Before I describe the physiological basis of Parkinson I would like to give a brief history of Parkinson and the number of people who have it. Parkinson was not formally recognized and its symptoms were not documented until the year 1817 by a British apothecary named James Parkinson. He wrote an Essay on the Shaking Palsy. In this essay he listed six cases that he had seen and in each case the person was a male over the age of fifty with trouble walking and had shaking limbs. What he described were the symptoms that would latter take his name (Jankovic J. 2008). Parkinson back then was known as paralysis agitans (shaking palsy). He described shaking palsy as an involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forwards, and to pass from a walking to a running pace: the senses and intellects being uninjured (Parkinson J. 2002). Parkinson has the second highest number of neurodegenerative disease patients; only Alzheimer’s is higher. It is estimated that there are almost 1.5 million people who have Parkinson in the US alone and more than 5.5 million globally. The numbers point to more men than women developing Parkinson and to more whites with Parkinson than Black Americans of African ancestory, Africans or Asians (Parkinsonsfocustoday 2010).
Now that you know a little about Parkinson’s history I am going to describe the physiological basis of the Parkinson. The physiological basis for Parkinson’s is the decreasing balances between the excitatory neurotransmitters and the inhibitory neurotransmitters, in this case it would be the dopamine and norepinephrine. Dopamine plays in a role in regulation of behaviour, voluntary movement, cognition, motivation, reward, attention, learning and mood. The degeneration of the dopamine neurons is usually gradual and may take place over many years. This results in precursor symptoms which are just being recognized by the medical profession (Carlson 2008). Once there is significant loss of norepinephrine triggered by the extreme loss of dopamine, its precursor, then the diagnosis begins. By this time between 60-80% of the dopamine found in the pars compacta substantia nigra of the basal ganglia has occurred and people begin to see TRAP. TRAP stands for Tremors, rigidity/stiffness, akinesia/bradykinesia or slow movements and postural instability (Parkinsonsfocustoday 2010).
I would now like to move on to the prognosis or the diagnosis of the Parkinson disorder. Parkinson is both chronic and progressive. Chronic meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time. Although some people become severely disabled, others experience only minor motor disruptions. Tremor is the major symptom for some patients, while for others tremor is only a minor complaint and other symptoms are more troublesome. No one can predict which symptoms will affect an individual patient, and the intensity of the symptoms also varies from person to person (NINDS 2010). Parkinson is diagnosed on clinical criteria; there is no definitive test for diagnosis. Historically, pathological confirmation of the hallmark Lewy body on autopsy has been considered the criterion standard for diagnosis. In clinical practice, diagnosis is typically based on the presence of a combination of cardinal motor features, associated and exclusionary symptoms, and response to levodopa. Although the diagnosis of Parkinson is straightforward when patients have a classical presentation, differentiating Parkinson from other forms of parkinsonism can be challenging early in the course of the disease, when signs and symptoms overlap with other syndromes (Parkinsonsfocustoday 2010).
The National Institute of Neurological Disorders and Stroke (NINDS) have diagnostic criteria for Parkinson’s disease. They have two groups, group (A) which is the characteristics of Parkinson and group (B) which is suggestive of alternative diagnoses of Parkinson. Group (A) consists of Resting tremor, Bradykinesia, Rigidity, Asymmetric onset. Group (B) consists of features unusual early in the clinical course, prominent postural instability in the first three years after symptom onset, freezing phenomenon in the first three years, hallucinations unrelated to medications in the first three years, dementia preceding motor symptoms or in the first year, supranuclear gaze palsy or slowing of vertical saccades, severe, symptomatic dysautonomia unrelated to medications, documentation of condition known to produce parkinsonism and plausibly connected to the patient’s symptoms. To meet the criteria for definite Parkinson all criteria for probable Parkinson’s are met and histopathological confirmation of the diagnosis is obtained at autopsy. To meet the criteria for probable Parkinson at least three of the four features in group (A) are present and None of the features in group (B) is present and substantial and sustained response to levodopa or a dopamine agonist has been documented. To meet the criteria for possible Parkinson at least two of the four features in group (A) are present; at least one of these is tremor or bradykinesia and either none of the features in group (B) is present or symptoms have been present more than three years and none of the features in group (B) is present and either substantial and sustained response to levodopa or a dopamine agonist has been documented or the patient has not had an adequate trial of levodopa or a dopamine agonist (Jankovic J. 2008).
