Knee hyperextension, known medically as Genu Recurvatum, is a condition where the knee joint extends backward beyond its normal, straight position of zero degrees. This abnormal extension primarily occurs during the stance phase of the gait cycle. During typical walking, the knee maintains a slight bend to absorb shock and ensure smooth forward progression. When the knee locks backward into hyperextension, it creates an extension gait pattern, sacrificing dynamic control for passive stability. Understanding the causes requires examining the interaction between muscles, joint structure, and nervous system control.
Primary Causes: Insufficient Muscular Control
Muscles surrounding the knee act as active restraints, providing the dynamic control necessary to prevent the joint from collapsing into hyperextension during walking. The most common mechanical cause of genu recurvatum is weakness in the quadriceps muscle group. When the quadriceps are too weak to control the natural flexion moment as the body’s weight shifts onto the leg, the individual compensates by pushing the knee backward.
This hyperextension is a functional strategy that locks the joint and moves the ground reaction force vector in front of the knee axis. Locking the knee allows the person to walk using the passive stability of the ligaments and bony structures, requiring minimal effort from the weakened quadriceps. While this provides stability, it places excessive strain on the posterior structures of the knee over time.
The hamstring muscles, which flex the knee, provide a dynamic “brake” to terminal knee extension during the swing phase of gait. Weakness in the hamstrings reduces this braking capacity, allowing the knee to snap into hyperextension as the leg prepares for initial contact. Weakness in the gluteal muscles, particularly the gluteus maximus, can also indirectly contribute. This hip extensor weakness causes the pelvis to tilt forward, forcing a compensatory extension moment at the knee to maintain an upright posture.
Structural Instability and Ligamentous Laxity
Beyond muscular control, the inherent structure of the knee joint and its passive restraints can predispose an individual to hyperextension. Ligamentous laxity refers to increased looseness in the ligaments, which normally stop the knee from moving too far backward. This laxity can be congenital, often associated with generalized hypermobility syndromes like Ehlers-Danlos syndrome, or result from previous traumatic injuries.
When ligaments are stretched or torn, they lose their passive “braking” function, allowing the knee to extend past the zero-degree point without restriction. The posterior oblique ligament is a powerful soft tissue restraint against hyperextension, and injury to this structure significantly increases the risk of recurvatum. Chronic hyperextension itself stretches the posterior capsular structures, creating a cycle of progressive instability.
The bony alignment of the knee also influences stability. Most people have a slight posterior slope to the tibial plateau, which naturally encourages a slight flexion moment and protects against excessive extension. Structural variations, such as a flatter or anteriorly tilted tibial plateau, reduce this bony protection. In these cases, the knee relies more heavily on surrounding soft tissues and muscles to prevent genu recurvatum.
Neurological Impairments and Compensatory Patterns
Genu recurvatum is often a symptom of a neurological condition that disrupts motor control pathways. Conditions such as stroke, cerebral palsy, multiple sclerosis, and poliomyelitis can cause weakness, spasticity, or poor motor planning, leading to a loss of dynamic knee control. In some instances, spasticity (involuntary tightness) in the quadriceps can actively force the knee into hyperextension during the stance phase.
A more common neurological cause is functional weakness or impaired timing in the leg muscles. For example, after a stroke, the brain may fail to activate the hamstrings or calf muscles at the correct moment to stabilize the knee. This forces the person to lock the knee for static stability. Hyperextension becomes an unconscious, acquired strategy used to secure the limb during weight-bearing despite the underlying motor impairment.
Compensatory Patterns
Hyperextension is frequently a consequence of compensatory patterns originating at the joints above or below the knee, known as the kinetic chain. A limitation of ankle dorsiflexion (the inability to pull the foot upward) is a significant contributor. If the foot is stuck in a plantarflexed position, such as with a tight Achilles tendon, the tibia cannot move forward properly over the foot during mid-stance.
To prevent the body from falling forward due to this blocked movement, the knee must hyperextend. This shifts the ground reaction force vector forward and stabilizes the limb. Similarly, issues at the hip can induce knee hyperextension. A hip flexion contracture restricts the hip’s ability to extend fully during the stance phase.
The body compensates for this lack of hip movement by pushing the knee backward into hyperextension, which helps keep the body’s center of mass aligned vertically over the foot. This multi-joint compensation shows that the cause of genu recurvatum is often a downstream effect of problems elsewhere in the leg.