Blog

Dystonia Symptoms Explained: A New Theory on Neural Disruption and Muscle Selectivity

profile-picture
Joaquin Farias PHD, MA, MS

In this article, Dr. Farias presents his models explaining why dystonia affects certain muscle groups while sparing others. He explores the concept that all forms of dystonia may be linked to a common neural disruption. By examining the selective involvement of specific cranial and peripheral nerves—such as the facial, accessory, ulnar, and peroneal—through neuroanatomical, developmental, and functional lenses, this piece offers a unified framework for understanding the disorder’s diverse manifestations.

Dystonia-and-nerves

 

Dystonia encompasses a group of neurological conditions marked by involuntary muscle contractions that compel the body into abnormal, occasionally painful, movements and postures.1 This heterogeneous disorder can affect various parts of the body and arise from diverse causes.1 A perplexing aspect of dystonia is the apparent selective involvement of certain nerve groups, notably specific cranial nerves and, among somatic nerves, the ulnar and peroneal branches. Understanding why these particular nerves are more prone to the effects of dystonia is crucial for unraveling the underlying mechanisms of this debilitating condition. The impact of dystonia on individuals can range considerably, from mild, intermittent symptoms to severe, incapacitating manifestations that significantly diminish their quality of life.1 The diverse clinical presentations observed across the spectrum of dystonias suggest that the etiological underpinnings may involve a range of mechanisms, with varying degrees of influence on different neural circuits. The preferential targeting of specific nerve groups could therefore offer vital clues to these intricate mechanisms. Furthermore, the contribution of both genetic and non-genetic factors to the development of dystonia 1 implies that the selective vulnerability of these nerve groups might stem from a combination of inherent predispositions and environmental factors that impact particular neural structures or pathways. Investigating this interplay could pave the way for more refined diagnostic and therapeutic interventions.

Typical Patterns of Nerve Involvement in Dystonia

Dystonia is clinically categorized based on the distribution of affected body parts, including focal (affecting a single body part), segmental (affecting adjacent areas), multifocal (affecting non-contiguous areas), generalized (affecting the trunk and two other regions), and hemidystonia (affecting one side of the body).1 Several focal dystonias commonly involve cranial nerves. Blepharospasm, characterized by involuntary muscle contractions in the eyelids, is a frequent manifestation.1 Cervical dystonia, also known as spasmodic torticollis, affects the neck muscles, leading to abnormal head movements and postures.1 Oromandibular dystonia involves forceful contractions of the face, jaw, and tongue muscles, interfering with chewing and speech.1 Laryngeal dystonia, or spasmodic dysphonia, affects the vocal cords, causing speech disturbances.1 Limb dystonias are also common, with hand dystonia, such as writer’s cramp, being a well-recognized task-specific form.1 Lower limb involvement is frequently observed, often as an initial symptom that can progress to generalized dystonia.1 Notably, dystonia can sometimes spread from a focal presentation to affect more generalized areas of the body, particularly in cases with an earlier age of onset.1 The consistent involvement of specific cranial nerves across various dystonia classifications suggests a shared underlying vulnerability within the neural circuits controlling these structures. For instance, the frequent co-occurrence of blepharospasm and oromandibular dystonia in Meige’s syndrome 2 points to a non-random pattern of involvement, implying that the pathophysiology of dystonia might preferentially target these motor and sensory pathways. Furthermore, the observation that upper limb dystonia, especially affecting the hand, is often linked to specific tasks 1, while lower limb involvement can be an early indicator of generalized dystonia 3, might indicate different mechanisms or stages of the disease affecting upper versus lower extremities and their neural control.

Cranial/Peripheral Nerve  Typical Dystonia Type Muscles Primarily Affected Typical Manifestations
Facial (VII) Blepharospasm, Oromandibular Dystonia Orbicularis oculi, facial expression muscles Eyelid spasms, jaw clenching, grimacing
Accessory (XI) Cervical Dystonia Sternocleidomastoid, Trapezius Head twisting, abnormal neck postures
Trigeminal (V) Oromandibular Dystonia, Meige’s Syndrome Muscles of mastication Jaw clenching, teeth grinding, facial spasms
Vagus (X) Laryngeal Dystonia, Oromandibular Dystonia Vocal cords, pharyngeal muscles Strained or whispering voice, swallowing difficulties
Ulnar Nerve Focal Hand Dystonia Intrinsic hand muscles (interossei, lumbricals, hypothenar) Involuntary finger flexion, impaired fine motor control
Peroneal Nerve Lower Limb Dystonia Anterior and lateral compartment leg muscles Plantarflexion posture, foot drop–like gait

Neuroanatomical Pathways and Connections

Cranial Nerves Commonly Affected in Dystonia

The facial nerve (CN VII) originates in the brainstem, specifically within the pons.47 Its primary function is motor innervation of the muscles responsible for facial expression.47 This nerve plays a crucial role in dystonias affecting the face, such as blepharospasm (involuntary eyelid closure) and oromandibular dystonia (involuntary movements of the jaw, mouth, and tongue).7 Additionally, the facial nerve carries sensory fibers for taste from the anterior two-thirds of the tongue and parasympathetic fibers that control salivation and lacrimation.49

The accessory nerve (CN XI) possesses a unique dual origin, arising from the medulla oblongata (cranial root) and the spinal cord (spinal root, originating from approximately C1 to C5 or C6).53 Its primary motor function is to innervate the sternocleidomastoid and trapezius muscles53, which are essential for movements of the head and neck. Consequently, the accessory nerve is significantly involved in cervical dystonia (torticollis), a condition characterized by involuntary twisting and tilting of the head.3

