Updated: Oct 22, 2018
Author: Michael C Kruer, MD; Chief Editor: Selim R Benbadis, MD 



Torticollis is the common term for various conditions of head and neck dystonia, which display specific variations in head movements (phasic components) characterized by the direction of movement (horizontal, as if to say "no", or vertical, as if to say "yes"). Such to-and-fro movements of the head can be equal (as in a tremor) or unequal (ie, rapid clonic movements of the head and neck with slow recovery, termed spasmodic). Torticollis is derived from the Latin, tortus, meaning twisted and collum, meaning neck.

Torticollis results in a fixed or dynamic posturing of the head and neck in tilt, rotation, and flexion.[1] Spasms of the sternocleidomastoid, trapezius, and other neck muscles, usually more prominent on one side than the other, cause turning or tipping of the head.[2, 3] Note the images below.

Female patient presenting with torticollis. Image Female patient presenting with torticollis. Image courtesy of Danette C Taylor, DO, MS.
Female patient presenting with torticollis. Image Female patient presenting with torticollis. Image courtesy of Danette C Taylor, DO, MS.
Female patient presenting with torticollis. Image Female patient presenting with torticollis. Image courtesy of Danette C Taylor, DO, MS.

Characteristic head tilt often occurs from a tonic component. One example is laterocollis, in which the head is displaced with the ear moved toward the shoulder from increased tone in the ipsilateral cervical muscles. Another is rotational torticollis, in which partial rotation or torsion of the head occurs along the longitudinal axis. In anterocollis, the head and neck are held in forward flexion with increased tone of anterior cervical muscles; in retrocollis, the head and neck are held in hyperextension with increased tone in the posterior cervical muscles.

No matter which term is preferred in communicating about these conditions, the implication is that they all represent differing degrees of the same phenomenon. Jankovic et al[4] and Chan et al[5] preferred to avoid the popular term spasmodic torticollis and instead preferred cervical dystonia, because many patients have neither simple rotation nor spasmodic movements. In fact, several patients have combinations of movements, not as simple tremors but as responses to dystonic motor control.

Torticollis is not a diagnosis but a symptom of diverse conditions. Presentations of torticollis or cervical dystonia are often defined using causal terms—acute torticollis, congenital torticollis, chronic torticollis, or acquired torticollis, idiopathic or secondary. The last implies a chronic etiology, often of a structural nature (eg, odontoid fracture, cystic mass, cervical adenitis). Some of the more common causes include congenital problems, trauma, and infections.[2, 3, 6, 7, 8, 9, 10, 11]


Congenital torticollis

Congenital muscular torticollis is rare (< 2%) and is believed to be caused by local trauma to the soft tissues of the neck just before or during delivery.[7] The most common explanation involves birth trauma to the sternocleidomastoid (SCM) muscle, resulting in fibrosis or that intrauterine malpositioning leads to unilateral shortening of the SCM.[12] There may be resultant hematoma formation followed by muscular contracture. These children often have undergone breech or difficult forceps delivery.

The fibrosis in the muscle may be due to venous occlusion and pressure on the neck in the birth canal because of cervical and skull position. Another hypothesis includes malposition in utero resulting in intrauterine or perinatal compartment syndrome. Other causes of congenital torticollis include postural torticollis, pterygium colli (webbed neck), SCM cysts, vertebral anomalies, odontoid hyperplasia, spina bifida, hypertrophy or absence of cervical musculature, and Arnold-Chiari syndrome. It can also be seen with clavicular fractures, especially in neonates secondary to birth trauma. Up to 20% of children with congenital muscular torticollis have congenital dysplasia of the hip as well.[13, 14, 15, 16, 17, 18, 19]

Acquired torticollis

The pathophysiology of acquired torticollis depends on the underlying disease process. Cervical muscle spasm causing torticollis can result from any injury or inflammation of the cervical muscles or cranial nerves from different disease processes.

Acute torticollis can be the result of blunt trauma to head and neck, or from simply sleeping in an awkward position. Acute torticollis may be self-limited in days to weeks or the result of idiosyncrasy to certain medications (eg, traditional dopamine receptor blockers, metoclopramide, phenytoin, or carbamazepine.) After stopping medication, it quickly resolves without further action. After the resolution of acute traumatic torticollis, a chronic or persistent form may reappear after days or weeks of a quiescent interval. This situation often has legal implications regarding liability associated with the acute traumatic incident.

Atlantoaxial rotary subluxation (AARS) of C1 on C2 is important to consider and leads to a presentation similar to torticollis. It is predominant in children and generally occurs after minor trauma, pharyngeal surgery, an inflammatory process, or upper respiratory tract infection. It is thought to be precipitated by retropharyngeal edema leading to laxity of ligaments and structures at the atlantoaxial level, permitting the rotational deformity. In contrast to congenital muscular torticollis, the head tilts away from the affected SCM muscle. Known as the "cock robin" position, the head is rotated to the side opposite the facet dislocation and laterally flexed in the opposite direction.[20] Patients may also complain of unilateral occipital pain. AARS can also be a result of torticollis, although extremely rare.

Idiopathic spasmodic torticollis (IST) is a chronic, progressive form of torticollis classified as a focal dystonia. The etiology is unclear, although a thalamic lesion has been suspected. It is characterized by having an acquired, nontraumatic origin consisting of episodic tonic and/or clonic involuntary contractions of neck muscles. Symptoms last more than 6 months and result in considerable somatic and psychologic disability.

Benign paroxysmal torticollis is a self-limited condition common in infants characterized by repetitive episodes of head tilting with vomiting, pallor, irritability, ataxia, or drowsiness and usually presents in the first few months of life. Episodes can alternate sides. It is thought to be a migraine equivalent disorder, with some cases associated with underlying channelopathy.

Basal ganglia circuit abnormalities

As a neurodegenerative disease, torticollis, or idiopathic cervical dystonia, is believed to arise from basal ganglia circuit abnormalities stemming from selective vulnerability of these structures to an abnormal biochemical process that leads to neuronal dysfunction. Some indication of involvement of dopamine-secreting circuits comes from findings of low levels of metabolites of dopamine in the cerebrospinal fluid (CSF) and some minor improvements reported from individual trials of levodopa and traditional neuroleptics, both of which possess equal D1 and D2 receptor-binding properties. Neither moderate-dose levodopa nor high-dose anticholinergics are as effective in idiopathic torsion dystonias as in inherited dystonias, which therefore have clearly different receptor responses and circuit abnormalities.

