PARKINSON’S DISEASE

Definition

- Parkinson’s disease is a slowly progressive degenerative disorder of the nervous system characterized by tremor when muscles are at rest (resting tremor), slowness of voluntary movements, and increased muscle tone (rigidity).Source: Beers M. MD. , Fletcher A. MB., Thomas J The Merck Manual of medical information. 2nd edition. United States of America: Merck and Co., 2003. Page 495

- Parkinson disease is a degenerative disorder of the basal ganglia that results in variable combinations of tremor, rigidity, and bradykinesia. The disorder is characterized by progressive destruction of the nigrostriatal pathway with a subsequent reduction in striatal concentrations of dopamine. Source: Porth, Carol Mattson (2007). Essentials of Pathophysiology Concepts of Altered Health Status Wisconsin: Lippincott Williams & Wilkins.page 806

- Parkinson’s disease is a slowly progressing neurologic movement disorder that eventually leads to disability. It is associated with decreased levels of dopamine resulting from destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia region of the brain.

Source: Smeltzer, Suzanne and Bare, Brenda (2004). Brunners and Suddarth’s Textbook of Medical Surgical Nursing 10th Edition. Philadelphia: Lippincott Williams & Wilkins, Vol 2 page 2311

Anatomy and PhysiologyNervous System

ROLE OF THE NERVOUS SYSTEM(1) The nervous system is able to sense change both inside the body and change in the environment surrounding the body.(2) The nervous system is able to interpret these changes.(3) The nervous system causes the body to react to these changes by either muscular contraction or glandular secretion.

Homeostasis is a good example of the nervous system sensing change, interpreting change, and adjusting to change. (In homeostasis, the equilibrium of factors such as temperature, blood pressure, and chemicals are kept in relative balance.) In the case of homeostasis, the nervous system and

the endocrine system operate together to maintain equilibrium in the body.

The nervous system is broken down into two major part: the central nervous system, which includes the brain and spinal cord, and the peripheral nervous system, which includes all nerves, which carry impulses to and from the brain and spinal cord. These include our sense organs, the eyes, the ears, our sense of taste, smell and touch, as well as our ability to feel pain.

Central Nervous SystemSpinal Cord

The spinal cord is a long bundle of neural tissue continuous with the brain that occupies the interior canal of the spinal column and functions as the primary communication link between the brain and the rest of the body. The spinal cord receives signals from the peripheral senses and relays them to the brain.Brain Stem

The brain stem is the part of the brain that connects the cerebrum and diencephalons with the spinal cord.Medulla Oblongata

The medulla oblongata is located just above the spinal cord. This part of the brain is responsible for several vital autonomic centers including:

the respiratory center, which regulates breathing.

the cardiac center that regulates the rate and force of the heartbeat.

the vasomotor center, which regulates the contraction of smooth muscle in the blood vessel, thus controlling blood pressure.

The medulla also controls other reflex actions including vomiting, sneezing, coughing and swallowing.Pons

Continuing up the brain stem, one reaches the Pons. The pons lie just above the medulla and acts as a link between various parts of the brain. The pons connect the two halves of the cerebellum with the brainstem, as well as the cerebrum with the spinal cord. The pons, like the medulla oblongata, contain certain reflex actions, such as some of the respiratory responses.Midbrain

The midbrain extends from the pons to the diecephalon. The midbrain acts as a relay center for certain head and eye reflexes in response to visual stimuli. The midbrain is also a major relay center for auditory information.

Diencephalon The diencephalons is located between the

cerebrum and the mid brain. The diencephalons houses important structures including the thalamus, the hypothalamus and the pineal gland.Thalamus

The thalamus is responsible for "sorting out" sensory impulses and directing them to a particular area of the brain. Nearly all sensory impulses travel through the thalamus.Hypothalamus

The hypothalamus is the great controller of body regulation and plays an important role in the connection between mind and body, where it serves as the primary link between the nervous and endocrine systems. The hypothalamus produces hormones that regulate the secretion of specific hormones from the pituitary. The hypothalamus also maintains water balance, appetite, sexual behavior, and some emotions, including fear, pleasure and pain.Cerebellum

The functions of the cerebellum include the coordination of voluntary muscles, the maintenance of balance when standing, walking and sitting, and the maintenance of muscle tone ensuring that the body can adapt to changes in position quickly.Cerebrum

The largest and most prominent part of the brain, the cerebrum governs higher mental processes including intellect, reason, memory and language skills. The cerebrum can be divided into 3 major functions:

Sensory Functions - the cerebrum receives information from a sense organ; i.e., eyes, ears, taste, smell, feelings, and translates this information into a form that can be understood.