The trigeminal nerve (CN V) is the largest of the cranial nerves.23 It is primarily responsible for sensory innervation of the face, mouth, and nasal cavity24, as well as motor innervation of the muscles of mastication.24 The trigeminal nerve is implicated in oromandibular dystonia and Meige’s syndrome, which often involves a combination of blepharospasm and oromandibular dystonia.2 The trigeminal sensory nuclear complex (TSNC) within the brainstem is believed to play a significant role in the pathophysiology of craniocervical dystonia.19

The vagus nerve (CN X) is the longest cranial nerve and has both motor and sensory functions.45 It innervates a wide range of structures, including the pharynx, larynx, heart, and gastrointestinal system.45 The vagus nerve can be involved in laryngeal dystonia (spasmodic dysphonia), affecting the vocal cords, and potentially in oromandibular dystonia.2 Interestingly, stimulation of the auricular branch of the vagus nerve has shown potential as a treatment for cervical dystonia.34

Peripheral Nerves Commonly Affected in Dystonia

Ulnar Nerve

The ulnar nerve originates from the brachial plexus, specifically from nerve roots C8 and T1.61 It travels along the medial aspect of the arm and forearm, passing through several key anatomical landmarks including the arcade of Struthers in the arm, the cubital tunnel at the elbow, and Guyon’s canal at the wrist.61 The ulnar nerve provides motor innervation to specific forearm muscles, namely the flexor carpi ulnaris and the medial half of the flexor digitorum profundus, as well as to most of the intrinsic muscles of the hand, including the hypothenar muscles, interossei, the medial two lumbricals, and the adductor pollicis.61 It also provides sensory innervation to the medial one and a half fingers (the little finger and the ulnar half of the ring finger) and the associated palm area.61 The ulnar nerve has been strongly associated with focal hand dystonia, particularly affecting the ring and small fingers.67

Peroneal Nerve

The peroneal nerve, also known as the fibular nerve, originates as one of the two major branches of the sciatic nerve (L4-S2) in the popliteal fossa behind the knee.70 It courses laterally around the neck of the fibula, where it is relatively superficial, and then divides into the superficial and deep peroneal nerves.70 The superficial peroneal nerve provides motor innervation to the muscles in the lateral compartment of the leg (fibularis longus and brevis), responsible for eversion of the foot. The deep peroneal nerve innervates the muscles in the anterior compartment of the leg (tibialis anterior, extensor hallucis longus, extensor digitorum longus), which are crucial for dorsiflexion of the foot and extension of the toes.72 Sensory innervation of the peroneal nerve includes the anterolateral aspect of the leg and most of the dorsum of the foot (superficial peroneal), and the web space between the first and second toes (deep peroneal).70 Foot dystonia, sometimes mimicking foot drop (weakness in foot dorsiflexion), has been associated with the peroneal nerve.71

The diversity of functions among the affected cranial nerves, which innervate muscles controlling facial expressions, head and neck movements, mastication, and vocalization, suggests that dystonia can impact a broad spectrum of motor functions governed by the brainstem. This implies that the underlying pathology is not confined to a single functional system within the brainstem but may affect more widespread regulatory mechanisms. Similarly, the selective involvement of the ulnar and peroneal nerves, both peripheral nerves innervating distal limbs essential for fine motor control (hand) and gait (foot), points towards a potential vulnerability related to the length of their axons, their susceptibility to peripheral injury or compression, or the specific motor tasks they govern. The distal location and specialized functions of these nerves might render them more susceptible to the effects of dystonia, possibly due to the complex neural control demanded for these movements.

Shared Developmental Origins, Anatomical Proximity, and Functional Relationships

Developmental Origins

During embryonic development, the trigeminal nerve originates from the 1st branchial arch (mandibular arch).47 The facial and vagus nerves arise from the 2nd and 4th branchial arches, respectively.45 Notably, the accessory nerve shares an embryological origin with the vagus nerve, both developing from the same ganglionic crest of the ectoderm.53 In contrast, the somatic nerves, including those contributing to the brachial plexus (C8, T1, which form the ulnar nerve) and the lumbosacral plexus (L4-S2, which form the peroneal nerve), originate from the neural tube, a structure distinct from the branchial arches. The shared developmental origin of the accessory and vagus nerves might suggest common molecular pathways or regulatory mechanisms that could be disrupted in dystonia, potentially contributing to their co-involvement, particularly in cervical and laryngeal dystonias. This common lineage could predispose these nerve groups to similar vulnerabilities or responses to pathological processes. Conversely, the distinct origins of the somatic nerves (ulnar and peroneal) from the spinal nerve roots, unlike the cranial nerves’ brainstem origins, suggest that their selective vulnerability might be attributed to factors other than their initial developmental pathway, such as their peripheral course or the specific types of motor neurons they comprise. This disparity in origin implies that different etiological factors or mechanisms might underlie the selective involvement of cranial and somatic nerves in dystonia.

Anatomical Proximity

Several cranial nerves exit the skull through various foramina located in the skull base, often in close proximity to one another. For example, the glossopharyngeal (CN IX), vagus (CN X), and accessory (CN XI) nerves all pass through the jugular foramen.45 There is also the potential for ephaptic cross-talk, a form of neuronal communication without direct synaptic connection, between the trigeminal nerve and adjacent nerves within the brainstem, such as the facial, glossopharyngeal, and vagus nerves.23 In the periphery, the ulnar nerve follows a superficial course as it passes behind the medial epicondyle of the humerus at the elbow, making it vulnerable to compression or trauma.61 Similarly, the peroneal nerve’s superficial location as it wraps around the fibular neck increases its susceptibility to injury from external pressure or direct trauma.70 The anatomical proximity of certain cranial nerves at the skull base, along with the potential for cross-talk within the brainstem23, could explain the frequent co-occurrence of certain cranial dystonias, such as blepharospasm and oromandibular dystonia, as seen in Meige’s syndrome. Close anatomical relationships can lead to shared vulnerabilities to mechanical stress, vascular compression, or the spread of pathological processes. Furthermore, the superficial peripheral course of both the ulnar and peroneal nerves makes them susceptible to external compression or trauma.61 While this explains their vulnerability to peripheral neuropathy, it raises the question of whether dystonia might exacerbate or be triggered by such peripheral nerve insults in individuals with an underlying susceptibility to the disorder. The shared anatomical vulnerability to external factors might contribute to the selective involvement of these somatic nerves in dystonia, possibly through altered sensory feedback mechanisms.