The use of selective D2 ligands with single-photon emission computerized tomography (SPECT) scanning in 10 patients with torticollis has shown reduced D2-receptor binding in the basal ganglia.[21] Similar results have been noted in focal hand dystonia by using SPECT[22] and positron emission tomography (PET) scanning.[23] The implication is that underactivity occurs in the D2 dopamine receptors located in the indirect pallidal outflow pathway in both conditions. Such underactivity can be expected to cause disinhibited thalamocortical output and dystonic postures.

This relative imbalance between direct (D1-related) and indirect (D2-related) pallidal outflow pathways (see the image below) explains the failure of levodopa to adequately improve torticollis and the transient improvement from traditional neuroleptic agents, which initially may reduce D1 activity and eventually both D1 and D2 activity in both pathways.

Pallidal outflow pathways from basal ganglia to th Pallidal outflow pathways from basal ganglia to thalamus. E = excitatory; i = inhibitory; STN = subthalamic nucleus. Image courtesy of Norman C. Reynolds, MD, and Wisconsin Medical Journal.

Pramipexole is a dopamine agonist with selective, highly potent binding properties to D2 and D3 receptors. The authors have tried pramipexole in an open label trial in 14 patients with idiopathic cervical dystonia who displayed uncomplicated torticollis (unpublished results). Reduction in stiffness of neck muscles and head movements was reported in 6 patients who received 1.5 mg 3 times per day for at least 2 years. Five of 8 patients improved on 5 mg olanzapine, a dopamine-receptor blocker with minimal D1-blocking potency compared with its major D2- and D3-blocking potency. Atypical neuroleptic action suggests a bilateral relative binding effect, in which blocking the D2 action on the opposite indirect pathway may enhance the ipsilateral D2 receptor effect by comparison. This observation may suggest a mechanism of bilateral rather than unilateral basal ganglia control of torticollis.

Another approach to increasing the inhibitory output of the indirect pathway (an alternative to increasing D2 receptor action in the same pathway) is to deplete or block glutamate action. Selective glutamate release inhibition can be achieved with riluzole or with glutamate receptor blocking with amantadine, lamotrigine, or memantine.

Although the D3 activity of pramipexole has been linked to improvement in mood,[24] D3 receptors are also found in the striatum of the basal ganglia and may provide a role complementary to the expected increased activity in the indirect pathway provided by D2 action of the drug. The action of the atypical neuroleptics such as olanzapine or risperidone is quite interesting and needs far more extensive evaluation before a mechanism of rebalance can be offered.

Further studies of receptor binding are needed to clarify the unknown process leading to the slow evolution and progression of torticollis. Such understanding is also necessary in providing viable medication alternatives to repeated botulinum toxin injections every few months and the surgical alternatives offered in cases of injection failure.


Because idiopathic cervical dystonia is a neurodegenerative process, the confluence of etiologic factors in modern popular explanations applies here as it does in idiopathic Parkinson disease. Patients have a genetically determined susceptibility to environmental toxins, which, if encountered in threshold doses, activate free radical production in susceptible brain regions, leading to neuronal deterioration.

Because both idiopathic and delayed posttraumatic cervical dystonia wax and wane with emotional tone, the patient may believe an unjustified assertion that the dystonic problem is psychiatric in nature. This belief is easily reinforced by others who are not medically trained and actually was presumed by medical practitioners before the advent of synaptic chemistry and neurophysiology.

Occasionally, torticollis with dystonic components or major cervical dystonia occurs as part of the overall clinical picture of Parkinson disease. The entire degenerative disease process should not be considered 2 processes but rather 1 process (ie, Parkinson disease). When head tremors without dystonic components occur with postural tremors of the upper extremities, consider the entire syndrome essential tremor. When torticollis with dystonic components occurs with postural tremors of the upper extremities, regard the entire syndrome as a form of cervical dystonia.

Nondystonic torticollis can occur as an abnormal head position due to spinal deformity. In these patients, no palpable muscle hypertonus or hypertrophy and no record of sensory tricks should be present.

Local etiology in adults and children

In adults, acute wryneck is the most prevalent type of torticollis and develops overnight without provocation. It is self-limited, and symptoms resolve in 1-2 weeks.

Any abnormality or trauma of the cervical spine can present with torticollis. Trauma, including minor trauma (sprains/strains), fractures, dislocations, and subluxations, often result in spasms of cervical musculature. Other causes may involve infection, spondylosis, tumor, scar tissue, or ligamentous laxity in the atlantoaxial region. Spinal epidural hematomas are a potential life-threatening cause to consider. Torticollis also rarely presents secondary to intervertebral disk calcifications, cervical spine tumors, spondylitis, arteriovenous malformations, and other bony abnormalities.

Upper respiratory and soft-tissue infections of the neck can cause an inflammatory torticollis secondary to muscle contracture or adenitis. Torticollis has been associated with retropharyngeal abscesses and is important to consider, because it is potentially life-threatening.[25, 26] It is most commonly seen in children aged 2-4 y, but the incidence in adults is increasing. Patients typically present with neck discomfort, fever, stridor, dysphagia, drooling, odynophagia, and respiratory distress.

A 69-year-old woman presents with torticollis and A 69-year-old woman presents with torticollis and a fever.

Torticollis may also occur from infection following trauma or any infection involving surrounding tissue or structures of the neck including pharyngitis, tonsillitis, epiglottitis, sinusitis, otitis media, mastoiditis, nasopharyngeal abscess (see the image below), and upper lobe pneumonias.

Soft-tissue neck radiograph demonstrates retrophar Soft-tissue neck radiograph demonstrates retropharyngeal abscess appearing as torticollis.

Pediatric local etiology may include the following:

  • Congenital causes, such as pseudotumor of infancy, hypertrophy or absence of cervical musculature, spina bifida, hemivertebrae, and Arnold-Chiari syndrome

  • Otolaryngologic causes, such as vestibular dysfunction, otitis media, cervical adenitis, pharyngitis, retropharyngeal abscess, and mastoiditis

  • Esophageal reflux, particularly if episodic (ie, Sandifer syndrome)

  • Syrinx with spinal cord tumor

  • Traumatic causes, such as birth trauma, cervical fracture or dislocation, and clavicular fractures

  • Juvenile rheumatoid arthritis, with associated risk of atlanto-axial subluxation

Compensatory etiology in adults and children

Torticollis is also often seen as a compensatory mechanism for another disease or symptoms. Patients present with a head tilt to compensate for an essential head tremor or for diplopia secondary to an ocular muscle or nerve palsy.

