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Tone

Original Editor - Vidya Acharya

Top Contributors - Vidya Acharya and Ewa Jaraczewska  


Introduction

Muscle tone is the residual tension in the relaxed muscle and the most widely used definition of muscle tone is the resistance to passive movements or stretching. [1][2] It is a continuous and passive partial contraction of the muscles, which maintains posture and is felt as resistance when passively stretching a muscle or performing the passive movement of a limb at a joint. [3] Although often assessed through resistance to passive movement, the concept of muscle tone varies in interpretation. Some clinicians have noted that this definition lacks precision, potentially influencing tone assessment and contributing to inconsistent findings due to subjective variation between examiners. [1][4]

Brief overview of normal muscle tone

The ongoing tension within skeletal muscle is attributed to result of passive viscoelasticity of multiple tissues and active low-level sustained muscle contraction.[5] The active or contractile components resulting from the activation of the motor unit are detectable by EMG, whereas the passive or viscoelastic components are independent of neural activity and not detected by EMG. [1]So, the muscle tone is dependent on two factors: nonneural (mechanical properties of muscle) and neural (neurophysiological properties of the skeletal muscle). [1]

Non-neural: The viscoelastic component depends upon several factors like the sarcomeric actin-myosin cross-bridges, the viscosity, elasticity, and extensibility of the contractile filaments, filamentous connection of the sarcomeric non-contractile proteins, osmotic pressure of the cells, and also on the surrounding connective tissues.[1]

Neural: Muscle tone is centrally controlled and regulated by a complex, dynamically adaptive neural system that is interconnected across the body and highly sensitive to postural demands. It is closely connected with excitability of lower levels of the nervous system, which is tuned by tonic descending neural drive. [5]

Types of Muscle Tone

Muscle tone can be classified as:[1]

Postural tone: Seen in axial muscles where gravity is the most important inciting factor. It results from a steady stretch on the muscles and tendons and manifests as prolonged muscle contraction.

Phasic tone is what is commonly assessed clinically in the extremities as a rapid and short duration response. It results from the rapid stretching of a tendon and attached muscle and more precisely, the muscle spindle.

Regulation of Muscle Tone

Muscle tone is regulated by spinal and supraspinal mechanisms:[1]

  • spinal control depends on the interaction between muscle spindle and spinal cord along with the interneurons, and
  • supraspinal control is regulated by facilitatory and inhibitory long tracts and cerebellum.
Stretch Reflex


Corticospinal Pathway


It is also influenced by various sources of sensory feedback in relation to postural demands, gravity, and arousal levels.[5]

Abnormal Tone

Hypertonia

Hypertonia: is the abnormal increase in muscle tone as a result of upper motor neuron lesions. It is defined as abnormally increased resistance to externally imposed movement about a joint. Hypertonia and spasticity are sometimes used synonymously. There are three following clinical types: spasticity, dystonia, and rigidity.[6]

Spasticity: is a motor disorder marked by an increase in muscle tone or tonic stretch reflexes associated with hypertonia. It arises as a result of damage to the corticoreticulospinal (pyramidal) tracts. It is both amplitude and velocity-dependent and is best assessed using rapid movements of the relevant joint to cause abrupt stretching of the muscle group involved. At a certain threshold of velocity, angle, or amplitude, a sudden increase in muscle tone can be observed as a distinct “catch.”[7] Clasp knife phenomenon is seen when limb initially resists movement and then suddenly gives way. It is seen in Cerebral Palsy, Multiple Sclerosis, Stroke, Hypoxic Brain Injury, Traumatic Brain Injury, Parkinson's Disease, Spinal cord injury.

Rigidity: is resistance to passive movement irrespective of posture and velocity. It is one of the cardinal features of Parkinson's disease, and is usually present in extrapyramidal disorders. It is different than spasticity, doesn’t depend on the velocity of movement and equally affects flexors and extensors and gives rise to uniform resistance to passive stretching in all directions known as ‘lead pipe’ phenomenon. [1] Also, a superimposed tremor, or “an underlying, not yet visible, tremor” could result in intermittent increase in tone during the passive movement of a joint and gives rise to an interrupted “cogwheeling” effect or ‘cog wheel’ rigidity in PD. [7]

Dystonia: is a hyperkinetic movement disorder characterised by sustained muscle contractions and abnormal postures of the trunk, neck, face, arms, and legs, often resulting in twisting and repetitive patterned movements, as well as abnormal postures related to the co-contraction of agonist and antagonist muscles. The pathophysiology involves several brain regions, including the basal ganglia, cerebellum, thalamus, and sensorimotor cortex, resulting in the development of abnormal neural motor programs. [8]

Opisthotonus: is defined as a dramatic abnormal posture due to spastic contraction of the extensor muscles of the neck, trunk, and lower extremities that produces a severe backward arching from neck to heel. It is usually sudden in onset and can be sustained or repetitive and can manifest at any stage of the disorder.Also, at times it is only symptom that identifies the correct disease. It is seen in infectious diseases (like meningitis, encephalitis, tetanus, rabies); in poisoning; developmental and metabolic (cerebral palsy, Krabbe disease, hyperbilirubinemia, and kernicterus, Gaucher disease); in increased intracranial pressure (intracranial hemorrhage, subarachnoid hemorrhage, hydrocephalus, or space-occupying lesion); neurodegenerative syndromes (due to brain iron accumulation, Wilson disease, cerebral palsy, and Parkinson disease); anoxic injury (after near-drowning, cardiac arrest, suffocation, or birth asphyxia. [9]