Let’s move on to the treatment considerations of Parkinson. There are several types of treatments that are used to relieve the symptoms of Parkinson, but I will only mention a couple of the treatments. The first treatment that I would like to talk about is medication. People with Parkinson are given L-DOPA. L-DOPA is the precursor to dopamine. We know that dopamine can’t cross the blood-brain barrier but L-DOPA can. When the L-DOPA reaches the brain it is taken up by the dopaminergic neurons and is converted into dopamine. The increased synthesis of dopamine cause more dopamine to be released by the surviving dopaminergic neurons in patients with Parkinson (Carlson 2008).
There are also three sterotaxic procedures designed to alleviate the symptoms of Parkinson. The first one is transplantation of fetal tissue. It is used to reestablish the secretion of dopamine in the neostriatum. In a study of thirty-two patients with fetal transplants Freed found that those who symptoms responded to L-DOPA were most likely to benefit from the surgery (Carlson 2008). The second procedure involves destruction of the globus pallidus, which provides an inhibitory output from the basal ganglia through the thalamus to the motor cortex. The third stereotaxic procedure aimed at relieving the symptoms of Parkinson’s disease is a therapy called deep brain stimulation. Deep brain stimulation has been approved by the U.S. Food and Drug Administration and this therapy involves implanting electrodes in the brain and connected to a small electrical device called a pulse generator that can be externally programmed. This device permits the patient to electrically stimulate the brain through the electrodes. This surgery may be appropriate if the disease doesn’t respond to drugs In DBS (NINDS 2010).
I have mentioned the physiological basis of the disorder, I described the prognosis and I discussed the treatments of Parkinson now I would like to talk about the impact Parkinson has on one’s self and the family. Depending on how bad you have Parkinson in my opinion determines how it will impact you and or your family. I am giving my point because my dad has Parkinson and it did not keep him from working. He has the resting tremors. The resting tremors started on his left side first and then about five years later he got the tremors on his right side. My dad’s doctor helped to stop his tremors by doing a procedure that is called Deep Brain Stimulation. Deep Brain Stimulation stops resting tremors by implanting electrodes in the subthalamic nucleus and attaching a square shaped device called the implanted pulse generator. The implanted pulse generator permits the patient to electrically stimulate the brain through the electrodes which is called the lead.
The deep brain stimulation system consists of three components: the implanted pulse generator, the lead, and the extension. The implanted pulse generator is a battery-powered neurostimulator encased in a titanium housing, which sends electrical pulses to the brain to interfere with neural activity at the target site. The lead is a coiled wire insulated in polyurethane with four platinum iridium electrodes and is placed in one of three areas of the brain. All three of these components are surgically implanted inside the body. Under local anesthesia, a hole about 14 mm in diameter is drilled in the skull and the electrode is inserted, with feedback from the patient for optimal placement. The installation of the implanted pulse generator and lead occurs under general anesthesia. The right side of the brain is stimulated to address symptoms on the left side of the body and vice versa (NINDS 2010).
I put a picture at the end of this paper that would show you what the implanted electrodes would look like in the body. You would not be able to see the electrodes in the head but you can see the outlines of the square shaped stimulation devices or implanted pulse generators that are underneath the skin near the collar bone.
Let’s say that all you have is the resting tremors. Having this will not affect you too much because it would not keep you from working, driving, walking, or any other thing like that, But if you have all four of the symptoms then that would affect you and your family because now you have to depend on other people for a lot of help. You could need help walking so that you would not fall and you can even need help feeding yourself just to name a few things.
On a side note the reason I chose this topic is because my dad has Parkinsons and I was concerned that I could end up with it too because I thought that it is hereditary. The more information I read about Parkinson the more that I found out that only about 15% or at most 20% has been identified as being genetic. There are several genes which have protein mutations associated with Parkinson, but they are each more common to specific geographic areas for specific gene lines although there are almost certainly trade route connections and migration or emigration patterns (Parkinsonsfocustoday 2010).
In the picture above you can see what the deep brain stimulation would look like if we had x-ray vision like superman and could see inside the body. You can see from this picture that there are electrodes which are called leads that are implanted deep into the brain. This is why it is called deep brain stimulation because of the electrodes that are implanted deep into the brain. These electrodes that are implanted in the brain have wires that run down the side of the neck, behind the ear to the square shaped stimulation devices which are called the implanted pulse generator. The implanted pulse generator is placed underneath the skin below the collarbone or in some cases, the abdomen. This square shaped device sends impulses to the electrodes that are in the brain to stimulate the brain to stop the resting tremors. You can also see from the picture above that you can see the outlines of these square shaped stimulation devices from underneath the skin (NINDS 2010). These square shaped stimulation devices are powered by batteries. The batteries of the stimulation devices last roughly about five years before they will need to be changed out.
In this paper I described the physiological basis of the disorder, prognosis, treatment considerations and impact on self and family unit.
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