Functional Relationships

The trigeminal nerve’s sensory input from the face and mouth has extensive connections to motor nuclei within the brainstem that control facial and jaw muscles, which is highly relevant to the manifestation of cranial dystonias affecting these regions.19 The accessory nerve functions in collaboration with the vagus nerve to innervate the muscles of the larynx53, a relationship that is pertinent to laryngeal dystonia. Notably, there is evidence suggesting that peripheral nerve injury, such as to the ulnar or peroneal nerve, can influence central motor control circuits, potentially leading to the development of dystonia in susceptible individuals.67 The functional integration of trigeminal sensory input with motor control of facial and jaw muscles19 indicates that disruptions in sensorimotor processing within the trigeminal system could be a key factor in the development of cranial dystonias affecting these areas. Dystonia is increasingly understood as a disorder involving aberrant sensorimotor integration, and the trigeminal system’s role in facial sensation and motor control makes it a likely candidate for involvement in cranial dystonias. Moreover, the observed link between ulnar neuropathy and focal hand dystonia67, as well as the use of functional electrical stimulation of the peroneal nerve to treat leg dystonia71, highlight a potential bidirectional relationship between peripheral nerve function and the central mechanisms underlying dystonia. Peripheral nerve issues might trigger or exacerbate dystonia, and conversely, dystonia might manifest in specific ways in nerves already susceptible to peripheral dysfunction. This interplay between the peripheral and central nervous systems in dystonia warrants further investigation to fully understand the underlying pathophysiological mechanisms.

Selective Vulnerability of Specific Nerve Groups in Dystonia

The concept of selective neuronal vulnerability is well-established in the context of neurodegenerative diseases, where specific populations of neurons are preferentially affected while others remain relatively spared.81 While primary dystonia is not typically characterized by overt neurodegeneration15, similar principles of selective vulnerability might apply to explain the preferential involvement of certain nerve groups. This could involve cellular or molecular mechanisms leading to dysfunction rather than cell death. Several factors could contribute to this selective vulnerability. The high metabolic demands of neurons86 might render specific motor neuron populations within the cranial nerves and the ulnar and peroneal nerves more susceptible to subtle energy imbalances or mitochondrial dysfunction that could be present in dystonia. Neurons with higher firing rates or more extensive axonal arborizations might be particularly vulnerable to disruptions in energy supply. Additionally, the peripheral nerves (ulnar and peroneal) are inherently more susceptible to mechanical compression and injury due to their anatomical course.61 This could lower their threshold for manifesting dystonic symptoms if the central nervous system’s motor control is already compromised in individuals with a predisposition to dystonia. A “two-hit” hypothesis could be considered, where a subtle central motor control issue combined with a peripheral nerve vulnerability leads to the manifestation of dystonia in those specific nerves. Furthermore, distinct patterns of gene expression within different neuronal populations81 might influence their susceptibility to the molecular mechanisms underlying dystonia.

Role of the Basal Ganglia and Other Relevant Brain Structures

The basal ganglia, a group of interconnected nuclei deep within the brain, play a central role in the control of movement, including the initiation, inhibition, and modulation of voluntary actions.4 Dysfunction of the basal ganglia is widely considered a primary factor in the pathophysiology of dystonia.4 The basal ganglia have extensive connections with the motor cortex and brainstem motor nuclei that control the cranial nerves.88 This direct connectivity provides a pathway through which basal ganglia dysfunction can manifest as dystonia affecting muscles innervated by cranial nerves. The basal ganglia play a critical role in refining motor commands from the cortex before they reach the brainstem and spinal cord; disruptions in this filtering process can lead to the involuntary muscle contractions characteristic of dystonia. Emerging evidence also highlights the involvement of the cerebellum and cerebello-basal ganglia circuits in the development of dystonia.5 This suggests that a network dysfunction involving both the basal ganglia and the cerebellum, along with the cortex, might be crucial in the pathophysiology of dystonia affecting both cranial and somatic nerves. Dystonia is increasingly viewed as a network disorder, and the interplay between the cerebellum, basal ganglia, and cortex in motor control and learning makes this network a likely substrate for the development of dystonic symptoms in various body regions. Furthermore, the sensorimotor cortex, responsible for integrating sensory feedback with motor commands, is likely disrupted in dystonia.5 This disruption could lead to abnormal muscle co-contraction and the overflow of motor activity observed in the disorder, potentially contributing to the selective involvement of nerve groups that are particularly reliant on precise sensorimotor integration for their function, such as the hand and face. Impaired sensorimotor integration can result in a mismatch between intended and actual movements, leading to compensatory or involuntary muscle activity.