Pediatric patients need a thorough eye examination to rule out a cranial nerve palsy or congenital nystagmus. Pediatric compensatory etiologies may include the following:

  • Strabismus with fourth cranial nerve paresis

  • Congenital nystagmus

  • Posterior fossa tumor

Central etiology in adults and children

Torticollis often presents as a dystonic reaction secondary to medications including phenothiazines, metoclopramide, haloperidol, carbamazepine, phenytoin, and L-dopa therapy. Dystonic reactions cause acute muscle spasms of certain muscle groups often resulting in torticollis, trismus, fixed upper gaze, grimace, clenched jaw, and difficulty with speech. It is treated with diphenhydramine or benzodiazepines.

Idiopathic spasmodic torticollis occurs more frequently in females, and onset typically occurs in those aged 30-60 years.[27]

Pediatric central etiology dystonias include torsion dystonia, drug-induced dystonia, and cerebral palsy.[28]


Reports of torticollis incidence are available primarily from the United States and Canada. Posttraumatic cases account for 10-20% of cases; the others are idiopathic. Consky and Lang reviewed several series to determine the relative frequency of torticollis types, with the following conclusions[29] :

  • Most cases of torticollis have mixtures of movements

  • Spasmodic features presumably dominate and relate to the classic descriptor of head jerks and spasms, hence the term spasmodic torticollis (no consensus exists regarding that description; the term cervical dystonia is preferred)

  • Torticollis with some degree of rotation is the most common individual type

  • After rotational torticollis in frequency come laterocollis and then retrocollis, with anterocollis being the rarest form

Although no racial predominance is reported for torticollis, females are affected twice as often as males,[30] and there are age-related differences. Onset of idiopathic cervical dystonia typically occurs when patients are aged 30-50 years (average age of onset, 40 y). Onset of posttraumatic cervical dystonia is within days of injury for the acute form and 3-12 months after injury for the delayed form. Congenital muscular torticollis occurs in less than 0.4% of newborns.[7]


Torticollis conditions do not usually lead to death, and the life span of affected individuals is normal. However, morbidity from this condition concerns 3 areas that may require additional treatment:

  • Chronic pain due to dystonia or strain in attempts to compensate for abnormal postures

  • Cervical spondylosis from chronic abnormal dystonic posture, which can lead to radiculopathies and/or spinal stenosis

  • Social embarrassment or the extreme of social isolation with depression

Ninety percent of patients with congenital muscular torticollis respond to passive stretching within the first year of life. For patients who undergo selective denervation, 65-80% experience satisfactory results, and these patients can be expected to maintain their improvement. No long-term prognosis for sternocleidomastoid release is available in the current literature.

Patient Education

Patients must understand that their condition is expected to wax and wane with emotions and that this phenomenon does not make their condition a psychologic problem.

Patient electromagnetic field precautions

Patients must be wary of any interaction with major electromagnetic fields associated with electrical generators in industrial applications, field detectors used in library screening to prevent book stealing, and metal detectors in general. Preflight check-in to airlines or other security checkpoints should avoid electromagnetic probes or wands that can turn off the deep brain stimulator (DBS). Nevertheless, the patient has a handheld magnetic trigger and can either turn on or off the pacemaker controller.

Magnetic resonance imaging (MRI) has special considerations because of massive fluctuations of magnetic fields that can cause the generator to cycle on and off. Before scanning, the pacemaker should be turned off (the patient can do this), and the amplitude setting of the controller should be set to zero (done by a physician or technician with special interrogator needs). Recycling at zero amplitude is not problematic.

Similar issues occur if electroconvulsive therapy is anticipated. When electric cardioversion is needed in a cardiopulmonary resuscitation (CPR) emergency, postsurvival adjustments can be made to maximize motor performance and the status of the DBS being on or off should not detract from needed lifesaving measures.


Certain motor activities or prolonged postural vocational requirements may exacerbate pain. An ergonomics evaluation in the workplace can be helpful. Changing or selecting positions can also be beneficial (ie, sitting to the left or the right of a speaker to avoid cervical strain).

For patient education information, see Torticollis and Whiplash.




Of patients with torticollis (cervical dystonia), 80-90% fall into the idiopathic category, typically without a family history. A positive family history suggests that the case in question may in fact be a residual form of an inherited generalized dystonia. The remaining 10-20% of patients with torticollis (cervical dystonia) fall into the posttraumatic category.

Other neurologic problems can mimic torticollis, and the practitioner should be alert to a history of adversive seizures, homonymous hemianopsia, and various ocular disturbances that lead to head tilt, including a variety of cervical spinal deformities, ocular palsies, congenital nystagmus, labyrinthine disease, and probable cervical adenitis. A positive history of chronic neuroleptic drug use may call attention to possible tardive dystonia.

Psychological factors such as depression or anxiety also may play a role. A very careful history should be taken, and thorough physical examination should be performed to try to discover the cause.

Idiopathic cervical dystonia

Idiopathic cervical dystonia demonstrates a slowly progressive course initiated in patients aged 30-50 years. Details of the extent of dystonia (including dystonic speech, involvement of upper limbs, other body parts with painful sustained contractures) may suggest a genetic or more generalized form of dystonia but can also occur as a natural progression of cervical symptoms over time.

Jahanshahi et al reported progression of dystonic symptoms to extranuchal but still cervical innervated sites (hand, arm, oromandibular region) in 32% of 72 patients with adult-onset cervical dystonia.[31] In addition, Comella et al observed both clinical dysphagia and subclinical swallowing motility disturbances in such patients.[32]

Action-induced or activity-induced worsening of torticollis and dystonia are typical, as are variable periods of lessened symptoms in the morning (ie, morning benefit). The symptoms are usually worsened by standing, walking, and stressful situations. Patients often discover certain sensory tricks (ie, gestes antagonistiques) that reduce head and neck movement (eg, touching the face in a particular spot with the thumb). The absence of sensory tricks can help distinguish acute traumatic torticollis and nondystonic torticollis from idiopathic and delayed dystonic torticollis.

