Bradykinesia · What Is It, Causes, Diagnosis, and More

Bradykinesia is a hallmark symptom of Parkinson disease, a movement disorder where the dopamine-producing neurons in the substantia nigra of the brain undergo degeneration. The substantia nigra is part of the basal ganglia, a group of brain regions that help control movement through their connections with the motor cortex. Bradykinesia is also a symptom of other movement disorders, such as Lewy body dementia, multiple system atrophy, and progressive supranuclear palsy. These disorders are collectively called atypical parkinsonism or “Parkinson-plus” syndromes because they display characteristics of Parkinson disease along with additional clinical features.   

Finally, bradykinesia may be a side effect of medication, including antipsychotics such as haloperidol, which blocks dopamine receptors; and metoclopramide, a dopamine antagonist used to treat vomiting. 

Bradykinesia is diagnosed when an individual has difficulty performing rapidly alternating movements, such as tapping the finger and thumb together, rotating the palms up and down, or tapping the foot up and down. Individuals with bradykinesia typically show a decrease in speed or amplitude of movement in addition to slowness. This pattern can help distinguish bradykinesia from other disorders that cause difficulty with repetitive movements, such as cerebellar ataxia.   

The bradykinesia-akinesia incoordination test (BRAIN) is a keyboard-tapping task used to assess upper limb motor function in individuals with movement disorders. The BRAIN test involves tapping the keys “S” and “;” on the keyboard with alternating fingers as rapidly as possible for 30 seconds. Individuals with bradykinesia may be unable to complete this task or do so slower than expected. While the BRAIN test is not used to diagnose Parkinson’s disease, it can serve as a useful tool for screening motor dysfunction, monitoring disease progression, or assessing treatment response. 

The diagnosis of Parkinson disease requires the presence of bradykinesia in addition to other typical symptoms, such as tremors, rigidity, or postural instability. Ruling out other potential causes of motor dysfunction, like medication-induced parkinsonism, is also necessary for diagnosis. 

Treatment of bradykinesia depends on the underlying cause. In individuals with Parkinson disease, treatment focuses on increasing the amount of dopamine signaling in the brain. This can be done by administering levodopa; a precursor molecule converted into dopamine by a decarboxylase enzyme. Levodopa is often administered along a peripheral decarboxylase inhibitor called carbidopa, which decreases the conversion of levodopa to dopamine in the peripheral circulation, thereby allowing a higher concentration of it to enter the brain.   

Levodopa/carbidopa is usually the first-line treatment for Parkinson disease and is particularly effective at controlling motor symptoms like bradykinesia. However, its effectiveness can decrease over time, individuals can develop motor fluctuations, and symptoms may begin to reappear. In such cases, treatment involves increasing the frequency of levodopa/carbidopa doses. Another option is to add medications that help increase dopamine levels by preventing its breakdown outside the brain. These include COMT-inhibitors, like tolcapone and entacapone, and MAO-B inhibitors, like selegiline.  

An alternative to levodopa/carbidopa is dopamine agonists (e.g., bromocriptine, cabergoline, apomorphine, pramipexole, ropinirole), which directly stimulate dopamine receptors in the brain. However, these medications are generally less effective than levodopa/carbidopa and are associated with significant  side effects, such as nausea, dizziness, headaches, orthostatic hypotension, cardiac arrhythmias, and impulse control disorders such as compulsive shopping, gambling, or hypersexuality. Finally, anticholinergic medications, such as benztropine, may be used when tremor or rigidity are the predominant motor symptoms, but they are not as effective for bradykinesia.  

In cases where medications are ineffective at controlling the symptoms, a surgical treatment called deep brain stimulation (DBS) can be considered. DBS involves implanting a device that sends electrical impulses to the brain's basal ganglia, which improves dopamine’s effects in the brain for those with Parkinson’s disease. 

Individuals with bradykinesia caused by atypical parkinsonism may also benefit from the same treatment strategies as Parkinson’s disease, though effectiveness may vary depending on the disorder's characteristics. Finally, in cases where bradykinesia is a side effect of medication, withholding the offending medication can generally resolve the symptoms.