Motor Functions - all voluntary movement and some involuntary movement.

Intellectual Functions - responsible for learning, memory and recall.Meninges

The meninges are made up of three layers of connective tissue that surround and protect both the brain and spinal cord. The layers include the dura mater, the arachnoid and the pia matter.Cerebrospinal Fluid

The cerebrospinal fluid is a clear liquid that circulates in and around the brain and spinal cord. Its function is to cushion the brain and spinal cord, carry nutrients to the cells and remove waste products from these tissues.

Peripheral Nervous SystemNerves

Nerves are made up of specialized cells, which act as little wires, transmitting information to and from the central nervous system and brain. Nerves form the network of connections that receive signals (known as sensory input) from the environment and within the body, and transmit the body's responses, or instructions for action, to the muscles, organs, and glands. Nerve cells are located outside the central nervous system or spinal cord.

Two main components of the PNS:1. sensory (afferent) pathways that

provide input from the body into the CNS.2. motor (efferent) pathways that

carry signals to muscles and glands (effectors).Most sensory input carried in the PNS

remains below the level of conscious awareness. Input that does reach the conscious level contributes to perception of our external environment. Somatic Nervous System

The Somatic Nervous System (SNS) includes all nerves controlling the muscular system and external sensory receptors. External sense organs (including skin) are receptors. Muscle fibers and gland cells are effectors. The reflex arc is an automatic, involuntary reaction to a stimulus. When the doctor taps your knee with the rubber hammer, she/he is testing your reflex (or knee-jerk). The reaction to the stimulus is involuntary, with the CNS being informed but not consciously controlling the response. Examples of reflex arcs include balance, the blinking reflex, and the stretch reflex.

Sensory input from the PNS is processed by the CNS and responses are sent by the PNS from the CNS to the organs of the body.

Motor neurons of the somatic system are distinct from those of the autonomic system. Inhibitory signals, cannot be sent through the motor neurons of the somatic system. Autonomic Nervous System

The Autonomic Nervous System is that part of PNS consisting of motor neurons that control internal organs. It has two subsystems. The autonomic system controls muscles in the heart, the smooth muscle in internal organs such as the intestine, bladder, and uterus. The Sympathetic Nervous System is involved in the fight or flight response. The Parasympathetic Nervous System is involved in relaxation. Each of these subsystems operates in the reverse of the other (antagonism). Both systems innervate the same organs and act in opposition to maintain homeostasis. For example:

when you are scared the sympathetic system causes your heart to beat faster; the parasympathetic system reverses this effect.

Motor neurons in this system do not reach their targets directly (as do those in the somatic system) but rather connect to a secondary motor neuron which in turn innervates the target organ.The Neuron

Nervous tissue is composed of two main cell types: neurons and glial cells. Neurons transmit nerve messages. Glial cells are in direct contact with neurons and often surround them.

The neuron is the functional unit of the nervous system. Humans have about 100 billion neurons in their brain alone! While variable in size and shape, all neurons have three parts. Dendrites receive information from another cell and transmit the message to the cell body. The cell body contains the nucleus, mitochondria and other organelles typical of eukaryotic cells. The axon conducts messages away from the cell body.

Three types of neurons occur. Sensory neurons typically have a long dendrite and short axon, and carry messages from sensory receptors to the central nervous system. Motor neurons have a long axon and short dendrites and transmit messages from the central nervous system to the muscles (or to glands). Interneurons are found only in the central nervous system where they connect neuron to neuron.