Of patients with cervical dystonia, 10-20% experience spontaneous self-limited remissions that may be quite brief or last as long as 2-3 years. Patients most frequently present with torticollis unprovoked or after sleeping in an awkward position. Acute torticollis develops overnight and results in painful, palpable neck spasms the following morning. Symptoms usually resolve spontaneously within a few days, lasting no more than 1-2 weeks. It is treated with conservative, symptomatic management like analgesics, massage, exercise, and stretching.

Posttraumatic cervical dystonia

Posttraumatic cervical dystonia is divided into 2 subtypes, acute onset (initiated immediately to a few days after head and neck trauma) and delayed onset (3-12 mo after head and neck trauma).

Characteristics of acute posttraumatic cervical dystonia include local pain immediately following trauma such as concussion or whiplash injury, followed within days by a marked limitation in range of motion (ROM) of the neck and an abnormal posture of the head (without phasic components), elevation of the shoulder, and eventual hypertrophy of the trapezius. Two characteristics distinguish acute posttraumatic from idiopathic and delayed posttraumatic cervical dystonia: (1) no increase in symptoms with effort and (2) no inhibitory response to sensory tricks.

Delayed-onset posttraumatic cervical dystonia is nearly identical to idiopathic cervical dystonia and includes activation by effort and the ability to minimize symptoms by the use of sensory tricks.

Whether occupational overuse or subacute recurring trauma can lead to cervical dystonia, as hypothesized with focal hand dystonia (writer's cramp) or musicians' syndromes, is uncertain.[33]

Physical Examination

The primary goal in physical examination is to locate evidence for torticollis or cervical dystonia as the obvious primary finding representing the primary process, with additional dystonic features in the limb or hand being minimal and typically unilateral. Generalized dystonia does not reinforce the diagnosis but draws attention to idiopathic torsion dystonia/genetic forms of dystonia. The presence of craniofacial asymmetry indicates congenital or long-standing torticollis.

Patients with traumatic torticollis should be immobilized. Midline cervical tenderness suggests cervical spine trauma or osteomyelitis. In other cases, active and passive range of motion (ROM) should be evaluated.

The posterior pharynx should be examined for signs of inflammation and infection. The neck should be palpated for masses, adenopathy, or focal tenderness. A complete neurologic examination should be performed, including strength testing, sensory deficits, and gait.

Characterization of head and/or neck posture includes tonic components and dystonic head movements (phasic components).

Tonic head and neck posture (when chronic, may cause scoliosis)

In rotational torticollis, the head is turned around the long axis with nose and chin toward the shoulder; this is the most common head and neck deviation. This is not synonymous with torsion dystonia, a generalized dystonia named for rare athetoid components. Tone and bulk increase are appropriate in the sternomastoid contralateral to the direction of turn.

With simple torticollis, no head tilt is present. Document the increased tone of neck muscles as symmetric or absent, hypertrophied, or normal. In laterocollis, the head tilts to one side with the ear toward the shoulder; asymmetric tone and muscle bulk are also present. In anterocollis, the head tilts forward with chin toward the chest, and the anterior cervical muscles are increased in tone and bulk. In retrocollis, the head tilts in hyperextension, with increased tone and bulk in the posterior cervical muscles.

Phasic head components include the following:

  • Spasmodic jerks:- Rapid, irregular clonic jerks with less rapid recovery toward the neutral position

  • High-frequency oscillations: Horizontal, vertical, mixed, or irregular tremors

Other dystonic features

Extranuchal dystonias may occur on the side ipsilateral to the cervical dystonia (if bilateral or contralateral, consider more generalized or torsion dystonias). Oral, facial, or mandibular dystonias occasionally are associated with blepharospasm and laryngeal dystonia but not with neuroleptic use.

Nondystonic findings include the following:

  • Swallowing difficulty (trouble initiating)

  • Cervical radiculopathies (secondary to bony changes)

  • Ulnar neuropathy secondary to performing sensory tricks

  • Reactive depression, self-consciousness

Congenital torticollis

Patients with congenital muscular torticollis often have a firm, nontender, palpable soft-tissue mass in the sternocleidomastoid (SCM) muscle shortly after birth. This mass, which is more often localized near the clavicular attachment of the SCM, usually enlarges during the first 4-6 weeks of life and then gradually decreases in size. By age 4-6 months, the mass is usually absent, and the only clinical finding is the contracture of the sternocleidomastoid muscle and the torticollis posture. The head characteristically tilts toward the side of the mass with the chin rotated in the opposite direction.



Diagnostic Considerations

Distinguishing acute cervical trauma from traumatic torticollis may be difficult, but this is a recurring theme for car accident victims with persisting whiplash symptoms or for patients with industrial injuries when legal interest or chronic pain is an issue. Precise chronologic history is required in providing testimony to distinguish acute cervical trauma from posttraumatic torticollis. To maintain credibility during testimony, consistent statements of chronology are critical and must be prepared by careful review of the medical record by the physician giving testimony.

With postconcussive syndrome, whiplash head and neck injury from rapid acceleration and/or deceleration involves sprained and painful neck muscles, usually on both sides and the posterior muscles, along with global headache, inability to concentrate, and often dizziness and blurred vision.

Although beginning a few days or immediately following whiplash or other trauma, acute posttraumatic torticollis can be defined clearly only when the postconcussive syndrome is minimal. When the postconcussive syndrome is of great magnitude and persistent, acute posttraumatic torticollis can be identified clearly only after the acute strain and other postconcussive symptoms are eliminated in time or by analgesic medication (short-term narcotics or nonsteroidal anti-inflammatory drugs [NSAIDs]). "Residuals" of consistent abnormal head and neck posture with marked limitation of motion are not from the postconcussive syndrome (which is self-limited) but rather from acute posttraumatic torticollis (which is likely to be a chronic syndrome requiring botulinum toxin or a D2 agonist for long-term treatment).

Delayed posttraumatic torticollis is not a recurrence of the postconcussive or whiplash syndrome in the absence of a new injury but an identifiable torticollis syndrome with persistent abnormal posture of head and neck with major limitation in motion. The history of a previous whiplash or postconcussive syndrome establishes the original trauma that may eventually lead to torticollis due to intracranial brain changes in physiology as a delayed response to the original trauma.

