Distinguishing Spasticity vs Rigidity: Stanford Bedside Exam

The stretch reflex (also called deep tendon reflex) is a monosynaptic reflex arc: stretching a muscle activates muscle spindle receptors → Ia afferent fibers → spinal cord → alpha motor neuron → muscle contraction. This negative feedback mechanism maintains muscle length. Gamma motor neurons continuously activate intrafusal muscle fibers, maintaining muscle spindle sensitivity and contributing to muscle tone. Without gamma motor neuron activity, muscle spindles would become less sensitive to stretch, reducing the stretch reflex response.

The stretch reflex is a monosynaptic reflex arc where tendon tapping stretches extrafusal fibers, which stretches intrafusal fibers and activates Ia afferents directly on alpha motor neurons, causing contraction that returns the spindle to original length. However, gamma motor neurons continuously discharge to prevent spindle slack, maintaining constant afferent discharge for continuous muscle tone monitoring. Spindle loading occurs through extrafusal stretching (exogenous) or gamma motor neuron discharge (endogenous). Spindle unloading occurs when extrafusal fibers contract. This continuous loading ensures the brain constantly monitors muscle length and tension for posture and movement control.

The myotatic stretch reflex is a monosynaptic reflex arc that maintains muscle tone. Muscle spindles (intrafusal fibers arranged in capsules) detect muscle stretch and send feedback via Ia and II afferent fibers to the spinal cord. These afferents synapse directly with alpha motor neurons in the ventral horn, which then cause the stretched muscle to contract. Gamma motor neurons modulate spindle sensitivity by adjusting intrafusal fiber tension, allowing central nervous system control over reflex sensitivity.

The stretch reflex is a fundamental reflex arc that regulates muscle length. It consists of: (1) a receptor (muscle spindle) that detects muscle stretch, (2) sensory fibers (type Ia or II) that transmit information to the spinal cord, (3) a sensory neuron that synapses directly with a motor neuron, and (4) an effector (skeletal muscle) that contracts in response. When a muscle is stretched, the reflex causes contraction, which reduces the muscle length. This reflex operates continuously to maintain muscle tone and posture, as muscles are constantly being stretched during daily activities like standing or walking.

The stretch reflex is a fundamental reflex arc that regulates muscle length through a specific pathway: muscle spindle receptors detect stretch, afferent Ia fibers transmit this information to the spinal cord, motor neurons cause the stretched muscle to contract, and gamma motor neurons adjust spindle sensitivity. Gamma motor neurons innervate intrafusal fibers within muscle spindles, allowing the nervous system to continuously adjust muscle tone based on desired muscle length. This gamma loop enables the body to maintain appropriate muscle tension for different postures and movements, from standing to sitting, by modulating the sensitivity of the stretch reflex. Muscle tone is defined as the resistance to stretch that skeletal muscle presents even when voluntarily relaxed, and is fundamental for maintaining posture and performing movements like standing and walking.

Passive movement assessment involves evaluating range of motion for shoulders (flexion, extension, abduction, adduction, rotation), elbows (flexion, extension, forearm rotation), wrists, hips, knees, and ankles while encouraging patient relaxation. Lift each arm/leg and allow it to fall freely to assess muscle tone, noting rigidity types: clasp-knife (upper motor neuron), lead-pipe/plastic rigidity (Parkinson's), and cog-wheel rigidity (Parkinson's with tremor). Active movement assessment requires the patient to move limbs in all normal planes of movement, noting range achieved and control. Demonstrate movements rather than issuing complex instructions. This comprehensive assessment helps identify limitations due to neurological or musculoskeletal pathology.

The neurological examination of the limbs involves a systematic assessment of muscle tone, power, coordination, and sensation in both arms and legs, following a standardized sequence that begins with gait observation and Romberg's test, followed by inspection for muscle wasting and posture abnormalities, then testing tone through passive movements, assessing power through resisted movements, evaluating coordination with finger-nose tests and heel-shin tests, examining reflexes using a tendon hammer, and finally testing four sensory modalities (pin prick, light touch, proprioception, and vibration) across dermatomal patterns to identify neurological deficits.

Passive range of motion examination involves moving each joint through its full range of motion, typically 10-20 repetitions per joint, proceeding systematically through the body. Muscle tone assessment involves evaluating resistance to passive movement: in hypotonia, the limb moves easily with minimal resistance; in hypertonia, resistance is increased. The neck tone can be assessed by supporting the chin with fingers and gently pushing downward. These examination techniques are essential for neurological assessment.

