Back To Search Results


Editor: Orlando De Jesus Updated: 8/23/2023 12:39:10 PM


Dysdiadochokinesia (diadochokinesia) is the inability to perform rapid alternating muscle movements. These can be quick and synchronous and can include pronation/supination, fast finger tapping, opening and closing of the fists, and foot tapping. It is an essential component to evaluate in patients suspected of having a cerebellar disease. These activities correlate well with numerous lifelong measures of disability. It is a form of ataxia that leads to the loss of coordination of speech and limbs. It is measurable by using the alternate motion rate (AMR). For example, speech AMR is measurable through verbal commands such as counting the number of syllable repetitions within a specific time (less than 1 minute).[1]


Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care


Dysdiadochokinesia is present with cerebellar dysfunction. Cerebellar lesions producing dysdiadochokinesia include:

  • Vascular (ischemic stroke, intracranial hemorrhage)[2]
  • Medications (barbiturates and sedatives)[3][4]
  • Toxins (alcohol abuse, illicit drug use, botulinum)[5]
  • Metabolic (Hashimoto disease, celiac disease)[6][7][8]
  • Vitamin deficiency (B, E, and thiamine deficiency)[9]
  • Hereditary (Friedrich ataxia, spinocerebellar muscle atrophy)[10][11][12][13]
  • Structural causing hydrocephalus/herniation (brain malignancy)[14]
  • Trauma[15][16]
  • Neuroinfectious (Lyme disease, cerebellar encephalitis, abscess)[17]
  • Neuroinflammatory (multiple sclerosis)[18][19]
  • Neurodegenerative(Huntington disease, Parkinson disease)[20][21][22]
  • Psychiatric (schizophrenia)[23]


Dysdiadochokinesia is an important definition to understand cerebellar dysfunction in the context of clinical disease. It should be routinely assessed in patients who elicit deficits in the coordination of speech and movement, as it is a common finding. As it can be present or absent in cerebellar disease, no incidence or prevalence has been reported. Tapping performance showed a decline with increasing age, and male subjects were faster than females in forearm diadochokinesia.[24]

Dysdiadochokinesia can be present in small children without other focalizing neurological deficits or mental retardation. Children under the age of 13 years can present dysdiadochokinesia in 8% to 20% of the cases if tested.[25] It is highest in the 7 to 8-year range. This presentation could be due to decreased myelination at younger ages with improved corticocerebellar connections later in life.


The cerebellum is organized into:

  1. primary sensorimotor region- anterior, part of lobule VI,
  2. secondary sensorimotor, lobule VIII
  3. cognitive and limbic region-posterior lobe, lobule VI-VIIA/B

The posterior vermis represents the limbic cerebellum. The corticopontocerebellar and cerebellothalamocortical loops connect the cerebellum to the motor and limbic tracts in the brain; any damage to these loops disrupts complex tasks involved in cognition, mood, and sensorimotor coordination. Complex white matter tracts involved include vestibulocerebellar and vestibulospinal (cerebellar oculomotor systems).

The cerebellum coordinates the function of agonist and antagonist movements required for specific alternating movements. This altered coordination forms the basis for dysdiadochokinesia in cerebellar injury or dysfunction.[26] The cerebellum also coordinates the acceleration and velocity of muscular activity.

History and Physical

Dysdiadochokinesia is one of the features of cerebellar dysfunction, but other clinical findings associated with cerebellar dysfunction can help you localize and narrow the differential diagnosis of the patient.

Clinical Symptoms

Typically affects the coordination of alternating movements and ambulation of the proximal and distal upper and lower extremity.[24] It can also affect the laryngeal muscles that control speech. It is a form of dysmetria/ataxia that can manifest as rigidity, bradykinesia, dysarthria, dysphagia, dysesthesias, or tremors. Ocular movements related to alignment, stability, and calibration also fall in the realm of cerebellar function.

