Weakness with a particular accent
In the previous guide you saw a stroke as a plumbing accident in the brain — a clot or a bleed, ischaemic or haemorrhagic — and met the organised stroke unit that catches it early. Now we follow what that injury does to movement. Because each cerebral hemisphere drives the opposite side of the body, a stroke on one side typically weakens the *other* side: the face, arm, and leg of one half of the body. Weakness of one side is [[hemiparesis-hemiplegia|hemiparesis]]; complete paralysis of one side is hemiplegia. They are not separate diseases — hemiplegia is simply the severe end of the same line.
But this is not the soft, floppy weakness of a cut nerve out in the arm. The stroke sits *above* the spinal cord, so it is an upper-motor-neuron problem — the same family of signs you met when studying tone. Picture a patient, Mr Lin, three weeks after a stroke: his right hand is weak, yes, but his fingers also curl shut, his elbow tends to bend, and a tap on his knee makes the leg jump more than it should. Weakness is only half the story. The injured side speaks with a particular accent — too little useful movement on one side of the ledger, and too much of the wrong kind on the other.
The film of recovery, played in fast-forward
Here is the part that surprises most beginners. The weak side does not simply get stronger in a straight line, the way a muscle does after a few weeks in a cast. It comes back in a recognisable *sequence*, almost as if the nervous system is replaying motor development in fast-forward. A Swedish physiotherapist, Signe Brunnstrom, watched this carefully and named the steps — the [[brunnstrom-stages-of-recovery|Brunnstrom stages]] of motor recovery. Knowing the sequence lets a clinician say roughly *where* a patient is, and what is likely to come next.
Brunnstrom stages of motor recovery (after stroke)
1 Flaccid no movement; the limb is limp, tone is absent
2 Synergy onset spasticity appears; first weak movements arrive only
as the basic synergy (all-or-nothing patterns)
3 Synergy peak synergies are strong & voluntary; spasticity at its worst
4 Out of synergy a few movements break free of the synergy pattern
5 Independence most movement now independent of the synergy
6 Near-normal spasticity gone; isolated, coordinated movement returns
(7 Normal) full recovery (often not reached)
Note: stages may stop at any point; not every patient finishes the film.Notice the strange middle of that list. Movement does not return one clean muscle at a time. It returns first as a [[synergy-patterns|synergy]] — a fixed, all-or-nothing package of muscles that fire together whether you want them to or not. In the arm, the *flexor* synergy yanks the whole limb into a tight bundle: shoulder pulled in, elbow bent, forearm turned palm-down, fingers clenched. In the leg, the *extensor* synergy stiffens it straight, which is awkward but, by luck, useful — a stiff leg is a leg you can stand on. Ask Mr Lin to reach for a cup and the whole arm flexes as one block; he cannot yet pick out elbow alone. The synergy is real, returning movement; it is simply coarse, like a piano with the keys glued in groups.
Recovery, then, is largely the slow *un-gluing* of those keys: moving out of synergy until a hand can do one finger at a time. Be honest about the timeline, though. Most spontaneous recovery happens in the first weeks to a few months, riding the brain's own repair, and then the curve flattens — this is the [[stroke-recovery-natural-history|natural history]] that any therapy is layered on top of. The Brunnstrom stages tell you the *shape* of the journey, not its *speed* or its *destination*, and many people simply stop part-way up the list.
Spasticity: not simply the enemy
You met [[spasticity-defined|spasticity]] in the tone-management rung as a *velocity-dependent* increase in muscle tone: the faster you stretch the muscle, the harder it resists, like a seat-belt that locks when you tug it sharply but lets you lean forward slowly. After stroke it usually emerges as the flaccid stage passes — that is exactly the spasticity that climbs and then peaks in Brunnstrom stages 3 and 4. Left to itself it can hold a joint short, and over months a permanently shortened joint becomes a fixed contracture — a hardware problem that no amount of relaxation will undo.
So far this reads like a villain. Here is the honest twist that this field works hard to teach: not all spasticity should be reduced. Spasticity is one of the *positive* signs of the upper-motor-neuron syndrome — the added behaviours like brisk reflexes and clonus — but it sits on a foundation of the *negative* signs, which are weakness and clumsiness. Sometimes the extensor tone in a leg is the only thing letting a patient stand and walk. Relax that leg with a drug, and you may trade a stiff but functional limb for a soft, useless one. The right question is never "is there spasticity?" but "is this spasticity doing harm, or doing a job?"
The shoulder that quietly falls apart
The flaccid early days carry their own hidden danger, and it lives in the shoulder. The shoulder is the most mobile joint in the body, and it pays for that freedom with almost no bony stability — it is held together mostly by muscles and a thin capsule, rather like a golf ball balanced on a tee. When the muscles around a paralysed shoulder go slack, the dead weight of the dangling arm can drag the head of the bone partly out of its socket. That is [[hemiplegic-shoulder-pain|shoulder subluxation]], and the ache and damage that follow are among the most common — and most *preventable* — problems in stroke rehabilitation.
It is also a place where well-meaning hands cause harm. A common, painful scenario: a helper grabs the weak arm to pull a patient up from bed, and the unguarded shoulder is wrenched. Pain feeds a vicious cycle — the patient guards the arm, moves it less, and the joint stiffens. So the management is mostly *gentle and preventive*: support the arm so it is never left dangling, position it with care, and protect it during every transfer. The order matters too — protect the shoulder first, and address tone or movement once the joint is safe.
Be careful, though, not to pin every sore shoulder on subluxation alone. The hemiplegic shoulder hurts for many reasons that often overlap — a torn rotator cuff, an inflamed and frozen capsule, an impinged tendon, or pain coming straight from the brain itself as central post-stroke pain. And a subluxed shoulder is not always a painful one. Sorting out *why* this particular shoulder hurts is part of the careful detective work the rehab team does, rather than reaching for one tidy label. It also feeds back into the spasticity question: a clenched, painful shoulder can drive tone up, and tone left unchecked can in turn worsen the pain.
Recovery is not the same as getting around
There is one last distinction that quietly governs everything you have just read, and it is the one most worth carrying forward: [[recovery-vs-compensation|recovery is not the same as compensation]]. True recovery is the weak side actually moving more normally again — the synergy un-gluing, isolated finger movement returning. Compensation is reaching the *same goal by a different route*: buttoning a shirt one-handed, or swinging a stiff leg out in an arc to clear the floor instead of bending the knee. Both are valuable, and a good rehab plan uses both, but they are not the same achievement, and confusing them muddies what is really happening.
Keep one more honest line clear, the same one that opened this rung: rehabilitation does not cure the lesion. The dead patch of brain stays dead. What therapy does is help the *rest* of the nervous system relearn — re-mapping, finding new routes — which is why repetition and real-world tasks matter so much, and why a limb left out of use can sink into learned non-use. So the motor story of stroke is not a tale of erasing damage. It is a story of a person, with a particular pattern of weakness and overactivity, learning to move and to live again around an injury that does not go away.