Genetic Predispositions and Molecular Mechanisms

Genetic factors play a significant role in the etiology of many forms of dystonia.1 Numerous genes have been associated with dystonia, including TOR1A (DYT1), THAP1 (DYT6), KMT2B (DYT28), GNAL, ANO3, GCH1, TH, SPR, CIZ1, TUBB4A, PRRT2, SLC30A10, ATP1A3, and VPS16.1 Some genetic dystonias exhibit specific patterns of nerve involvement. For instance, TOR1A dystonia often begins in a limb and progresses to a generalized form1, while THAP1 dystonia is characterized by more prominent cranial involvement.11 KMT2B-related dystonia typically starts with focal dystonia in the lower limbs and advances to generalized dystonia with significant involvement of the cervical, cranial, and laryngeal regions.17 Mutations in the DYT6 gene can cause dystonia in the head, neck, and arms.20 Dopa-responsive dystonia (DRD) often manifests initially in the legs and shows a characteristic worsening of symptoms later in the day (diurnal fluctuation).2 Furthermore, mutations in the ATP1A3 gene have been linked to rapid-onset dystonia-parkinsonism.3 The identification of specific genes associated with dystonia and their correlation with particular patterns of body involvement provides compelling evidence for genetic predispositions influencing the selective vulnerability of certain nerve groups. These genetic links suggest that dysfunctions in specific proteins can disrupt neural circuits controlling particular body regions or types of movement. The involvement of genes like ATP1A3, which encodes a subunit of the sodium-potassium pump87, suggests that disruptions in fundamental cellular processes such as ion transport can selectively affect neuronal populations involved in the motor control of specific nerve groups. The sodium-potassium pump is essential for maintaining neuronal excitability, and its malfunction in specific brain regions or neuron types could lead to the development of dystonia in the corresponding body parts.

Motor and Sensory Functions and Manifestation of Dystonia

Ulnar Nerve

The ulnar nerve plays a crucial role in the fine motor control of the hand, contributing to grip strength and the abduction and adduction of the fingers.61 It also provides sensory innervation to the small and ring fingers.61 In dystonia, the ulnar nerve’s involvement can manifest as involuntary adduction and flexion of the small finger67, significantly impacting hand dexterity and overall function.1 Notably, ulnar neuropathy, a condition affecting the ulnar nerve, can present with similar motor abnormalities, potentially exacerbating or mimicking the symptoms of dystonia.63

Peroneal Nerve

The peroneal nerve is essential for motor functions related to gait, including foot dorsiflexion, eversion, and toe extension.70 It also provides sensory innervation to the top and lateral aspects of the foot and the area between the first two toes.70 Dystonia affecting the peroneal nerve can manifest as dystonic plantarflexion, leading to a characteristic steppage gait71, or it can present in a way that mimics foot drop, a condition of weakness in foot dorsiflexion.79

Comparison with other peripheral nerves

While dystonia can affect other limbs, such as radial nerve involvement in writer’s cramp, the ulnar and peroneal nerves are frequently highlighted in the context of focal limb dystonias. The manifestation of dystonia in the ulnar nerve’s distribution often involves specific hand movements like finger flexion and adduction67, which are critical for fine motor skills. This suggests that dystonia might preferentially affect nerve pathways involved in highly coordinated and skilled movements. The complex neural control required for intricate hand movements might make the ulnar nerve and its associated central pathways more susceptible to the disruptions in motor programming seen in dystonia. Similarly, the presentation of leg dystonia involving the peroneal nerve often impacts gait71, emphasizing the role of this nerve in controlling movements essential for locomotion. This suggests that dystonia can selectively affect nerves critical for specific functional domains, potentially based on the underlying neural circuits involved. Furthermore, the frequent association between ulnar neuropathy and hand dystonia67 compared to other common entrapment neuropathies like carpal tunnel syndrome (median nerve)67 raises questions about the specific role of the ulnar nerve’s innervation of intrinsic hand muscles in the development or manifestation of dystonia. The ulnar nerve’s unique distribution of motor innervation in the hand might make it particularly susceptible to the interplay between peripheral nerve dysfunction and central dystonic mechanisms.

Existing Hypotheses and Models

Current hypotheses regarding the pathophysiology of dystonia emphasize a network dysfunction involving the basal ganglia, cerebellum, and cerebral cortex.4 The selective vulnerability of cranial, ulnar, and peroneal nerves might be attributed to their specific roles within these networks and their sensitivity to disruptions in inhibition, sensorimotor integration, or plasticity. Understanding how these particular nerve pathways interact within the broader dystonia network could explain their preferential involvement. A key feature of dystonia is often a reduction in inhibition within the central nervous system, affecting areas such as the sensorimotor cortex5, basal ganglia, brainstem, and spinal cord. This loss of inhibition can lead to the co-contraction of agonist and antagonist muscles and the overflow of motor activity seen in dystonia. Abnormalities in sensorimotor integration and plasticity are also considered crucial in the development of dystonia.5 The cerebellum and its connections within cerebello-cortical pathways are increasingly recognized for their role in dystonia.5 The observation that peripheral nerve lesions can sometimes trigger or sustain dystonia67 suggests a model where altered sensory feedback from these nerves, possibly due to subclinical peripheral nerve issues or anatomical vulnerabilities, could contribute to the development or exacerbation of central motor control abnormalities in dystonia. The phenomenon of sensory tricks, where specific sensory stimuli can temporarily alleviate dystonic symptoms1, further underscores the importance of sensorimotor integration in this disorder.

Cortical Involvement in Selective Nerve Vulnerability in Dystonia

My theory suggests that the selective vulnerability of certain nerve groups in dystonia could be related to the level of cortical activation necessary for their regulation. Research indicates that movements demanding finer motor control and more complex motor planning engage more extensive cortical areas. For instance, ankle dorsiflexion, which requires precise foot placement during gait, has been shown to involve greater cortical activity compared to the more automatic movement of plantarflexion.118 Functional MRI studies have demonstrated that ankle active dorsiflexion excites several cortical areas, including the bilateral primary motor area (M1), the primary somatosensory area, the bilateral supplementary motor area (SMA), and the primary visual area, suggesting a greater reliance on cortical resources for this more demanding kinematic task requiring a synchronized neural network for precise foot placement. This increased cortical involvement could potentially make dorsiflexion more vulnerable to disruptions in neural circuitry that occur in dystonia, potentially explaining the foot drop observed in some presentations of the disorder.

