Parkinson’s Disease



Parkinson’s Disease


Joanne V. Hickey



Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease (AD). PD is characterized by a loss of dopaminergic neurons in the substantia nigra of the basal ganglia. The major signs and symptoms include tremors

(at rest), rigidity, bradykinesia, and gait and balance disorders. PD causes significant disability and decreased quality of life.1 There are also many nonmotor features of PD which will be discussed. The etiology of PD is unknown, and there is no cure.

PD can occur from 10 to 20 years of age (juvenile onset) through 21 to 40 years of age (young onset), through the 90s years of age. The most frequent time of diagnosis is between 60 and 70 years although the disease often begins between 45 and 70 years of age. Approximately 1% to 2% of people over the age of 65 years have PD.1, 2 Over one million people live with PD in the United States, and with current demographic trends of increased older persons, the number is expected to increase significantly in the next three decades.3 Early-onset PD affecting persons as early as in their 20s is being recognized with greater frequency. More than ten autosomal dominant and recessive genes or gene loci have been linked to PD.4 PD is a progressive degenerative disorder of multifactorial etiology. A small proportion of patients have a direct inherited causative mutation for PD; multiple genetic predisposing factors and environmental factors are more commonly involved.5


NEUROANATOMY

The basal ganglia is a collective term for the subcortical motor nuclei of the cerebrum. The structures that compose the basal ganglia include the substantia nigra, striatum, globus pallidus, subthalamic

nucleus, and red nucleus. Symptoms of PD are caused by loss of nerve cells in the pigmented substantia nigra pars compacta, including the locus ceruleus in the midbrain. Cell loss also occurs in the globus pallidus and putamen.3 Depletion of the dopaminergic neurons (pars compacta) of the substantia nigra results in reduction of dopamine, the main biochemical abnormality in PD. Normally, the pars compacta neurons of the substantia nigra provide dopaminergic input to the striatum, a part of the basal ganglia. In PD, loss of pars compacta neurons leads to striatal dopamine depletion and reduced thalamic excitation of the motor cortex.3 Although the central problem in PD is dopaminergic loss in the basal ganglia, other neurotransmitters are also involved and the disease extends to other areas of the brain.5






Figure 31-1 ▪ Understanding Parkinson’s disease. Asset provided by Anatomical Chart Co.




SIGNS AND SYMPTOMS

Because symptoms develop insidiously, diagnosis may be delayed, with symptoms sometimes attributed to aging. The disease is progressive, so that eventually the patient’s ability to perform activities of daily living (ADLs) and other independent functions is reduced. The signs and symptoms of PD are divided into major manifestations and secondary manifestation. The major motor manifestations include the following: tremors (resting tremors), rigidity of muscles, bradykinesia/akinesia, and gait and balance disorders (Fig. 31-1). These are briefly described below.


Major Motor Manifestations

In about 75% of patients, motor problems are unilateral. However, as the disease advances, symptoms become bilateral.


Tremors. The classic tremor of PD is a resting tremor in a limb, most commonly one hand, which disappears with voluntary movement.1 Tremors occur most often in the distal portions of extremities and especially in the hands. A so-called pill-rolling motion of the fingers is characteristic. Handwriting becomes small, tremulous, and cramped. Other areas where tremors are seen include the foot, lip, tongue, and jaw. Tremors are present when the hand is motionless and thus are termed resting tremors (Fig. 31-2). Tremors are absent during sleep.

Rigidity. Muscle rigidity may be felt as stiffness by the examiner, and is associated with vague aching and discomfort of a limb. The muscle feels stiff and requires much effort to move. Initiation of purposeful movement is slow. During movement, the patient may become momentarily frozen.






Figure 31-2 ▪ Tremors of Parkinson’s disease.






Figure 31-3 ▪ The clinical features of Parkinson’s disease.


Bradykinesia/akinesia. Movement is slow. Gait is slowed with decreased arm swing on the affected side. As a result, difficulty in rising from a chair, getting into a car, and performing ADLs is common. Slow or absent movement renders the patient at high risk for deep vein thrombosis, constipation, and pressure ulcers.

Gait and balance disorders. As the disorder of movement worsens, all basic activities and ADLs are affected. Patients walk in a stooped-over position with small, shuffling steps and often a broad base on turns. The forearms are semiflexed, and the fingers are flexed at the metacarpophalangeal joints. The characteristic appearance and posture of the patient with PD are illustrated in Figure 31-3. After movement is initiated, it frequently accelerates to series of small steps. The patient may fall forward (propulsion) or backward (retropulsion). If pushed, he or she makes no attempt to brace or to reach out and protect himself or herself. As a result, the patient is at high risk for injury, especially from falls. Patients have difficulty in maintaining balance and sitting erect. When walking, an obstacle such as a threshold in a doorway may cause the patient to “freeze” in place. Getting in and out of a chair or car or walking into a room becomes difficult.6


Secondary Manifestations

There are several secondary manifestations; they are included in Table 31-1. Practice parameters are available for the treatment of nonmotor symptoms of PD.12