Some axons are wrapped in a myelin sheath formed from the plasma membranes of specialized glial cells known as Schwann cells. Schwann cells serve as supportive, nutritive, and service facilities for neurons. The gap between Schwann cells is known as the node of Ranvier, and serves as points along the neuron for generating a signal. Signals jumping from node to node travel hundreds of times faster than signals traveling along the surface of the axon. This allows your brain to communicate with your toes in a few thousandths of a second.

The action potential begins at one spot on the membrane, but spreads to adjacent areas of the membrane, propagating the message along the length of the cell membrane. After passage of the action potential, there is a brief period, the refractory period, during which the membrane cannot be stimulated. This prevents the message from being transmitted backward along the membrane.

Steps in an Action Potential1. At rest the outside of the

membrane is more positive than the inside. 2. Sodium moves inside the cell

causing an action potential, the influx of positive sodium ions makes the inside of the membrane more positive than the outside.

3. Potassium ions flow out of the cell, restoring the resting potential net charges.

4. Sodium ions are pumped out of the cell and potassium ions are pumped into the cell, restoring the original distribution of ions.

SynapsesThe junction between a nerve cell and

another cell is called a synapse. Messages travel within the neuron as an electrical action potential. The space between two cells is known as the synaptic cleft. To cross the synaptic cleft requires the actions of neurotransmitters. Neurotransmitters are stored in small synaptic vessicles clustered at the tip of the axon.

Arrival of the action potential causes some of the vesicles to move to the end of the axon and discharge their contents into the synaptic cleft. Released neurotransmitters diffuse across the cleft, and bind to receptors on the other cell's membrane, causing ion channels on that cell to open. Some neurotransmitters cause an action potential, others are inhibitory.

Neurotransmitters tend to be small molecules, some are even hormones. The time for neurotransmitter action is between 0,5 and 1 millisecond. Neurotransmitters are either destroyed

by specific enzymes in the synaptic cleft, diffuse out of the cleft, or are reabsorbed by the cell. More than 30 organic molecules are thought to act as neurotransmitters. The neurotransmitters cross the cleft, binding to receptor molecules on the next cell, prompting transmission of the message along that cell's membrane. Acetylcholine is an example of a neurotransmitter, as is norepinephrine, although each acts in different responses. Once in the cleft, neurotransmitters are active for only a short time. Enzymes in the cleft inactivate the neurotransmitters. Inactivated neurotransmitters are taken back into the axon and recycled.

Diseases that affect the function of signal transmission can have serious consequences. Parkinson's disease has a deficiency of the neurotransmitter dopamine. Progressive death of brain cells increases this deficit, causing tremors, rigidity and unstable posture. L-dopa is a chemical related to dopamine that eases some of the symptoms (by acting as a substitute neurotransmitter) but cannot reverse the progression of the disease.

The bacterium Clostridium tetani produces a toxin that prevents the release of GABA. GABA is important in control of skeletal muscles. Without this control chemical, regulation of muscle contraction is lost; it can be fatal when it effects the muscles used in breathing.

Clostridium botulinum produces a toxin found in improperly canned foods. This toxin causes the progressive relaxation of muscles, and can be fatal. A wide range of drugs also operate in the synapses: cocaine, LSD, caffeine, and insecticides.Basal Ganglia

The basal ganglia (or basal nuclei) are a group of nuclei in the brains of vertebrates, situated at the base of the forebrain and strongly connected with the cerebral cortex, thalamus and other areas. The basal ganglia are associated with a variety of functions, including motor control and learning. Currently popular theories implicate the basal ganglia primarily in action selection, that is, the decision of which of several possible behaviors to execute at a given time. Experimental studies show that the basal ganglia exert an inhibitory influence on a number of motor systems, and that a release of this inhibition permits a motor system to become active. The "behavior switching" that takes place within the basal ganglia is influenced by signals from many parts of the brain, including the prefrontal cortex, which is widely believed to play a key role in executive functions.

The main components of the basal ganglia are the striatum, pallidum, substantia nigra, and subthalamic nucleus. The largest component, the striatum, receives input from many brain areas but sends output only to other components of the basal ganglia. The pallidum receives its most important input from the striatum (either directly or indirectly), and sends inhibitory output to a number of motor-related areas, including the part of the thalamus that projects to the motor-related areas of the cortex. The substantia nigra consists of two parts, one that functions similarly to the pallidum, and another that provides the source of dopamine input to the striatum. The subthalamic nucleus receives input mainly from the striatum and cortex, and projects to the pallidum. Each of these areas has a complex internal anatomical and neurochemical organization.

