Dystonias
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Dystonia (from Greek, meaning altered muscle tone) refers to a syndrome of involuntary sustained or spasmodic muscle contractions involving co-contraction of the agonist and the antagonist. The movements are usually slow and sustained, and they often occur in a repetitive and patterned manner; however, they can be unpredictable and fluctuate.
The frequent abnormal posturing and twisting can be painful, and the functional impact of dystonia can vary from barely noticeable to severely disabling. Consequently, dystonias can have a profound effect on the personal, vocational, and emotional life of a patient and can impact his/her ability to live independently.
The options to medically manage dystonic movements have traditionally been 4-fold; they consist of the following:
Rehabilitative therapies
Oral medications
Neurochemolytic interventions
Surgery
Psychological counseling and participation in support groups are vital adjuncts to medical and physical approaches in the multidisciplinary management of dystonia.
Surgical options for intractable dystonias include altering the location or length of problematic muscles, but this is rarely successful. Other techniques include transection of the spinal accessory nerve for cervical dystonia, stereotactic thalamotomy or pallidotomy for generalized dystonia, and deep brain stimulation (DBS). [1, 2, 3]
Thorough neurologic, physiatric, neuropsychologic, and physical therapy evaluations are important prior to consideration for surgery. Because of the risk of significant comorbidity, surgical approaches are reserved for patients with disabling dystonia in whom other treatment modalities have been exhausted.
For patient education information, see Torticollis.
Regardless of the cause, dystonic contractions can have a chronic course and can lead to severe persistent pain and disability. Because each type of dystonia is treated in a different manner, the distinction between the various types is therapeutically important. [4]
Dystonias can be classified according to the following characteristics:
Age of onset
Etiology
Anatomic distribution
With regard to patient age, dystonias can be classified as follows:
Infantile dystonia – Begins before age 2 years
Childhood dystonia – Begins at age 2-12 years
Juvenile dystonia – Begins at age 13-20 years
Adult dystonia – Begins after age 20 years
Primary (idiopathic) dystonia
Primary, or idiopathic, dystonias can present in a sporadic, autosomal dominant, autosomal recessive, or X-linked recessive manner. Heritable childhood-onset dystonia is particularly common among Ashkenazi Jewish people.
Currently, at least 12 types of dystonia can be distinguished on a genetic basis (see Table 1, below). Identification of more dystonia genes may lead to better understanding and treatment of these largely nondegenerative disorders.
Table 1. Classification of Primary Dystonia (Open Table in a new window)
Type
Affected Chromosome Arm
Clinical Features
Mode of Inheritance
DYT1
9q34
Early onset, generalized; starts in a limb
Autosomal dominant
DYT2
Not known
Early onset, generalized or segmental
Autosomal recessive
DYT3
Xq13.1
Approximately 50% of patients with parkinsonism
X-linked recessive
DYT4
Not known
Whispering dysphonia
Autosomal dominant
DYT5a
14q22.1-22.2
Onset in the first decade of life; starts distally in the leg and spreads to the proximal limb; diurnal fluctuation; dopa-responsive mutations in the guanosine triphosphate (GTP) cyclohydrolase I and tyrosine hydroxylase genes
Autosomal dominant
DYT5b
11p15.5
Dopa-responsive dystonia
Autosomal recessive
DYT6
8p21-22
Onset in adolescence; segmental
Autosomal dominant
DYT7
18p
Adult onset, focal (writer’s cramp, torticollis, dysphonia, blepharospasm)
Autosomal dominant
DYT8
DYT82q33-25
Paroxysmal dystonia-choreoathetosis triggered by stress, fatigue, alcohol
Autosomal dominant
DYT9
1p21-13.8
Paroxysmal dystonia; paresthesias, diplopia; spastic paraplegia between attacks
Autosomal dominant
DYT10
Not known
Paroxysmal dystonia-choreoathetosis precipitated by sudden movements
Autosomal dominant
DYT11
11q23
Myoclonus and dystonia
Autosomal dominant
DYT12
19q
Rapid-onset dystonia and parkinsonism
Not known
Secondary dystonia
This may result from a wide variety of neurologic diseases or inherited metabolic defects, including the following:
Huntington disease
Hallervorden-Spatz disease
