Understanding Spasticity: Navigating the Recovery Pathway After Neurological Injury

Neurological injury presents us with one of the most complex challenges in medicine—how does the brain rewire itself after damage, and why do we see such an intricate dance of recovery, spasticity, and functional loss?

Spasticity, the hallmark of upper motor neuron damage, offers a prime example of the intricacies of recovery following injury. Whether it’s the result of a stroke, traumatic brain injury, or spinal cord injury, spasticity brings about both positive and negative symptoms—a dichotomy that has fascinated and frustrated clinicians and researchers alike.

Let’s break this down:

On one hand, positive symptoms—spasticity, clonus, exaggerated reflexes—are excesses. They reflect an overactivity, a failure of the inhibitory pathways that usually govern smooth muscle control. Muscles stiffen, reflexes amplify, and the body seems to develop a mind of its own.

Conversely, negative symptoms are deficiencies. The brain, in its damaged state, struggles to send signals to muscles, leading to weakness, loss of voluntary control, and atrophy. These are the deficits of function that, from the outside, appear passive but are far more disabling than we often acknowledge.

Signe Brunnstrom’s seven stages of recovery offer us a structured view of this progression from flaccid paralysis to near-normal movement, but the journey is far from linear. Patients move through stages not by checklist, but through a complex interplay of spontaneous neural reorganization, therapy, and often, pure biological chance. At first, muscles are limp (Stage 1: Flaccidity), and over time, spasticity kicks in (Stage 2: Early Synergy), eventually leading to the reclamation of voluntary control (Stage 3-4) as abnormal synergy patterns give way to more refined, deliberate movement.

However, spasticity is not a static phenomenon. As patients attempt to reclaim control, the battle between overactivity and loss of function intensifies. Early in recovery, we see primitive motor patterns—stiff, stereotypical, and devoid of purpose—but later stages reveal a dance between reemerging volitional movements and residual spasticity.

The positive symptoms we see in patients—the jerks, rigidity, and uncontrolled movements—are often viewed as the villains in this narrative. But in truth, it is the negative symptoms—the absence of movement, the loss of dexterity—that represent the more formidable adversary. Without strength, without volition, even the ability to manage the positive symptoms is reduced.

So, what’s the way forward?

As our understanding deepens, timely interventions matter more than ever. Early rehabilitation, pharmacological management with antispasmodics, botulinum toxin injections, cryoneurolysis or even intrathecal baclofen—these tools can reduce the hyperactivity of spasticity. But they must be accompanied by a nuanced understanding of neuroplasticity and the motor learning principles that guide recovery.

Rehabilitation is not merely about loosening stiff muscles, it’s about reshaping movement patterns and guiding the brain back to purposeful control.

At the intersection of spasticity and recovery lies a hopeful frontier: the possibility that with early, targeted, and multidisciplinary interventions, we can reawaken volition—helping patients move from rigidity and helplessness to dynamic, functional movement.

It’s time we stop seeing spasticity as a singular phenomenon and instead understand it as a biological marker of recovery in flux. With positive and negative symptoms, recovery is both a presence and an absence—two sides of the same coin in the quest for a return to functional independence.

In the end, spasticity is not the enemy—it’s a call for action.

#Neurorehabilitation #StrokeRecovery #Spasticity #MotorLearning #Neuroplasticity #Neurology #MovementScience #UpperMotorNeuron #RecoveryJourney

José López Sánchez

CEO @ Centro Europeo de Neurociencias | Intensive Therapy Specialist