Other conditions that should be considered in the evaluation of torticollis include the following:

  • Spinal deformity: Early childhood "dropped head syndrome" seen in myopathies and myasthenia, may mimic anterocollis

  • Juvenile cerebral palsy with cervical dystonia

  • Phenothiazine-induced acute dystonic reactions of childhood

  • Juvenile-onset Wilson disease: Often dystonic rather than dyskinetic

  • Juvenile-onset Huntington disease: Often dystonic and cervical

  • Acquired dystonia of childhood, such as hematoma or other tumor of sternocleidomastoid muscle

  • Gastroesophageal reflux (Sandifer syndrome) producing rapid flexion and odd postures reminiscent of torticollis subtypes: Sandifer syndrome is a term used to describe gastroesophageal reflux with abnormal posturing including torticollis in infants; torticollis occurs intermittently and can alternate sides; other symptoms of reflux may be present including regurgitation, anorexia, irritability, anemia, failure to thrive, coughing, asthma, and hoarseness; treatment is antireflux therapy

  • Anterior horn disease

  • Radiculopathy

  • C1 and C2 fractures

  • Movement disorders in individuals with developmental disabilities

Differential Diagnoses



Approach Considerations

When a positive family history suggests a familial dystonia rather than idiopathic cervical dystonia, DNA tests for specific genetic dystonias are available that detect causative mutations. Plain cervical spine films are useful in distinguishing sequelae of bony buildup and scoliosis or spondylosis secondary to chronic dystonia from structural changes of the spine that may mimic cervical dystonia per se (ie, nondystonic torticollis).

Magnetic resonance imaging (MRI) of the cervical cord is useful in documenting cord impingement leading to either spinal stenosis or multiple radiculopathy, all of which can be secondary to bony changes from chronic dystonia. Cranial imaging (computed tomography [CT] scanning or MRI) of cervical dystonias is indicated when the physical examination includes abnormal long tract findings (eg, in pyramidal tracts), ophthalmoplegia, and/or dementia.

Contrast swallowing studies can be performed in consultation with a speech pathologist to evaluate and treat patients for swallowing disorders that accompany cervical dystonia. Indications for these studies are to plan botulinum toxin injections, which, if too extensive, may worsen the swallowing mechanism.

Electromyography is useful in distinguishing myopathic from neuropathic processes, as follows:

  • Myopathic upper girdle muscles versus dystonic hypertrophied upper girdle muscles

  • Multiple cervical root entrapment (polyradiculopathy) versus brachial plexus or single nerve involvement versus combinations of the above associated with bony cervical changes from dystonia

  • Anterior horn disease shows fibrillations in involved root distributions (eg, amyotrophic lateral sclerosis, Charcot-Marie-Tooth disease).



Approach Considerations

A comprehensive approach to the medical care of torticollis includes several treatment goals. All underlying reversible causes of torticollis should be explored and treated appropriately.

Medications include nonsteroidal anti-inflammatory drugs (NSAIDs), benzodiazepines and other muscle relaxants, anticholinergics, and local intramuscular injections of botulinum toxin,[17, 34, 35, 36] or phenol. Physical therapy includes stretching exercises, massage, local heat, analgesics, sensory biofeedback, and transcutaneous electrical nerve stimulation (TENS).[37]

When conservative treatment measures fail, patients may undergo brain stimulation procedures, a sternocleidomastoid release, selective denervation, or dorsal cord stimulation. Surgical therapy may consist of the following:

  • Unipolar sternocleidomastoid release

  • Bipolar sternocleidomastoid release

  • Selective denervation

  • Dorsal cord stimulation

Conservative Management

In torticollis, the conventional dopamine agonists and antagonists are not effective (dopamine receptors D1=D2), as distinguished from the L-dopa–responsive dystonias (a set of inherited generalized dystonias). Anticholinergics (eg, trihexyphenidyl, benztropine) may be somewhat effective but are typically less so than in generalized or torsion dystonias.

Try unconventional dopamine agonists (dopamine receptors D2 >D1, such as pramipexole or ropinirole) or antagonists with D2, D3, D4 blocking activity, such as olanzapine or risperidone, or try glutamate release inhibitors (eg, riluzole) or glutamate receptor blockers (eg, high-dose amantadine, lamotrigine, memantine).

Botulinum toxin injection is the current popular treatment of choice. Selective medication choices may include clonazepam, especially if blepharospasm is part of the syndrome, or baclofen, especially if oromandibular dystonia is part of the syndrome.

Nonspecific medication choices include propranolol or primidone if prominent oscillatory components, or nonsteroidal anti-inflammatory drugs (NSAIDs) for arthritic components.

Patients may respond well to sensory feedback training. Muscle relaxation techniques may be tried. Cervical braces occasionally are made that reproduce the tactile advantage of a sensory trick, which controls movement and/or reduces dystonia.

Surgical Intervention

Typically, surgical care has been tried as a last resort for patients whose symptoms are refractory to botulinum injections; however, advances in brain stimulation technology and popular use has encouraged US Food and Drug Administration (FDA) approval for stimulator use, especially in the subthalamic nucleus (STN), as follows:

  • Selective ramisectomy for cervical musculature (late delayed recurrence can be a problem)

  • Deep brain stimulator electrode implants in the globus pallidus (GP) or the STN to control contralateral dystonia

Other procedures such as sternocleidomastoid release (unipolar/bipolar), selective denervation, or dorsal cord stimulation may be indicated. Preoperative electromyography (EMG) may be helpful in defining the exact muscles and nerves involved.

Surgery is contraindicated in patients in whom underlying reversible causes have not been excluded and in those in whom conservative therapy has not been attempted. In congenital muscular torticollis, a trial of nonoperative treatment for 12-24 months is allowed before surgical intervention is pursued, because 90% of these patients respond to passive stretching within the first year of life.[38]

Stereotactic neurosurgery

Stereotactic neurosurgery using brain stimulator technology is now a subspecialty that was originally confined to conditions of Parkinson disease (STN or GP placement) and non-Parkinsonian tremor (ventrointermediated thalamic nucleus [VIM] or STN placement) but has been expanded to include FDA-approved brain stimulator applications for dystonia (STN or GP placement) and experimental adaptations to Tourette syndrome (STN or GP placement), obsessive-convulsive disorder (OCD) and major affective disorders (cingulate placement), and phantom pain.

