Muscle Tone
Muscle tone is the resistance a muscle offers to passive stretch when the patient is at rest and not voluntarily contracting. It is not a single, static property but the dynamic product of the muscle stretch reflex arc—the spindle afferent, its synapse in the spinal cord, and the lower motor neuron—operating under the continuous influence of descending pathways from the cortex, basal ganglia, brainstem, and cerebellum. Because tone integrates so many levels of the motor system, the manner in which a limb resists passive movement is one of the most informative observations in the neurologic examination. The character of the resistance, its dependence on the velocity of movement, and its anatomical distribution each point toward a different part of the nervous system, allowing the examiner to separate corticospinal disease from extrapyramidal disease, and central lesions from disease of the lower motor unit.
Assessing tone correctly requires deliberate technique. The findings are subtle, and they are easily abolished by the patient's voluntary participation or masked by anxiety. The examiner must obtain genuine relaxation, move the limb in a way that loads the reflex arc, and pay attention not only to whether resistance is increased or decreased but to its precise quality.
Examining Tone
Tone is tested by passively moving the relaxed limb through its range of motion while the patient does nothing. The goal is to feel the muscle's response to stretch without the contamination of voluntary effort.
- Ensure relaxation. Ask the patient to let the limb go completely limp and to allow the examiner to do all the work. Casual conversation or asking the patient to count or recite a list can distract a tense patient and unmask abnormal tone—the basis of the activation, or reinforcement, maneuver.
- Move at varying velocities. Flex and extend the limb both slowly and quickly. Velocity is the single most important variable, because it is what separates the velocity-dependent resistance of spasticity from the velocity-independent resistance of rigidity.
- Test multiple joints. Examine tone at the elbow, wrist, knee, and ankle. In the upper limb, supination–pronation and elbow flexion–extension are sensitive; in the lower limb, the classic test is to roll the relaxed thigh and watch the foot, or to briskly lift the knee and observe whether the heel leaves the bed.
- Compare sides. As with most of the motor examination, asymmetry between homologous muscle groups is more reliable than an absolute judgment of "normal."
Hypertonia
Hypertonia is an abnormal increase in resistance to passive stretch. It is not a single entity: spasticity, rigidity, and paratonia are physiologically distinct, localize differently, and feel different in the examiner's hands. Distinguishing among them is the central task when increased tone is found.
Spasticity
Spasticity is a velocity-dependent increase in tone: the faster the limb is moved, the greater the resistance. When the joint is moved briskly, resistance builds and then, at a certain point in the range, abruptly releases—the so-called "clasp-knife" phenomenon, named for the sudden give of a folding pocket-knife. Spasticity is a cardinal feature of corticospinal (upper motor neuron) disease and characteristically travels with the other signs of an upper motor neuron lesion: hyperreflexia, clonus, and an extensor plantar (Babinski) response. Its distribution is selective rather than uniform; it preferentially affects the antigravity muscles—the flexors of the upper limb and the extensors of the lower limb—producing, when chronic and severe, the characteristic hemiparetic posture of a flexed, adducted arm and an extended leg.
Rigidity
Rigidity is an increase in tone that is present throughout the range of motion and is independent of the velocity of movement, so that the resistance feels uniform whether the limb is moved slowly or quickly. This even, sustained resistance is described as "lead-pipe." When a superimposed tremor is present, as in Parkinson disease, the smooth resistance is interrupted by a regular ratchet-like series of catches and gives, producing "cogwheel" rigidity. Rigidity is a feature of extrapyramidal (basal ganglia) disease, most familiarly parkinsonism. Unlike spasticity, it affects flexors and extensors more equally and is not accompanied by the hyperreflexia, clonus, or extensor plantar response of corticospinal disease.
Paratonia (Gegenhalten)
Paratonia, also called gegenhalten ("counter-holding"), is a variable, irregular resistance that appears to oppose the examiner's movement, seeming to increase the more vigorously the examiner moves the limb and to fluctuate in a way that neither spasticity nor rigidity does. The patient is unable to relax voluntarily, and the resistance feels like an involuntary active opposition. It is associated with frontal lobe dysfunction and diffuse cerebral disease, including the dementias, and its presence often signals a more global disturbance of cerebral function. A related facilitatory phenomenon, mitgehen ("going with"), in which the limb moves excessively and involuntarily in the direction the examiner nudges it, may coexist.
Hypotonia and Flaccidity
Hypotonia is an abnormal reduction in resistance to passive stretch; when tone is lost altogether the limb is described as flaccid. The hypotonic limb feels floppy, falls limply under gravity, and may show an excessive range of passive movement. Hypotonia has several causes:
- Lower motor neuron lesions—disease of the anterior horn cell, root, plexus, peripheral nerve, neuromuscular junction, or muscle interrupts the efferent limb of the reflex arc, abolishing the tone it normally maintains.
