Hypertonia

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Hypertonia
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Hypertonia is a term sometimes used synonymously with spasticity and rigidity in the literature surrounding damage to the central nervous system, namely upper motor neuron lesions. [1] Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition. [2] These consequences result in abnormally increased muscle tone of symptomatic muscles. [3] Some authors suggest that the current definition for spasticity, the velocity-dependent over-activity of the stretch reflex, is not sufficient as it fails to take into account patients exhibiting increased muscle tone in the absence of stretch reflex over-activity. They instead suggest that "reversible hypertonia" is more appropriate and represents a treatable condition that is responsive to various therapy modalities like drug or physical therapy. [4]

Contents

Presentation

Symptoms associated with central nervous systems disorders are classified into positive and negative categories. Positive symptoms include those that increase muscle activity through hyper-excitability of the stretch reflex (i.e., rigidity and spasticity) where negative symptoms include those of insufficient muscle activity (i.e. weakness) and reduced motor function. [5] Often the two classifications are thought to be separate entities of a disorder; however, some authors propose that they may be closely related. [6]

Pathophysiology

Characteristic features, analogy, and pathophysiology of common types of hypertonia. GTO - Golgi Tendon Organ 02 Types of hypertonia.svg
Characteristic features, analogy, and pathophysiology of common types of hypertonia. GTO – Golgi Tendon Organ

Hypertonia is caused by upper motor neuron lesions which may result from injury, disease, or conditions that involve damage to the central nervous system. The lack of or decrease in upper motor neuron function leads to loss of inhibition with resultant hyperactivity of lower motor neurons. Different patterns of muscle weakness or hyperactivity can occur based on the location of the lesion, causing a multitude of neurological symptoms, including spasticity, rigidity, or dystonia. [3]

Spastic hypertonia involves uncontrollable muscle spasms, stiffening or straightening out of muscles, shock-like contractions of all or part of a group of muscles, and abnormal muscle tone. It is seen in disorders such as cerebral palsy, stroke, and spinal cord injury. Rigidity is a severe state of hypertonia where muscle resistance occurs throughout the entire range of motion of the affected joint independent of velocity. It is frequently associated with lesions of the basal ganglia. Individuals with rigidity present with stiffness, decreased range of motion and loss of motor control. Rigidity is a nonselective increase in the tone of agonist and antagonist without velocity dependence, and the increased tone remains uniform throughout the range of movement. On the contrary, spasticity is a velocity-dependent increase in tone resulting from the hyper excitability of stretch reflexes. [7] It primarily involves the antigravity muscles – flexors of the upper limb and extensors of the lower limb. During the passive stretch, a brief “free interval” is appreciated in spasticity but not in rigidity because the resting muscle is electromyographically silent in spasticity. In contrast, in rigidity, the resting muscle shows firing. [8] Dystonic hypertonia refers to muscle resistance to passive stretching (in which a therapist gently stretches the inactive contracted muscle to a comfortable length at very low speeds of movement) and a tendency of a limb to return to a fixed involuntary (and sometimes abnormal) posture following movement.[ citation needed ]

Management

Therapeutic interventions are best individualized to particular patients.[ citation needed ] Basic principles of treatment for hypertonia are to avoid noxious stimuli and provide frequent range of motion exercise.[ citation needed ]

Physical interventions

Physiotherapy has been shown to be effective in controlling hypertonia through the use of stretching aimed to reduce motor neuron excitability. [9] The aim of a physical therapy session could be to inhibit excessive tone as far as possible, give the patient a sensation of normal position and movement, and to facilitate normal movement patterns. While static stretch has been the classical means to increase range of motion, PNF stretching has been used in many clinical settings to effectively reduce muscle spasticity. [10]