Torticollis involves cervical dystonia and, as such, qualifies as a candidate for consideration of treatment with deep brain stimulation. Now FDA approved, deep brain stimulation (DBS)[39] should be considered a competitive option to botulinum injections in consultation with a stereotactic neurosurgeon familiar with this application.

Stereotactic procedures targeting the pallidofugal fibers or Forel field have not had results encouraging enough for them to become widely accepted.

Sternocleidomastoid release

Sternocleidomastoid muscle release is often used in congenital muscular torticollis. For mild deformity, unipolar release of the muscle is performed distally. For moderate and severe torticollis, bipolar technique is used to release the muscle proximally and distally.

Although sternocleidomastoid release is described mainly for congenital torticollis, it may also be used in the other forms as well. Some patients may ultimately require a combination of several different surgical procedures for correction of torticollis.

Unipolar sternocleidomastoid release for congenital muscular torticollis

Make an incision 5 cm long just superior and parallel to the medial end of the clavicle and to the depth of the tendons of the sternal and clavicular attachments of the sternocleidomastoid muscle. Incise the tendon sheath longitudinally and pass a hemostat or other blunt instrument posterior to the tendons. Next, using traction on the hemostat, draw the tendons outside the wound and then superior and inferior to the hemostat; clamp them and resect 2.5 cm of their inferior ends. If contracted, divide the platysma muscle and adjacent fascia. Next, with the patient's head turned toward the affected side and the chin depressed, explore the wound digitally for any remaining bands of contracted muscle or fascia and, if any are found, divide them under direct vision until the deformity can, if possible, be overcorrected.

If overcorrection is not possible after this procedure, make a small transverse incision inferior to the mastoid process and carefully divide the muscle near the bone. Take care to avoid damaging the spinal accessory nerve. Close the wound or wounds and apply a bulky dressing that holds the head in the overcorrected position.

Bipolar sternocleidomastoid release

The bipolar sternocleidomastoid release, as described by Ferkel et al, for congenital muscular torticollis involves making a short transverse proximal incision behind the ear and dividing the sternocleidomastoid muscle insertion transversely just distal to the tip of the mastoid process.[7, 40] With this limited incision, the spinal accessory nerve is avoided, although the possibility that the nerve may take an anomalous route should be considered. Next, make a distal incision 4-5 cm long in line with the cervical skin creases 1 fingerbreadth proximal to the medial end of the clavicle and the sternal notch. Divide the subcutaneous tissue and platysma muscle, exposing the clavicular and sternal attachments of the sternocleidomastoid muscle. Carefully avoid the anterior and external jugular veins and the carotid vessels and sheath during the dissection.

Next, cut the clavicular portion of the muscle transversely and perform a Z-plasty on the sternal attachment in order to preserve the normal V-contour of the sternocleidomastoid muscle in the neckline. Obtain the desired degree of correction by manipulating the head and neck during the release. Occasionally, release of additional contracted bands of fascia or muscle is necessary before closure. Close both wounds with subcuticular sutures.

Selective denervation

Selective denervation is primarily used in the treatment of torticollis, and varying success rates have been reported since its introduction in the early 1980s by Claude Bertrand, MD, and his colleagues in Montreal, Canada.[41, 42, 43] Denervation involves resecting the nerves that supply the specific muscles involved and is irreversible. Because of this, an EMG is sometimes performed to correctly identify all muscles involved before the procedure.

Selective denervation using the Bertrand method involves dissection through fascial planes to expose and section the posterior primary rami throughout all cervical levels. Preoperative EMG isolates the exact muscles involved and their nerve supply, and only the involved segments are denervated. Once the nerve supply has been cut, the associated muscles will atrophy permanently.

Dorsal cord stimulation

In dorsal cord stimulation, the electrodes are inserted into the subarachnoid space laterally at the C1-C2 level, with a monopolar electrode threaded down to the C4-C5 level for a 7-10–day trial of stimulation. About two thirds of the patients have improvement in their symptoms, and most patients respond best to higher frequencies between 1100 and 1500 Hz. Patients who have significant relief and tolerate stimulation are considered candidates for permanent dorsal column stimulator electrode implantation. The epidural electrode is placed midline at the C1-C2 level and sutured in place so that it cannot become dislodged with neck movement.

Surgical complications

As with any surgical procedure within the calvarium, the possibility of bleeding or infection exists, but in the hands of a subspecialty trained stereotactic neurosurgeon, this is less than 2-3%. Previously, electrode displacement was a risk due to translational forces, but this problem has been overcome by proper technical advance in mechanical stabilization. Other complications include injury to spinal accessory nerve or nearby vasculature (including the jugular veins and carotid artery), neck muscle atrophy, loss of muscle control, instability, variable numbness or sensory loss, pain, and neck deformity.

Certain neuropsychiatric conditions may occur in a minority of postsurgical cases but are typically corrected by recalibration of impulse parameters (pulse width, frequency, and amplitude). These behavioral side effects include visual hallucinations, obsessive gambling, hypersexuality, and depression. This same set of issues occurs with medication adjustment in anti-Parkinson medications.

Electromagnetic field precautions post surgery

Patients must be wary of any interaction with major electromagnetic fields associated with electrical generators in industrial applications, field detectors used in library screening to prevent book stealing, and metal detectors in general. Preflight check-in to airlines or other security checkpoints should avoid electromagnetic probes or wands that can turn off the deep brain stimulator (DBS). Nevertheless, the patient has a handheld magnetic trigger and can either turn on or off the pacemaker controller.

Magnetic resonance imaging (MRI) has special considerations because of massive fluctuations of magnetic fields that can cause the generator to cycle on and off. Before scanning, the pacemaker should be turned off (the patient can do this), and the amplitude setting of the controller should be set to zero (done by a physician or technician with special interrogator needs). Recycling at zero amplitude is not problematic.

Similar issues occur if electroconvulsive therapy is anticipated. When electric cardioversion is needed in a cardiopulmonary resuscitation (CPR) emergency, postsurvival adjustments can be made to maximize motor performance and the status of the DBS being on or off should not detract from needed lifesaving measures.

Long-Term Monitoring

Regular outpatient visits are needed for routine medication checkups, repeat botulinum toxin injections, or recalibration of deep brain stimulation settings.

