Abstract
A 62 year old male worker sustained a head contusion from a fall in the workplace. When assessing the mechanism of the fall, it was noted that the worker stated that his feet became “stuck” and would not move. He also stated that he could not move fast enough to break his fall. Upon physical examination, a resting tremor was noted as well as upper and lower body rigidity, and a festinating gait. The worker was evaluated by a neurologist and diagnosed with early Parkinson’s disease.
Keywords
SW was a 62-year-old male, who presented to an employee health clinic for re-evaluation of a facial contusion sustained during a fall at work 3 days prior. SW stated that the floor was “sticky,” his feet became “stuck,” and he fell forward and hit the right side of his face on a table sustaining the facial contusion. By way of explanation, SW stated that he could not move fast enough to break his fall with his arms and hands. Because no occupational health and safety personnel were onsite during this particular shift, SW was evaluated in an emergency department. A CT scan without contrast was ordered; fortunately, findings were normal. SW was then released and told to visit the employee health service on Monday.
SW did not complain of any pain; however, he did exhibit bruising and swelling on the right upper side of his face. He stated that his eye was unaffected. SW denied any past medical or surgical problems and that his health was “good.” SW was not currently taking any medications, prescribed or over-the-counter. He denied any history of smoking, alcohol use, or illegal drug use. SW had worked as a housekeeper for the same hospital for the past 25 years.
A full neurological examination in response to the head injury found that cranial nerves two to 12 were grossly intact. However, a resting tremor of the right hand was noted and when asked to hold a cup, the tremor disappeared. Romberg’s sign was negative; however, increased swaying was noted. When SW was asked to extend his arms forward with palms up and to close his eyes, bilateral mild tremors were noted. When SW was asked whether he ever experienced any episodes of his “feet getting stuck,” he stated that sometimes he felt “frozen” and could not walk. Turning from one room into another room was also difficult. With musculoskeletal testing, upper body stiffness and rigidity were noted.
Based on the preliminary findings by the occupational health nurse practitioner, SW was referred to his primary care provider for evaluation of Parkinson’s disease.
Parkinson’s Disease
Parkinson’s disease is classified as a progressive neurodegenerative disorder (Fauci et al., 2015). The disease seems to have a genetic connection that involves proteins (e.g., alpha-synuclein and Parkin; Fauci et al., 2015). However, patients with a history of stroke or head injury are at increased risk of Parkinson’s disease. A link between environmental factors and genetic predisposition has also been proposed (Fauci et al., 2015). Oxidative stress and the production of free radicals result from dopamine and melanin metabolism that can lead to the destruction of substantia nigra (Fauci et al., 2015).
Parkinson’s disease appears to result from the degeneration of dopaminergic cells in the presence of Lewy bodies within the substantia nigra that is located in the basal ganglia. Dopaminergic cells produce a neurotransmitter called dopamine that is responsible for movement, cognition, mood, and neuroendocrine secretion. Lewy bodies are abnormal proteins that can be found in the central nervous system. These Lewy bodies appear in high concentration within the alpha-synuclein protein. As the disease progresses, Lewy bodies invade extranigral areas causing sleep disturbances, autonomic dysfunction, cognitive impairment, and mood disorders. As the dopaminergic cells are destroyed, levodopa levels are decreased resulting in postural instability, gait disturbances, and bulbar symptoms.
Epidemiology
According to the National Institute of Neurological Disorders and Stroke (NINDS; 2015), 500,000 Americans live with Parkinson’s disease and approximately 50,000 new cases are diagnosed every year. However, as the population of the United States ages, the incidence and prevalence of Parkinson’s disease may increase. The onset of Parkinson’s disease often begins when patients reach their 60s; the risk of Parkinson’s disease increases with age. However, patients have exhibited signs and symptoms of Parkinson’s disease as early as age 40 (NINDS, 2015). Researchers have suggested that the onset of Parkinson’s disease may actually be even earlier, but undiagnosed with isolated signs and symptoms such as constipation or stiff muscles that may be misdiagnosed as osteoarthritis (Tolosa, Gaig, Santamaria, & Compta, 2009).
Signs and Symptoms
Three primary symptoms are associated with Parkinson’s disease. The first is resting tremor in the extremities beginning in the upper extremities. Later stages of tremors may cause individuals to exhibit “pill rolling.” Rigidity is characterized by stiffness in the extremities and bradykinesia and slowness in movement. Later stages of the disease include postural instability, impaired balance, and coordination. Gait disturbances are described as shuffling with short steps or “festinating gait,” a flexed posture and loss of postural reflexes which results in acceleration in walking to “catch up” with the body’s center of gravity. Workers also experience “freezing,” while walking and hypotonia, softer speech. Micrographia, unusually small handwriting, is also present.
Final stages of Parkinson’s disease include dementia, anxiety disorders, depression, and sleep disturbances. Impulsive disorders are noted that may include hypersexuality or compulsive eating. Masked facies and decreased eye blinking are common. Autonomic dysfunction such as urinary retention or constipation are common. Orthostatic hypotension and excessive sweating can also occur.
Diagnosing Parkinson’s disease is based on signs and symptoms. Magnetic resonance imaging (MRI) with and without contrast is used to determine damage to basal ganglia and rule out other disease processes such as normal pressure hydrocephalus (Fauci et al., 2015).
Interventions
Medications are the mainstay of Parkinson’s disease management. Dopamine agonists, pramipexole and ropinirole, work by directly affecting dopamine receptors. They are neuroprotective and reduce endogenous dopamine turnover. Dopamine agonist may be used as monotherapy or with carbidopa/levodopa formulations. Sinemet is a common medication in this category and slows the progression of the disease by slowing the degeneration of dopamine neurons in the substantia nigra and reducing free radical damage via oxidative stress. Monoamine oxidase is also neuroprotective and blocks free radical formation from oxidative metabolism of dopamine. Anticholinergic agents are used to control bradykinesia and gait disturbances.
Surgical interventions include deep brain stimulation to control motor fluctuations associated with Parkinson’s disease. The surgery involves the suppression of excessive neuronal activity and activates efferent fiber pathways that decrease thalamocortical activity.
Physical therapy may be consulted for gait and balance training including the need for assistive devices (Tomlinson, Herd, & Clarke, 2014). Occupational therapy may be consulted as well for upper body assistance (e.g., weighted instruments to reduce tremors). Regular physical exercise may slow the progressive of akinesia, rigidity, and gait disturbances (Ahiskog, 2011).
Implications for the Occupational Health Nurse
When soliciting fall histories, it is essential to not only focus on the environment but also on the mechanism of the fall as well. Personal risk factors may predispose workers to falls. During physical examinations, occupational health nurses and nurse practitioners should not only focus on injuries that have occurred but also assess for risk factors that could have contributed to the fall. Once workers are evaluated and treated by a neurologist, the occupational health nurse must consider whether the workers are fit for duty.
Footnotes
Conflict of Interest
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
Author Biography
Ann R. Lurati lives in Monterey, California and works as a nursing professor at San Jose State University and as a nurse practitioner in a private dermatology practice.