The basal ganglia play a central role in a number of neurological conditions, including several movement disorders. The most notable are Parkinson's disease, which involves degeneration of the dopamine cells in the substantia nigra, and Huntington's disease, which primarily involves damage to the striatum. Basal ganglia disfunction is also implicated in some other disorders of behavior control such as Tourette's syndrome and obsessive–compulsive disorder, although the neural mechanisms underlying these are not well understood.

The basal ganglia have a limbic sector whose components are assigned distinct names: the nucleus accumbens (NA), ventral pallidum, and ventral tegmental area (VTA). The VTA provides dopamine to the nucleus accumbens (ventral striatum) in the same way that the substantia nigra provides dopamine to the dorsal striatum. The VTA→NA dopaminergic projection has attracted a great deal of attention, because there is much evidence that it plays a central role in reward learning. A number of highly addictive drugs, including cocaine, amphetamines, and nicotine, are thought to work by increasing the efficacy of the VTA→NA dopamine signal. There is also evidence implicating overactivity of the VTA dopaminergic projection in schizophrenia.

The basal ganglia form a fundamental component of the vertebrate telencephalon (forebrain). In contrast to the pallial or cortical layer that lines the surface of the forebrain, the basal ganglia are a collection of distinct masses of gray matter lying in the interior, not far from the junction with the thalamus. Like most parts of the brain, the

basal ganglia consist of left and right sides that are virtual mirror images of each other.

At the highest level, the basal ganglia are divided by anatomists into four distinct structures. Two of them, the striatum and pallidum, are relatively large; the other two, the substantia nigra and subthalamic nucleus, are smaller. In the illustration to the right, two coronal sections of the human brain show the location of the basal ganglia. The subthalamic nucleus and substantia nigra lie farther back in the brain than the striatum and pallidum.Connections

Connectivity diagram showing excitatory glutamatergic pathways as red, inhibitory GABAergic pathways as blue, and modulatory dopaminergic as magenta.

The flow of neural signals through the basal ganglia is strongly directional. The striatum is the primary recipient of input from other brain areas, most notably the cerebral cortex. The internal segment of the globus pallidus (GPi), together with the reticular part of the substantia nigra (SNr), give rise to the primary output, most notably to the thalamus. The striatum projects to the pallidum both directly and indirectly via the subthalamic nucleus, which also receives cortical input. The substantia nigra consists of two parts, one of which functions similarly to the pallidum, the other of which sends a modulatory dopaminergic input to the striatum and other structures.

The adjoining figure shows some of the most important connections between components. On the largest scale, the basal ganglia form a loop that begins and ends in the cortex. Anatomists have distinguished two main circuits, known as the "direct" and "indirect" pathways. The direct pathway runs cortex→striatum→GPi→thalamus→cortex. Two of these links are excitatory, and two inhibitory, so the net effect of the whole sequence is excitatory: the cortex excites itself via the direct pathway. The indirect pathway runs cortex→striatum→GPe→STN→GPi→thalamus→cortex. Three of these links are inhibitory and two excitatory, so the net effect of the sequence is inhibitory: the cortex inhibits itself via the indirect pathway. The total effect of basal ganglia upon the cortex is believed to result from a complex interplay between these two pathways.Striatum

The striatum is the largest component of the basal ganglia. The term "striatum" comes from the observation that this structure has a striped

appearance when sliced in certain directions, arising from numerous large and small bundles of nerve fibers (white matter) that traverse it. Early anatomists, examining the human brain, perceived the striatum as two distinct masses of gray matter separated by a large tract of white matter called the internal capsule. They named these two masses the "caudate nucleus" and "putamen". More recent anatomists have concluded, on the basis of microscopic and neurochemical studies, that it is more appropriate to consider these masses as two separated parts of a single entity, the "striatum", in the same way that a city may be separated into two parts by a river. Numerous functional differences between the caudate and putamen have been identified, but these are taken to be consequences of the fact that each sector of the striatum is preferentially connected to specific parts of the cerebral cortex.