Icing and other topical anesthetics may decrease the reflexive activity for short period of time in order to facilitate motor function. Inhibitory pressure (applying firm pressure over muscle tendon) and promoting body heat retention and rhythmic rotation (slow repeated rotation of affected body part to stimulate relaxation) [11] have also been proposed as potential methods to decrease hypertonia. Aside from static stretch casting, splinting techniques are extremely valuable to extend joint range of motion lost to hypertonicity. [12] A more unconventional method for limiting tone is to deploy quick repeated passive movements to an involved joint in cyclical fashion; this has also been demonstrated to show results on persons without physical disabilities. [9] For a more permanent state of improvement, exercise and patient education is imperative. [11] Isokinetic, [13] [14] [15] [16] aerobic, [17] [18] [19] and strength training [20] [21] [22] [23] exercises should be performed as prescribed by a physiotherapist, and stressful situations that may cause increased tone should be minimized or avoided. [11]

Pharmaceutical interventions

Baclofen, diazepam and dantrolene remain the three most commonly used pharmacologic agents in the treatment of spastic hypertonia. Baclofen is generally the drug of choice for spinal cord types of spasticity, while sodium dantrolene is the only agent which acts directly on muscle tissue. Tizanidine is also available. Phenytoin with chlorpromazine may be potentially useful if sedation does not limit their use. Ketazolam, not yet available in the United States,[ needs update ] may be a significant addition to the pharmacologic set of options. Intrathecal administration of antispastic medications allows for high concentrations of drug near the site of action, which limits side effects. [12]

See also

Related Research Articles

Hemiparesis, or unilateral paresis, is weakness of one entire side of the body. Hemiplegia is, in its most severe form, complete paralysis of half of the body. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke.

<span class="mw-page-title-main">Cerebral palsy</span> Group of movement disorders that appear in early childhood

Cerebral palsy (CP) is a group of movement disorders that appear in early childhood. Signs and symptoms vary among people and over time, but include poor coordination, stiff muscles, weak muscles, and tremors. There may be problems with sensation, vision, hearing, and speaking. Often, babies with cerebral palsy do not roll over, sit, crawl or walk as early as other children of their age. Other symptoms include seizures and problems with thinking or reasoning, each of which occur in about one-third of people with CP. While symptoms may get more noticeable over the first few years of life, underlying problems do not worsen over time.

Spasticity is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles.

Hereditary spastic paraplegia (HSP) is a group of inherited diseases whose main feature is a progressive gait disorder. The disease presents with progressive stiffness (spasticity) and contraction in the lower limbs. HSP is also known as hereditary spastic paraparesis, familial spastic paraplegia, French settlement disease, Strumpell disease, or Strumpell-Lorrain disease. The symptoms are a result of dysfunction of long axons in the spinal cord. The affected cells are the primary motor neurons; therefore, the disease is an upper motor neuron disease. HSP is not a form of cerebral palsy even though it physically may appear and behave much the same as spastic diplegia. The origin of HSP is different from cerebral palsy. Despite this, some of the same anti-spasticity medications used in spastic cerebral palsy are sometimes used to treat HSP symptoms.

<span class="mw-page-title-main">Muscle spindle</span> Innervated muscle structure involved in reflex actions and proprioception

Muscle spindles are stretch receptors within the body of a skeletal muscle that primarily detect changes in the length of the muscle. They convey length information to the central nervous system via afferent nerve fibers. This information can be processed by the brain as proprioception. The responses of muscle spindles to changes in length also play an important role in regulating the contraction of muscles, for example, by activating motor neurons via the stretch reflex to resist muscle stretch.

<span class="mw-page-title-main">Clonus</span> Set of involuntary and rhythmic muscular contractions and relaxations

Clonus is a set of involuntary and rhythmic muscular contractions and relaxations. Clonus is a sign of certain neurological conditions, particularly associated with upper motor neuron lesions involving descending motor pathways, and in many cases is accompanied by spasticity. Unlike small spontaneous twitches known as fasciculations, clonus causes large motions that are usually initiated by a reflex. Studies have shown clonus beat frequency to range from three to eight Hz on average, and may last a few seconds to several minutes depending on the patient’s condition.

