James Parkinson's essay, An Essay on the Shaking Palsy, published, in 1817, described a disease characterized by involuntary tremors. The term Shaking Palsy was used throughout the essay to describe the disease. In this article, Parkinson compares other reported cases of the Shaking Palsy by medical doctors to the symptoms and presentations of the clients he was observing, but not treating. Parkinson states the progression of the disease. He discusses the possibility that an individual may have this disease substantially long before the individual can detect its presence. Because of its slow progression, the patient is only inconvenienced slightly and is able to self-compensate for the deficits. As the disease progresses, however, the individual with the Shaking Palsy will experience extreme inconvenience (Parkinson 1817/2002). Though referred to as the Shaking Palsy in the essay by Parkinson and in a variety of previous medical literature, Jean Martin Charcot renamed the disease. In recognition of the importance of the research completed by James Parkinson, the disease is now referred to as Parkinson's disease (PD) (Ross & Farrer, 2005). TRAN
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PD is a subgroup of the general syndrome, Parkinsonism. Parkinsonism is broken into subgroups based upon the etiology of the disease. Loss of dopaminergic neurons in the basal ganglia and the brainstem are associated with Parkinsonism Syndrome. Though Parkinsonism and PD have comparable symptoms, they are not the same disorder. Parkinsonism is used to describe the syndrome when an individual has the symptoms but the cause is known. For example, the term Parkinsonism would be used if the individual has the associated symptoms but are caused by repeated trauma. Idiopathic PD is the diagnosis made when the cause of the disease is unknown. (Yorkston, beukelman, Strand, Hakel 463-464). PD is not considered to be a fatal disease but does shorten life expectancy. TRAN TO DIAGNOSIS
With approximately 85% of individual's with PD being over the age of 50, age is a risk factor of the disease (Mosley, Romaine, & Samii, 2009.) PD affects approximately one person per 2,000 older than the age of 50. Though the exact cause of the loss of dopaminergic neuron in the basal ganglia has not been found, it is suspected that genes and/or environmental triggers are responsible. It has been found that those with two or more affected first degree, (i.e. parents, offspring, and siblings), relatives are more likely to acquire the disease (Duffy, 190). However, twin studies do not suggest there is a genetic basis for the disease. The primary focus of epidemiological studies has been on potential environment risk factors. (Farrer, 306). More recent studies, however, have determined that a genetic component to the disease exists. It has been found that at least 10 genetic loci are associated with PD. Four genes with mutations have also been identified. Of the genes that have been linked to familial PD, four have been identified to have the phenotype of earlier onset PD with slow progression (Moore, West, Dawson, and Dawson, 59). TRAN
Previous studies have indicated that incidence and prevalence of PD is 1.5-2 times higher for men than women. Gender Differences in Parkinson's disease investigate the gender differences found in PD further. Of the 253 patients eligible for the study, age at onset was later for women. On average, the age of disease onset was 51.3 for men while it was 53.4 for women. The study also found that women were slightly more likely to have a tremor dominant form of PD. If either gender did have a tremor dominant form of PD, age of onset was 3.6 years later. The approximate two year age of onset difference between genders could be explained by the higher initial striatal dopamine levels in women (Haaxma, 819-825). In addition to the loss of dopminergic neurons, disrupted function of areas that substantia nigra connects, such as cortical and subcortical areas has also been noted (Murray & Clark, 2006).
To evaluate the severity of the PD symptoms, the Hoehn and Yahr (H&Y) scale is commonly used. Originally a 5-point scale, it has been modified as a 7-point scale, with 1.5 and 2.5 being added to better describe the stages (Zhao, et. al., 2010). Stage one is described as the period of time when the symptoms of PD are mild and present on only one side of the body. Stage two is reached when the both sides of the individual's body is affected as well as their gait and posture. Markers of stage three include impairment of equilbirum and moderately severe generalized dysfunction. At stage four, rigidity and bradykinesia are seen. The individual is not able to live alone. When stage five occurs, the individual must use a wheelchair because of inability to stand or walk without significant support (Eskandar, 2005). As reported in a study completed by Y. J. Zhao, et. al., by the 60th month of the study all participants had transitioned from stage one to stage two of Y & H scale. Transition time from stage three to four and four to five was similiar of the that from stage one to two. the rate of transition from stage two to two and a half varied significantly among the participants. It was found that the age of onset was the determiner of the varying length of time of the transitions (Zhao, et. al., 2010).Another commonly used scale system is the Unified Parkinson Disease Rating Scale (UPDRS).
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The UPDRS is a commonly used rating tool that follows the course of PD. The UPDRS consists of the following parts: 1) Mentation, Behavior, and Mood, 2)Activities of Daily Living, and 3) Motor Exam. With the UPDRS, areas such as motivation/initiative, depression, handwriting, ability to care for oneself, and tremor at rest (Eskandar, 2005).Behavior, and MORE!!!!!!!!!!!!!!!!!!
