Parkinson\'s Disease a Brief Description of Parkinson\'s

Parkinson's Disease

A Brief Description of Parkinson's Disease

Parkinson's disease (PD) is a progressive neuromuscular disorder that occurs in middle-age to older adults. The disorder has a mean beginning of about 55 years of age. The incidence of Parkinson's disorder increases with age. PD affects about 0.15% percent of the population (American Psychiatric Association [APA], 2000). PD was first described in 1817 by James Parkinson's "Essay on the Shaking Palsy."

In 95% of PD cases diagnoses there is no genetic association (no one in the family has it) and these cases are designated as sporadic PD. In the small number of remaining cases the disorder is inherited (Dauer & Przedborski, 2003). A condition known as secondary Parkinsonism that resembles the physical presentation of PD can be brought on by a number of drugs or other conditions such as dopamine antagonist medications, hypoxia, and from brain tumors (APA, 2000).

The Cause of PD

The etiology (cause) of PD is not known but there are distinct neuropathological signs of PD that have been relatively well described. The neural loops that connect the basal ganglia and the thalamus in midbrain are composed of both inhibitory and excitatory pathways. These pathways combine together to form two basic routes: a direct route that induces physical actions (composed of excitatory neural loops) and an indirect neural route that decreases or inhibits actions (composed of inhibitory neural loops). PD results from involvement in both of these areas. The two major neuropathological characteristics of PD are (Goetz, Emre & Dubois, 2009):

1. A massive loss of the nirgrostriatal dopaminergic neurons. The loss of dopaminergic neurons means that a deficiency of the brain neurotransmitter dopamine is the characteristic feature of PD (Goetz, Emre & Dubois, 2009). The nirgrostriatal tract is one of the major projections in the brain that is involved in movement. However, the principal pathology of PD appears to affect the dopamine-producing neurons in an area of the brain known as the substantia nigra pars compacta. The neurotransmitter dopamine is produced by neurons in the substantia nigra from DOPA (which is a precursor of melanin) and then is transported along the axons of these particular neurons to a brain area known as the striatum (Goetz, Emre & Dubois, 2009). The striatum is the major input center of the basal ganglia and is divided by the internal capsule (a large white matter tract) into two sections that are known as the putamen and the caudate nucleus (Bear, Connors, & Paradiso, 2001). By the time that the symptoms of PD appear in the person the dopamine levels in the putamen (which plays a role in movement) are depleted by nearly 80% and there is a total 60% loss of dopaminergic neurons in the substantia nigra (Fearnley, & Lees, 1991). As the disorder gets worse there is an even greater loss of dopaminergic neurons in the basal ganglia. The loss of these particular neurons, which normally contain large amounts of darker neuro-melanin, leads to the depigmentation of the substantia nigra in PD patients (the substantia nigra typically appears black owing to high levels of melanin and low levels of dopaminergic neurons).

2. The appearance of am overabundance of Lewy bodies. The other trademark feature of PD is the emergence of Lewy bodies. Lewy bodies are intra-neuronal inclusion bodies that are comprised of protein. The buildup of high levels of these Lewy bodies in the brain results in neuronal degeneration and cell death in the brain. While the brain is capable of some repair it cannot repair a massive loss of tissue like say a deep cut in your arm is repaired. Once a considerable number of neurons die in a particular area of the brain certain functions are adversely affected. If a significant number of neurons are lost one cannot regain that function (Goetz, Emre & Dubois, 2009).

Major Symptoms of PD

The loss of a significant proportion of the dopaminergic neurons in the basal ganglia that affect both excitatory and inhibitory pathways in the basal ganglia results in the typical triad of symptoms found in PD (Forno, 1996):

1. Tremor. Tremors that occur in PD consist of include a fine motor tremor that is usually most pronounced at rest (thus it is termed a "resting tremor"). This type of tremor gets worse with movement of the limb and in the arms results in the classic pill-rolling tremor observed in individuals with PD. Other similar fine tremors can be observed elsewhere in the patient, often in the head.

2. Rigidity. The rigidity observed in PD patients consists of increased "tone" of the muscles (tone means that passive movement of the legs or arms is difficult). Often when a PD patient's arm or leg is forcibly bent by another person one gets the feeling of a "ratchet" type movement in the limb (Dauer & Przedborski, 2003).

3. Bradykinesia or slowed movements. Bradykinesia is defined as a reduction of speed of most of the normal movements in PD, especially with movements that have to do with fine motor control. Bradykinesia can also be evidenced in the general lack of expressive movements, such as a mark reduction of expressive gestures, a marked decrease in facial movements, and a significant reduction of facial expressions in PD patients. Bradykinesia also leads to the "shuffling gait" observed in PD patients. The shuffling gait occurs when the person walks as if their feet are magnetized and are stuck to a metal floor resulting in a sort of sliding on the floor. The movement disorder in PD can be intermittent at times as there is an additional subcortical route that is involved in gross motor movements that circumvents the basal ganglia. This route operates by way of the cerebellum, so PD patients are sometimes able to run or to walk normally in emergency situations.

Other PD symptoms are comprised of sudden cessations of movement (freezing), difficulty beginning or getting certain movements started (akinesia), and deceased speed of thought (bradyphrenia). In later stages of PD the cognitive abilities of the person also become affected. There is a high rate of dementia as PD progresses (Forno, 1996).