Wilson disease (hepatolenticular degeneration)
Leigh disease
Lipid storage disease
Parkinsonism
Central nervous system infections
Cerebral or cerebellar tumors
Drug intoxication – Dopamine antagonists, neuroleptics, metoclopramide, and haloperidol, among others
Structural or hypoxic injury to the basal ganglia brainstem structures
On the basis of its clinical distribution, dystonia is classified as follows:
Focal dystonia – Involves a single body part
Segmental dystonia – Affects 2 or more contiguous regions of the body; examples of segmental dystonias of the head and neck include craniocervical dystonia, blepharospasm, oromandibular dystonia, and laryngeal dystonia
Multifocal dystonia – Consists of abnormalities in noncontiguous body parts
Generalized dystonia – Involves segmental crural dystonia and at least 1 other body part; dystonia musculorum deformans (or torsion dystonia), a generalized form of the disease, involves the trunk and limbs. [5]
Hemidystonia – Also called unilateral dystonia; usually associated with abnormalities in the contralateral basal ganglia [1]
Cervical dystonia, or torticollis, is the most common focal dystonia. Local limb dystonias often begin as action or task-specific dystonias, such as writer’s cramp dystonia or musician’s dystonia (repetitive wrist or finger movements). [6, 7] In 20-30% of patients, focal dystonias become segmental or multifocal.
Pseudodystonia encompasses a group of movement disorders that may express dystonialike movements as one of the clinical features of a syndrome. Sandifer syndrome, stiff-man syndrome, and Isaacs syndrome may fall into this category.
Cervical dystonia, or torticollis, is the most common focal dystonia. It has an insidious onset in people aged 30-50 years, although it can begin earlier. Cervical dystonia commonly affects women.
Intermittent spasms of the neck muscles or abnormal head movements occur because of contractions of the sternocleidomastoid, trapezius, and posterior cervical muscles. This effect results in a patterned, repetitive, and spasmodic movement that causes the head to twist (rotational torticollis), extend (retrocollis), flex (anterocollis), or tilt toward the shoulder (laterocollis). The patient may display more than 1 of these head movements simultaneously.
Patients may report psychiatric symptoms associated with depression or anxiety. These may be due to the chronic course of the illness rather than to real psychopathology.
Upper limb dystonia causes cramping and posturing of the elbows, hands, and fingers that lead to the inability to perform certain occupational tasks. The literature describes at least 55 occupations in which individuals are affected by this condition. Men and women are affected with equal frequency. Onset is in persons aged 10-50 years.
A common upper limb dystonia is known as writer’s cramp, occupational cramp, or graphospasm. This task-specific dystonia, manifesting as hyperextension or hyperflexion of the wrist and fingers, may be triggered by repetitive activities such as writing and attempting to play the piano or other musical instruments. [6, 7, 8] After cessation of the task, the spasm disappears. Although torticollis, tremor, and pain are accompanying symptoms, the spasm itself usually limits further activities.
The results of general physical and neuromusculoskeletal examinations are usually unremarkable. Some clinicians inadvertently label these conditions as occupational neuroses.
This may occur in stroke or dystonia-parkinsonism syndrome and lead to painful positioning of the leg, impaired gait, and altered bone development.
A study by Martino et al indicated that lower limb dystonia is an uncommon condition in adulthood. [9] Evaluating 579 patients with adult-onset primary dystonia, the investigators found 11 patients (8 women, 3 men) with lower limb dystonia, with the condition existing either alone (4 patients) or as part of a segmental/multifocal dystonia (7 patients). In 63.6% of the patients, the dystonia spread to the lower limb from another site, while in the remaining patients, the condition originated in the lower limb. The authors noted that 64% of the patients required treatment.
Oromandibular, facial, and lingual dystonias are grouped together because of their possible coexistence. Cranial dystonia, commonly known as Meige syndrome, is the most common craniocervical dystonia. Women are more commonly affected, and onset is in the sixth decade of life.