Similarly, finger extension, especially the fine, independent control of fingers, relies heavily on cortical input.121 Studies using fMRI have shown that the brain volume activated during thumb extension is substantially larger than that during flexion, even when the relative muscle activity is similar.122 This suggests that finger extension, requiring more precision, inhibition of grasp, and modulation of grip, demands greater cortical resources compared to flexion. Hand dystonia frequently manifests as abnormal postures and involuntary movements of the fingers, often due to a lack of proper modulation of finger extension, which leads to excessive and unmodulated flexion. The complex control needed for these movements might be more vulnerable to the sensorimotor integration deficits and loss of inhibition seen in dystonia.

Furthermore, if dystonia affects the sensory and frontal cortex, areas crucial for motor planning and execution, it could lead to a functional failure in muscle groups that require larger cortical activation. The sensorimotor cortex plays a vital role in integrating sensory feedback with motor commands, and disruptions in this area are implicated in dystonia.5 Aberrant processing in these cortical regions could disproportionately impact movements that demand a higher degree of conscious control and sensorimotor integration, potentially explaining the selective involvement of cranial nerves and the ulnar and peroneal nerves in dystonia.

Conclusion

The selective involvement of cranial nerves and the ulnar and peroneal nerves in dystonia likely arises from a complex interplay of neuroanatomical, pathophysiological, and potentially genetic factors. The affected cranial nerves control a diverse set of motor functions in the head and neck, suggesting a broad impact of dystonia on brainstem-mediated movements. The ulnar and peroneal nerves, innervating distal parts of the limbs crucial for skilled hand movements and gait, might be selectively vulnerable due to their peripheral course, susceptibility to injury, or their specific roles in complex motor tasks. Current hypotheses emphasize a network disorder involving the basal ganglia, cerebellum, and cortex, with disruptions in inhibition and sensorimotor integration playing key roles. Genetic predispositions can also influence the patterns of nerve involvement. The observation that peripheral nerve issues can sometimes trigger or exacerbate dystonia highlights the potential for bidirectional interactions between the peripheral and central nervous systems. Future research should focus on detailed neurophysiological studies of these specific nerve pathways, genetic analyses exploring differential vulnerability, and investigations into the role of peripheral nerve health in the onset and progression of dystonia to further elucidate the mechanisms underlying this selective vulnerability in dystonia.

