Parkinson’s disease (PD) has been defined as a steady progressive central neuro-degenerative disorder. The disease affects the body movement and is typified by severe symptoms which include significant rigidity in muscle, tremors in hands and legs among other body parts, loss of facial expression as well as hypophonia, diminished blinking and akinesia.
The nerve cells (or the neurons) are located in the substantia nigra of the brain which is pigmented part of the brain that secrete a chemical substance known as dopamine. Dopamine is a neurotransmitter that assists in the transmition and modulation of signals between the substantia nigra and the corpus striatum which is a relaxation point of the brain and functions in smooth muscle activity.
Corpus striatum functions in balancing the body as it works dependently between the two neurotransmitters namely the dopamine and acetylcholine. Consequently, neurons may get impaired or damaged or die which leads to non-production of dopamine in the brain.
This as a result will create imbalance between the neurotransmitters. Accordingly this causes the corpus striatum non-functional in transmitting and modulating of movement rendering those people with PD to result to posture abnormalities and difficulties in mobility. The lack of dopamine also leads to excitation of the medial segment of the globus pallidus resulting in bradykinesia (Tandberg 1995, p. 541).
Parkinsonian is a central nervous system (CNS) disorders. Insightful research have reported that PD the pigmented substantia nigra located in the brain stem gives rise to the dopaminergic nigrostriatal pathway and the locus ceruleus giving rise to a noradrenergic pathway.
The motor disabilities that characterize PD are chiefly due to the failure of dopaminergic neurons in the substantia nigra resulting in a dramatic decrease in the dopamine levels in the brain. Once the dopamine neuronal cell dies at the critical level of 85-90%, the neurological symptoms of PD appear.
The current treatment for PD is the systematic administration of levodopa (L-DOPA); a precursor to dopamine which enters the brain via a carrier mediated transport system and then converted to DA by the enzyme L-aromatic amino acid decarboxylase (L-AAAD).
It was discovered that striatal dopamine is deficient in PD and that its substitution with high dosages of L-DOPA could revolutionize the symptoms of Parkinsonism. However, wide ranges of problem are associated with the current treatment especially of during the chronic use of L-DOPA.
On the same note, dramatic increase on research involving PD in the recent years has been experienced. The most common and vexing problems are dyskinesias. Researchers have tried to gain imminent into the mechanism of these worrying harmful effects by studying the metabolism of L-DOPA using animal models.
Numerous suggestion have been put forth to explain the main side effects but none of them have been inherently proven. Investigation efforts focusing on the treatment of PD are therefore needed because PD affects 1 person in 500 of the population in general and also its occurrence augments with advancing age to 2-3% of the population over 50.
The etiology and possible means of prevention are unknown (Cummings 1992, p. 1445). However, there are three theories regarding the etiology of Parkinson’s disease, but none of them have been fully studied. This includes; ageing, toxic factors or infection and genetic factors. One of the most explored hypotheses is that PD may be caused by contaminating with the environmental agents or endogenous toxins.
This accelerates the ageing of the brain that causes decline in the substantia niagra neurons. Further, epidemiological studies have indicated that the commonness of Parkinson’s disease is quite high in highly industrialized countries.
These results however support the premise that environmental or endogenous factors play a role in the development of PD (Tandberg 1995, p. 545).
Categories of Parkinson’s disease
Two categories of Parkinson’s disease have been distinguished as the idiopathic or primary PD and secondary PD. Idiopathic or Primary PD is defined by the presence of a certain symptom-complex but its main cause is still unknown.
Idiopathic PD falls under the ICD-10 Category G20. Secondary PD has similar symptoms to PD but the cause is known. These diseases fall under ICD-10 Category G21 (such as Syphilitic Parkinsonism, fall under the ICD-10 category G22).
Secondary PD includes the malignant neuroleptic syndrome as well as other drug-induced Parkinsonism such as those caused by neuroleptic drugs (for example antipsychotics), antiemetic agents (such as prochlorperazine), gastro-intestinal anti-motility drugs (such as metaclopramide), antihypertenstive drugs (reserpine) and some calcium-channel blockers.
Other secondary Parkinsonism is caused by the environmental factors such as toxicity, trauma, metabolic derangement and brain tumor. The knowledge of the cause of Parkinson’s symptoms hints the best treatment. For instance, Parkinsonism induced by drug usually disappears within weeks to months after medication is discontinued.
However, recent studies have reported that symptoms can be permanent in about 15% of people. The diagnosis of the two types of Parkinson’s disease is the same but both have different medical treatment and prognosis. In addition, supporting evidence has also shown that both idiopathic and secondary PDs have similar impact on the individuals (Christen 2000, p. 626).
Causes of Parkinson’s disease
Causes of Parkinson’s disease Surprisingly, the cause of Parkinson’s disease has not been identified. However, four causes have been linked to PD namely; ageing, oxidative damage, environmental toxins and genetic predisposition. PD has been associated with accelerated ageing of the normal, age related deterioration of neurons.
This is supported by the connection between antioxidants and PD and the fact that loss of anti-oxidative protective mechanisms is also age related. The second factor involves the oxidative damage caused by free radicals which are unstable and accumulates to damage molecules generated through normal chemical reactions in the body.
The reason why free radicals are potential in damaging of molecules is that they are deficient of one electron and thus attempts to replace the missing electrons through reactions with other molecules. This process is referred to as oxidation. However, antioxidants are known to protect the cells from damage.
