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Dysdiadochokinesia
Introduction
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]
Etiology
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Etiology
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]
Epidemiology
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.
Pathophysiology
The cerebellum is organized into:
- primary sensorimotor region- anterior, part of lobule VI,
- secondary sensorimotor, lobule VIII
- 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]
Evaluation
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
Prognosis
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.
Complications
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.
Consultations
- 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.
Media
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References
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