For unipolar sternocleidomastoid release, physical therapy that includes manual stretching of the neck to maintain the overcorrected position is begun 1 week after surgery. Manual stretching should be continued 3 times daily for 3-6 months. The use of plaster casts or braces is usually unnecessary.

For bipolar sternocleidomastoid release, physical therapy involving range of motion and muscle stretching and strengthening is started early. A cervical collar may be used for the first 6-12 weeks after surgery.



Medication Summary

The goals of pharmacotherapy in the treatment of torticollis are to reduce morbidity and prevent complications. Medication categories are as follows: (1) dystonia reducing (eg, trihexyphenidyl, pramipexole, glutamate release inhibitors and receptor blockers, botulinum toxin) and (2) selective adjunctive (eg, clonazepam for blepharospasm, baclofen for oromandibular dystonia, propranolol or primidone for prominent tremor).


Class Summary

Anticholinergic agents reduce dystonia.


Central cholinergic blockade is often an effective treatment strategy in dystonias in all categories, not just torticollis. Doses used in nontorticollis dystonias are often much higher than those suggested here. Anticholinergic agents should be tried initially and may be more effective in children than in adults. Children tend to tolerate much higher doses than adults.

Antiparkinson Agents, Dopamine Agonists

Class Summary

Agents with high potency at the D2 receptor, relative to lower potency at the D1 receptor, can be used to enhance activity in the indirect pallidal outflow pathway. This is especially useful in treating the cervical dystonias.

Pramipexole hydrochloride (Mirapex)

Pramipexole is an especially appropriate agent in treatment of torticollis, because its D2 specificity fits single photon emission computed tomography (SPECT) and positron emission tomography (PET) scanning evidence of D2 underactivity in the indirect pallidal outflow pathway. In addition, antidepressant properties are most appropriate to this group of patients and stem from the additional specificity of pramipexole for D3 receptors. Because of the tedium of regular painful injections that are required in botulinum toxin use, try administration of pramipexole before using the toxin.

Ropinirole hydrochloride (Requip)

Ropinirole is a nonergot dopamine agonist that has high relative in vitro specificity and full intrinsic activity at the D2 subfamily of dopamine receptors, binding with higher affinity to D3 than to D2 or D4 receptor subtypes. This agent has moderate affinity for opioid receptors. The precise mechanism of action of ropinirole as treatment for torticollis is unknown. However, it is possibly related to the stimulation of dopamine receptors in the striatum.

To avoid malignant hyperthermic complications when stopping the drug, discontinue ropinirole gradually over a 7-day period. Decrease the frequency of administration from tid to bid for 4 days. For the remaining 3 days, decrease the frequency to once daily before complete withdrawal.

Ropinirole serves as an alternative agent to pramipexole if that drug has objectionable adverse effects. Its dopamine receptor profile is similar to that of pramipexole.

Neurologics, Other

Class Summary

Glutamate release inhibition and glutamate receptor blockade are alternatives to potentiating D2 receptors in the indirect pallidal outflow pathway by reducing the glutamate-related excitatory circuit in this outflow pathway.

Riluzole (Rilutek)

Riluzole appears to block glutamatergic neurotransmission in the central nervous system (CNS) through indirect mechanisms. This agent may inactivate voltage-dependent sodium channels; it may also activate guanosine triphosphate-binding signal transduction proteins (G-proteins), which may cause inhibition of glutamate release.

This agent has the least adverse effects of the 3 drugs mentioned for glutamate release inhibition, but its expense is prohibitive unless the insurance carrier has a low copay. Because riluzole is classified as an orphan drug, the carrier is required to make payment by law (Federal Orphan Drug Act). Amantadine must be dosed above a threshold amount (usually 300 mg) to provide release inhibition above and beyond the dopamine receptor agonism. Lamotrigine is an acceptable alternative, but its effective dosing is not as clear and ranges from 25 to 100 mg tid. Memantine can also be tried as 10 mg bid.

Nevertheless, if riluzole is not covered by the insurance carrier, one can try amantadine, lamotrigine, or possibly memantine.


Amantadine inhibits N-methyl-D-aspartic acid (NMDA) receptor-mediated stimulation of acetylcholine release in rat striatum. This agent may enhance dopamine release, inhibit dopamine reuptake, stimulate postsynaptic dopamine receptors, or enhance dopamine receptor sensitivity. Glutamate receptor inhibition occurs at high doses only. Use amantadine only at 100 mg orally (PO) tid (lower doses or frequencies only provide dopamine agonism).

Memantine (Namenda)

Memantine is an N-methyl-D-aspartate (NMDA) antagonist.

Lamotrigine (Lamictal)

Lamotrigine blocks glutamate receptors and inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membrane. This drug is a back-up alternative to amantadine.

Beta-Blockers, Nonselective

Class Summary

Adrenergic beta-blocking agents offer antitremor action when overt tremor complicates torticollis.

Propranolol (Inderal LA, InnoPran XL)

Propranolol is often the first choice for tremor control in essential tremor and can be used as adjunctive medical therapy when tremor complicates torticollis.

Anticonvulsants, Other

Class Summary

Primidone is an anticonvulsant drug used in low doses for its antitremor effect.

Primidone (Mysoline)

The low-dose form of primidone is the traditional second choice agent for treatment of essential tremor. This drug is also possibly effective as an adjunct in treatment of torticollis with prominent tremor.

Antiparkinson Agents, Anticholinergics

Class Summary

The use of anticholinergics may improve morbidity.

Benztropine (Cogentin)

By blocking striatal cholinergic receptors, benztropine may help balance cholinergic and dopaminergic activity in striatum. This agent can be used as an alternative to trihexyphenidyl.

Nonsteroidal Anti-Inflammatory Agents (NSAIDs)

Class Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other possible mechanisms may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Aspirin (Ecotrin, Bayer Aspirin, Ascriptin)

Aspirin treats mild to moderately severe pain by inhibiting prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.