Dystonia musculorum deformans, or torsion dystonia, is the term used to describe a generalized form of dystonia that involves the trunk and limbs. There are at least 2 types, and onset may begin in childhood or adolescence, infrequently occurring as abnormal movement of a limb after an activity. The movements progress in severity and frequency until they become a continuous spasm, resulting in contortion of the body.
At first, rest relieves the spasms, but as the disease progresses, the level of activity and positioning have no effect. The shoulder, trunk, and pelvic muscles undergo spasmodic twisting, as do the limbs. The hands are seldom involved. The orofacial muscles also may be affected, leading to dysarthria and dysphagia.
The pathology of dystonia musculorum deformans has yet to be described. In some cases, genetics appear to play a role. [5] Autosomal dominant and recessive patterns of inheritance have been reported. A rare, sex-linked form associated with parkinsonism has been described in the Philippines.
This is a common complication of long-term antipsychotic drug treatment due to dopamine receptor antagonism. The precise mechanism is unknown, but the risk appears to increase with advancing age. When medication is withdrawn relatively early in a patient’s treatment, the dyskinesia may reverse, whereas after 6 months of exposure, the movement disorder may persist indefinitely. The clinical features of tardive dyskinesia include abnormal choreoathetoid movements, especially involving, in adults, the face and mouth (ie, blepharospasm, torticollis, oromandibular dystonia), and in children, the limbs. [10, 11]
Impaired basal ganglia outflow is thought to play a role in the genesis of some dystonias. Lesions in the putamen have been linked to hemidystonia. Bilateral putaminal involvement may be responsible for generalized dystonia.
Torticollis and hand dystonia are thought to result from involvement of the head of the caudate nucleus and thalamus, respectively. Disease of the thalamus and subthalamus, as well as derangement of hypothalamic function, also has been suspected.
Because the basal ganglia play a role in maintaining normal head posture, the basal ganglia and the vestibulo-ocular reflex pathway have been implicated in the development of cervical dystonia. Disturbances of neurotransmitter systems also have been described in dystonias. [5, 12] Abnormalities in blink reflex recovery suggest involvement of the brainstem. Cervical and upper limb traumas have been implicated as well.
A study by McClelland et al indicated that there are significant differences in the rate and pattern of pallidal firing according to the etiology and phenotype of dystonia. For example, the median firing frequency of the internal globus pallidus was higher in patients with primary dystonia than in those with secondary static dystonia and was higher in patients with progressive dystonia secondary to neuronal brain iron accumulation than in the other two groups. [13]
Drug-induced supersensitivity of striatal dopamine receptors and abnormality of gamma-aminobutyric acid (GABA)–ergic neurons are proposed mechanisms for some drug-induced dystonias. Although supersensitivity is an inevitable accompaniment of long-term antipsychotic drug treatment, tardive dyskinesia does not always occur.
Abnormalities of serotonin, dopamine, and norepinephrine in specific cerebral structures also have been associated with dystonia musculorum deformans. In a literature review of human and animal studies, Smit et al pointed out that reduced levels of the serotonin metabolite 5-hydroxyindolacetic acid have been found in association with dystonia. The investigators also identified 89 cases, reported in 49 papers, that demonstrated a relationship between dystonia and drugs that impact the serotonergic system. [14]
In dystonia, as in all neuromuscular disorders, history taking and physical examination are necessary. Family history is important; as many as 44% of patients have a family history of similar or other movement disorders.
Dystonia may be a clinical manifestation of many treatable neurologic conditions; therefore, a thorough screening should be performed to exclude Wilson disease (ie, hepatolenticular degeneration), hypoxic brain injury, traumatic brain injury, Huntington disease, Leigh disease, lipid storage disease, and Parkinson disease.