Works cited

  1. Dystonia – Symptoms, Causes, Treatment – National Organization for Rare Disorders, accessed April 20, 2025, https://rarediseases.org/rare-diseases/dystonia/
  2. Forms of Dystonia and Their Treatment – Premier Neurology & Wellness Center, accessed April 20, 2025, https://premierneurologycenter.com/blog/forms-of-dystonia-and-their-treatment/
  3. Dystonia: Symptoms, Causes, and Treatment Options – Brain Foundation, accessed April 20, 2025, https://brainfoundation.org.au/disorders/dystonia/
  4. Dystonia – AANS, accessed April 20, 2025, https://www.aans.org/patients/conditions-treatments/dystonia/
  5. How Many Types of Dystonia? Pathophysiological Considerations – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2018.00012/full
  6. What is Dystonia? – PX Docs, accessed April 20, 2025, https://pxdocs.com/developmental-delays/what-is-dystonia/
  7. Dystonia – Symptoms and causes – Mayo Clinic, accessed April 20, 2025, https://www.mayoclinic.org/diseases-conditions/dystonia/symptoms-causes/syc-20350480
  8. The Dystonias – PMC – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC10226676/
  9. Hyperkinetic Movement Disorders (Section 3:) – Cambridge University Press, accessed April 20, 2025, https://www.cambridge.org/core/books/international-compendium-of-movement-disorders/hyperkinetic-movement-disorders/AA98F0615154BB1A83F4B5D0F7CD7F5C
  10. Classification of Dystonia – MDPI, accessed April 20, 2025, https://www.mdpi.com/2075-1729/12/2/206
  11. Hereditary Dystonia Overview – GeneReviews® – NCBI Bookshelf, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK1155/
  12. genetics of dystonia: new twists in an old tale | Brain – Oxford Academic, accessed April 20, 2025, https://academic.oup.com/brain/article/136/7/2017/277430
  13. Understanding dystonia: diagnostic issues and how to overcome them – SciELO, accessed April 20, 2025, https://www.scielo.br/j/anp/a/MGTVkXMr56fx8wC4jMY4rXw/
  14. Understanding Dystonia – Christopher Duma, MD, FACS, accessed April 20, 2025, https://www.cduma.com/blog/understanding-dystonia
  15. Dystonia – StatPearls – NCBI Bookshelf, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK448144/
  16. Dystonia: What It Is, Causes, Symptoms, Treatment & Types – Cleveland Clinic, accessed April 20, 2025, https://my.clevelandclinic.org/health/diseases/6006-dystonia
  17. Genetic Update and Treatment for Dystonia – PMC – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC11011602/
  18. Practice Essentials, Classification, Common Types of Dystonias – Medscape Reference, accessed April 20, 2025, https://emedicine.medscape.com/article/312648-overview
  19. The Role of the Trigeminal Sensory Nuclear Complex in the Pathophysiology of Craniocervical Dystonia – PMC – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC6618800/
  20. Dystonia: Causes, Symptoms, and Treatments – WebMD, accessed April 20, 2025, https://www.webmd.com/brain/dystonia-causes-types-symptoms-and-treatments
  21. Cranial dystonia, blepharospasm and hemifacial spasm: clinical features and treatment, including the use of botulinum toxin – PMC, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC1268337/
  22. CT-guided radiofrequency ablation of the extracranial cranial nerve for the treatment of Meige’s syndrome – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2022.1013555/full
  23. Neuropathy as an inductor of Tourette’s syndrome, cervical dystonia and chronic cough, accessed April 20, 2025, https://mskneurology.com/neuropathy-tourettes-syndrome-cervical-dystonia-chronic-cough/
  24. www.jneurosci.org, accessed April 20, 2025, https://www.jneurosci.org/content/jneuro/33/47/18358.full.pdf
  25. Spreading of Trigeminal Neuralgia and Hemifacial Spasm to Blepharospasm: What the Role for Neurovascular Compression of the V th Cranial Nerve? – ClinMed International Library, accessed April 20, 2025, https://clinmedjournals.org/articles/ijbdt/international-journal-of-brain-disorders-and-treatment-ijbdt-8-043.php?jid=ijbdt
  26. Hemifacial spasm and involuntary facial movements | QJM – Oxford Academic, accessed April 20, 2025, https://academic.oup.com/qjmed/article/95/8/493/1698426
  27. Oromandibular Dystonia | Dystonia Medical Research Foundation, accessed April 20, 2025, https://dystonia-foundation.org/what-is-dystonia/types-dystonia/oromandibular/
  28. Facial dystonia, essential blepharospasm and hemifacial spasm – PubMed, accessed April 20, 2025, https://pubmed.ncbi.nlm.nih.gov/2042553/
  29. Shortened cortical silent period in facial muscles of patients with cranial dystonia, accessed April 20, 2025, https://www.neurology.org/doi/10.1212/WNL.54.1.130
  30. Cervical Dystonia | PM&R KnowledgeNow, accessed April 20, 2025, https://now.aapmr.org/cervical-dystonia/
  31. Cervical Dystonia – The Bertrand Procedure: Selective Peripheral Denervation, accessed April 20, 2025, https://dystoniacanada.org/cervical-dystonia
  32. Spinal dystonia and other spinal movement disorders – Frontiers Publishing Partnerships, accessed April 20, 2025, https://www.frontierspartnerships.org/journals/dystonia/articles/10.3389/dyst.2023.11303/full
  33. Cervical dystonia and spasmodic torticollis treatment – – Caring Medical, accessed April 20, 2025, https://caringmedical.com/prolotherapy-news/getting-help-cervical-dystonia-spastic-torticollis/
  34. Expected Effects of Auricular Vagus Nerve Stimulation in Dystonia – ResearchGate, accessed April 20, 2025, https://www.researchgate.net/publication/256665402_Expected_Effects_of_Auricular_Vagus_Nerve_Stimulation_in_Dystonia
  35. Motor and Sensory Features of Cervical Dystonia Subtypes: Data From the Italian Dystonia Registry – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2020.00906/full
  36. Modulation of Muscle Tone and Sympathovagal Balance in Cervical Dystonia Using Percutaneous Stimulation of the Auricular Vagus Nerve – PubMed, accessed April 20, 2025, https://pubmed.ncbi.nlm.nih.gov/26450637/
  37. Redrawing the brain’s motor map – Emory News Center, accessed April 20, 2025, https://news.emory.edu/stories/2015/06/motor_homunculus_jinnah/index.html
  38. The basal ganglia are hyperactive during the discrimination of tactile stimuli in writer’s cramp, accessed April 20, 2025, https://academic.oup.com/brain/article/129/10/2697/290089
  39. Focal dystonia in musicians: linking motor symptoms to somatosensory dysfunction – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/human-neuroscience/articles/10.3389/fnhum.2013.00297/full
  40. Child Neurology: KMT2B-Related Dystonia in a Young Child With Worsening Gait Abnormality, accessed April 20, 2025, https://www.neurology.org/doi/10.1212/WNL.0000000000207300
  41. Research Priorities in Limb and Task-Specific Dystonias – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2017.00170/full
