Tone in Clinical Medicine

Dr Neeraj Manikath , claude.ai

Abstract

Tone, or tonus, represents the continuous partial contraction of skeletal muscles and reflects the complex interplay between the central and peripheral nervous systems. While often overlooked in clinical practice, abnormalities in muscle tone serve as critical diagnostic indicators across numerous neurological and systemic conditions. This review synthesizes contemporary understanding of tone assessment, pathophysiology, and clinical interpretation, providing internists with practical frameworks for evaluation and diagnosis.

Introduction

Muscle tone represents one of the fundamental components of the neurological examination, yet its assessment remains challenging for many practitioners. The ability to accurately evaluate and interpret tone abnormalities distinguishes experienced clinicians and often provides the first clue to serious underlying pathology. This review addresses the physiological basis, clinical assessment techniques, differential diagnosis, and practical pearls for mastering this essential clinical skill.

Physiological Foundations

Muscle tone arises from the baseline firing of alpha motor neurons, modulated by supraspinal influences, local spinal reflexes, and intrinsic muscle properties. The gamma motor neuron system maintains muscle spindle sensitivity, creating a continuous feedback loop that sustains resting tension. The extrapyramidal system, particularly the basal ganglia and cerebellum, exerts profound modulatory effects, while the corticospinal tracts provide inhibitory control.

Understanding this neuroanatomical substrate explains why tone abnormalities localize lesions. Upper motor neuron lesions produce spasticity through disinhibition of spinal reflexes, while extrapyramidal disorders generate rigidity through altered basal ganglia output. Lower motor neuron damage results in hypotonia through loss of the reflex arc itself.

Clinical Assessment Techniques

The Art of Examination

Proper tone assessment requires a relaxed, comfortable patient in a warm environment. Anxiety, pain, and cold all increase tone artificially. The examiner should establish rapport before testing, as voluntary resistance ("gegenhalten") commonly confounds assessment.

Pearl #1: Always warm your hands before examination. Cold hands trigger reflexive muscle contraction, falsely elevating perceived tone.

Technique Essentials:

• Support the limb throughout the examination
• Move joints through their full range at varying speeds
• Test multiple joints in each limb
• Compare side-to-side symmetry
• Assess tone with patient distracted when possible

Upper Limbs

Assess shoulder internal/external rotation, elbow flexion/extension, forearm pronation/supination, and wrist movements. The "dropped arm test" provides valuable information: lift the relaxed arm and release it suddenly. Normal tone allows smooth, controlled descent, while hypotonia causes the arm to fall limply, and increased tone produces slow, resistant dropping.

Pearl #2: Check for pronator drift simultaneously. Position the arms outstretched with palms supinated and eyes closed. Subtle pyramidal weakness causes downward drift with pronation, often before tone changes become apparent.

Lower Limbs

Roll the thigh externally and internally on the examination table, observing foot movement. Normally, the foot moves smoothly with slight lag. In rigidity, the foot moves as though "bolted" to the leg. In spasticity, initial resistance yields suddenly (clasp-knife phenomenon). Test hip flexion/extension, knee flexion/extension, and ankle dorsiflexion/plantarflexion.

Pearl #3: The "pendulum test" reveals subtle tone abnormalities. With the patient seated, legs dangling, passively extend the knee then release. Normal tone produces 3-5 oscillations before the leg settles. Increased tone reduces oscillations; hypotonia increases them.

Classification of Tone Abnormalities

Hypotonia

Reduced muscle tone manifests as decreased resistance to passive movement, hyperextensible joints, and diminished deep tendon reflexes. The differential diagnosis spans neurological and systemic etiologies.

Neurological Causes:

• Acute cerebral or cerebellar lesions (stroke, hemorrhage)
• Lower motor neuron disorders (Guillain-Barré syndrome, poliomyelitis, peripheral neuropathy)
• Neuromuscular junction disorders (myasthenia gravis, botulism)
• Myopathies (polymyositis, muscular dystrophies)
• Spinal shock (acute spinal cord injury)

Systemic Causes:

• Electrolyte disturbances (hypokalemia, hypercalcemia, hypomagnesemia)
• Endocrine disorders (hypothyroidism, Cushing's syndrome)
• Sepsis
• Medications (benzodiazepines, baclofen, dantrolene)

Oyster #1: In acute stroke, initial hypotonia paradoxically predicts subsequent spasticity development. Document early hypotonia carefully, as it has prognostic implications for rehabilitation planning.

Hypertonia: Spasticity

Spasticity demonstrates velocity-dependent resistance—faster movements encounter greater resistance. The "clasp-knife" phenomenon, where initial resistance suddenly yields, typifies spasticity. Distribution patterns provide localizing value: upper limb flexor predominance with lower limb extensor predominance suggests cortical lesions, while varied patterns indicate spinal pathology.

Common Etiologies:

• Stroke (most common in clinical practice)
• Multiple sclerosis
• Traumatic brain injury
• Cerebral palsy
• Spinal cord injury or compression
• Hereditary spastic paraplegia

Modified Ashworth Scale remains the standard clinical grading tool:

• 0: No increase in tone
• 1: Slight increase, catch and release at end range
• 1+: Slight increase, catch followed by resistance throughout less than half the range
• 2: Marked increase through most of range
• 3: Considerable increase, passive movement difficult
• 4: Rigid in flexion or extension

Hack #1: When assessing potential spinal cord compression, check for sensory level carefully. Spasticity below the level with normal tone above localizes the lesion and warrants urgent imaging.

