currently, there is no established method to diagnose or exclude visual field defects in children in whom a standardised perimetry cannot be performed. Frequency and severity have only been indirectly characterised in this population on the presence of electroretinogram or visual evoked potential anomalies.
Electroretinography is recommended in infants and children who are unable to cooperate with perimetry. Based on the available data the first oscillatory potential and 30 Hz flicker responses of the electroretinogram appear to be correlated with a vigabatrin associated VFD.
These responses are delayed and reduced beyond the normal limits. Such changes have not been seen in vigabatrin treated patients without a VFD. The parents and/or caregivers must be given a thorough description of the frequency and Implications of the development of VFD during vigabatrin treatment.
VFD may not be detected until it is severe and undetected moderate defects may affect child integrity. Therefore, vision assessment is required at baseline (no later than 4 weeks after starting treatment) and at least every 6 months while on therapy.
The assessment must be continued 6 to 12 months after the discontinuation of therapy. Available data suggests that visual field defects are irreversible. If a visual field constriction is observed during follow-up, consideration should be given to gradual discontinuation of vigabatrin.
If the decision to continue treatment is made, consideration should be 7 given to more frequent follow-up (perimetry) in order to detect progression or sight threatening defects. Vigabatrin should not be used concomitantly with other retinotoxic medicinal products.
3) it is recommended that patients treated with vigabatrin are closely observed for adverse reactions on neurological function. Rare reports of encephalopathic symptoms such as marked sedation, stupor and confusion in association with non-specific slow wave activity on electroencephalogram have been described soon after the initiation of vigabatrin treatment.
Risk factors for the development of these reactions include higher than recommended starting dose, faster dose escalation at higher steps than recommended and renal failure. 8). Abnormal magnetic resonance imaging signals Abnormal magnetic resonance imaging (MRI) signal changes characterised by increased T2 signal and restricted diffusion in a symmetric pattern involving the thalamus, basal ganglia, brain stem, and cerebellum have been observed in some infants treated with vigabatrin for infantile spasms.