Physical Exam

It is relevant to include in the neurological exam other areas to increase the degree of certainty of the clinical findings and help with the diagnosis, which includes:

  • Cognition- impairments in executive functions, visual-spatial procedural memory, language, and mood regulation
  • Language- impairments in articulation and speech planning, verbal fluency, semantic word retrieval, syntax, reading, and writing
  • Oculomotor deficits- impaired ocular stability-misalignment, horizontal or vertical nystagmus, saccades smooth pursuit, and vestibulo-ocular reflex[27]
  • Dysarthria- ataxic speech (impairments in saying "papa," "kaka," "tata," "lala")[28][29][30][31]
  • Dysdiadochokinesia slowed or clumsy alternating supination/pronation of upper extremities, turning a doorknob, changing lightbulb movements, foot-tapping, and abdomen tapping.
  • Dysmetria-inaccurate finger-to-nose and heel-to-shin testing
  • Tone- decreased[20]
  • Tremors-including intention or kinetic tremors in finger-to-nose testing, difficulties grabbing objects, and impaired kinetic proprioception
  • Gait ataxia-wide based, impaired heel walk, tandem and Romberg test[32]


The underlying cause of the symptom will determine the evaluations needed.

  • Vascular: Risk factor stratification (Hgb A1c, lipid panel), plain head computed tomographic (CT) scan, or vessel imaging (CT angiography/magnetic resonance angiography) and appropriate use of magnetic resonance imaging, digital subtraction angiography, positron emission tomography
  • Trauma: Head CT scan to screen for increased intracranial pressure and correlate clinical symptoms with concerning findings such as midline shift or herniation syndromes 
  • Metabolic: A complete metabolic panel, blood panel, and screen for thyroid disease
  • Malnutrition: Vitamin deficiency panel (B-subtypes, E, and thiamine) should be considerations.
  • Toxic: Urine and serum toxicology screen  (home medications, bacterial toxins, or recreational drugs)
  • Hereditary: Inherited ataxias undergo screening through the clinical and family history before being sent to the geneticist for formal counseling and testing.
    • DNA southern blot, RNA Northern blot, methylation assays, karyotyping, whole-genome sequencing
  • Neuroinflammatory or autoimmune: Lumbar puncture with cerebrospinal fluid glucose, protein, cell count oligoclonal bands, IgG index, aquaporin-4 antibody, MOG antibody
  • Neuroinfectious: Lumbar puncture with basic cerebrospinal fluid laboratories, meningoencephalitis panel, VDRL, HSV-1, HSV-2, VZV, cryptococcus antigen, toxoplasmosis antigen
  • Psychogenic: Psychiatric evaluation to uncover conversion disorders or psychogenic dysdiadochokinesia
  • Neurodegenerative: a thorough neuropsychiatric evaluation, well-documented history of clinical progression, behavioral changes, motor changes, and genetic testing, if indicated

Treatment / Management

Dysdiadochokinesia and cerebellar ataxia are challenging to treat, and the underlying etiology requires attention. Physical, speech, and occupational therapy, including strength training, balance exercises, treadmill, cycling, and Romberg exercises, can help improve functional outcomes in patients with cerebellar lesions. Home safety evaluation and durable medical equipment may be necessary to prevent falls.[4]

Differential Diagnosis

  • Ataxic dysarthria
  • Dysarthria
  • Friedreich ataxia
  • Lesions to either the frontal lobe or cerebellar hemispheres or both
  • Multiple sclerosis
  • Mutation in SLC18A2, which encodes vesicular monoamine transporter 2


It depends on the etiology of the slowed alternating movements. For example, acute traumatic, vascular, or fast progressing hereditary ataxias may have a poorer prognosis on elderly patients with multiple medical comorbidities. Infectious, inflammatory, and metabolic etiologies can have a better prognosis if identified and diagnosed quickly and treated aggressively.


There are no known complications, as dysdiadochokinesia is a clinical finding of cerebellar dysfunction.

Complications of cerebellar dysfunction include frequent falls, dysarthric speech, swallowing problems, and visual-spacial coordination. Surgery for the cerebellum may become complicated by hemorrhage, edema, and hydrocephalus. As the posterior fossa is a small compartment, any complication that can potentially cause hydrocephalus or brainstem compression requires emergency treatment. Delay in the management can cause irreversible brainstem damage, producing coma or death.