A diagnosis of PD is based on a patient's medical history as well as a neurological exam. A lab test to diagnose this disease is unavailable. Certain tests, however, can be used to rule out the possiblity of other diseases. Magnetic resonance imaging (MRI) or computed tomograph (CT) scan are unable to detect the levels of dopamine found in individual's brain but may be used to rule out the possibility of a stroke. A positron emission tomography (PET), though it is an imaging test, can detect low levels of dopamine. Though it can detect low levels, a necessary characteristic of PD, it is only occasionally used in the diagnosing process. In addition to no lab tests being available for the diagnosis of PD, there is also not a screening test. This makes early detection of the disease nearly impossible (http://www.webmd.com/parkinsons-disease/guide/parkinsons-disease-exams-and-tests). TRAN
Many symptoms are present in a person with PD. A clinical diagnosis of PD is made by identifying the following classic signs: tremor-at-rest, rigidity, akinesia/bradykinesia, and loss of postural reflexes (Yorkston, Beukelman, Strand, Hakel, 465). A resting tremor, as found in PD, refers to a tremor that occurs when an individual's muscles are relaxed, not moving. The rigidity refers to the increased muscle tone that causes stiffness of the muscles. A person with PD, because of the rigidity, may struggle to swing his arms when walking. Bradykinesia refers to a struggle with initiating movements as well as a sudden halt of movement. Both bradykinesia and rigidity can be found in the facial muscles. Facial expressions can be severely reduced because of this. The loss of postural reflexes refers to the individual's instability while standing (http://www.pdf.org/en/symptoms). In addition to these symptoms, patients may experience poor handwriting, slowness of motor initiation, speech issues, and swallowing problems (Yorkston, Beukelman, Strand, Hakel, 465). Many nonmotor symptoms coexist with the motor symptoms of tremor-at-rest, rigidity, akinesia/bradykinesia, and loss of postural reflexes.
Nonmotor symptoms such as vision problems, drenching sweats, and impaired sense of smell can be present in patients with PD. For some patients, the nonmmotor symptoms can cause greater discomfort than the motor symptoms, causing a decrease in quality of life. Sensory symptoms include pain that is not connected to rigidity, which can be found in up to 38% of PD patients as well as the impaired sense of smell and poor vision. Autonomic symptoms that may be found in a patient with PD include the following: orthostatic hypotension, postprandial hypotension, cold limbs, dysphagia, constipation, urinary problems, and sexual dysfunction. Orthostatic hypotension is either experienced as a side effect from medicine or it is a manifestation of the disease. Patients with PD experience the gastrointestinal symptoms more than any other age-matched control. The severity of the gastrointestinal symptoms is linked to the stage of PD the patient is experiencing. Cognitive-behavioral problems - depression, apathy, anxiety disorders, classic obsessive-compulsive disorder, visual hallucinations, psychosis, and dementia - commonly co-occur with the motor symptoms. (Pandaya, Kubu, and Giroux, 856-864). Though prevalence estimations for patients with PD and dementia vary widely, it is noted that approximately 15% meet the criteria necessary for a diagnosis of demintia (Yorkston, Beukelman, Strand, Hakel, 465). Another nonmotor area that is a possible symptom of PD is the likeliness of sleep disorders. Sleep disorders commonly seen in patients with PD include excessive daytime sleepiness, insomnia, and restless legs syndrome. It is estimated that up to 74% of PD patients have difficulty sleeping or some form of a sleep disorder (Pandaya, Kubu, and Giroux, 856-864). TRAN to dementia
Dementia, a symptom found in approximately 10% to 40% of individuals with PD, is predominately found in the individuals who were older when symptoms of PD were first detected. The progression of the disease is also significantly quicker than those who do not experience dementia (Murray & Clark, 2006). Dementia experienced by individuals with PD is typically characterized by slow thinking and difficulty with problem-solving because of disruption of the frontal-subcortical circuits. Hallucinations and depression are also noted characteristics of dementia of individuals with PD (Pandaya, Kubu & Giroux, 2008). Though dementia is not seen in all individuals with PD, over half will develop mild cognitive deficits (Murray & Clark, 2006). Cognitive deficits commonly seen include the following: decreased ability to plan, sequence, concept formation and active memory. All of the deficits relate to dysfunction of the frontal lobe (Padovani, Costanzi, Gilberti, & Borroni, 2006). Tran
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Speech and Voice Characteristics
Individuals with PD typically develop voice and speech problems at some point in the progression of the disease. Common voice and speech problems include decreased vocal loudness, breathy, harsh, or hoarse voice quality, reduced prosodic pitch inflection, imprecise and reduced range of articulatory movements, and short rushes of speech (Sapir, Spielman, Ramig, Story, and Fox, 900). Changes in communication of a patient with PD is unavoidable with ap[proximately 80 to 90% of patients experiencing voice changes while 45 to 50% show changes in articulation (Miller, Nhoble, Jones, and Burn, 2006). Collectively, the speech and voice impairments experienced by an individual who experiences speech impairments because of a leasion of the peripheral or central nervous system are referred to as dysarthria (Pinto et. al., 2004).
Typically, individuals with PD experience hypokinetic dysarthria, however 10 to 20% of patients show charactereristics of hypokinetic/hyperkinetic dysarthria (Tajden, 2008). The following characteristics are typical of hypokinetic dysarthria: monotony with reduced loudness, reduced pitch range,
As reported in a study comparing spoken language results of individual's with PD to a control group, the mean scores of individuals PD consistently fall below the mean scores of the control group. The mean intelligibility percentage on the Assessment of Intelligibility of Dysarthric Speech (AIDS) for those with PD is 91.40 while for the control group it is 99.11. This allows the possibility of reduced intelligibility because of aging to be dismissed. The mean length of utterance for speakers with PD was only slightly lower than the control group, 9.67 and 10.85 respectively. Mean length of utterance, a measurement traditionally used to calculate a child's level of language abilities, is calculated by collecting 100 spoken utterances. Then, the number of morphemes is divided by the number of utterances. The total number of words used by patients with PD compared to the control group is comparable, 178.60 and 178.89 respectively. Comprehension was also found to be lower (Murray, 1350-1366). TRAN
Speech intelligibility is greatly impaired as well. The voice and speech deficits are hypokinetic dysarthria
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Death among people with PD is frequently caused by and attributed to abnormalities of respiration. The abnormalities of respiration can be the cause of many of the speech changes found in people with PD. When compared to typical speakers, the respitory function of individual's with PD is l