Decorticate and decerebrate posturing: are abnormal posturing responses that typically occur in response to noxious stimuli. They involve stereotypical movements of the trunk and extremities indicative of significant brain or spinal injury. [10] Decerebrate posturing is seen in brainstem lesions, whereas the decorticate posture follows lesions at the cerebral cortex level.[11] In decorticate posture, flexor posturing is observed along with internal rotation of the upper limbs, accompanied by extensor posturing of the lower limbs. The decorticate posturing suggests that the integrity of the rubrospinal tract is intact, and the extent of damage from the lesion has not extended below it. [12] Whereas in decerebrate posturing,  extensor posturing with internal rotation of both the upper and the power limbs is seen, which suggests that the vestibulospinal tract is spared and is intact. The damage from the injury has not extended beyond it.[12]

Hypotonia

Hypotonia: is characterised by poor muscle tone, resulting in floppiness. It is abnormally decreased resistance encountered with passive movement of the joint. It can be caused by dysfunction at any level of the motor pathway, including the central nervous system (brain and spinal cord), peripheral nerves, neuromuscular junction, or muscles. Hypotonia is seen in genetic disorders (e.g., Down syndrome , Joubert Syndrome), Spinal Muscular Atrophy, congenital myopathies.

Flaccidity: A severe form of hypotonia is flaccidity, characterised by muscles that offer no resistance to passive movement and appear completely limp.

Spinal shock: It is characterised by flaccid paralysis and loss of all reflexes below the level of the injury and occurs immediately after an acute spinal cord injury. [13] It is temporary and can last days to weeks; as spinal shock resolves, reflexes often return and may progress into spasticity.

Cerebral shock: Refers to a transient phase of decreased muscle tone and reflexes following an acute injury to the brain, such as a stroke or traumatic brain injury. Like spinal shock, it can resemble lower motor neuron weakness early on, but, over time may evolve into hypertonia as upper motor neuron pathways regain activity in a dysregulated way.

This video explains the pathways from the brain to the muscles and provides a general overview of upper and lower motor neuron lesions, focusing particularly on their causes and associated signs and symptoms:

[14]

Assessment

The tone is assessed clinically by performing passive movements around a joint to determine muscular resistance. The tone is perceived by the examiner, not by the patient. Assessment should include palpation of muscles to estimate the resting (baseline) state of muscle activation. It is important to note that tone is not rated by the presence or absence of muscle contraction at rest. Additionally, tone can be measured in muscles at rest or in those with involuntary active contraction, but it should not be measured during voluntary muscle contraction.[6]

Modified Ashworth Scale: is utilized to assess spasticity in various conditions: stroke, spinal cord injury, multiple sclerosis, cerebral palsy, traumatic brain injury, paediatric hypertonia and central nervous system lesions.

Tardieu Scale and the Modified Tardieu Scale: are used clinically to measure spasticity in patients with neurological conditions.

Hypertonia Assessment Tool: is a standardized clinical tool used to identify different forms of hypertonia in the paediatric population.

The video below demonstrates the examination of tone:

[15]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Ganguly J, Kulshreshtha D, Almotiri M, Jog M. Muscle tone physiology and abnormalities. Toxins. 2021 Apr 16;13(4):282.
  2. ↑ Kopecka B, Ravnik D, Jelen K, Bittner V. Objective methods of muscle tone diagnosis and their application—a critical review. Sensors. 2023 Aug 15;23(16):7189.
  3. ↑ Madhok SS, Shabbir N. Hypotonia.
  4. ↑ Shortland A. Muscle tone is not a well-defined term. Developmental Medicine and Child Neurology. 2018 Jul;60(7).
  5. ↑ 5.0 5.1 5.2 Cacciatore TW, Anderson DI, Cohen RG. Central mechanisms of muscle tone regulation: implications for pain and performance. Frontiers in Neuroscience. 2024 Dec 9;18:1511783.
  6. ↑ 6.0 6.1 Sanger TD, Delgado MR, Gaebler-Spira D, Hallett M, Mink JW, Task Force on Childhood Motor Disorders. Classification and definition of disorders causing hypertonia in childhood. Pediatrics. 2003 Jan 1;111(1):e89-97.
  7. ↑ 7.0 7.1 Fearon C, Doherty L, Lynch T. How do I examine rigidity and spasticity?. Movement Disorders Clinical Practice. 2015 Jun;2(2):204-.
  8. ↑ Stephen CD, Simonyan K, Ozelius L, Breakefield XO, Sharma N. Dystonia. Neurobiology of brain disorders. 2023 Jan 1:713-51.
  9. ↑ Shahade A, De Jesus O. Opisthotonus.
  10. ↑ Knight J, Decker LC. Decerebrate and decorticate posturing.
  11. ↑ Wei Y, Cui Y, Pang X, Wang W. A systematic review and meta-analysis on abnormal posturing among brain injury patients. Arquivos de Neuro-psiquiatria. 2024 Apr;82(04):001-10.
  12. ↑ 12.0 12.1 Munakomi S, Das JM. Decorticate Posturing. InStatPearls [Internet] 2023 May 1. StatPearls Publishing.
  13. ↑ Ziu E, Weisbrod LJ, Mesfin FB. Spinal shock. InStatPearls [Internet] 2024 Feb 12. StatPearls Publishing.
  14. ↑ Palindrome Upper vs Lower Motor Neuron Lesions Explained | UMN vs LMNAvailable from: https://www.youtube.com/watch?v=blmQ-v0lt3Y
  15. ↑ UCD MedicineNeurology - Topic 6 - Motor examination of the upper limbsAvailable fromhttps://www.youtube.com/watch?v=5knyQRCTHzw