  • Speech therapy
  • Occupational therapy
  • Physical therapy

Deterrence and Patient Education

Patients with cerebellar dysfunction will often present signs that the patient will notice in the daily activities. Incoordination of hand or foot should prompt a patient to seek medical evaluation. Most cerebellar lesions are unpreventable, but those patients with arterial hypertension, hypercholesterolemia, and untreated or uncontrolled high blood triglycerides should seek medical treatment and normalize them. All of them are risk factors for vertebrobasilar atherosclerosis and strokes.

Clinical Symptoms

  • Coordination of movements
  • Muscles that control speech
  • Muscles that control the movement of the eyes
  • Decision-making processes with problems with memory, solving puzzles, and mood

Enhancing Healthcare Team Outcomes

No evidence-based study is specific for dysdiadochokinesia; however, depending on the etiology, an interdisciplinary team that consists of a neurologist, physical therapist, occupational therapist, speech therapist, social workers, nursing, mental health counselors, psychiatrist, and, at times, geneticist should be consulted to provide the best quality of life for the patient. [Level 5] Prompt consultation with an interprofessional group of specialists is recommended to improve outcomes. Collaboration, shared decision-making, and communication are crucial elements for a good outcome.


Contributed by Dr. Raju S. Menon (



Bodranghien F, Bastian A, Casali C, Hallett M, Louis ED, Manto M, Mariën P, Nowak DA, Schmahmann JD, Serrao M, Steiner KM, Strupp M, Tilikete C, Timmann D, van Dun K. Consensus Paper: Revisiting the Symptoms and Signs of Cerebellar Syndrome. Cerebellum (London, England). 2016 Jun:15(3):369-91. doi: 10.1007/s12311-015-0687-3. Epub     [PubMed PMID: 26105056]

Level 3 (low-level) evidence


Pereira AC, Brasolotto AG, Berretin-Felix G, Padovani CR. [Oral and laryngeal diadochokinesia in post cerebrovascular accident patients]. Pro-fono : revista de atualizacao cientifica. 2004 Sep-Dec:16(3):283-92     [PubMed PMID: 15609583]


Kim CK, Kalynchuk LE, Pinel JP, Kippin TE. Tolerance to the anticonvulsant and ataxic effects of pentobarbital: effect of an ascending-dose regimen. Pharmacology, biochemistry, and behavior. 1995 Dec:52(4):825-9     [PubMed PMID: 8587926]

Level 3 (low-level) evidence


Pirker W, Katzenschlager R. Gait disorders in adults and the elderly : A clinical guide. Wiener klinische Wochenschrift. 2017 Feb:129(3-4):81-95. doi: 10.1007/s00508-016-1096-4. Epub 2016 Oct 21     [PubMed PMID: 27770207]


Rodriquez AA, Ford CN, Bless DM, Harmon RL. Electromyographic assessment of spasmodic dysphonia patients prior to botulinum toxin injection. Electromyography and clinical neurophysiology. 1994 Oct-Nov:34(7):403-7     [PubMed PMID: 7859668]


Algahtani HA, Fatani AN, Shirah BH, Algahtani RH. Hashimoto`s Encephalopathy Presenting with Progressive Cerebellar Ataxia. Neurosciences (Riyadh, Saudi Arabia). 2019 Oct:24(4):315-319. doi: 10.17712/nsj.2019.4.20190016. Epub     [PubMed PMID: 31872812]


Ercoli T, Defazio G, Muroni A. Cerebellar Syndrome Associated with Thyroid Disorders. Cerebellum (London, England). 2019 Oct:18(5):932-940. doi: 10.1007/s12311-019-01059-9. Epub     [PubMed PMID: 31388971]