  42. The Role of the Trigeminal Sensory Nuclear Complex in the Pathophysiology of Craniocervical Dystonia | Journal of Neuroscience, accessed April 20, 2025, https://www.jneurosci.org/content/33/47/18358.short
  43. Case report: Peripheral nerve stimulation relieves post-traumatic trigeminal neuropathic pain and secondary hemifacial dystonia – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2023.1107571/full
  44. Trigeminal Nerve Anatomy Illustrated Using Examples of Abnormalities | AJR, accessed April 20, 2025, https://ajronline.org/doi/10.2214/ajr.176.1.1760247
  45. Neuroanatomy, Cranial Nerve 10 (Vagus Nerve) – StatPearls – NCBI …, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK537171/
  46. The Vagus Nerve (CN X) – Course – Functions – TeachMeAnatomy, accessed April 20, 2025, https://teachmeanatomy.info/head/cranial-nerves/vagus-nerve-cn-x/
  47. Neuroanatomy, Cranial Nerve 5 (Trigeminal) – StatPearls – NCBI …, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK482283/
  48. Neuroanatomy, Trigeminal Reflexes – StatPearls – NCBI Bookshelf, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK551641/
  49. Neuroanatomy, Cranial Nerve 7 (Facial) – StatPearls – NCBI Bookshelf, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK526119/
  50. Facial Nerve Anatomy – Medscape Reference, accessed April 20, 2025, https://emedicine.medscape.com/article/835286-overview
  51. Facial Nerve (CN VII): What It Is, Function & Anatomy, accessed April 20, 2025, https://my.clevelandclinic.org/health/body/22218-facial-nerve
  52. Anatomy and Pathology of the Facial Nerve | AJR – American Journal of Roentgenology, accessed April 20, 2025, https://ajronline.org/doi/10.2214/AJR.14.13444
  53. Neuroanatomy, Cranial Nerve 11 (Accessory) – StatPearls – NCBI Bookshelf, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK507722/
  54. Accessory nerve – Wikipedia, accessed April 20, 2025, https://en.wikipedia.org/wiki/Accessory_nerve
  55. The Accessory Nerve: Anatomy, Function, and Treatment – Verywell Health, accessed April 20, 2025, https://www.verywellhealth.com/accessory-nerve-anatomy-4783765
  56. Accessory nerve (CN XI): Anatomy, pathways and function | Kenhub, accessed April 20, 2025, https://www.kenhub.com/en/library/anatomy/the-accessory-nerve
  57. The Accessory Nerve (CN XI) – Course – Motor – TeachMeAnatomy, accessed April 20, 2025, https://teachmeanatomy.info/head/cranial-nerves/accessory/
  58. Bilateral trapezius hypertrophy with dystonia and atrophy – PMC, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC1877850/
  59. Vagus Nerve Anatomy – Medscape Reference, accessed April 20, 2025, https://emedicine.medscape.com/article/1875813-overview
  60. Vagus Nerve: What It Is, Function, Location & Conditions – Cleveland Clinic, accessed April 20, 2025, https://my.clevelandclinic.org/health/body/22279-vagus-nerve
  61. Anatomy, Shoulder and Upper Limb, Ulnar Nerve – StatPearls …, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK499892/
  62. Body Anatomy: Upper Extremity Nerves | The Hand Society, accessed April 20, 2025, https://www.assh.org/handcare/safety/nerves
  63. Ulnar Nerve – Physiopedia, accessed April 20, 2025, https://www.physio-pedia.com/Ulnar_Nerve
  64. Nerves of the Upper Limb – TeachMeAnatomy, accessed April 20, 2025, https://teachmeanatomy.info/upper-limb/nerves/
  65. The Ulnar Nerve – Course – Motor – Sensory – TeachMeAnatomy, accessed April 20, 2025, https://teachmeanatomy.info/upper-limb/nerves/ulnar-nerve/
  66. Ulnar Neuropathy: Background, Anatomy, Pathophysiology – Medscape Reference, accessed April 20, 2025, https://emedicine.medscape.com/article/1141515-overview
  67. Focal hand dystonia in a patient with ulnar nerve neuropathy at the elbow – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC2988118/
  68. Does ulnar neuropathy predispose to focal dystonia? – PubMed, accessed April 20, 2025, https://pubmed.ncbi.nlm.nih.gov/7753123/
  69. Ulnar neuropathy and dystonic flexion of the fourth and fifth digits: Clinical correlation in musicians | Semantic Scholar, accessed April 20, 2025, https://www.semanticscholar.org/paper/Ulnar-neuropathy-and-dystonic-flexion-of-the-fourth-Charness-Ross/ae4019f1831fd0b9bbe9f3c9f42405127827b26e
  70. Common Peroneal Nerve – Also Known As Foot Drop – Neuroaxis, accessed April 20, 2025, https://neuroaxis.com.au/conditions-treated/peripheral-neuropathy/common-peroneal-nerve/
  71. Functional electrical stimulation for the treatment of lower extremity dystonia – PMC, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC3703504/
  72. Anatomy, Bony Pelvis and Lower Limb: Calf Common Peroneal …, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK532968/
  73. Common fibular (peroneal) nerve: origin, course, function – Kenhub, accessed April 20, 2025, https://www.kenhub.com/en/library/anatomy/common-fibular-nerve
  74. Neuroanatomy: Peroneal & Tibial Nerves – Essentials | ditki medical & biological sciences, accessed April 20, 2025, https://ditki.com/course/neuroanatomy/peripheral-nerve-innervation/lower-extremity/1339/peroneal–tibial-nerves—essentials/notes
  75. The Sciatic Nerve – Course – Motor – Sensory – TeachMeAnatomy, accessed April 20, 2025, https://teachmeanatomy.info/lower-limb/nerves/sciatic-nerve/
  76. Peroneal Nerve Injury – StatPearls – NCBI Bookshelf, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK549859/
  77. Common Peroneal Nerve – Physiopedia, accessed April 20, 2025, https://www.physio-pedia.com/Common_Peroneal_Nerve
  78. The Deep Fibular Nerve – Course – Motor – Sensory – TeachMeAnatomy, accessed April 20, 2025, https://teachmeanatomy.info/lower-limb/nerves/deep-fibular/
  79. Dystonic Pseudo Foot Drop – PMC, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC6178651/
  80. A Patient With Focal Dystonia That Occurred Secondary to a Peripheral Neurogenic Tumor: A Case Report, accessed April 20, 2025, https://www.e-arm.org/journal/view.php?number=580
  81. Motor pool selectivity of neuromuscular degeneration in type I spinal muscular atrophy is conserved between human and mouse – Oxford Academic, accessed April 20, 2025, https://academic.oup.com/hmg/article/34/4/347/7926930
  82. Special Issue : Selective Vulnerability in Neurodegenerative Diseases – MDPI, accessed April 20, 2025, https://www.mdpi.com/journal/biology/special_issues/mr_selectivevulnerability
  83. Molecular determinants of selective dopaminergic vulnerability in Parkinson’s disease: an update – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/neuroanatomy/articles/10.3389/fnana.2014.00152/full
  84. Motor Neuron Susceptibility in ALS/FTD – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2019.00532/full
