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PARKINSON]S DISEASE (Paralysis Agitans)


Parkinsons Disease is a chronic degenerative movement disorder that arises in the basal ganglia in the cerebrum. It usually begins in the fourth of fifth decade of life, with symptoms becoming progressively worse as the patient ages. The disease is characterized by tremors, changes in posture and gait, rigidity, and slowness of movements. Named after James Parkinson, described PD as Shaking Palsy in 1817. PD is also known as IDIOPATHIC PARKINSONISM. Understanding Medical-Surgical Nursing Neurologic System Cerebrum Basal Ganglia Substantia Nigra Production of Dopamine and its functions Balanced released of Dopamine and Acetylcholine Anatomy Parkinson disease is predominantly a disorder of the basal ganglia, which are a group of nuclei situated at the base of the forebrain. The striatum, composed of the caudate and putamen, is the largest nuclear complex of the basal ganglia. The striatum receives excitatory input from several areas of the cerebral cortex, as well as inhibitory and excitatory input from the dopaminergic cells of the substantia nigra pars compacta (SNc). These cortical and nigral inputs are received by the spiny projection neurons, which are of 2 types: those that project directly to the internal segment of the globus pallidus (GPi), the major output site of the basal ganglia; and those that project to the external segment of the globus pallidus (GPe), establishing an indirect pathway to the GPi via the subthalamic nucleus (STN). For an illustration of the subthalamic nucleus, see the image below.

Anatomy and Physiology

Sagittal section, 12 mm lateral of the midline, demonstrating the subthalamic nucleus (STN) (lavender). The STN is one of the preferred surgical targets for deep brain stimulation to treat symptoms of advanced Parkinson disease. The actions of the direct and indirect pathways regulate the neuronal output from the GPi, which provides tonic inhibitory input to the thalamic nuclei that project to the primary and supplementary motor areas.

PARKINSON]S DISEASE (Paralysis Agitans)



1.) Genetics Recent discovery of inherited forms of Parkinson disease suggest that genetic factors may play a role in the pathogenesis of early-onset Parkinson disease. Eight genetic loci for monogenic forms of Parkinson disease or doparesponsive parkinsonism have been identified. Mutations in the parkin gene (Park2) have been identified in a high percentage of family members with early-onset Parkinson disease (i.e., persons who developed symptoms before 45 years of age). A second gene mutation involves the -synuclein gene (Park1). Synuclein is a member of a small family of proteins that are expressed preferentially in the substantia nigra. Although mutations in this gene appear to be a rare cause of Parkinson disease, synuclein has received much attention because it is one of the major components of the Lewy bodies (intracytoplasmic inclusions found in the substantia nigra neurons) that are found in brain tissue of persons with Parkinson disease.

PRECIPITATING: 1.) Antipsychotic Drugs Drug-induced parkinsonism can follow the administration of antipsychotic drugs in high doses (e.g., phenothiazines, butyrophenones). These drugs block dopamine receptors and dopamine output by the cells of the substantia nigra. Of interest in terms of research was the development of Parkinson disease in several persons who had attempted to make a narcotic drug and instead synthesized a compound called MPTP (1-methyl-phenyl-2, 3,6 tetrahydropyridine).28 This compound selectively destroys the dopaminergic neurons of the substantia nigra. This incident prompted investigations into the role of toxins that are produced by the body as a part of metabolic processes and those that enter the body from outside sources in the pathogenesis of Parkinson disease. 2.) Toxins/ Chemical Agent 3.) Carbon Monoxide Poisoning 4.)


1.) Tremors at Rest 2.) Rigidity 3.) Bradykinesia

The brain is no longer able to direct the muscles to perform in the usual manner. This lack of communication between the brain and the muscles can have a profound impact on the patients ability to ambulate safely, perform ADLs and job functions, or enjoy leisure
4.) Postural Instability 5.) Dementia

PARKINSON]S DISEASE (Paralysis Agitans)

It occurs in approximately 20% of persons with the disease and develops late in the course of the disease. The mental state of some persons with Parkinson disease may be indistinguishable from that seen in Alzheimers disease. It has been suggested that many of the brain changes in both diseases may result from degeneration of acetylcholinecontaining neurons in a region of the brain called the nucleus basalis of Meynert, which is the main source of cholinergic innervation of the cerebral cortex. Persons with Parkinson disease also have other neurochemical disturbances that can account for some of the features of dementia.


The substantia nigra is a group of cells located within the basal ganglia, which is situated deep within the brain. These cells are responsible for the production of dopamine, an inhibitory neurotransmitter. Dopamine facilitates the transmission of impulses from one neuron to another. Parkinsons disease is caused by destruction of the cells of the substantia nigra, resulting in decreased dopamine production. Loss of dopamine function results in impairment of semiautomatic movements.