The internal organization of the striatum is extraordinarily complex. The great majority of neurons (about 96%) are of a type called "medium spiny neurons". These are GABAergic cells (meaning that they inhibit their targets) with small cell bodies and dendrites densely covered with dendritic spines, which receive synaptic input primarily from the cortex and thalamus. Medium spiny neurons can be divided into subtypes in a number of ways, on the basis of neurochemistry and connectivity. The next most numerous type (around 2%) are a class of large cholinergic interneurons with smooth dendrites. There are also several other types of interneurons making up smaller fractions of the neural population.

Numerous studies have shown that the connections between cortex and striatum are generally topographic; that is, each part of the cortex sends stronger input to some parts of the striatum than to others. The nature of the topography has been difficult to understand, however—perhaps in part because the striatum is organized in three dimensions whereas the cortex, as a layered structure, is organized in two. This dimensional discrepancy entails a great deal of distortion and discontinuity in mapping one structure to the other.Pallidum

The pallidum consists of a large structure called the globus pallidus ("pale globe") together with a smaller ventral extension called the ventral pallidum. The globus pallidus appears as a single neural mass, but can be divided into two functionally distinct parts, called the internal (sometimes "medial") and external (sometimes "lateral")

segments, abbreviated GPi and GPe. Both segments contain primarily GABAergic neurons, which therefore have inhibitory effects on their targets. The two segments participate in distinct neural circuits. The external segment, or GPe, receives input mainly from the striatum, and projects to the subthalamic nucleus. The internal segment, or GPi, receives signals from the striatum via two pathways, called "direct" and "indirect". The direct pathway consists of direct projections from the striatum to the GPi. The indirect pathway consists of projections from the striatum to the GPe, followed by projections from the GPe to the subthalamic nucleus (STN), followed by projections from the STN to the GPi. These pathways have opposite net effects: striatal activity inhibits the GPi via the direct pathway because striatal outputs are GABAergic, but has a net excitatory effect on the GPi via the indirect pathway because this three-link pathway consists of two inhibitory links plus one excitatory link.

Pallidal neurons operate using a "disinhibition" principle. These neurons fire at steady high rates in the absence of input, and signals from the striatum cause them to "pause". Because pallidal neurons themselves have inhibitory effects on their targets, the net effect of striatal input to the pallidum is a reduction of the tonic inhibition exerted by pallidal cells on their targets.Function

Information about the functions of the basal ganglia comes from anatomical studies, from physiological studies carried out mainly in rats and monkeys, and from the study of diseases that damage them.

The greatest source of insight into the functions of the basal ganglia has come from the study of two neurological disorders, Parkinson's disease and Huntington's disease. For both of these disorders, the nature of the neural damage is well understood and can be correlated with the resulting symptoms. Parkinson's disease involves major loss of dopaminergic cells in the substantia nigra; Huntington's disease involves massive loss of medium spiny neurons in the striatum. The symptoms of the two diseases are virtually opposite: Parkinson's disease is characterized by gradual loss of the ability to initiate movement, while Huntington's disease is characterized by an inability to prevent parts of the body from moving unintentionally. It is noteworthy that although both diseases have cognitive symptoms, especially in their advanced stages, the most salient symptoms relate

to the ability to initiate and control movement. Thus, both are classified primarily as movement disorders.

Eye movementsOne of the most intensively studied

functions of the BG is their role in controlling eye movements.Eye movement is influenced by an extensive network of brain regions that converge on a midbrain area called the superior colliculus (SC). The SC is a layered structure whose layers form two-dimensional retinotopic maps of visual space. A "bump" of neural activity in the deep layers of the SC drives an eye movement directed toward the corresponding point in space.