Casella G, Bordo BM, Schalling R, Villanacci V, Salemme M, Di Bella C, Baldini V, Bassotti G. Neurological disorders and celiac disease. Minerva gastroenterologica e dietologica. 2016 Jun:62(2):197-206     [PubMed PMID: 26619901]

Level 3 (low-level) evidence


Adam MP, Feldman J, Mirzaa GM, Pagon RA, Wallace SE, Bean LJH, Gripp KW, Amemiya A, Schuelke M. Ataxia with Vitamin E Deficiency. GeneReviews(®). 1993:():     [PubMed PMID: 20301419]


Cisnéros E, Braun CM. [Vocal and respiratory diadochokinesia in Friedreich's ataxia. Neuropathological correlations]. Revue neurologique. 1995 Feb:151(2):113-23     [PubMed PMID: 7676138]


Konstantopoulos K, Zamba-Papanicolaou E, Christodoulou K. Quantification of dysarthrοphonia in a Cypriot family with autosomal recessive hereditary spastic paraplegia associated with a homozygous SPG11 mutation. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology. 2018 Sep:39(9):1547-1550. doi: 10.1007/s10072-018-3453-8. Epub 2018 May 26     [PubMed PMID: 29804168]


Brendel B, Synofzik M, Ackermann H, Lindig T, Schölderle T, Schöls L, Ziegler W. Comparing speech characteristics in spinocerebellar ataxias type 3 and type 6 with Friedreich ataxia. Journal of neurology. 2015 Jan:262(1):21-6. doi: 10.1007/s00415-014-7511-8. Epub 2014 Sep 30     [PubMed PMID: 25267338]


Ackermann H, Hertrich I, Hehr T. Oral diadochokinesis in neurological dysarthrias. Folia phoniatrica et logopaedica : official organ of the International Association of Logopedics and Phoniatrics (IALP). 1995:47(1):15-23     [PubMed PMID: 7728177]


Dennis M, Salman MS, Jewell D, Hetherington R, Spiegler BJ, MacGregor DL, Drake JM, Humphreys RP, Gentili F. Upper limb motor function in young adults with spina bifida and hydrocephalus. Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery. 2009 Nov:25(11):1447-53. doi: 10.1007/s00381-009-0948-x. Epub 2009 Aug 12     [PubMed PMID: 19672605]

Level 2 (mid-level) evidence


Ergun A, Oder W. Oral diadochokinesis and velocity of narrative speech: a prognostic parameter for the outcome of diffuse axonal injury in severe head trauma. Brain injury. 2008 Sep:22(10):773-9. doi: 10.1080/02699050802372182. Epub     [PubMed PMID: 18787987]


Wang YT, Kent RD, Duffy JR, Thomas JE, Weismer G. Alternating motion rate as an index of speech motor disorder in traumatic brain injury. Clinical linguistics & phonetics. 2004 Jan-Feb:18(1):57-84     [PubMed PMID: 15053268]


Herkert PF, Hagen F, de Oliveira Salvador GL, Gomes RR, Ferreira MS, Vicente VA, Muro MD, Pinheiro RL, Meis JF, Queiroz-Telles F. Molecular characterisation and antifungal susceptibility of clinical Cryptococcus deuterogattii (AFLP6/VGII) isolates from Southern Brazil. European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology. 2016 Nov:35(11):1803-1810     [PubMed PMID: 27477855]


Rusz J, Benova B, Ruzickova H, Novotny M, Tykalova T, Hlavnicka J, Uher T, Vaneckova M, Andelova M, Novotna K, Kadrnozkova L, Horakova D. Characteristics of motor speech phenotypes in multiple sclerosis. Multiple sclerosis and related disorders. 2018 Jan:19():62-69. doi: 10.1016/j.msard.2017.11.007. Epub 2017 Nov 8     [PubMed PMID: 29149697]


Tjaden K, Watling E. Characteristics of diadochokinesis in multiple sclerosis and Parkinson's disease. Folia phoniatrica et logopaedica : official organ of the International Association of Logopedics and Phoniatrics (IALP). 2003 Sep-Oct:55(5):241-59     [PubMed PMID: 12931058]


