Download Parkinson`s Disease Rigidity Quantification Kylen Bares1, Eddie

Parkinson’s Disease Rigidity Quantification
Kylen Bares1, Eddie Cao1
1
Vanderbilt University, Department of Biomedical Engineering, Nashville, TN
37235
ABSTRACT:
Parkinson’s disease is a neurodegenerative disorder caused by the lack of
sufficient release of dopamine, which is needed to act on the motor neurons to enable
effective control of muscle activity. It occurs among at least a million people every year,
and it is prevalent mostly in elderly white males as well as those with a genetic
predisposition for it and proneness due to a history of other illnesses. It is characterized
by various symptoms, such as rigidity, tremors, loss of postural coordination, and
reduction in eye blinking rate. While various forms of treatment exist for Parkinson’s
patients, they do not have a reliable method of quantifying the symptoms that occur,
which is needed to maximize therapy. Thus, we decided to focus on measuring rigidity
of a Parkinson’s patient’s arm and fingers. For our design project, we designed and
constructed a pneumatic device that uses pressurized air cylinders to force movement in
a patient’s arm and fingers and display the pressure that is required to induce movement
in said arm or fingers.
Although our completed device discarded measurements of
finger rigidity, it had minimal success in quantifying arm muscle rigidity by displaying
higher values of pressure for greater amounts of rigidity.
INTRODUCTION:
Parkinson’s disease is a neurodegenerative disorder caused by damage or lack
of neurons in the substantia nigra which release a neurotransmitter called dopamine.
Dopamine is responsible for the stimulation of motor neurons in the basal ganglia. In a
human being with a normally functioning brain, the stimulation of the basal ganglia
neurons counteracts the inhibition induced by acetylcholine to enable control of motor
activities by the reticular formation. If dopamine is not released by the substantia nigra
in sufficient amounts to act on motor neurons, then the inhibition of acetylcholine on the
basal ganglia predominantly
prevents the reticular formation
from
controlling
muscular
activity very well. In a person
with Parkinson’s, at least about
80%
of
dopamine-releasing
neurons in the substantia nigra
are defective [3].
Parkinson’s affects at
least a million people every
year in the United States. It is
more prevalent among white
males, and people with Parkinson’s begin to develop noticeable symptoms when they
reach the age of 60 on average. Risk factors for developing Parkinson’s can be related
to age, genetics, and history of previous illnesses.
Being older, having a genetic
predisposition, and having had another illness may affect likeliness of the disease’s
onset [3].
The symptoms of Parkinson’s are all related to inability to control one’s motor
activities. They include tremor or trembling in the hands, arms, legs, jaw, and face as
well as rigidity or stiffness of the limbs and trunk [8]. Other examples of symptoms are
slowness of motor movements and reduction in rate at which one can blink his or her
eyes. As one’s muscles also control one’s ability to control his or her posture, loss of
coordination or stability in one’s posture can also be symptomatic of Parkinson’s.
Currently, there exist three common forms of treatment for Parkinson’s disease.
The first treatment is the administration of a drug called levodopa. The second type of
treatment involves surgical removal of a section of brain. The third form is deep brain
stimulation.
Levodopa (3,4-dihydroxy-L-phenylalanine), or L-DOPA, when administered into
the body, undergoes transformation into dopamine by L-aromatic decarboxylase. Thus,
it aids in the increase of dopamine levels to compensate for the insufficient amount of
dopamine-releasing neurons in the substantia nigra. However, only a small percentage
of administered L-DOPA reaches and is able to enter the dopaminergic neurons. The
majority of the L-DOPA is transformed into dopamine elsewhere, thereby causing
various side effects.
Moreover, administering L-DOPA as a pro-drug inhibits the
endogenous production of L-DOPA, reducing the amount of dopamine produced within
the body, which contributes to its counterproductivity [5].
Pallidotomy is the surgical removal of a portion of the basal ganglia called the
globus pallidus. The procedure is performed by inserting a wire probe into the globus
pallidus, followed by the emission of radio waves through the wire probe. The heat that
is induced by the radio waves, as a result, destroys the surrounding tissue. Effects of
pallidotomy include reduction of muscle rigidity and tremor by 25% to 50%, and
successful surgery reduces the necessity of treatment by L-DOPA administration.
However, the treatment is not without its adverse effects, including deficits in vision and
speech as well as sensations of weakness and confusion [6].
Deep brain stimulation is the surgical implantation of a battery-powered
neurostimulator to electrically stimulate targeted brain areas that are responsible for
control of motor activities. The area of the brain is pre-designated using MRI or CT
scanning, prior to the procedure.