<span class="mw-page-title-main">Functional electrical stimulation</span> Technique that uses low-energy electrical pulses

Functional electrical stimulation (FES) is a technique that uses low-energy electrical pulses to artificially generate body movements in individuals who have been paralyzed due to injury to the central nervous system. More specifically, FES can be used to generate muscle contraction in otherwise paralyzed limbs to produce functions such as grasping, walking, bladder voiding and standing. This technology was originally used to develop neuroprostheses that were implemented to permanently substitute impaired functions in individuals with spinal cord injury (SCI), head injury, stroke and other neurological disorders. In other words, a person would use the device each time he or she wanted to generate a desired function. FES is sometimes also referred to as neuromuscular electrical stimulation (NMES).

Hypotonia is a state of low muscle tone, often involving reduced muscle strength. Hypotonia is not a specific medical disorder, but a potential manifestation of many different diseases and disorders that affect motor nerve control by the brain or muscle strength. Hypotonia is a lack of resistance to passive movement, whereas muscle weakness results in impaired active movement. Central hypotonia originates from the central nervous system, while peripheral hypotonia is related to problems within the spinal cord, peripheral nerves and/or skeletal muscles. Severe hypotonia in infancy is commonly known as floppy baby syndrome. Recognizing hypotonia, even in early infancy, is usually relatively straightforward, but diagnosing the underlying cause can be difficult and often unsuccessful. The long-term effects of hypotonia on a child's development and later life depend primarily on the severity of the muscle weakness and the nature of the cause. Some disorders have a specific treatment but the principal treatment for most hypotonia of idiopathic or neurologic cause is physical therapy and/or occupational therapy for remediation.

The primary goals of stroke management are to reduce brain injury and promote maximum patient recovery. Rapid detection and appropriate emergency medical care are essential for optimizing health outcomes. When available, patients are admitted to an acute stroke unit for treatment. These units specialize in providing medical and surgical care aimed at stabilizing the patient's medical status. Standardized assessments are also performed to aid in the development of an appropriate care plan. Current research suggests that stroke units may be effective in reducing in-hospital fatality rates and the length of hospital stays.

<span class="mw-page-title-main">Baclofen</span> Medication for muscle movement disorders

Baclofen, sold under the brand name Lioresal among others, is a medication used to treat muscle spasticity such as from a spinal cord injury or multiple sclerosis. It may also be used for hiccups and muscle spasms near the end of life, and off-label to treat alcohol use disorder or opioid withdrawal symptoms. It is taken orally or by intrathecal pump. It is also sometimes used transdermally in combination with gabapentin and clonidine prepared at a compounding pharmacy.

In physiology, medicine, and anatomy, muscle tone is the continuous and passive partial contraction of the muscles, or the muscle's resistance to passive stretch during resting state. It helps to maintain posture and declines during REM sleep. Muscle tone is regulated by the activity of the motor neurons and can be affected by various factors, including age, disease, and nerve damage.

Primary lateral sclerosis (PLS) is a very rare neuromuscular disease characterized by progressive muscle weakness in the voluntary muscles. PLS belongs to a group of disorders known as motor neuron diseases. Motor neuron diseases develop when the nerve cells that control voluntary muscle movement degenerate and die, causing weakness in the muscles they control.

<span class="mw-page-title-main">Stretch reflex</span> Muscle contraction in response to stretching

The stretch reflex, or more accurately "muscle stretch reflex", is a muscle contraction in response to stretching a muscle. The function of the reflex is generally thought be maintaining the muscle at a constant length but the response is often coordinated across multiple muscles and even joints. The term deep tendon reflex is often wrongfully used by many health workers and students to refer to this reflex. "Tendons have little to do with the response, other than being responsible for mechanically transmitting the sudden stretch from the reflex hammer to the muscle spindle. In addition, some muscles with stretch reflexes have no tendons ".

