Botulinum Toxin versus Oral Antispasmodics for Spasticity in Hereditary Spastic Paraplegia
A single patient with progressive lower-limb spasticity in a specific, gait-driving pattern layered over milder diffuse tone. The disagreement is whether a targeted injection or a systemic drug actually matches what her exam shows.
K.V.'s mother spent her last years explaining away a slow, stiffening gait as ordinary aging — an explanation that stopped making sense three years ago, when genetic testing confirmed that K.V., a 43-year-old part-time accountant, carries the same hereditary spastic paraplegia mutation herself. For K.V. it has been, unlike what she'd braced for, not a sudden loss but a slow tightening, most visible now in the way her legs scissor across each other with each step, forcing her onto a cane for anything beyond short distances. Exam confirms what her gait already shows: marked spasticity concentrated in her hip adductors and calf muscles bilaterally, the specific pattern driving the scissoring, with milder, more diffuse increased tone throughout both legs beyond those focal points. She has never tried a pharmacologic spasticity treatment, relying on physical therapy alone until her functional decline made that insufficient on its own.
The choice in front of the team isn't simply "treat the spasticity" — it's which tool matches her specific distribution without costing her something she can't afford to lose. Botulinum toxin injected directly into her hip adductors and gastrocnemius reliably reduces tone in exactly this kind of focal spasticity, and critically avoids the systemic sedation that limits oral antispasmodics like baclofen and tizanidine. What it has not clearly bought, in the one randomized trial run specifically in hereditary spastic paraplegia — SPASTOX, Diniz de Lima and colleagues, 2021 — is functional improvement: injections into the adductor magnus and triceps surae lowered adductor tone but did not significantly improve gait velocity — a genuine consideration for a part-time accountant whose job depends on staying alert through an afternoon. But her tone isn't confined to those two muscle groups alone; it's milder but present diffusely throughout both legs, territory injections aimed at her worst muscles won't reach.
Targeted injection against a diffuse tone distribution
I'd start with botulinum toxin injections targeted at her hip adductors and gastrocnemius — the specific muscle groups actually driving her scissoring gait. I'll concede the headline evidence up front: SPASTOX, the only randomized trial of botulinum toxin in hereditary spastic paraplegia, reduced adductor tone without producing a significant gain in gait velocity. But its own critics noted it enrolled by diagnosis rather than by whether a patient was actually hindered by adductor or calf spasticity while walking, which is precisely how K.V. was selected — her scissoring is visible and the target muscles are the ones producing it. And it avoids the systemic sedation that would directly interfere with her work. For a patient this borderline-ambulatory, preserving alertness and coordination matters as much as reducing tone itself.
Injections make sense for her most limiting muscles, but her exam shows milder tone diffusely throughout both legs beyond just the adductors and gastrocnemius — territory botulinum toxin, by its mechanism, simply can't reach without injecting far more muscle groups than is practical, repeated every three to four months indefinitely at real, recurring cost.
Treating this as "inject the worst spots and you've addressed her spasticity" undersells how much of her total tone burden sits outside whatever muscles get injected — a diffuse component needs a systemic answer, even if it's a lower dose than would be needed to treat everything with oral therapy alone.
I don't think this needs to be either-or. Botulinum toxin for the adductors and gastrocnemius specifically — the muscles actually producing her scissoring gait and limiting her speed — addresses the functionally worst problem directly and without sedation risk.
Alongside that, a low, carefully titrated dose of baclofen can handle the milder diffuse tone elsewhere, kept low enough that sedation stays manageable for her work. Each therapy does the part it's actually suited for, rather than asking either one to cover the whole distribution alone.
Resolved: combined regimen started, botulinum toxin to her worst muscle groups plus low-dose oral baclofen for diffuse tone, with a follow-up gait assessment scheduled after her first injection cycle.