Dyskinesia vs Dystonia: Differences and Similarities

Both dyskinesia and dystonia are two types of movement disorder, with shared neurobiological factors and overlap in conditions such as Parkinson’s Disease. This article will compare and contrast these two conditions, discussing their symptoms, prevalence, causes, and characteristics.
Klara Hatinova

Klara Hatinova

Klara is postgraduate researcher in experimental psychology at the
University of Oxford.

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Symptoms: Dyskinesia vs Dystonia

Dyskinesia is a disorder that affects an individual’s ability to carry out or initiate movement. It encompasses various conditions, including chorea, tremors, ticks and athetosis, and dystonia. Dyskinesia symptoms include involuntary, rapid movements. Chorea, a specific form of dyskinesia, presents as a whole-body dance movement and is frequently seen in Parkinson’s Disease. Dyskinesia symptoms often include fidgeting, wriggling, swaying, nodding, twitching, restlessness, and facial twitches. [1, 2]

Dystonia symptoms include sustained, involuntary muscle contractions, causing slow, repetitive movements or abnormal postures [1, 3, 4]. These can also include tremors, voice problems, and dragging foot. Dystonia as a disorder can also present through non-motor symptoms, which include increased anxiety, depression, restless leg syndrome, excessive sleepiness throughout the day, problems with cognition, and reduced quality of sleep [5].

Dyskinesia vs Dystonia: Causes and Characteristics

A spectrum of factors causes dyskinesia. These include conditions that damage the brain, such as stroke, infection, brain injury, or schizophrenia, through elevated dopamine levels. The second main cause of dyskinesias is medication side-effects, such as levodopa in Parkinson’s disease, and, in rare cases, anti-nausea medication such as metoclopramide or anti-psychotic medication used for schizophrenia treatment. [1, 6, 7]

Dystonia is more complex, with several potential causes and contributors to this neurological condition. Dystonia can be primary, where sustained or intermittent muscle contractions are the sole symptom, or secondary, which includes dystonia as a symptom of Parkinson’s disease, Wilson’s disease, or dopamine-blocking medication.

Genetic factors can also cause both dyskinesia and dystonia. These can be mutations in genes regulating neurotransmitters in the brain, such as dopamine or glutamate, or their receptors [8, 9, 10, 11].

Prevalence: Dyskinesia vs Dystonia

The prevalence of dyskinesia and dystonia varies widely depending on the population studied and the specific type of the disorder it is associated with. The prevalence of dyskinesia and dystonia differ because there are neurobiological changes and medications that can increase their relative risk. Here, we will focus on the prevalence of dyskinesia and dystonia in Parkinson’s disease. Dyskinesia can be a side effect of levodopa medication, so its prevalence is 34% in Parkinson’s disease patients.

Dystonia, on the other hand, is a symptom of unmedicated Parkinson’s disease. In unmedicated Parkinson’s disease patients, the prevalence is also around 30%. However, here the prevalence is higher in patients who exhibited Parkinson’s disease symptoms before the age of 40 – so-called early onset Parkinson’s disease [12]. Dyskinesia and dystonia prevalence increases gradually with age, but increasingly more so in women [13].

Characteristics and Pathology: Dyskinesia

Dyskinesia pathology is primarily associated with elevated dopamine levels, which facilitate movement initiation. The pathology of dyskinesia involves disrupted connections between the cortex and the midbrain structures, including the thalamus and basal ganglia. Dopamine acts as a neuromodulator, which controls the activity of excitatory and inhibitory connections in the brain. Too much dopamine can reduce the suppression of motor circuits in the basal ganglia, leading to increased movement.

More recently, dyskinesia is also linked to changes in the cerebellum, which controls fine movement and coordination [14, 15].

Characteristics and Pathology: Dystonia

The pathology of dystonia involves multiple brain regions, including the basal ganglia, cerebellum, and sensorimotor cortex. These areas are linked to changes to motor inhibition, deficits in integrating sensory information to guide future movement, or difficulty planning movement. Like dyskinesia, dystonia pathology can also include dysfunction of the cerebellum [16, 17].

ConditionDyskinesiaDystonia
NeurobiologyElevated dopamine levelsReduced dopamine levels
SymptomsJittery movements and tremorInability to initiate movement, tensions, stiffness or twisting movements
CausesSchizophrenia, stroke, brain injury, multiple sclerosis, anti-psychotic medication, anti-nausea medicationParkinson’s disease, Wilson’s disease, brain lesions, peripheral nerve injury, sensorimotor cortex damage
PathologyLoss of inhibition between the basal ganglia, thalamus, and cortex.Disrupted communication between the basal ganglia, cerebellum and sensorimotor cortex.
Prevalence in PD patients34% in medicated patients30% in all patients

In summary, although dyskinesia and dystonia share common features of disrupted motor control, their underlying mechanisms and presentations differ. Dystonia is neurologically more complex, spanning across multiple brain regions and presenting as stiffening of the muscles and slow, twisting movements. Dyskinesia is a broad category of movement disorders characterized by involuntary and jittery movements. Awareness of differences between dystonia and dyskinesia can significantly aid in delivering appropriate treatment strategies.

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Klara Hatinova

Klara Hatinova

Klara is a postgraduate researcher in experimental psychology at the University of Oxford. She has worked across a spectrum of hot topics in neuroscience, including her current project measuring reinforcement learning strategies in Parkinson’s disease. Previously, she studied the efficacy of psilocybin as a therapy for critical mental health conditions and examined molecular circadian rhythms of migraine disorders. She completed her undergraduate degree in Neuroscience at the University of Glasgow and participated in a year abroad at the University of California, where she worked on a clinical trial for spinal cord injury.