Ibuprofen (Motrin, I-Prin, Ultraprin)

Ibuprofen is the drug of choice (DOC) for patients with mild to moderately severe pain. This drug inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Neuromuscular Blockers, Botulinum Toxins

Class Summary

Paralysis of dystonic muscles by direct injection is used to reduce pain and abnormal posture. The various botulinum toxins possess individual potencies, and care is required to assure proper use and avoid medication errors. Changes to the established drug names by the US Food and Drug Administration (FDA) were intended to reinforce these differences and prevent medication errors. The products and their approved indications include the following:

- OnabotulinumtoxinA (Botox, Botox Cosmetic): Botox (cervical dystonia, blepharospasm)

- AbobotulinumtoxinA (Dysport): Cervical dystonia, moderate-to-severe glabellar lines

- IncobotulinumtoxinA (Xeomin): Cervical dystonia, blepharospasm

- RimabotulinummtoxinB (Myobloc): Cervical dystonia

OnabotulinumtoxinA (Botox)

Although botulinum toxin type A (Botox) is considered treatment of choice because of its degree of effectiveness, the duration of paralysis is limited to a few months, multiple sites must be injected, and electromyographic (EMG)–guided injections in neuromuscular junction are tedious and painful. On this basis, early oral (PO) medication trials with other drugs are desirable.

Alternatives to botulinum toxin type A (especially B and F) can be used if a patient develops resistance to type A by producing type A antibodies.

Botulinum toxin type A must be reconstituted from vacuum-dried toxin into 0.9% sterile saline without preservative according to manufacturer's instructions to provide an injection volume of 0.1 mL; this agent must be used within 4 hours of storage in a refrigerator at 2-8°C. Preconstituted dry powder must be stored in a freezer at less than 5°C.

IncobotulinumtoxinA (Xeomin)

IncobotulinumtoxinA is botulinum toxin type A that is free of complexing proteins found in the natural toxin from Clostridium botulinum. This drug is an acetylcholine release inhibitor and neuromuscular blocking agent. IncobotulinumtoxinA is indicated in adults for cervical dystonia in botulinum toxin–naive patients, and it is also indicated for blepharospasm in adults previously treated with onabotulinumtoxinA (Botox).

Antispastic/Gamma-Aminobutyric Acid Inhibitors

Class Summary

As an inhibitor of the neurotransmitter gamma-aminobutyric acid (GABA), baclofen can be used as an adjunctive medication when torticollis is complicated by oromandibular dystonia.

Baclofen (Lioresal, Gablofen)

Baclofen can be used to supplement other medications used to treat torticollis when oromandibular dystonia is present.

Anxiolytics, Benzodiazepines

Class Summary

Benzodiazepine agents provide adjunctive treatment for patients with blepharospasm.

Clonazepam (Klonopin)

Clonazepam is the preferred benzodiazepine for movement disorders. This agent can be used alone or to supplement other medications used to treat torticollis that is complicated by blepharospasm.

Antipsychotics, 2nd Generation

Class Summary

Antipsychotic agents are useful for treating dystonia that is associated with torticollis.

Olanzapine (Zyprexa, Zyprexa Zydis)

Olanzapine may inhibit serotonin, muscarinic, and dopamine effects. This agent exerts dopamine receptor blockade in both striatal (D2 > D1 receptor blockade) and in nonstriatal sites (D3, D4).

Risperidone (Risperdal, Risperdal M-Tab, Risperdal Consta)

Risperidone is an atypical neuroleptic. This agent binds to dopamine D2-receptor with 20 times lower affinity than for serotonin subtype 2 (5-HT2)–receptor affinity. Has weak affinity for dopamine D1 receptors and no affinity for muscarinics or beta-1 and beta-2 receptors.


Questions & Answers


What is torticollis?

What is the pathophysiology of congenital torticollis?

What is the pathophysiology of acquired torticollis?

What is the role of basal ganglia circuit abnormalities in the pathophysiology of torticollis?

What causes torticollis?

What causes torticollis in adults?

What causes torticollis in children?

What is the compensatory etiology of torticollis?

What is the central etiology of torticollis?

What is the prevalence of torticollis?

Which patient groups have the highest prevalence of torticollis?

What is the morbidity associated to torticollis?

What is the prognosis of torticollis?

What is included in patient education about torticollis?


What are the signs and symptoms of posttraumatic cervical dystonia in torticollis?

Which clinical history findings are characteristic of torticollis?

What is the progression of idiopathic cervical dystonia in torticollis?

What is included in the physical exam for torticollis?

What are the head and neck findings characteristic of torticollis?

Which dystonic features suggest torticollis?

Which nondystonic findings are characteristic of torticollis?

Which physical findings are characteristic of congenital torticollis?


How is acute cervical trauma differentiated from traumatic torticollis?

Which conditions should be included in the differential diagnosis of torticollis?

What are the differential diagnoses for Torticollis?


How is torticollis diagnosed?

What is the role of electromyography in the workup of torticollis?


What are the treatment options for torticollis?

What is included in the conservative management of torticollis?

What is the role of surgery in the treatment of torticollis?

What is the role of stereotactic neurosurgery in the treatment of torticollis?

What is the role of sternocleidomastoid release in the treatment of torticollis?

How is unipolar sternocleidomastoid release performed for the treatment of congenital muscular torticollis?

How is bipolar sternocleidomastoid release performed for the treatment of torticollis?

What is the role of selective denervation in the treatment of torticollis?

What is the role of dorsal cord stimulation in the treatment of torticollis?

What are the possible complications of the surgery for torticollis?

What electromagnetic field precautions are necessary after surgery for torticollis?

What is included in the long-term monitoring of patients with torticollis?


What is the role of medications in the treatment of torticollis?

Which medications in the drug class Antipsychotics, 2nd Generation are used in the treatment of Torticollis?

Which medications in the drug class Anxiolytics, Benzodiazepines are used in the treatment of Torticollis?

Which medications in the drug class Antispastic/Gamma-Aminobutyric Acid Inhibitors are used in the treatment of Torticollis?

Which medications in the drug class Neuromuscular Blockers, Botulinum Toxins are used in the treatment of Torticollis?

Which medications in the drug class Nonsteroidal Anti-Inflammatory Agents (NSAIDs) are used in the treatment of Torticollis?

Which medications in the drug class Antiparkinson Agents, Anticholinergics are used in the treatment of Torticollis?

Which medications in the drug class Anticonvulsants, Other are used in the treatment of Torticollis?

Which medications in the drug class Beta-Blockers, Nonselective are used in the treatment of Torticollis?

Which medications in the drug class Neurologics, Other are used in the treatment of Torticollis?

Which medications in the drug class Antiparkinson Agents, Dopamine Agonists are used in the treatment of Torticollis?

Which medications in the drug class Anticholinergics are used in the treatment of Torticollis?