A thin, insulated wire called a lead electrode is
inserted through the skull and implanted in the targeted area. Another insulated wire
called the extension is inserted under the skin passing through the head, neck, and
shoulder and is connected to the lead. Finally, the neurostimulator is implanted through
the skin by the collarbone, in the chest, or near the abdomen.
After all three
components have been placed, the neurostimulator sends electrical impulses along the
extension wire and lead, thus entering the brain to block abnormal electrical signals that
lead to Parkinson’s symptoms. Deep brain stimulation has been regarded as a very
effective of treatment, as for many patients, Parkinson’s symptoms have been reduced
significantly.
A possible drawback is that despite the effectiveness of deep brain
stimulation, some patients may still be required to take medications such as L-DOPA,
albeit in smaller dose prescriptions [7].
All three forms of treatment offer individual advantages and disadvantages.
However, no matter how effective each of them is, the study of Parkinson’s symptoms
still has one major setback: there is currently no known reliable method for making
quantitative measurements of any of the symptoms. Finding and verifying a method for
quantification of symptoms would help maximize the effects of therapy such as the
aforementioned types of treatment. The aim in our project was to design and construct a
medical device that is intended to make quantitative measurements of symptoms of
Parkinson’s. While symptoms range from rigidity and tremors to lack of coordination and
balance, we focused primarily on measuring rigidity and tension of muscles in the arms.
METHODOLOGY:
Our design project focused on the quantitative detection of Parkinson’s disease
symptoms. The advisor who supervised our work was Dr. Chris Kao, M.D., Ph.D, a
research associate professor in the Vanderbilt University Department of Neurosurgery.
His clinical studies centered
on
microelectrode
brain
mapping to localize brain
targets
for
stimulation
deep
to
brain
treat
movement disorders, and his
research
focused
electrophysiology
in
on
nerve
stimulation, epilepsy, pain control, and head injury.
Our device focus centered on the design and
construction of a pneumatic-actuated frame that fits
around specifically the right arm of a patient. It was
designed to be tested on the rigidities of the arm and
fingers.
It utilizes air pressure to enable the
individual flexion of the fingers and forearm and
measures that pressure for fingers and forearm
exerted on the actuator piston.
This pressure
corresponds to the force that the patient needs to
exert to move his arm or fingers.
In turn, the
pressure measurements will enable us to quantify the
rigidity of said arm or finger. Ultimately, our device
should be able to force movement in the arms and fingers of actual Parkinson’s patients
and accurately display the values of pressure required to induce movement.
The pneumatic actuator is composed of two main components: a control box
(see Fig. 2) and an arm frame (see Fig. 3). The control box contains the pneumatic air
pressure valves and pressure manifold. The control box allows slow circulation of air
into the desired side of the cylinder actuator, thus applying force on the actuator piston
and the arm via the arm frame. The arm frame encloses the arm and translates the
motion of the pneumatic cylinders into the motion of the arm.
In addition to our pneumatic-actuated arm frame, a glove was also designed and
constructed to attach a pneumatic air cylinder between the opposable thumb and the
index finger. This enables us to detect rigidity of the fingers by translating the motion of
the pneumatic air cylinder attached to the glove into the motion of the fingers. Since inhouse air pressure would not be available in the operating room, the actuator would be
tested using a household air compressor with pressure values up to around 125 psi. In
the operating room, we would likely use a compressed air tank with a regulator set to
around 125 psi, likewise.
RESULTS:
For the actual experiment, the glove was discarded, and it was determined that
only the arm frame would be used to assess the rigidity of one’s arm muscle. The
pneumatic actuated device was tested on Eddie’s right arm. After the arm was inserted
through the frame and held in place, and an air compressor was attached to the control
box, air pressure was released by Kylen from the compressor by activating the control
box switch.
Eddie was required to hold his arm in flexion, while pressure was applied into the
air cylinder to exert force on his arm to make it extend. There were two trials in which
this was done. In the first trial, Eddie was told to hold his arm rigidly, and air pressure
released from the compressor was slowly increased until his arm was forced to extend.
This determined how much pressure was needed to be applied to the air cylinder to
force his arm, when rigid, into extension. In the second trial, Eddie was told to hold his
arm in flexion, but to keep it relaxed, and air pressure, again, was slowly released
incrementally until his arm was forced to extend. This, in turn, determined how much
pressure was needed to be applied to the air cylinder to force his arm, when relaxed,
into extension. All pressure values were measured in units of pounds per square inch.