Disease-Specific Rating Scales

Scales developed to rate the severity of signs and symptoms of PD objectively are useful clinically and in drug trials for staging the disease and for monitoring deterioration. The categorical, nonlinear
scale described by Hoehn and Yahr is frequently used to characterize the severity of illness (Table 31-2).12, 13 The standard tool for tracking PD progress and response to therapy is the United Parkinson’s Disease Rating Scale (UPDRS). The UPDRS is a standard rating scale used for tracking PD progress and response to therapy in patients with PD. The UPDRS is subdivided into three scales including cognitive and mood aspects, motor aspects, and ADLs. The UPDRS is available at http://www.mdvu.org/library/ratingscales/pd/. Items include mentation, behavior, and mood (e.g., intellectual impairment, thought disorder, depression, motivation/initiative); ADLs (e.g., speech, salivation, swallowing handwriting, etc.); and motor examination (e.g., facial expression, rigidity, hand movements, arising from a chair, etc.). Most items scored on a scale from 0 to 4 (0 = normal to 4 = most severe). There are a few items scored on a scale of 0 to 1. The scores on the subscales are added together to yield a total score (higher scores indicate a higher degree of disability).14 The scale has good inter-rater reliability. In addition, other standardized scales, such as the Beck Depression Inventory for depression are helpful for assessing and monitoring other symptoms common in PD.








TABLE 31-1 SECONDARY MANIFESTATIONS OF PARKINSON’S DISEASE


















































































SIGNS/SYMPTOMS

DESCRIPTION


Face and Cranial Nerves


• Mask-like face

Face has reduced facial expression and the eyes stare straight ahead; blinking is less frequent than normal— 5-10 times per minute rather than the normal 15-20 times


• Sialorrhea (drooling)

Drooling: secondary to decreased frequency of swallowing


• Soft monotone voice (hypophonia)

Voice gradually becomes soft to whisper-like, monotonic, and muffled; changes result in impaired verbal communications


• Anosmia (loss of sense of smell)

Cause unclear


• Visual impairments

Impaired upward gaze and convergence


• Dysphagia (difficulty swallowing)

Secondary to the neuromuscular incoordination of the hypopharyngeal musculature; can interfere with normal fluid and dietary intake, eats very slowly


• Dysarthria (difficulty with speech)

Difficulty pronouncing words5


Sensory Changes


• Paresthesia

Tingling, pricking, or numbness reported


• Pain

40-60% have chronic pain that frequently includes more than one type of pain7, 8; 70% musculoskeletal pain (muscle cramps of the legs, neck, and trunk), 40% dystonic pain; 20% radicular-neuropathic pain, and 10% central neuropathic pain;9 pain increases and decreases with fluctuation of dopamine


Autonomic Changes


• Urinary disturbance

Urinary hesitation and frequency: secondary to autonomic dysfunction


• Constipation

Secondary to hypomotility of the gastrointestinal tract associated with prolonged gastric emptying time. Decreased fluid intake, lack of roughage, and decreased activity contribute to the development of constipation


• Sexual dysfunction

Erectile dysfunction and impotence secondary to autonomic dysfunction


• Excessive perspiration

Autonomic disorder of the hypothalamic heat regulatory mechanism, as well as impairment of perspiration controls. The patient may be diaphoretic even in cold weather and may have a fever in warm weather


• Orthostatic hypotension

Result of peripheral autonomic failure; can contribute to falls; is also a side effect of levodopa therapy


Neuropsychiatric Manifestations


• Apathy

Common neuropsychiatric finding


• Anxiety

Common neuropsychiatric finding


• Depression

Depression (very common) is seen in over 50% of persons with PD and may even occur before classic symptoms of PD are noted


• Dementia

Dementia is noted in 20-40% of patients.10 About 65% of patients over 80 years of age will have dementia6


• Psychosis

Common neuropsychiatric finding


Other


• Fatigue

Fatigue is a common complaint, especially when ADLs are attempted


• Sleep disorders

Very common; there are many causes and thus need individual assessment to determine the best treatment approach11; many experience fragmented sleep with excessive daytime sleepiness


• Seborrheic dermatitis

Oily, greasy skin; attributable to hypothalamic dysfunction, which causes release of an increased amount of sebotrophic hormone.





DIAGNOSIS

Guidelines for the diagnosis and prognosis of PD are available.15, 16 The diagnosis of PD is based on a careful history, physical examination, and clinical presentation. In addition to the motor findings, the best test is a good response to dopaminergic treatment with levodopa. If these findings are verified, the diagnosis of PD is made.17 There are no laboratory tests or imaging tests currently available to confirm the diagnosis of PD.18 Magnetic resonance imaging (MRI) is usually normal. Single photon emission computed
tomography (SPECT) imaging with DaTSCAN has been recently approved for diagnosis of PD. DaTSCAN is a dopamine transporter ligand that tags presynaptic dopaminergic neurons in the basal ganglia; in patients with PD, there is a decreased signal on SPECT.5

Only gold members can continue reading. Log In or Register to continue

Related posts:

  1. Nutritional Support for Neuroscience Patients
  2. Rehabilitation of Patients with Neurological Disorders
  3. Headaches
  4. Cerebral Aneurysms

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 14, 2016 | Posted by in NURSING | Comments Off on Parkinson’s Disease

Full access? Get Clinical Tree
Get Clinical Tree app for offline access