A number of medications can induce acute dystonic movements, and a careful investigation of the patient’s medication list must be performed to rule out iatrogenic causes. Common drugs that can induce movement disorders and dystonias include, but are not limited to, the following:
Dopamine antagonists
Haloperidol
Metoclopramide
Antiepileptics
Phenytoin
Carbamazepine
Valproic acid
Felbamate
Dopamine agonists
Levodopa
Monoamine oxidase inhibitors (MAOIs)
Adrenergic agents
Amphetamines
Methylphenidate
Caffeine
Beta agonists
Antihistamines
Tricyclic antidepressants
Buspirone
Lithium
Cimetidine
Oral contraceptives
Cocaine
Various laboratory studies should be considered in the evaluation of dystonia. Blood chemistries, liver functions, ceruloplasmin levels, and blood copper levels may be appropriate. [15]
Magnetic resonance imaging (MRI) and computed tomography (CT) scanning of the brain are especially important in the pediatric population and may identify hypoxic, hemorrhagic, or tumorous lesions. Slit-lamp eye examination for Kayser-Fleischer rings and 24-hour urine copper analysis also may be useful. [15]
Genetic screening for DYT gene abnormalities and genetic counseling are important for patients who have had an onset of primary dystonia before age 30 years or for persons who have an affected relative. [2]
As with most movement disorders, dystonia may be influenced by fatigue, anxiety, relaxation, or sleep. Thus, attention to overall health, environment, and stressors can make dystonia more manageable. [16, 17]
Dystonic movements are often exacerbated or triggered by voluntary or intentional movements of the same or other body parts. Involuntary movements can be transiently suppressed by a contact stimulus, such as placing a hand on the ipsilateral or contralateral side of the face or neck of a patient with spasmodic torticollis.
Some dystonic movements may last seconds or minutes, but others may last hours or weeks. They can lead to permanent contractures, boney deformity, or significantly impaired function. Appropriate use of upper and lower extremity splints and orthotics to support, guide, reduce, or stabilize movements can help to prevent orthopedic deformities.
Physical therapy techniques (eg, massage), slow stretching, and physical modalities (eg, ultrasonography, biofeedback) are sometimes helpful in persons with focal or regional dystonias. Patients with generalized dystonia often benefit from gait and mobility training, as well as from instruction in the use of assistive devices.
Various physiatric therapies and modalities have been used with limited success in the symptomatic treatment of dystonias. These include relaxation training, sensory stimulation, biofeedback, transcutaneous electrical nerve stimulation, and percutaneous dorsal column stimulation. [18]
Occupational therapy is an important means of training patients to perform activities of daily living (ADLs); it is also important for proper positioning and seating in patients whose mobility is impaired. Adaptive equipment should be provided to enhance function.
Speech therapists can offer training and communication aids to patients with oromandibular or laryngeal dystonia, and they can help in preventing complications in patients with transient dysphagia resulting from botulinum toxin injections.
Vocational rehabilitation may aid individuals in job retraining or in adapting to the workplace, as appropriate.
Medications can be somewhat effective in controlling dystonic movements, but the lack of knowledge about the exact pathophysiology of dystonia has made the development of specific pharmacologic therapies difficult. Systemic medications benefit about one third of patients and consist of a wide variety of options, including the following [2] :
Cholinergics
Benzodiazepams
Antiparkinsonism drugs
Anticonvulsants
Baclofen
Carbamazepine
Lithium
Successful drug therapy often requires combinations of several medications, with choices generally guided by empirical trials and adverse effect profiles. Doses should be slowly increased over the course of weeks or months until the therapeutic benefit is optimized or until adverse effects occur. In most patients, discontinuation of the drugs requires tapering to prevent withdrawal symptoms.
Baclofen, given intrathecally by an implanted pump, can be very effective in certain types of dystonia, especially if spasticity coexists. [2] Due to the low prevalence of side effects when the medicine is delivered into the cerebrospinal fluid, the ability to deliver the medicine continuously, and the ability to test the therapeutic effect prior to proceeding with surgery, this option may provide effective treatment for many patients.
Neurochemolysis of dystonic muscles is another important therapeutic option. Botulinum toxins or phenol/alcohol injections have become powerful tools in improving the symptomatic treatment of focal dystonias. [2, 19, 20, 21] These injections temporarily reduce the ability of the muscles to contract and may be the treatment of choice for blepharospasm, cervical dystonia, and hemifacial spasm.
Botulinum toxins are produced by the gram-negative bacterium Clostridium botulinum and act by inhibiting the presynaptic release of acetylcholine at the neuromuscular junction. Of the 7 immunologically distinct botulinum toxin serotypes, only types A and B are approved for clinical use. The onset of effect takes several days after injection.