The SC receives a strong inhibitory projection from the BG, originating in the substantia nigra pars reticulata (SNr). Neurons in the SNr usually fire continuously at high rates, but at the onset of an eye movement they "pause", thereby releasing the SC from inhibition. Eye movements of all types are associated with "pausing" in the SNr; however, individual SNr neurons may be more strongly associated with some types of movements than others. Neurons in some parts of the caudate nucleus also show activity related to eye movements. Since the great majority of caudate cells fire at very low rates, this activity almost always shows up as an increase in firing rate. Thus, eye movements begin with activation in the caudate nucleus, which inhibits the SNr via the direct GABAergic projections, which in turn disinhibits the SC.Role in motivation

Although the role of the basal ganglia in motor control is clear, there are also many indications that it is involved in the control of behavior in a more fundamental way, at the level of motivation. In Parkinson's disease, the ability to execute the components of movement is not greatly affected, but motivational factors such as hunger fail to cause movements to be initiated or switched at the proper times. The immobility of Parkinsonian patients has sometimes been described as a "paralysis of the will". These patients have occasionally been observed to show a phenomenon called kinesia paradoxica, in which a person who is otherwise immobile responds to an emergency in a coordinated and energetic way, then lapses back into immobility once the emergency has passed.

The role in motivation of the "limbic" part of the basal ganglia—the nucleus accumbens (NA), ventral pallidum, and ventral tegmental area (VTA)—is particularly well established. Thousands of

experimental studies combine to demonstrate that the dopaminergic projection from the VTA to the NA plays a central role in the brain's reward system. Animals with stimulating electrodes implanted along this pathway will bar-press very energetically if each press is followed by a brief pulse of electrical current. Numerous things that people find rewarding, including addictive drugs, good-tasting food, and sex, have been shown to elicit activation of the VTA dopamine system. Damage to the NA or VTA can produce a state of profound torpor.

Although it is not universally accepted, some theorists have proposed a distinction between "appetitive" behaviors, which are initiated by the basal ganglia, and "consummatory" behaviors, which are not. For example, an animal with severe basal ganglia damage will not move toward food even if it is placed a few inches away, but if the food is placed directly in the mouth, the animal will chew it and swallow it.

Comparative anatomy and naming

The basal ganglia form one of the basic components of the forebrain, and can be recognized in all species of vertebrates. Even in the lamprey (generally considered one of the most primitive of vertebrates), striatal, pallidal, and nigral elements can be identified on the basis of anatomy and histochemistry.

A clear emergent issue in comparative anatomy of the basal ganglia is the development of this system through phylogeny as a convergent cortically re-entrant loop in conjunction with the development and expansion of the cortical mantle. There is controversy, however, regarding the extent to which convergent selective processing occurs versus segregated parallel processing within re-entrant closed loops of the basal ganglia. Regardless, the transformation of the basal ganglia into a cortically re-entrant system in mammalian evolution occurs through a re-direction of pallidal (or "paleostriatum primitivum") output from midbrain targets such as the superior colliculus, as occurs in sauropsid brain, to specific regions of the ventral thalamus and from there back to specified regions of the cerebral cortex that form a subset of those cortical regions projecting into the striatum. The abrupt rostral re-direction of the pathway from the internal segment of the globus pallidus into the ventral thalamus—via the path of the ansa lenticularis--could be viewed as a footprint of this evolutionary transformation of basal ganglia outflow and targeted influence. The evolutionary emergence

of cortical re-entrant systems in the brain has been postulated by Gerald Edelman as a critical basis for the emergence of primary consciousness in the theory of Neural Darwinism.Neurotransmitters

In most regions of the brain, the predominant classes of neurons use glutamate as neurotransmitter and have excitatory effects on their targets. In the basal ganglia, however, the great majority of neurons use GABA as neurotransmitter and have inhibitory effects on their targets. The inputs from the cortex and thalamus to the striatum and STN are glutamatergic, but the outputs from the striatum, pallidum, and substantia nigra pars reticulata all use GABA. Thus, following the initial excitation of the striatum, the internal dynamics of the basal ganglia are dominated by inhibition and disinhibition.

Other neurotransmitters have important modulatory effects. The most intensively studied is dopamine, which is used by the projection from the substantia nigra pars compacta to the striatum, and also in the analogous projection from the ventral tegmental area to the nucleus accumbens. Acetylcholine also plays an important role, being used both by several external inputs to the striatum, and by a group of striatal interneurons. Although cholinergic cells make up only a small fraction of the total population, the striatum has one of the highest acetylcholine concentrations of any brain structure.Medical Management

*Assessment and Diagnostic Methods

Patient’s history and presence of two of the three cardinal manifestations: tremor, muscle rigidity and bradykinesia.

