What is Bradykinesia?

Bradykinesia is very slow motion of all muscle movements.  You can describe it as impaired muscle activity. It includes slow reflexes.  Examples are weightless spaceflight motion and catatonic schizophrenia.   [1]

Bradykinesia Definition

Bradykinesia is most often seen as a sign of Parkinson’s Disease, though there are other causes for it. The loss of motor control in sequential activities that once were typically fast and easy and now have become dreadfully slow is a form of bradykinesia.  It can be a symptom of a central nervous system disorder or even a side effect  from some prescriptions. [3]

Bradykinesia Causes

Bradykinesia starts within the central nervous system. The appropriate communication between the brain and the basal ganglia is inadequate to produce the desired movement.  Essentially the basal ganglia is hyperactive and therefore unable to deliver the required messages to the muscles in a timely and typical fashion. [11]

Bradykinesia Symptoms

Primary clinical symptoms of bradykinesia include:

  • Slow movements,
  • Weakness,
  • Tremor,
  • Rigidity,
  • Inaccuracy in movements. [11 ]
  • Akinesia -slow to initiate
  • Hypokinesia-decreased muscle movement [13]

Bradykinesia describes the inability to move your body in a typical fashion.  Movement of muscles requires thought and the action is slowed or sometimes non-existent.  This is one primary symptom of Parkinson’s Disease.  The onset of bradykinesia is sudden and stressful for the patient. In its own way it is a beginning of the loss of individual independence.  [15]

The diminished spontaneous movement generates a reduction of facial expressions and has the appearance of unusual stillness.  The individual experiencing bradykinesia may find it difficult to do routine tasks like preparing food, brushing teeth or even buttoning a shirt. [16]

Bradykinesia Diagnosis

  • Because the symptom of slow motor activity can be seen in several different medical conditions, it is really important to take the extra time to get a clear diagnosis of bradykinesia.  One simple and popular test is done by your physician during your exam. Checking to see how fast you can tap your fingers up and down, or how slowly do you tap your foot, upon request, will give the doctor valuable information.
  • Meanwhile, your doctor will be asking questions to obtain a very complete medical history of you and of your family.
  • Sometimes an MRI test will help determine if a tumor or a stroke has been the cause of this change in your movements.
  • Be sure to tell your doctor all of your prescriptions and other supplements you are taking because some of them can create bradykinesia as a side effect.
  • Physicians must rule out metabolic disorders when diagnosiing Bradykinesia. Some medications can cause bradykinesia.  Because the issue with bradykinesia is within the central nervous system, it is not very responsive to simple training.
  • Misdiagnosis is plausible because the symptom of bradykinesia is also presented by diabetic neuropathy, muscular  sclerosis, peripheral neuropathy among other conditions.   [9]

Bradykinesia Treatment

Nearly one million Americans have some level of bradykinesia.  For many it never becomes a serious condition. Yet, some of the conditions which cause bradykinesia are progressive and over time the patient’s symptoms are more pronounced and other complications may arise.  Many people choose treatments which are not chemical prescriptions.[14]

Multiple sources list these treatments for bradykinesia.  Do not attempt to handle this without consulting a medical professional.

  • Provide  clear education to the patient about what is happening.
  • Encourage attention to each movement.   [oxford]
  • Minimize multi-tasking to reduced mixed messages in the basal ganglia.
  • Focus on one task at a time – do not multi-task.
  • Seek medical help as early as you can.
  • Walking sticks – use them.

Two types of therapies rely on other strategies:

  • Neuroprotective therapies and
  • Restorative Therapies.

The goal of neuroprotective therapies is to slow the progression of this condition by interfering with the degeneration of nerve cells.

Restorative therapies are intended to replace neurons which have been lost. This is accomplished by transplanting embryonic cells which may perform normal function of nervous system pathways.  Sometimes genetic modification of cells can help restore normal function. [17]

Various prescriptions can alleviate the symptoms of bradykinesia.

  • Amantadine
  • Bromocriptine
  • Sinemet
  • Cardidopa
  • Levodopa
  • Selegilline
  • Pergolide

In more severe cases surgical intervention may be considered, though it is not a preferred choice of action. Deep brain stimulation is preferred today over the more invasive surgical procedures of the past. [11 ]

  • Pallidotomy is a surgical procedure for advanced Parkinson’s disease. It treats rigidity and tremors by creating scar tissue in an appropriate and precise location in the brain. It was once quite common. Now the diverse medications available are more likely to be used. [11]
  • Stereotactic thalmotomy is rarely used in these times. It is essentially a last resort when all other treatments have failed. The surgery is performed while the patient is awake and can answer questions. Basically, it makes the thalamus non-functional and reduces tremors and some other symptoms of advanced Parkinson’s Disease. That is why it is so rarely used. [12]


Active research programs are looking into neurotrophic proteins.Once these proteins succeed in passing the blood to brain barrier, they can protect nerve cells from death.

Other neuroprotective agents include some enzymes which are naturally occuring. These operate by reducing free radicals which can damage nerve cells.

Transplants of neural tissue from fetal pigs into the brain have been intneded to restore neural activity to the damaged area.  The results are positive but  inconclusive because the population has been small.

In addition, genetic engineering may play a role in future treatments of bradykinesia by modifying skin cells to produce dopamine.  However, other studies show that dopamine is effective with reducing Parkinsons disease progression, but not particularly effective with  eliminating bradykinesia.

Clearly there is work to be pursued towards the goal of minimizing the condition of bradykinesia in many areas. It is not a simple solution to restore function to basal ganglia cells.[18]


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