The local injection of botulinum toxins into the offending muscles (often the sternocleidomastoid, trapezius, and splenius capitis) reduces muscle contraction for approximately 3 months. The treatment is not associated with significant complications, although dysphagia and dry mouth can occur. The medications can be used effectively for years, and although they are expensive, their cost is typically reimbursed by insurance. Most patients require repeated injections.
Phenol and alcohol nerve blocks also are temporary, but they last approximately 6 months and are significantly less expensive. However, only selected nerves can be injected, and a skilled practitioner is needed in order to avoid side effects.
The selection of appropriate muscles should be based on careful clinical assessment of the maximally involved muscles and on a clear delineation of the goals (eg, improved function, hygiene, pain relief). Initial needle placement in the chosen muscle, often with the aid of electromyelographic localization, is based on anatomic landmarks. The number of injection sites and overall dose vary depending on the size of the muscle, the degree of dystonia present, and the functional change desired.
DBS uses surgically implanted wires placed either unilaterally or bilaterally into target areas such as the thalamus, subthalamic nucleus, or globus pallidus. [22, 23] An implanted neurostimulator then delivers electrical stimulation through these wires to the brain. The best results have been obtained with pallidal stimulation in patients with primary dystonias, such as generalized DYT1 dystonia. [3, 24]
However, the optimal target point in different patients is still uncertain, and the long-term efficacy and side effects of DBS are unknown. [25, 26, 27, 28] Stereotactic placement of the electrodes requires a skilled neurosurgeon, and programming of the stimulator requires an experienced physiatrist or neurologist.
A prospective study by Volkmann et al found that the benefits of pallidal stimulation in patients with primary generalized or segmental dystonia were maintained at 5-year follow-up. In the study, significant improvements in dystonia were seen at 3-year follow-up to stimulation of the internal globus pallidus, with these improvements sustained by the patients at 5 years. Of 21 serious adverse events in the study, all resolved without permanent sequelae. [29]
Another study, by Romito et al, indicated that pallidal stimulation can improve dystonia occurring secondary to cerebral palsy. The study involved 15 patients with this condition who underwent stimulation of the internal globus pallidus; all had mild limb spasticity or mild static brain abnormalities on MRI. At last follow-up, the patients’ motor and disability scores, as measured using the Burke-Fahn-Marsden Dystonia Rating Scale, had improved by 49.5% and 30%, respectively, with health-related quality of life also having improved in the majority of patients. [30]
Using transcranial magnetic stimulation to study the physiologic effects of subthalamic nucleus deep brain stimulation (DBS) on cervical dystonia, Wagle Shukla et al found evidence that such DBS has only restricted effects on the physiology that underlies cervical dystonia. The investigators’ results indicated that DBS modulates sensorimotor integration and that this has good correlation with acute clinical improvement. However, DBS did not alter motor cortex excitability, and while it did normalize sensorimotor plasticity, this change was not found to be associated with clinical improvement. [31]
As previously mentioned, because of the risk of significant comorbidity, surgical approaches are reserved for patients with disabling dystonia in whom other treatment modalities have been exhausted.
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Jankovic J, Shale H. Dystonia in musicians. Semin Neurol. 1989 Jun. 9(2):131-5. [Medline].
Conti AM, Pullman S, Frucht SJ. The hand that has forgotten its cunning-lessons from musicians’ hand dystonia. Mov Disord. 2008 Apr 8. [Medline].
Zeuner KE, Knutzen A, Granert O, et al. Increased volume and impaired function: the role of the basal ganglia in writer’s cramp. Brain Behav. 2015 Feb. 5 (2):e00301. [Medline]. [Full Text].
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Hauser RA, Factor SA, Marder SR, et al. KINECT 3: A Phase 3 Randomized, Double-Blind, Placebo-Controlled Trial of Valbenazine for Tardive Dyskinesia. Am J Psychiatry. 2017 May 1. 174 (5):476-84. [Medline].
Assmann B, Kohler M, Hoffmann GF, et al. Selective decrease in central nervous system serotonin turnover in children with dopa-nonresponsive dystonia. Pediatr Res. 2002 Jul. 52(1):91-4. [Medline].
