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Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Most other authors who use the term “dysdiadochokinesia” define it as essentially synonymous with an inability to perform (rapid) alternating movements properly and describe relevant tests involving not only pronation-supination but some other movements as well. As examples: “Dysdiadochokinesis is the term applied to an inability to carry out alternating movements with rapidity and regularity. For example, the patient cannot smoothly alternately pronate and supinate his forearm or flex and extend his fingers.” (Bann, p. 106)“All the defects in volitional movement are more noticeable in acts that require alternation of movement, such as pronation-supination of the forearm or the successive touching of each finger to the thumb. The normal rhythm of these movements is interrupted by irregularities of force and speed, a disorder which Babinski named adiadochokinesis.” (A&V, p. 72: see, also, vaoA&R, p, 46–47; T&D, p. 107–110 [‘’dysdiadochokinesia” is defined on p, 109])
The nervous system
Published in Peter Kopelman, Dame Jane Dacre, Handbook of Clinical Skills, 2019
Peter Kopelman, Dame Jane Dacre
These are not worth attempting if the patient has significant weakness: Finger-to-nose test: ask the patient to touch the point of their nose first with the index finger, and then with the other, and then to touch one of your fingers with the same finger. Ask them to repeat this exercise as fast as possible. The patient can keep their eyes open while you change the position of your finger. If this is normal, there is no need to progress to additional tests. If the movement is not fluid, you should ask them to repeat the action of touching their nose with the eyes closed. Additional difficulty suggests an abnormality of joint position sense (Fig. 6.33).Dysdiadochokinesia: this is the term used to characterise an inability to perform rapidly repeated movements. It can be tested by asking the patient to pretend to screw a light bulb into a socket. Another useful test is to ask the patient to perform simple repetitive movements, such as drawing a circle with a finger on the back of one, and then the other, hand. Slow, awkward movements indicate dysdiadochokinesia.Heel-to-shin test: to assess lower limb coordination, ask the patient to slide the heel of one foot in a straight line down the shin of the other leg. In cerebellar ataxia, the heel wavers across the intended target.
Degenerative Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James A. Mastrianni, Elizabeth A. Harris
Limbs: Wasting of the intrinsic hand and distal lower leg muscles.Weakness (pyramidal) of the legs (paraparesis).Ataxia of the limbs, speech, and eye movements: Bilateral cerebellar tremor.Dysmetria (overshoot).Dysdiadochokinesia (poor coordination of rapid alternating movements).Absent deep tendon reflexes due to axonal degeneration of afferent fibers. This is reflected neurophysiologically by absence of sensory nerve action potential (SNAPs) and loss of the H-reflex. Note that rare patients present with late-onset symptoms, retained reflexes, and spasticity.Extensor plantar responses.Impaired touch, pain, and temperature sensations in the feet and distal lower limbs are unusual but found in a small fraction of patients.Impaired vibration sense in the feet and hands.Impaired joint position sense in the distal lower limbs and hands.
Clinical decision making and application of an active rehabilitation program for a person with the neuromuscular symptoms of Allgrove syndrome: a case report
Published in Physiotherapy Theory and Practice, 2020
The patient had intact sensation for light pressure and deep touch and was able to differentiate between sharp and dull stimuli. She has normal two-point discrimination and has intact vibration sense in bilateral upper and lower extremities as tested with a 128 Hz tuning fork. Her temperature perception threshold as tested with Neurosensory analyzer-TSA II-Medoc. Cold was normal but warm was mildly increased. Deep tendon reflexes of the patellar tendon were graded as 1+ bilaterally with absent Achilles and brachioradialis reflexes. She was able to perform isolated joint movements through full available range of motion and was able to perform coordination testing such as finger-to-nose and rapid alternating movements (RAMs) without dysmetria or dysdiadochokinesia. Cranial nerve testing showed uvula deviated to the left, however, all other cranial nerves were normal on clinical examination. She reported intolerance to heat and the inability to perspire which was confirmed with the Quantitative Sudomotor Axon Reflex Test (QSART).
A homozygote novel L451W mutation in CECR1 gene causes deficiency of adenosine deaminase 2 in a pediatric patient representing with chronic lymphoproliferation and cytopenia
Published in Pediatric Hematology and Oncology, 2019
Rabia Miray Kisla Ekinci, Sibel Balcı, Atil Bisgin, Ilgen Sasmaz, Goksel Leblebisatan, Faruk Incecik, Mustafa Yilmaz
Three months later, the patient was re-admitted to our department with fever lasting one day accompanied by reversible amnesia, refractory sudden-onset dizziness, and diplopia. Dysdiadochokinesia and a positive Romberg sing were present on neurological examination. Laboratory parameters showed markedly elevated ESR, CRP, and fibrinogen levels. Ophthalmologic examination and orbital Magnetic Resonance Imaging (MRI) were normal, besides diffusion brain MRI and angiography did not reveal any abnormalities. Due to recurrent inflammatory episodes accompanied by prominent splenomegaly, low IgM levels, and cytopenia, we suspected on DADA2 and performed CECR1 gene analysis. Next-generation sequencing of CECR1 disclosed a novel homozygote mutation, L451W (c.1352T > G) in CECR1 gene (Figure 1). Pathogenicity of the mutation was interpreted by in silico tools including, Mutation tester, PolyPhen-2, Provean, FATHMM, FATHMM-MKL, MetaSVM, and SIFT as causative with a high possibility. Parental studies confirmed that the mutations were inherited since parents were both heterozygote for the same mutation.
A speech measure for early stratification of fast and slow progressors of bulbar amyotrophic lateral sclerosis: lip movement jitter
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
Panying Rong, Yana Yunusova, Marziye Eshghi, Hannah P. Rowe, Jordan R. Green
Speech, as a finely-controlled oromotor behavior requiring spatiotemporal coordination of up to 70 muscles (5), has shown early and progressive changes throughout bulbar ALS (2,6,7). Among speech tasks, oral dysdiadochokinesis (DDK) tested via rapid syllable repetitions (e.g. repetitions of “ba” at a maximum rate on one breath) is particularly sensitive to early, subtle bulbar deficits in ALS (8) given its challenging nature as a “maximum performance” task. Moreover, due to the simplicity of the syllable structures, oral DDK tends to be less susceptible to cognitive-linguistic impairments.