A selective dorsal rhizotomy (SDR), also known as a rhizotomy, dorsal rhizotomy, or a selective posterior rhizotomy, is a neurosurgical procedure that selectively cut problematic nerve roots of the spinal cord. This procedure has been well-established in the literature as a surgical intervention and is used to relieve negative symptoms of neuromuscular conditions such as spastic diplegia and other forms of spastic cerebral palsy. The specific sensory nerves inducing spasticity are identified using electromyographic (EMG) stimulation and graded on a scale of 1 (mild) to 4. Abnormal nerve responses are isolated and cut, thereby reducing symptoms of spasticity.

<span class="mw-page-title-main">Paratonia</span>

Paratonia is the inability to relax muscles during muscle tone assessment. There are two types of paratonia: oppositional and facilitatory. Oppositional paratonia ("gegenhalten") occurs when subjects involuntarily resist passive movements, while facilitatory paratonia ("mitgehen") occurs when subjects involuntarily assist with passive movements.

Clasp-knife response refers to a Golgi tendon reflex with a rapid decrease in resistance when attempting to flex a joint, usually during a neurological examination. It is one of the characteristic responses of an upper motor neuron lesion. It gets its name from the resemblance between the motion of the limb and the sudden closing of a claspknife after sufficient pressure is applied.

Scissor gait is a form of gait abnormality primarily associated with spastic cerebral palsy. That condition and others like it are associated with an upper motor neuron lesion.

<span class="mw-page-title-main">Management of cerebral palsy</span>

Over time, the approach to cerebral palsy management has shifted away from narrow attempts to fix individual physical problems – such as spasticity in a particular limb – to making such treatments part of a larger goal of maximizing the person's independence and community engagement. Much of childhood therapy is aimed at improving gait and walking. Approximately 60% of people with CP are able to walk independently or with aids at adulthood. However, the evidence base for the effectiveness of intervention programs reflecting the philosophy of independence has not yet caught up: effective interventions for body structures and functions have a strong evidence base, but evidence is lacking for effective interventions targeted toward participation, environment, or personal factors. There is also no good evidence to show that an intervention that is effective at the body-specific level will result in an improvement at the activity level, or vice versa. Although such cross-over benefit might happen, not enough high-quality studies have been done to demonstrate it.

<span class="mw-page-title-main">Athetoid cerebral palsy</span> Type of cerebral palsy associated with basal ganglia damage

Athetoid cerebral palsy, or dyskinetic cerebral palsy, is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic–ischemic brain injury. Unlike spastic or ataxic cerebral palsies, ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques. While there are no cures for ADCP, some drug therapies as well as speech, occupational therapy, and physical therapy have shown capacity for treating the symptoms.

Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion.