McClelland VM, Valentin A, Rey HG, et al. Differences in globus pallidus neuronal firing rates and patterns relate to different disease biology in children with dystonia. J Neurol Neurosurg Psychiatry. 2016 Feb 4. [Medline].
Smit M, Bartels AL, van Faassen M, et al. Serotonergic perturbations in dystonia disorders-a systematic review. Neurosci Biobehav Rev. 2016 Apr 9. 65:264-75. [Medline].
Becker G, Berg D, Francis M, et al. Evidence for disturbances of copper metabolism in dystonia: from the image towards a new concept. Neurology. 2001 Dec 26. 57(12):2290-4. [Medline].
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Winter Y, von Campenhausen S, Popov G, et al. Social and clinical determinants of quality of life in Parkinson’s disease in a Russian cohort study. Parkinsonism Relat Disord. 2009 Dec 17. [Medline].
Cho HJ, Hallett M. Non-Invasive Brain Stimulation for Treatment of Focal Hand Dystonia: Update and Future Direction. J Mov Disord. 2016 May. 9 (2):55-62. [Medline].
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Starr PA, Turner RS, Rau G, et al. Microelectrode-guided implantation of deep brain stimulators into the globus pallidus internus for dystonia: techniques, electrode locations, and outcomes. J Neurosurg. 2006 Apr. 104(4):488-501. [Medline].
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Type
Affected Chromosome Arm
Clinical Features
Mode of Inheritance
DYT1
9q34
Early onset, generalized; starts in a limb
Autosomal dominant
DYT2
Not known
Early onset, generalized or segmental
Autosomal recessive
DYT3
Xq13.1
Approximately 50% of patients with parkinsonism
X-linked recessive
DYT4
Not known
Whispering dysphonia
Autosomal dominant
DYT5a
14q22.1-22.2
Onset in the first decade of life; starts distally in the leg and spreads to the proximal limb; diurnal fluctuation; dopa-responsive mutations in the guanosine triphosphate (GTP) cyclohydrolase I and tyrosine hydroxylase genes
Autosomal dominant
DYT5b
11p15.5
Dopa-responsive dystonia
Autosomal recessive
DYT6
8p21-22
Onset in adolescence; segmental
Autosomal dominant
DYT7
18p
Adult onset, focal (writer’s cramp, torticollis, dysphonia, blepharospasm)
Autosomal dominant
DYT8
DYT82q33-25
Paroxysmal dystonia-choreoathetosis triggered by stress, fatigue, alcohol
Autosomal dominant
DYT9
1p21-13.8
Paroxysmal dystonia; paresthesias, diplopia; spastic paraplegia between attacks
Autosomal dominant
DYT10
Not known
Paroxysmal dystonia-choreoathetosis precipitated by sudden movements
Autosomal dominant
DYT11
11q23
Myoclonus and dystonia
Autosomal dominant
DYT12
19q
Rapid-onset dystonia and parkinsonism
Not known
Elizabeth A Moberg-Wolff, MD Medical Director, Pediatric Rehabilitation Medicine Associates
Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Aathi R Thiyagarajah, MD Consulting Staff, Department of Rehabilitation Medicine and Pain Management, Oaktree Medical Centre
Aathi R Thiyagarajah, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Pain Society, American Society of Regional Anesthesia and Pain Medicine, Association of Academic Physiatrists, Massachusetts Medical Society, South Carolina Medical Association
Disclosure: Nothing to disclose.
Steven A Barna, MD Medical Director of MGH Pain Clinic, Instructor of Anaesthesia, Department of Anesthesia and Critical Care, Harvard Medical School, Massachusetts General Hospital
Steven A Barna, MD is a member of the following medical societies: American Society of Interventional Pain Physicians
Disclosure: Nothing to disclose.
Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans
Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.
Michael T Andary, MD, MS Professor, Residency Program Director, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine
Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists
Disclosure: allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching
Milton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and Ohio Valley General Hospital
Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.
Juan Santiago-Palma, MD Orthopedic Surgeon, Oak Orthopedics
Juan Santiago-Palma, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Association for the Study of Pain, and North American Spine Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Reference Salary Employment
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