Active range of movement testing includes cervical extension and flexion, rotation, and lateral side bending. Shoulder testing includes flexion, abduction, medial and lateral rotation, and elbow flexion and extension. Passive range of movement testing is performed by the examiner supporting and moving the patient's head through extension, flexion, rotation, and lateral side bending. The examiner observes for restriction or pain during both active and passive movements.

The neurological motor examination includes assessment of active voluntary movements, passive movements, and muscle tone. Active movements are performed by the patient at command, testing voluntary motor function. Passive movements are performed by the examiner to assess muscle tone. The examination evaluates head movements (flexion, extension, rotation), upper limb movements (flexion, extension, pronation, supination), and lower limb movements. This systematic approach helps identify motor deficits and localize neurological lesions.

Muscle tone alterations are classified into hypotonia and hypertonia. Hypotonia differs from flaccidity: hypotonia involves reduced excitatory influence on motor neurons with decreased stretch reflex sensitivity, while flaccidity represents complete loss of motor innervation with zero resistance. Hypertonia includes spasticity (hyperexcitability of stretch reflex with increased response magnitude and expanded stimulation area) and rigidity (increased resistance to passive movement that remains constant throughout the range). Spasticity presents with clasp-knife sign, clonus, hyperreflexia, and specific muscle group involvement. Rigidity shows uniform resistance without velocity dependence.

This section covers muscle tone disorders and their clinical significance. Muscle tone is the continuous passive partial contraction maintaining posture and readiness for movement, providing resistance to passive stretch through the stretch reflex. Hypotonia (decreased tone) results from lower motor neuron dysfunction, spinal cord lesions, or certain neurological conditions, presenting with reduced resistance to passive movement and floppy joints. Hypertonia (increased tone) results from upper motor neuron lesions and extrapyramidal disorders, presenting with increased resistance to passive movement. Hypertonia includes spasticity (velocity-dependent resistance increasing with faster movement) and rigidity (constant resistance regardless of velocity). Cogwheel rigidity shows rhythmic, ratchet-like resistance with clicking sounds, while lead pipe rigidity shows uniform resistance throughout movement.

Abnormal muscle tone includes hypotonia (decreased tone) and hypertonia (increased tone). Hypotonia indicates lower motor neuron disease from gamma loop disruption, with peripheral causes (motor unit/sensory nerve damage) showing weakness, while central causes (cerebral lesions) lack weakness. Cerebral/spinal shock shows transient hypotonia after acute pyramidal injury. Hypertonia manifests as rigidity (extrapyramidal, velocity-independent, diffuse involvement) or spasticity (pyramidal, velocity-dependent, focal involvement). Rigidity affects all muscle groups equally throughout range of motion, while spasticity varies by muscle group and movement speed.

Abnormal muscle tone includes: hypotonia - decreased resistance to passive movements, flabby muscles; hypertonia - increased resistance, dense muscles; dystonia - alternating areas of increased and decreased tone; asymmetry - increased tone in lower extremities with decreased in upper, or vice versa. Muscle hypertonia includes spasticity (resistance only at the beginning of active movement, then decreases - scissors phenomenon) and rigidity (constant or increasing resistance with repeated movements - waxy doll phenomenon, lead pipe phenomenon, cogwheel rigidity). Spasticity results from interruption of central nervous system influence on anterior horn cells and release of segmental reflex apparatus. Muscle hypotonia features include postural abnormalities, hypotonic flabby abdomen (frog-like abdomen), scapular winging, external clubfoot, and increased joint mobility with excessive extension.

Muscle tone is assessed by passive movement of the patient's limbs. Normal tone provides resistance to passive movement. Hypotonia (reduced tone) is felt as flaccidity during passive movement. Hypertonia (increased tone) is felt as resistance. Hypertonia has two main types: spastic and plastic (rigid). Spastic hypertonia is velocity-dependent, meaning resistance increases with faster passive movement. It is characteristic of pyramidal tract lesions. Plastic hypertonia (rigidity) is velocity-independent, providing constant resistance regardless of movement speed. It is characteristic of extrapyramidal disorders such as Parkinson's disease. Spastic hypertonia shows increased resistance with faster passive movement and may include clonus (rhythmic oscillations) and the clasp-knife phenomenon (initial resistance followed by sudden release).