  85. On Cell Loss and Selective Vulnerability of Neuronal Populations in Parkinson’s Disease, accessed April 20, 2025, https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2018.00455/full
  86. Selective Neuron Vulnerability in Common and Rare Diseases—Mitochondria in the Focus – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/molecular-biosciences/articles/10.3389/fmolb.2021.676187/full
  87. Dystonia – Wikipedia, accessed April 20, 2025, https://en.wikipedia.org/wiki/Dystonia
  88. Role of Basal ganglia in motor control – Physiopedia, accessed April 20, 2025, https://www.physio-pedia.com/Role_of_Basal_ganglia_in_motor_control
  89. Basal Ganglia – Physiopedia, accessed April 20, 2025, https://www.physio-pedia.com/Basal_Ganglia
  90. Basal ganglia: Gross anatomy and function | Kenhub, accessed April 20, 2025, https://www.kenhub.com/en/library/anatomy/basal-ganglia
  91. Neuroanatomy, Basal Ganglia – StatPearls – NCBI Bookshelf, accessed April 20, 2025, https://www.ncbi.nlm.nih.gov/books/NBK537141/
  92. Basal Ganglia: What It Is, Function & Anatomy – Cleveland Clinic, accessed April 20, 2025, https://my.clevelandclinic.org/health/body/23962-basal-ganglia
  93. Functional Neuroanatomy of the Basal Ganglia – PMC – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC3543080/
  94. Basal ganglia: Direct and indirect pathway of movement – Osmosis, accessed April 20, 2025, https://www.osmosis.org/learn/Basal_ganglia:_Direct_and_indirect_pathway_of_movement
  95. Cognitive-motor interactions of the basal ganglia in development – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/systems-neuroscience/articles/10.3389/fnsys.2014.00016/full
  96. Neuroanatomy 8: Basal Ganglia (Nuclei), accessed April 20, 2025, https://uomustansiriyah.edu.iq/media/lectures/2/2_2019_04_28!11_31_11_AM.pdf
  97. Functions and dysfunctions of the basal ganglia in humans – PMC – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC6117491/
  98. Basal Ganglia Circuits for Action Specification – Annual Reviews, accessed April 20, 2025, https://www.annualreviews.org/doi/pdf/10.1146/annurev-neuro-070918-050452
  99. Low-Pass Filter Properties of Basal Ganglia–Cortical–Muscle Loops in the Normal and MPTP Primate Model of Parkinsonism | Journal of Neuroscience, accessed April 20, 2025, https://www.jneurosci.org/content/28/3/633
  100. Function and dysfunction of the dystonia network: an exploration of neural circuits that underlie the acquired and isolated dystonias – ResearchGate, accessed April 20, 2025, https://www.researchgate.net/publication/377722461_Function_and_dysfunction_of_the_dystonia_network_an_exploration_of_neural_circuits_that_underlie_the_acquired_and_isolated_dystonias
  101. Basal Ganglia (Section 3, Chapter 4) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy – The University of Texas Medical School at Houston, accessed April 20, 2025, https://nba.uth.tmc.edu/neuroscience/m/s3/chapter04.html
  102. It’s not just the basal ganglia: cerebellum as a target for dystonia therapeutics – PMC, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC5815386/
  103. Cerebellar contributions to dystonia: unraveling the role of Purkinje cells and cerebellar nuclei – Frontiers Publishing Partnerships, accessed April 20, 2025, https://www.frontierspartnerships.org/journals/dystonia/articles/10.3389/dyst.2025.14006/full
  104. Emerging Concepts in the Physiological Basis of Dystonia – PMC – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC4159671/
  105. Convergent mechanisms in etiologically-diverse dystonias – PMC – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC3514401/
  106. Abnormal sensory homunculus in dystonia of the hand – ResearchGate, accessed April 20, 2025, https://www.researchgate.net/publication/13467634_Abnormal_sensory_homunculus_in_dystonia_of_the_hand
  107. Early-onset isolated dystonia: MedlinePlus Genetics, accessed April 20, 2025, https://medlineplus.gov/genetics/condition/early-onset-isolated-dystonia/
  108. Dopa-responsive dystonia: MedlinePlus Genetics, accessed April 20, 2025, https://medlineplus.gov/genetics/condition/dopa-responsive-dystonia/
  109. Ulnar Neuropathy Clinical Presentation – Medscape Reference, accessed April 20, 2025, https://emedicine.medscape.com/article/1141515-clinical
  110. Sensory Alterations in Patients with Isolated Idiopathic Dystonia: An Exploratory Quantitative Sensory Testing Analysis – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2017.00553/full
  111. Focal dystonia and the Sensory-Motor Integrative Loop for Enacting (SMILE) – Frontiers, accessed April 20, 2025, https://www.frontiersin.org/journals/human-neuroscience/articles/10.3389/fnhum.2014.00458/full
  112. The Basal Ganglia – Direct – Indirect – Nuclei- TeachMeAnatomy, accessed April 20, 2025, https://teachmeanatomy.info/neuroanatomy/structures/basal-ganglia/
  113. Sensorimotor Control in Dystonia – PMC – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC6523253/
  114. Sensory tricks in dystonia. Shown is a sensorimotor integration… | Download Scientific Diagram – ResearchGate, accessed April 20, 2025, https://www.researchgate.net/figure/Sensory-tricks-in-dystonia-Shown-is-a-sensorimotor-integration-mechanism-explaining-the_fig5_242334414
  115. Tricks in dystonia: ordering the complexity – CiteSeerX, accessed April 20, 2025, https://citeseerx.ist.psu.edu/document?repid=rep1&type=pdf&doi=b0df593efc31be393aed7b37d968b0181fc8b00a
  116. Abnormal central integration of a dual somatosensory input in dystonia. Evidence for sensory overflow – PubMed, accessed April 20, 2025, https://pubmed.ncbi.nlm.nih.gov/10611119/
  117. Abnormal somatosensory homunculus in dystonia of the hand – PubMed, accessed April 20, 2025, https://pubmed.ncbi.nlm.nih.gov/9818942/
  118. Activation of brain areas following ankle dorsiflexion versus plantar flexion: Functional magnetic resonance imaging verification – PubMed Central, accessed April 20, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC4348995/
  119. Activation of brain areas following ankle dorsiflexion versus plantar flexion: Functional magnetic resonance imaging verification – ResearchGate, accessed April 20, 2025, https://www.researchgate.net/publication/273154548_Activation_of_brain_areas_following_ankle_dorsiflexion_versus_plantar_flexion_Functional_magnetic_resonance_imaging_verification
  120. Role of ankle dorsiflexion in sports performance and injury risk: A narrative review, accessed April 20, 2025, https://www.ejgm.co.uk/download/role-of-ankle-dorsiflexion-in-sports-performance-and-injury-risk-a-narrative-review-13412.pdf
  121. Muscles in The Finger – JOI Jacksonville Orthopaedic Institute, accessed April 20, 2025, https://www.joionline.net/library/muscles-in-the-finger/