Positron emission tomography (PET) scanning.

Neurologic examination and response to pharmacologic management.

Goal of treatments is to CONTROL symptoms and maintain functional independence; NO APPROACH prevents disease progression.

* Pharmacologic Therapy

Levodopa therapy (converts to dopamine): most effective agent to relieve symptoms; usually given in combination with carbidopa (Sinemet), which prevent levodopa breakdown.

Budipine is a non-dopaminergic, antiparkinson medication that significantly reduces akinesia, rigidity and tremor.

Anithistamine drugs to allay tremors. Dopamine agonists (bromocriptine

mesylate, etc.) and pramipexole are used to postpone the initiation of carbidopa and levodopa therapy.

Anticholinergic therapy to control the tremor and rigidity.

Amantadine hydrochloride (Symmetrel), an antiviral agent, to reduce rigidity, tremor and bradykinesia.

Monoamine oxidase inhibitors (MAOIs) to inhibit dopamine breakdown.

Antidepressant drugs.* Surgical Management

Surgery to destroy a part of the thalamus (stereotactic thalamotomy and pallidotomy) to interrupt nerve pathways and alleviate tremor or rigidity.

Transplantation of neural cells from fetal tissue of human or animal source to re-establish normal dopamine release.

Deep brain stimulation with pacemaker-like brain implants shows promise but is waiting for FDA approval.

Nursing Diagnoses:

1. Impaired physical mobility related to muscle rigidity and motor weakness

2. Constipation related to medication and reduced activity

3. Imbalanced nutrition, less than body requirements, related to tremor, slowness in eating, difficulty in chewing and swallowing

4. Impaired verbal communication related to decreased speech volume, slowness of speech, inability to move facial muscles

5. Ineffective coping related to depression and dysfunction due to disease progression

6. Self care deficits (feeding, dressing, hygiene, and toileting) related to tremor and motor disturbance

Nursing Intervention

1. Monitor drug treatment to note adverse reactions and allow for dosage adjustments. Monitor for liver function changes and anemia during drug therapy.

2. Monitor the patient’s nutritional intake and check weight regularly.

3. Monitor the patient’s ability to perform activities of daily living.

4. To improve mobility, encourage the patient to participate in daily exercise, such as walking, riding stationary bike, swimming, or gardening.

5. Advise the patient to perform stretching and postural exercises as outlined by a physical therapist.

6. Teach the patient walking techniques to offset parkinsonian shuffling gait and tendency to lean forward.

7. Encourage the patient to take warm baths and massage muscles to help relax muscles.

8. Instruct the patient to rest often to avoid fatigue and frustration.

9. To improve the patient’s nutritional status, teach the patient to think through the sequence of swallowing.

10. Urge the patient to make a conscious effort to control accumulation of saliva (drooling) by holding head upright and swallowing periodically. Be alert for aspiration hazard.

11. Have the patient use secure, stabilized dishes and eating utensils.

12. Suggest the patient eat smaller meals and additional snacks.

13. To prevent constipation, encourage patient to consume foods containing moderate fiber content (whole grains, fruits, and vegetables), and to increase his or her water intake.

14. Obtained a raised toilet seat to help the patient sit and stand.

15. Teach the patient facial exercises and breathing methods to obtain appropriate pronunciation, volume, and intonation.

16. Teach the patient about the medication regimen and adverse reaction.

Prognosis:

PD is not considered to be a fatal disease by itself, but it progresses with time. The average life expectancy of a PD patient is generally lower than for people who do not have the disease. In the late stages of the disease, PD may cause complications such as choking, pneumonia, and falls that can lead to death.

The progression of symptoms in PD may take 20 years or more. In some people, however, the disease progresses more quickly. There is no way to predict what course the disease will take for an individual person. With appropriate treatment, most people with PD can live productive lives for many years after diagnosis. There are some indications that PD acquires resistance to drug treatment by evolving into a Parkinson-plus disorder, usually Lewy body dementia, although transitions to progressive supranuclear palsy or multiple system atrophy are not unknown.