- Cerebellar disease—lesions of the cerebellum or its connections reduce the facilitatory drive to the stretch reflex, producing hypotonia along with pendular reflexes.
- The acute phase of an upper motor neuron lesion—immediately after an acute corticospinal lesion, before spasticity develops, tone is paradoxically decreased. This state, known as spinal shock after acute spinal cord injury (or cerebral shock after an acute hemispheric lesion such as a large stroke), is characterized by flaccid weakness and areflexia that evolve over days to weeks into the expected spasticity and hyperreflexia. Recognizing this transient hypotonia prevents the early mislocalization of an upper motor neuron lesion as a lower motor neuron one.
Clonus
Clonus is a series of rhythmic, involuntary muscle contractions provoked by a sudden, sustained stretch of the muscle. It is elicited most reliably at the ankle, where a brisk dorsiflexion of the foot, held under tension, evokes repetitive beats of plantar flexion; it may also be demonstrated at the patella. Clonus reflects the same disinhibited, hyperexcitable stretch reflex that underlies spasticity and is therefore a sign of upper motor neuron disease. A few unsustained beats may occasionally be seen in anxious individuals with otherwise brisk reflexes, but sustained clonus—beats that continue as long as the stretch is maintained—is unequivocally pathologic and indicates corticospinal tract involvement.
Localizing Value
Each abnormality of tone carries a distinct localization, and reading the quality of the resistance is, in effect, a localization exercise:
- Spasticity (with hyperreflexia, clonus, extensor plantar) localizes to the corticospinal tract—anywhere from motor cortex through the internal capsule, brainstem, and spinal cord.
- Rigidity (lead-pipe or cogwheel, without pyramidal signs) localizes to the basal ganglia / extrapyramidal system.
- Paratonia localizes to the frontal lobes and diffuse cerebral cortex, signaling a more widespread disturbance.
- Hypotonia points to the lower motor unit or the cerebellum, or to the acute phase of a central lesion before spasticity emerges.
Comparing the Disorders of Tone
The four principal abnormalities of tone are most easily kept apart by their defining quality, their relationship to the velocity of passive movement, and the part of the nervous system to which they localize.
| Disorder | Quality | Velocity-dependence | Localization |
|---|---|---|---|
| Spasticity | Clasp-knife (resistance builds, then sudden give); favors antigravity muscles | Velocity-dependent (greater with faster movement) | Corticospinal tract (upper motor neuron) |
| Rigidity | Lead-pipe (uniform through range); cogwheel if tremor superimposed | Independent of velocity | Basal ganglia / extrapyramidal system |
| Paratonia (gegenhalten) | Variable, irregular active opposition to movement; may show mitgehen | Variable / inconsistent | Frontal lobes / diffuse cerebral disease |
| Hypotonia | Reduced or absent resistance; floppy, excessive passive range | Not applicable (resistance decreased) | Lower motor neuron, cerebellum, or acute UMN (spinal/cerebral shock) |
Two distinctions in this table deserve emphasis at the bedside. The contrast between spasticity and rigidity turns almost entirely on velocity: moving the limb at two different speeds will reveal the velocity-dependence and clasp-knife give of spasticity, while rigidity feels the same at any speed. And the contrast between true hypertonia and paratonia turns on consistency: spasticity and rigidity are reproducible, whereas paratonia is variable and seems to fight the examiner, often in proportion to how briskly the limb is moved.
Clinical Note
Spasticity is velocity-dependent and clasp-knife in character, the signature of a pyramidal (corticospinal) lesion, whereas rigidity is uniform and lead-pipe, the signature of an extrapyramidal (basal ganglia) lesion. Testing the limb at different velocities at the bedside is the simplest and most reliable way to distinguish the two: spasticity worsens as the movement quickens, while rigidity feels the same whether the limb is moved slowly or fast.
References
- Campbell WW, Barohn RJ. DeJong's The Neurologic Examination. 8th ed. Philadelphia: Wolters Kluwer; 2020.
- Ropper AH, Samuels MA, Klein JP, Prasad S. Adams and Victor's Principles of Neurology. 11th ed. New York: McGraw-Hill; 2019.
- Biller J, Gruener G, Brazis PW. DeMyer's The Neurologic Examination: A Programmed Text. 7th ed. New York: McGraw-Hill; 2017.
- Blumenfeld H. Neuroanatomy through Clinical Cases. 3rd ed. Sunderland, MA: Sinauer Associates / Oxford University Press; 2022.