Bradicinesia: Causes, Symptoms, Diagnosis, Treatment and Latest Studies


Bradykinesia is the slowing down of movements, incredibly complex voluntary movements. It can be described as altered muscle activity.

It is seen more frequently as a sign of Parkinson’s disease, although there are other causes. The loss of motor control in sequential activities that were once typically quick and easy and have now become slow is a form of bradykinesia.

It can be a symptom of a central nervous system disorder or even a side effect of some prescriptions.


Bradykinesia begins within the central nervous system, and communication between the brain and the basal ganglia is inadequate to produce the desired movement.

Essentially, the basal ganglia are hyperactive and therefore can not deliver the necessary messages to the muscles in a timely and typical manner.

Symptoms of Bradicinesia

  • Slow movements
  • Weakness
  • Temblor
  • Rigidity
  • Inaccuracy in movements
  • Akinesia
  • Hipocinesia

Bradykinesia describes the inability to move your body typically. The movement of the muscles requires thought, and the action slows down or, sometimes, does not exist. This is a primary symptom of Parkinson’s disease.


The onset of bradykinesia is sudden and stressful for the patient. In its way, it is the beginning of the loss of individual independence.

The diminished spontaneous movement reduces the facial expressions and appears an unusual stillness.

The individual who experiences bradykinesia may have difficulty performing routine tasks, such as preparing food, brushing teeth, or even buttoning the shirt.


Because the symptom of slow motor activity can be seen in several different medical conditions, it is essential to take extra time to obtain a precise diagnosis of bradykinesia.

Your doctor does a simple and common exam. By checking how quickly you can tap your fingers up and down or how slowly you touch your foot, with these data, you will give the doctor valuable information.

Meanwhile, your doctor will ask you questions to get a complete medical history of you and your family.

Sometimes an MRI (magnetic resonance imaging) test will help determine if a tumor or stroke has caused this change in your movements.

Tell your doctor about all of your prescriptions and other supplements you are taking, as some may create bradykinesia as a side effect.

Physicians should rule out metabolic disorders when diagnosing bradykinesia. Some medications can cause bradykinesia.

The wrong diagnosis is plausible because the symptom of bradykinesia is also presented by diabetic neuropathy, muscle sclerosis, and peripheral neuropathy, among other conditions.

Treatment of bradykinesia

For many, it never becomes a serious condition. However, some of the conditions that cause bradykinesia are progressive, and over time the patient’s symptoms are more pronounced, and other complications may arise.

Many people choose treatments that do not require chemical recipes.


  • Pay close attention to each movement
  • Concentrate on one task at a time, do not multitask
  • Seek medical help as soon as possible
  • The use of a cane is recommended

There are also neuroprotective therapies and restorative therapies:

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

Restorative therapies are designed to replace neurons that have been lost. This is achieved by transplanting embryonic cells that can perform the normal function of the nervous system pathways. Sometimes, genetic modification of the cells can help restore normal function.

Several prescriptions can relieve the symptoms of bradykinesia (ask your doctor):

  • amantadine
  • Bromocriptina
  • Sinemet
  • Cardidopa
  • Levodopa
  • Selegilline
  • Pergolida

Surgical intervention may be considered in more severe cases, although it is not a commonly preferred option. Deep brain stimulation is preferred today over the most invasive surgical procedures of the past.

Paedomotomy is a surgical procedure for advanced Parkinson’s disease. Treats stiffness and tremors by creating scar tissue in a proper and accurate location in the brain. It was once quite common. Now it is more likely that the various medications available are used.

Stereotaxic thalamotomy is rarely used in these times. It is essentially the last resort when all other treatments have failed. The surgery is done while the patient is awake and can answer questions.

It makes the thalamus non-functional and reduces tremors and some other advanced Parkinson’s disease symptoms, so it is used so little.


Active research programs study neurotrophic proteins. Once these proteins pass the blood barrier to the brain, they can protect the nerve cells from death.

Other neuroprotective agents include some enzymes that occur naturally—these work by reducing free radicals that can damage nerve cells.

Transplants of nervous tissue from fetal pigs to the brain have been performed to restore neuronal activity in the damaged area. The results are positive but not conclusive because the population is 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 effectively reduces the progression of Parkinson’s disease, but it is not particularly effective in eliminating bradykinesia.

Work must be done to achieve the goal of minimizing the condition of bradykinesia in many areas. It is not a simple solution to restore the function of basal ganglia cells.