Miller 2001.

Methods	Randomised, placebo‐controlled, double‐blind trial (2 × 2 block design)
Participants	84 participants who fulfilled international classification criteria for SMA types II or III and have an homozygous deletion of the SMN1 gene Inclusion criteria: clinical diagnosis of SMA, type II or III aged ≥ 21 years homozygous defect in the SMN gene FVC > 35% of predicted the ability to sit unsupported at some time in the disease course elbow flexion or handgrip strength (or both) > 3 kg Exclusion criteria: not mentioned
Interventions	Gabapentin 1200 mg 3 times a day or placebo Duration of treatment: 12 months Follow‐up: at quarterly time intervals while on treatment
Outcomes	Change in disability score (SMAFRS), change in muscle strength, development of walking, change in pulmonary function (FVC), change in quality of life (SIP), adverse events
Funding	Andrew's Buddies, MDA, Warner‐Lambert, and Families of SMA
Conflicts of interest	Not stated
Notes	Muscle strength of elbow flexion and hand grip was measured bilaterally.
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	Randomly assigned. Randomisation in blocks of 4 participants (2 placebo, 2 gabapentin) with equalised randomisation per centre. No methods of randomisation described.
Allocation concealment (selection bias)	Unclear risk	Randomisation performed by research pharmacist. Precise method of allocation concealment not known.
Blinding of participants and personnel (performance bias) All outcomes	Low risk	Only research pharmacist was not blinded.
Blinding of outcome assessment (detection bias) All outcomes	Low risk	Only research pharmacist was not blinded.
Incomplete outcome data (attrition bias) All outcomes	High risk	Reasons for dropout of 19 participants not mentioned. ITT analysis performed with a different number of participants than initially included.
Selective reporting (reporting bias)	Unclear risk	Adverse events not reported.
Other bias	Low risk	None identified