Hypertonia: Rigidity

Rigidity exhibits constant, velocity-independent resistance throughout the range of motion, affecting agonists and antagonists equally. "Lead-pipe" rigidity describes smooth, constant resistance, while "cogwheel" rigidity demonstrates ratchety, interrupted resistance.

Distinguishing Features:

• Present at all movement velocities (unlike spasticity)
• Equal in flexors and extensors
• Activated by voluntary movement in contralateral limbs (reinforcement)
• Associated with bradykinesia, tremor, and postural instability in Parkinson's disease

Pearl #4: Test for cogwheel rigidity with reinforcement. Have the patient perform circular movements with the contralateral hand while you assess tone. This maneuver unmasks subtle rigidity in early Parkinson's disease.

Etiologies:

• Parkinson's disease (most common)
• Parkinson-plus syndromes (progressive supranuclear palsy, multiple system atrophy)
• Drug-induced parkinsonism (antipsychotics, metoclopramide)
• Wilson's disease
• Diffuse Lewy body disease
• Vascular parkinsonism

Paratonia (Gegenhalten)

Paratonia represents involuntary, variable resistance that increases with examiner effort—the patient appears to actively resist, though unconsciously. This frontal lobe release sign indicates diffuse cerebral dysfunction.

Associated Conditions:

• Advanced dementia (Alzheimer's disease, frontotemporal dementia)
• Diffuse cerebrovascular disease
• Normal pressure hydrocephalus
• Hepatic encephalopathy
• Metabolic encephalopathies

Pearl #5: Distraction techniques help differentiate paratonia from voluntary resistance. Engage the patient in conversation or mental tasks (serial sevens, naming objects) during examination. Paratonia persists; voluntary resistance often diminishes.

Special Clinical Scenarios

Acute Tone Changes

Sudden tone alterations demand urgent evaluation. Acute hypotonia with areflexia suggests Guillain-Barré syndrome, requiring respiratory function monitoring. Acute asymmetric hypertonia with hyperreflexia indicates stroke until proven otherwise. Acute generalized rigidity with fever, altered consciousness, and autonomic instability defines neuroleptic malignant syndrome or serotonin syndrome—life-threatening emergencies requiring immediate intervention.

Hack #2: In suspected neuroleptic malignant syndrome, check creatine kinase immediately. Levels typically exceed 1,000 IU/L and may reach 100,000 IU/L, distinguishing this from functional rigidity.

Tone Assessment in Coma

Tone evaluation provides crucial information in unresponsive patients. Decerebrate posturing (extensor rigidity) indicates midbrain or pontine dysfunction with worse prognosis than decorticate posturing (flexor upper limbs, extensor lower limbs), which suggests cerebral hemisphere or diencephalic lesions. Flaccid tone with absent reflexes may indicate brainstem death, profound metabolic derangement, or spinal shock.

Medication Effects

Numerous medications alter tone. Benzodiazepines, baclofen, and tizanidine reduce tone therapeutically. Antipsychotics may induce rigidity. Selective serotonin reuptake inhibitors combined with other serotonergic agents risk serotonin syndrome with severe rigidity. Obtain meticulous medication histories when encountering unexplained tone abnormalities.

Oyster #2: Statin-induced myopathy typically produces weakness without tone changes. If a patient on statins develops rigidity rather than hypotonia, look for alternative explanations—drug-drug interactions or concurrent neurological disease.

Diagnostic Approach

Initial Evaluation

Characterize tone abnormalities systematically:

1. Hypotonia, spasticity, rigidity, or paratonia?
2. Symmetric or asymmetric?
3. Proximal, distal, or generalized?
4. Upper limbs, lower limbs, or both?
5. Acute, subacute, or chronic onset?
6. Associated neurological signs (weakness, sensory changes, reflex abnormalities)?

Directed Testing

Tailor investigations to clinical suspicion:

• Neuroimaging (CT/MRI): Stroke, structural lesions, demyelination
• Electrodiagnostic studies: Peripheral neuropathy, myopathy, neuromuscular junction disorders
• Laboratory testing: Electrolytes, thyroid function, creatine kinase, vitamin B12, copper/ceruloplasmin (Wilson's disease)
• Lumbar puncture: Guillain-Barré syndrome, inflammatory conditions
• Genetic testing: Hereditary conditions when clinically appropriate

Pearl #6: In unexplained progressive rigidity with cognitive changes in patients under 50, always check ceruloplasmin and 24-hour urinary copper. Wilson's disease remains treatable if caught early.

Therapeutic Considerations

While internists typically consult neurology for tone disorder management, understanding basic principles proves valuable. Spasticity management includes physical therapy, oral medications (baclofen, tizanidine, diazepam), and botulinum toxin injections for focal spasticity. Parkinson's disease requires dopaminergic therapy. Identifying and treating underlying systemic causes—correcting electrolyte abnormalities, treating infections, adjusting medications—often improves tone abnormalities without specific neurological interventions.

Conclusion

Mastering tone assessment enhances diagnostic accuracy across numerous conditions encountered in internal medicine practice. Systematic examination, understanding pathophysiological mechanisms, and recognizing clinical patterns enable internists to localize lesions, narrow differential diagnoses, and initiate appropriate management promptly. The skills outlined in this review, refined through deliberate practice, will serve clinicians throughout their careers.

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