References

  1. ↑ "Archived copy". Archived from the original on 2013-06-18. Retrieved 2012-12-17.{{cite web}}: CS1 maint: archived copy as title (link)[ full citation needed ]
  2. ↑ O'Sullivan, Susan (2007). Physical Rehabilitation . Philadelphia, Pennsylvania: F.A Davis Company. p.  234. ISBN   9780803612471.
  3. 1 2 Sheean, Geoffrey; McGuire, John R. (2009). "Spastic Hypertonia and Movement Disorders: Pathophysiology, Clinical Presentation, and Quantification". PM&R. 1 (9): 827–33. doi:10.1016/j.pmrj.2009.08.002. PMID   19769916. S2CID   30715890.
  4. ↑ Bakheit, A.M.; Fheodoroff, K.; Molteni, F. (2011). "Spasticity or Reversible Muscle Hypertonia?". Journal of Rehabilitation Medicine. 43 (6): 556–7. doi: 10.2340/16501977-0817 . PMID   21491075.
  5. ↑ Sanger, T. D.; Chen, D.; Delgado, M. R.; Gaebler-Spira, D.; Hallett, M.; Mink, J. W. (2006). "Definition and Classification of Negative Motor Signs in Childhood". Pediatrics. 118 (5): 2159–67. doi:10.1542/peds.2005-3016. PMID   17079590. S2CID   1974796.
  6. ↑ Damiano, Diane L; Dodd, Karen (2002). "Should we be testing and training muscle strength in cerebral palsy?". Developmental Medicine & Child Neurology. 44 (1): 68–72. doi:10.1111/j.1469-8749.2002.tb00262.x. PMID   11811654.
  7. ↑ Rushton, David N. (2008-04-24), "Intrathecal baclofen for the control of spinal and supraspinal spasticity", Upper Motor Neurone Syndrome and Spasticity, Cambridge University Press, pp. 181–192, doi:10.1017/cbo9780511544866.011, ISBN   9780521689786 , retrieved 2023-07-31
  8. ↑ Ramanathan, Venkateswaran; Baskar, Dipti; Pari, Hariswar (2022). "'Seatbelt Effect' of spasticity: Contrasting velocity dependence from the clasp knife phenomenon". Annals of Indian Academy of Neurology. 25 (3): 517–519. doi: 10.4103/aian.aian_817_21 . ISSN   0972-2327. PMC   9350785 . PMID   35936584.
  9. 1 2 Chang, Ya-Ju; Fang, Chia-Ying; Hsu, Miao-Ju; Lien, Hen-Yu; Wong, Mei-Kwan (2007). "Decrease of hypertonia after continuous passive motion treatment in individuals with spinal cord injury". Clinical Rehabilitation. 21 (8): 712–8. doi:10.1177/0269215507079137. PMID   17846071. S2CID   12538385.
  10. ↑ Sharman, Melanie J; Cresswell, Andrew G; Riek, Stephan (2006). "Proprioceptive Neuromuscular Facilitation Stretching". Sports Medicine. 36 (11): 929–39. doi:10.2165/00007256-200636110-00002. PMID   17052131. S2CID   3123371.
  11. 1 2 3 O'Sullivan, Susan (2007). Physical Rehabilitation . Philadelphia, PA: F.A Davis Company. p.  497. ISBN   9780803612471.
  12. 1 2 Katz, Richard T. (1988). "Management of spasticity". American Journal of Physical Medicine & Rehabilitation. 67 (3): 108–16. doi:10.1097/00002060-198806000-00004. PMID   3288246. S2CID   45292155.
  13. ↑ Giuliani, Carol A. (1997). "The Relationship of Spasticity to Movement and Considerations for Therapeutic Interventions". Neurology Report. 21 (3): 78–84. doi: 10.1097/01253086-199721030-00009 .
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  15. ↑ Giuliani, C A; Light, K E; Rose, D K. (1993). "The Effect of an Isokinetic Exercise Program on Gait Patterns in Patients with Hemiparesis". Neurology Report. 17 (4): 23–4. doi: 10.1097/01253086-199317040-00029 .
  16. ↑ Brown, D. A.; Kautz, S. A. (1998). "Increased Workload Enhances Force Output During Pedaling Exercise in Persons With Poststroke Hemiplegia". Stroke. 29 (3): 598–606. CiteSeerX   10.1.1.568.9281 . doi:10.1161/01.STR.29.3.598. PMID   9506599.
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  20. ↑ Damiano, Diane L.; Abel, Mark F. (1998). "Functional outcomes of strength training in spastic cerebral palsy". Archives of Physical Medicine and Rehabilitation. 79 (2): 119–25. doi:10.1016/S0003-9993(98)90287-8. PMID   9473991.
  21. ↑ Damiano, Diane L.; Vaughan, Christopher L.; Abel, Mark E. (1995). "Muscle response to heavy resistance exercise in children with spastic cerebral palsy". Developmental Medicine and Child Neurology. 37 (8): 731–9. doi:10.1111/j.1469-8749.1995.tb15019.x. PMID   7672470. S2CID   33519087.
  22. ↑ Miller, G T; Light, K E; Kellog, R. (1996). "Comparison of Isometric-Force Control Measures in Spastic Muscle of Poststroke Individuals Before and After Graded Resistive Exercise". Neurology Report. 20 (2): 92–3. doi: 10.1097/01253086-199620020-00041 .
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