People with Parkinson’s disease have high levels of iron and decreased levels of ferritin in the brain which is prone to the process of oxidation. In addition, oxidative damage may also contribute the development of dementia. Environmental toxins involve both an external or internal toxins which destroys the neurons. A number of such toxins have been identified by various investigators.
This includes; methylphenyltetrahydropyridine (MPTP) and neuroleptic drugs, which induce Parkinson’s disease symptoms. The forth suggested cause indicates that approximately 15-20% of people living with Parkinson’s disease have a close relative who has experienced PD symptoms.
Researchers have found that mutations of the gene for the proteins alpha-synuclein on chromosome 4 and parkin on chromosome 6 results in autosomal dominant Parkinsonism and autosomal recessive Parkinsonism, respectively. Age has been voted as the main risk factor for PD. PD usually begins between the ages of 40 and 70 years and around 10% of cases occur before the age of 50 years (Christen 2000, pp. 621-3).
Symptoms of Parkinson’s disease
The variety of symptoms and levels of severity can vary greatly from person to person and are often shared with other similar diseases. The four main symptoms of PD are tremor, rigidity, akinesia and bradykinesia as well as postural instability. Tremor is the trembling of arms, jaw, legs or face. Tremor is more prevalent in hands although it disappears when the patient is deep asleep.
Rigidity is the stiffness of the limbs and the trunk. The basic principle of the movement of muscles is that there are two opposing muscles and during movement one muscle moves while the other remains relaxed. Rigidity occurs when, due to brain signals, the opposing muscle remains contracted when one muscle moves. Facial expression may also become rigid and inflexible (Aarsland et al. 2003, p. 387).
Akinesia and bradykinesia is loss of spontaneous movement which affects the daily activity and increases dependency. Impaired imbalance and postural instability are common in patients with PD. The patience lacks balance and coordination and can therefore fall easily. Anxiety, depression and memory loss are common disorders experienced by patients (Aarsland et al. 2003, p. 387).
This is because dopamine is involved in the development of these conditions and partly because dopamine is a precursor for both adrenalin and noradrenalin.
Furthermore serotonin is depleted in PD, also contributing to the prevalence of depression in patients. Finally, some of the medications used to treat PD also result in these side effects. Other general symptoms include; sleep problems, speech problems, urinary problems as well as sex difficulties.
PD persists in the body and the symptoms get worse over time. The stages of PD are classified into five stages. The first stage involves minimal or non functional impairment (also referred to as unilateral involvement) associated with tremor, changes in posture and facial expression.
The second state is bilateral or midline involvement without impairment of balance. Here the posture is usually affected. The third stage exposes the first sigh of postural instability, significant slow of body movements. The patient at this stage can lead an independent life with mild disability.
The forth stage is associated with severe symptoms. Here, walking is limited, significant rigidity and bradykinesia. The patient is no longer independent. The fifth stage is known as cachectic stage. The patient is immobile either in bed or wheelchair.
Since there is no definite test for PD, diagnosis is widely based on medical history, significant symptoms and classic signs of PD. Mostly, individuals are given anti-PD medications to see whether they may respond. In addition, other tests are performed to rule out the possibility of PD.
The presence of other diseases like dementia and ageing hampers the symptoms of PD thus reducing the chance of accurate treatment. The accessibility of good referral clinic can also contribute to lack of right from the onset stages.
There is no cure for PD in the market today. Currently, the disease is treated with drugs that attempt to replenish or mimic dopamine in the brain. Knowing the cause of the PD symptoms can inform the best course of treatment. For example, drug-induced Parkinsonism usually disappears within weeks to months after discontinuing medication; however symptoms can be permanent in about 10% of people.
Although diagnosis, medical treatment and prognosis can be very different, both idiopathic and secondary PD have similar impacts on the individual. Needs are similar in terms of access to services and support. It is very complicated to treat PD since the drugs require continuity with slight adjustments in dosages and complex combinations. This requires significant medication management to reduce unnecessary disease burden.
Other effective treatments include physiotherapy, occupational therapy, speech therapy and surgery. Recent development in the treatment of PD involve planting an electrode in the brain to provide high frequency stimulation and block electrical signals in targeted areas of the brain that control movement blocking the abnormal nerve signals that cause tremor and PD symptoms (Whetten-Goldstein et al. 1997, p. 847).
The cornerstone of the approach to PD is the commitment to better health for the patients affected through prevention, care and cure. This involves the timely, accurate diagnosis and cost effective health interventions which reduces the immediate burden of the disease.
A future national strategy should include enhancing a collaborative medical research and training of doctors and nurses in relation to PD diagnosis, treatment, and knowledge of medication and hospitalization protocols. Considerable research to find a new effective therapy such as dopamine agonists ought to be employed to curb the disease (Whetten-Goldstein et al. 1997, p. 845).
Aarsland, D., Anderson, K., Larsen, J., et al. “Prevalence and Characteristics of Dementia in Parkinson Disease: An 8-Year Prospective Study”. Archives of Neurology, 60.3 (2003): 387-392.
Cummings, J. “Depression and Parkinson’s disease: a review”. American Journal of Psychiatry, 149 (1992): 1443-454.
Christen, Y. “Oxidative stress and Alzheimer disease”. American Journal of Clinical Nutrition, 71.2 (2000): 621-629.
Whetten-Goldstein, K., Sloan, F., Kulas, E., et al. “The Burden of Parkinson’s Disease on Society, Family and the Individual”. Journal of the American Geriatrics Society, 45.7 (1997): 844-849.
Tandberg, E. “The Epidemiology of Parkinson’s disease in the country of Rogaland, Norway”. Movement Disorders. 10 (1995): 541-9.