The three-month stroke clinic visit has a familiar script. The weakness has plateaued or even improved. But the wife mentions, almost in passing, that washing his palm has become a two-person job — the fingers curl closed and fight back. Or the patient's arm now rides flexed against the chest, and the elbow crease is macerated. Or walking has gotten slower even as strength returned, because the ankle now points down and in, and every step vaults over a stiff leg.

None of this was present in week one, and that is the first thing to understand about spasticity: it is a complication that develops during recovery, as the nervous system rewires around the injury. The flaccid limb of the acute stroke becomes, over weeks to months, the hypertonic limb of the chronic one. In population terms, spasticity emerges in roughly a quarter to a third of stroke survivors, with disabling spasticity in a smaller but meaningful minority; severe early paresis is its strongest predictor.12

What spasticity is — and what it is not

Spasticity is velocity-dependent resistance to passive stretch: move the limb slowly and it yields, move it fast and it catches. It is one piece of the upper motor neuron syndrome, traveling with hyperreflexia, clonus, and co-contraction, and it reflects the loss of descending inhibitory control over spinal stretch reflexes after corticospinal-system injury.

Two look-alikes matter at the bedside. Rigidity (as in parkinsonism) resists at every speed and direction. Contracture is not a neural phenomenon at all — it is shortened muscle and remodeled connective tissue, and it does not yield at any speed, to any drug. The distinction is not academic: spasticity is treatable and contracture is largely preventable-but-not-reversible, and the weeks in between are the window this entire article is about.

Grade what you find with the Modified Ashworth Scale — the imperfect but universal 0-to-4 tone vocabulary of rehabilitation notes3 — but document alongside it the thing the scale cannot capture: what the tone is costing this patient. "MAS 3 at the elbow flexors" matters less than "cannot extend the elbow enough to dress; palm hygiene failing."

The first decision: is this tone a problem at all?

Spasticity earns treatment when it causes something: pain, skin breakdown or hygiene failure (the clenched palm, the adducted axilla), positioning and caregiving difficulty, sleep disruption from spasms, orthosis intolerance, or lost function — the stiff leg that trips, the flexed arm that blocks dressing. But extensor tone in a weak leg can be the only reason a patient stands during transfers. Abolish that tone and you have traded stiffness for a fall.

The target is never a softer muscle. It is a cleaner palm, a wearable splint, a faster walk, a night without spasms.

Set the goal with the patient and the therapist before choosing the weapon — and revisit the goal, because a treatment that hit its stated target and helped nothing else should be stopped, not renewed by habit.

The treatment ladder

Rung 1 — Foundation: therapy, stretch, positioning, and the aggravator hunt

Everything else is layered on top of this rung, never instead of it. Daily stretching and range-of-motion, positioning programs, splinting and orthoses where indicated, and task-oriented therapy are the base of every guideline recommendation on the subject.4 This is also where prevention lives — the reason range-of-motion starts on the stroke unit, inside the same early-mobilization philosophy we cover in why early stroke rehab matters.

And before any escalation, hunt aggravators. Spasticity is a barometer of noxious input: a urinary tract infection, constipation, a pressure injury, an ingrown toenail, a tight strap, an occult fracture, pain of any source — each can crank tone in a limb that was manageable last month. A sudden worsening is a reason to examine the patient, not to double the baclofen.

Rung 2 — Focal spasticity: botulinum toxin is the evidence-backed workhorse

Most disabling post-stroke spasticity is focal or segmental — a clenched fist, a flexed elbow, an equinovarus foot — and for focal spasticity, botulinum toxin injection is the best-supported pharmacologic treatment we have: established as effective for reducing tone and improving passive function in adult limb spasticity in the AAN's evidence review.5 Honest framing for patients: the reliable wins are passive — easier cleaning, dressing, splint fit, less pain; gains in active hand function are less predictable and depend on what strength and control survive underneath the tone.

Practicalities worth knowing even if you never inject: effect begins within days, peaks by a few weeks, wears off by around three months (hence cycled reinjection); it must be paired with therapy and stretching during its window; and weakness of injected or neighboring muscles is the main dose-limiting effect.

Rung 3 — Oral agents: useful, sedating, and worth auditing

For diffuse spasticity or spasms, the oral options are baclofen and tizanidine most commonly, with dantrolene and benzodiazepines behind them. All work; all tax the patient. Baclofen and tizanidine sedate (tizanidine adds hypotension — mind the antihypertensive list), benzodiazepines sedate and dull a recovering brain, dantrolene spares cognition but needs liver-function monitoring. In an older stroke population the sedation cost is not a footnote: it is falls, fog, and blunted rehabilitation. Start low, titrate to the goal rather than the scale, and audit honestly — an oral agent that is not measurably helping should be tapered, and abrupt baclofen discontinuation must be avoided (withdrawal can be dangerous). Note what these drugs are not: none of them fixes contracture, and none substitutes for rung 1.

Rung 4 — Severe and refractory: intrathecal baclofen and targeted procedures

For severe, diffuse spasticity — especially in the legs — refractory to the rungs above, intrathecal baclofen delivers the drug where it acts at a fraction of the systemic dose, at the price of a pump, refills, and a specialized team. Phenol or alcohol neurolysis and orthopedic procedures (tendon lengthening for the fixed deformity that got away) round out the far end of the ladder. The realistic role of the stroke clinician is recognizing the candidate and referring before the joint is fixed.

Where this fits in the follow-up visit

Spasticity belongs on the same follow-up checklist as the rest of the quiet complications — mood (screen it: PHQ-9), late seizures, fatigue, and pain, including the burning variety we cover in the central post-stroke pain guide. Ask about the palm, the armpit, the splint, and the night spasms specifically; patients rarely volunteer them. And when documenting function over time, tone is one of the reasons a modified Rankin Scale can stall between visits even as strength improves.

The bottom line

Spasticity is a moving target that hardens into a fixed one. Catch it while it still yields: stretch and position from the start, treat the tone that causes problems and respect the tone that props a patient up, use botulinum toxin for the focal patterns where the evidence is strongest, prescribe oral agents like the sedatives they are, and read any sudden worsening as a symptom of something else until proven otherwise. The palm you can still open in month two is the palm you are fighting to keep open in year two.