PARKINSON]S DISEASE (Paralysis Agitans)

Parkinsons disease is sometimes referred to as an extrapyramidal disorder because the extrapyramidal tracts that contain motor neurons are affected. Acetylcholine, an excitatory neurotransmitter, is secreted normally in individuals with Parkinsons disease. The normal balance of acetylcholine and dopamine is interrupted in these patients, causing a relative excess of acetylcholine, which results in the tremor, muscle rigidity, and akinesia (loss of muscle movement) characteristic of Parkinsons disease.


The diagnosis of Parkinsons disease is made on the basis of two out of the four important symptoms: Tremors at rest, Rigidity, Bradykinesia, Postural instability; one of the 2 symptoms must be resting tremor or bradykinesia. Antiparkinson drugs act by increasing the functional ability of the underactive dopaminergic system, or they reduce the excessive influence of excitatory cholinergic neurons. Drugs that increase dopamine levels include: y levodopa and levodopa with the decarboxylase inhibitor (carbidopa), - drug of choice y amantadine, y bromocriptine y pergolide, and y selegiline. Because dopamine transmission is disrupted in Parkinson disease, there is a preponderance of cholinergic activity, which may be treated with anticholinergic drugs. Amantadine was introduced as an antiviral agent for prophylaxis of A2 influenza and was unexpectedly found to cause symptomatic improvement in persons with parkinsonism. Although the exact mechanism of action remains to be elucidated, it may augment release of dopamine from the remaining intact dopaminergic terminals in the nigrostriatal pathway of persons with Parkinson disease. It is used to treat persons with mild symptoms, but no disability. Bromocriptine, pergolide, pramipexole, and ropinirole are dopamine agonists that act directly to stimulate dopamine receptors. These drugs are used as adjunctive therapy in Parkinson disease. They often are used for persons who have become refractory to levodopa or have developed an onoff phenomenon. Selegiline is a monoamine oxidase type B inhibitor that inhibits the metabolic breakdown of dopamine. Selegiline may be used as adjunctive treatment to reduce mild onoff fluctuations in the responsiveness of persons who are receiving levodopa. It has been proposed that in inhibiting dopamine metabolism and the generation of destructive metabolites, selegiline also may delay the progression of the disease. Anticholinergic drugs (e.g., trihexyphenidyl, benztropine) are thought to restore a balance


PARKINSON]S DISEASE (Paralysis Agitans)

between reduced dopamine and uninhibited cholinergic neurons in the striatum. They are more useful in alleviating tremor and rigidity than bradykinesia. The anticholinergic drugs lessen the tremors and rigidity and afford some improvement of function. Treatment/Surgery Surgical treatment includes thalamotomy or pallidectomy that is performed using stereotactic surgery. With these procedures, part of the thalamus or globus pallidum in the basal ganglia is destroyed using an electrical stimulator or supercooled tip of a metal probe (cryothalamotomy). Brain mapping is done during the surgery to identify and prevent injury to sensory and motor tracts. Surgery is generally confined to one side of the brain and is usually restricted to persons who have failed to respond satisfactorily to drug therapy. Surgical transplantation of adrenal medullary tissue or fetal substantia nigra tissue is still experimental. Another surgical procedure involves the implantation of electrodes for deep brain stimulation into areas of the brain that are thought to account for rest tremors (thalamus) or motor dysfunction in Parkinson disease (subthalamic nuclei or the pars interna of the globus pallidus). Electrical stimulation has the advantage of being reversible and of causing minimal or no damage to the brain. Nursing Diagnosis 1.) Self-care deficit related to rigidity and tremors 2.) Risk for Injury 3.) Impaired physical mobility related to muscle stiffness and tremors 4.) Disturbed thought Processes related to dementia 5.) Imbalanced nutrition: Less than body requirements 1. Exercise therapy: Reinforce occupational and physical therapy recommendations 2. Ambulation, 3. Teach deep-breathing exercises to promote chest expansion and adequate air exchange. 4. To maintain nutritional status, monitor the patients ability to chew and swallow. 5. Muscle control; if painful during cramps, Do Warm Bath and/or Muscle Massage 6. Environmental management, 7. Self-care assistance; Encourage maximum participation in self-care activities. 8. Exercise promotion; 9. Energy management; Allow sufficient time to perform activities 10. Body image enhancement by emphasizing her or his abilities and by reinforcing success. The severity of Parkinson's disease symptoms vary greatly from individual to individual and it is not possible to predict how quickly the disorder will progress. Parkinson's disease itself is not a fatal disease, and the average life expectancy is similar to that of people without the disease. Secondary complications, such as pneumonia, falling-related injuries, and choking can lead to death. There are many treatment options that can reduce some of the symptoms and can prolong the quality of life of an individual with Parkinson's disease.

Nursing Intervention