Timmermann L, Braun M, Groiss S, Wojtecki L, Ostrowski S, Krause H, Pollok B, Südmeyer M, Ploner M, Gross J, Maarouf M, Voges J, Sturm V, Schnitzler A. Differential effects of levodopa and subthalamic nucleus deep brain stimulation on bradykinesia in Parkinson's disease. Movement disorders : official journal of the Movement Disorder Society. 2008 Jan 30:23(2):218-27     [PubMed PMID: 18044706]

Level 1 (high-level) evidence


Daneault JF, Carignan B, Sadikot AF, Duval C. Inter-limb coupling during diadochokinesis in Parkinson's and Huntington's disease. Neuroscience research. 2015 Aug:97():60-8. doi: 10.1016/j.neures.2015.02.009. Epub 2015 Mar 6     [PubMed PMID: 25747139]


Montaña D, Campos-Roca Y, Pérez CJ. A Diadochokinesis-based expert system considering articulatory features of plosive consonants for early detection of Parkinson's disease. Computer methods and programs in biomedicine. 2018 Feb:154():89-97. doi: 10.1016/j.cmpb.2017.11.010. Epub 2017 Nov 16     [PubMed PMID: 29249350]


Putzhammer A, Perfahl M, Pfeiff L, Ibach B, Johann M, Zitzelsberger U, Hajak G. Performance of diadochokinetic movements in schizophrenic patients. Schizophrenia research. 2005 Nov 15:79(2-3):271-80     [PubMed PMID: 15987669]

Level 2 (mid-level) evidence


Hermsdörfer J, Marquardt C, Wack S, Mai N. Comparative analysis of diadochokinetic movements. Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology. 1999 Aug:9(4):283-95     [PubMed PMID: 10437981]

Level 2 (mid-level) evidence


Bagchi DJ, Khanna R, Raju SS. Prevalence of soft neurological signs : a study among Indian school boys. Indian journal of psychiatry. 1996 Oct:38(4):196-200     [PubMed PMID: 21584130]


Diener HC, Dichgans J. Pathophysiology of cerebellar ataxia. Movement disorders : official journal of the Movement Disorder Society. 1992:7(2):95-109     [PubMed PMID: 1584245]


Simoceli L, Sguillar DA, Santos HM, Caputti C. Vestibular system paresis due to emergency endovascular catheterization. International archives of otorhinolaryngology. 2012 Apr:16(2):282-5. doi: 10.7162/S1809-97772012000200019. Epub     [PubMed PMID: 25991947]


Sinha P, Vandana VP, Lewis NV, Jayaram M, Enderby P. Evaluating the effect of risperidone on speech: A cross-sectional study. Asian journal of psychiatry. 2015 Jun:15():51-5. doi: 10.1016/j.ajp.2015.05.005. Epub 2015 May 11     [PubMed PMID: 26013669]

Level 2 (mid-level) evidence


Wertzner HF, Pagan-Neves Lde O, Alves RR, Barrozo TF. Implications of diadochokinesia in children with speech sound disorder. CoDAS. 2013:25(1):52-8     [PubMed PMID: 24408171]

Level 2 (mid-level) evidence


Andrade CR, Queiróz DP, Sassi FC. Electromyography and diadochokinesia--a study with fluent and stuttering children. Pro-fono : revista de atualizacao cientifica. 2010 Apr-Jun:22(2):77-82     [PubMed PMID: 20640368]


Padovani M, Gielow I, Behlau M. Phonarticulatory diadochokinesis in young and elderly individuals. Arquivos de neuro-psiquiatria. 2009 Mar:67(1):58-61     [PubMed PMID: 19330213]


Krishna R, Pathirana PN, Horne M, Power L, Szmulewicz DJ. Quantitative assessment of cerebellar ataxia, through automated limb functional tests. Journal of neuroengineering and rehabilitation. 2019 Feb 27:16(1):31. doi: 10.1186/s12984-019-0490-3. Epub 2019 Feb 27     [PubMed PMID: 30813963]