The amount of pressure required to force Eddie’s arm, while it was in flexion, to
extend it differed between when Eddie’s arm was relaxed and when his arm was held
rigid. When Eddie’s arm was in flexion and held relaxed, a pressure of 10 pounds per
square inch was needed to move his arm to make it extend. However, when Eddie’s
arm was in flexion but held rigid, a pressure of 22 pounds per square inch was needed
to move his arm to make it extend. Therefore, the amount of pressure required by the
device to move an arm from flexion into extension differs depending on whether the arm
was held relaxed or rigid.
DISCUSSION:
Our device was successful in quantifying muscle rigidity in terms of air pressure
to a certain degree. The data extracted from testing our device on Eddie’s arm provided
evidence that the amount of pressure that was required to be released into the air
cylinder to make one’s arm move depended upon the rigidity of the person’s arm. As
one’s arm muscle rigidity increases, we can expect that more pressure will need to be
released into the air cylinder of the arm frame to further exert force on his or her arm to
make it move. Likewise, if one relaxes his or her arm further, it can be safe to say the
amount of pressure that is needed to be released into the pneumatic air cylinder of the
arm frame is decreased until it reaches the minimum value of pressure equivalent to how
much pressure is needed to force arm movement if the person relaxes his or her arm
completely.
Although rigidity could be measured from our device, the efficiency of the actual
pneumatic actuated arm frame in determining muscle rigidity is not without its
drawbacks. The pressure values that were measured only referred to different amounts
of pressure released into the air cylinder that forced the arm to move from flexion into
extension. However, the amount of pressure required to force an arm to extend from
flexion may be significantly different from the amount of pressure required to force an
arm to flex an arm from extension, due to different muscle groups in the arm that are
predominantly in control of flexion and extension. Therefore, further specification may
be needed as to which muscle in the arm is being tested for rigidity. In addition, only
one test subject was used for data extraction.
A different person, who may have
different musculature, may have different corresponding pressure values for when his or
her arm is held fully relaxed or rigid.
Furthermore, no data was taken from actual
Parkinson’s patients. As it is more difficult for one with symptomatic tremors or rigidity to
control his or her muscles, it would be more difficult to assess if a Parkinson’s patient
has his or her arm held fully relaxed or rigid when taking pressure measurements.
There may be different ways to improve our device, at least some of which relate
to addressing part or all of the aforementioned drawbacks.
One possible way of
improvement is to refine our device to specify which muscle is being tested for rigidity.
As previously stated, different muscles may have rigidities corresponding to different
pressure values. Another possible way is to construct a control for each and every
individual, Parkinson’s or normal. It would be necessary to know if a Parkinson’s patient
were healthy, what his or her pressure values would be for arm muscle rigidity, and then
be able to compare that with the patient’s actual pressure values under his or her
present Parkinson’s conditions.
Additional ways to improve our design regard convenience and comfort for the
patient using it. Our device may not work for certain people with arms of enormous size
because a person’s arm, if too big, may not fit into the arm frame. Addressing the
problem may involve refining our device to make it able to adjust the width of the frame
to allow it to fit all. Another problem is that the device is constructed of aluminum and
consists of rough, sharp edges. If a patient’s arm is inserted into the frame, it cannot be
subject to abrasions and cuts, or the patient may reject its use. Therefore, a form of
protection may be necessary to provide safety and a sense of comfort upon placement
of the arm into the frame.
CONCLUSIONS:
Our device provided some efficacy in determining muscle rigidity of one’s arm. If
the arm is held rigid as opposed to being held relaxed, the amount of pressure that is
needed to be released into the air cylinder of the arm frame is greater, while the amount
of pressure is minimized as the person’s arm is further relaxed. However, it lacks further
specifications, such as the arm muscle, flexion or extension of the arm, amount of
musculature of each individual. The ways to improve our device involve addressing
these issues and providing convenience and comfort for the patient.
REFERENCES
[1] http://www.swedish.com/body.cfm?id=296
[2]
http://www.pdf.org/Ask/kb.cfm?selectedItem=6067&returnURL=kb.cfm%3Fcategory%3D
75
[3] http://neurologychannel.com/parkinsonsdisease/
[4] http://www.pdmdcenter.com/articles/HopkinsWeb/index.html
[5] http://en.wikipedia.org/wiki/Parkinson%27s_disease
[6] http://www.wemove.org/par/par_pal.html
[7]
http://www.ninds.nih.gov/disorders/deep_brain_stimulation/deep_brain_stimulation.htm
[8] Slowinski JL, Putzke JD, Uitti RJ, Lucas JA, Turk MF, Kall BA, Wharen RE. Unilateral
deep brain stimulation of the subthalamic nucleus for Parkinson disease. J Neurosurg.
2007 Apr;106(4):626-32.