Can you explain spasticity, its velocity‑dependent hypertonia, typical flexor or extensor muscle involvement, the clasp‑knife phenomenon, and how it differs from rigidity?

Spasticity: Velocity-Dependent Hypertonia and the Clasp-Knife Phenomenon

Spasticity is a velocity-dependent increase in muscle tone caused by hyperexcitable stretch reflexes, distinguished from rigidity by its speed-dependence and selective involvement of specific muscle groups (typically flexors in cerebral lesions, extensors in spinal lesions), with the clasp-knife phenomenon representing sudden release of resistance during passive stretch. 1, 2, 3

Core Pathophysiology

Velocity-Dependent Hypertonia:

• Spasticity manifests as increased resistance to passive muscle lengthening that intensifies with faster stretch velocities, reflecting hyperexcitability of the tonic stretch reflex 1, 3, 4
• The resistance is mediated by abnormal muscle spindle activity and altered spinal reflex circuits following upper motor neuron lesions 3, 4
• This velocity-dependence is the key distinguishing feature from rigidity, which shows constant resistance regardless of stretch speed 2, 4

Selective Muscle Group Involvement:

• Cerebral lesions typically cause rapid build-up of excitation with bias toward antigravity muscles (flexors in upper extremities, extensors in lower extremities) 4
• Spinal cord lesions produce slower excitation with overactivity of both flexors and extensors, with reactions spreading across multiple segments 4
• The pattern depends more on lesion location and extent than on the underlying pathology 2

The Clasp-Knife Phenomenon

Mechanism and Clinical Presentation:

• The clasp-knife phenomenon describes sudden, dramatic release of resistance during passive stretch after initial high resistance, resembling the closing of a pocket knife 2, 3
• This occurs when sustained stretch activates inhibitory Golgi tendon organ reflexes that override the hyperactive stretch reflex 2
• It is one of several "positive" upper motor neuron signs, alongside tendon hyperreflexia, clonus, and flexor/extensor spasms 2, 3

Clinical Significance:

• The presence of clasp-knife phenomenon confirms spasticity rather than other forms of hypertonia 2
• It reflects the preserved but disordered spinal reflex circuitry following supraspinal lesion 3

Distinguishing Spasticity from Rigidity

Critical Differences:

Feature	Spasticity	Rigidity
Velocity-dependence	Present (faster = more resistance) [1,4]	Absent (constant "lead-pipe") [2,4]
Muscle distribution	Selective (flexors or extensors) [4]	Uniform (all muscle groups) [2]
Clasp-knife	Present [2,3]	Absent [2]
Pathophysiology	Hyperactive stretch reflexes [3,4]	Increased alpha motor neuron activity [2]
Lesion location	Upper motor neuron (cortical/spinal) [1,2]	Extrapyramidal (basal ganglia) [2]

Associated Upper Motor Neuron Signs

"Positive" Phenomena (Muscle Overactivity):

• Exaggerated tendon reflexes with spread to adjacent segments 2, 3
• Clonus (rhythmic oscillations with sustained stretch) 2, 3
• Flexor and extensor spasms triggered by nociceptive stimuli 2, 3
• Babinski sign (extensor plantar response) 2
• Spastic dystonia (sustained abnormal posturing) 1, 2

"Negative" Phenomena (Loss of Function):

• Weakness and loss of dexterity, which invariably alter function more than spasticity itself 4
• These negative signs often contribute more to disability than the spasticity 4

Temporal Evolution and Plasticity

Delayed Onset:

• Spasticity develops over variable time periods following the primary lesion, not immediately 2, 3
• This delayed onset reflects plastic changes in spinal neuronal circuitries caudal to the lesion 3
• The mechanism involves reduction of spinal inhibitory mechanisms, particularly disynaptic reciprocal inhibition 3

Dynamic Changes:

• Reflex excitability frequently reduces over time, suggesting ongoing central nervous system adaptation 2, 3
• Chronic spasticity leads to secondary rheologic changes: muscle stiffness, contracture, atrophy, and fibrosis 4
• Distinguishing spasticity from these secondary contractures is therapeutically critical, as they require different interventions 4

Clinical Assessment Pitfalls

Key Examination Considerations:

• Always distinguish velocity-dependent resistance (true spasticity) from fixed contracture resistance (rheologic changes), as this determines treatment approach 4
• Nociceptive stimuli (urinary tract infections, pressure ulcers, ingrown toenails) can dramatically worsen spasticity and must be systematically eliminated 5
• Assess both the negative impact on function and any positive functional contributions of spasticity (e.g., assisting with transfers or standing) 5
• The Ashworth scale quantifies tone but does not capture functional impact, which should guide treatment decisions 6, 5