The learned non-use problem

After stroke, initial paresis leads to compensatory reliance on the unaffected limb. Over time, this becomes habitual—the brain literally suppresses motor commands to the affected limb even when some capacity remains (Taub et al., 2006). CIMT reverses this through massed practice with the affected limb while preventing compensatory strategies.

Evidence for cortical reorganization

Motor map expansion:

• Liepert et al. (2000) used transcranial magnetic stimulation to map motor cortex before and after 2 weeks of CIMT. The cortical representation of the affected hand enlarged significantly, with the expansion correlating with motor function gains (r=0.68).
• Hamzei et al. (2006) confirmed this with fMRI, showing increased activation in primary motor cortex and supplementary motor area during affected hand movements post-CIMT.

Interhemispheric balance:

• Normal motor control involves balanced interhemispheric inhibition. After stroke, the unaffected hemisphere becomes overactive and may suppress the affected hemisphere (Murase et al., 2004).
• Grefkes et al. (2008) showed CIMT reduces this abnormal interhemispheric inhibition, restoring more normal coupling between hemispheres.

The mechanism: competitive plasticity

The brain has limited cortical territory. When one body part is underused, its representation shrinks; when another is overused, it expands. CIMT combines:

1. Massed practice: 6+ hours/day of structured task practice with the affected limb
2. Constraint: The unaffected limb is immobilized (usually with a mitt), forcing problem-solving with the affected limb
3. Transfer package: Training that promotes generalization to real-world activities

This creates a use-dependent competition where the affected limb "reclaims" cortical territory.

Critical constraints on the hypothesis

Not all patients respond: CIMT requires some residual wrist and finger extension. Patients with complete paralysis don't benefit—there needs to be something to build on.

Dosage matters: The original CIMT protocol used 6 hours/day for 2 weeks. Modified versions with less intensity show smaller effects (Kwakkel et al., 2017 meta-analysis). The plasticity mechanism seems dose-dependent.

Persistence is questionable: Most studies show maintenance of gains at 6 months, but longer-term follow-up data is sparse. Whether the cortical reorganization is permanent or requires continued practice is unclear.

Compensation vs. recovery: Some critics argue CIMT teaches compensatory strategies (using trunk movement, altered movement patterns) rather than true neurological recovery. The fMRI evidence for motor map expansion suggests genuine reorganization, but the functional gains may combine true recovery with learned compensation.

Testable predictions

1. CIMT responders will show greater motor map expansion than non-responders, measurable by TMS
2. The magnitude of interhemispheric inhibition reduction will correlate with functional gains
3. Maintenance of gains at 1 year will require continued practice—cortical reorganization without continued use may revert
4. Combining CIMT with non-invasive brain stimulation (tDCS to affected M1) will enhance effects by amplifying the competitive plasticity mechanism

Clinical implications

CIMT is now standard of care for chronic stroke with residual hand function. The mechanism explains why it works best in subacute to chronic phases (some spontaneous recovery has occurred, but learned non-use has set in) and why intensity matters.

The competitive plasticity model also suggests CIMT principles could apply to other conditions—cerebral palsy, traumatic brain injury—where learned non-use develops. Early trials in these populations show promise but need larger studies.

Research synthesis via Aubrai