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Parkinson Disease and Other Movement Disorders P1: Trim: 8.375in × 10.875in Top: 0.373in Gutter: 0.664in LWBK915-57 LWW-KodaKimble-educational September 17, 2011 2:31 Parkinson Disease and Other 57 Movement Disorders Michael E. Ernst and Mildred D. Gottwald CORE PRINCIPLES CHAPTER CASES PARKINSON DISEASE 1 Parkinson disease (PD) is a chronic, progressive movement disorder resulting from Case 57-1 (Questions 1, 2) loss of dopamine from the nigrostriatal tracts in the brain, and is characterized by rigidity, bradykinesia, postural disturbances, and tremor. 2 Treatment for PD is aimed at restoring dopamine supply through one, or a Case 57-1 combination, of the following methods: exogenous dopamine in the form of a (Questions 3–18), precursor, levodopa; direct stimulation of dopamine receptors via dopamine Case 57-2 (Questions 1, 2) agonists; and inhibition of metabolic pathways responsible for degradation of levodopa. 3 Therapy for PD is usually delayed until there is a significant effect on quality of life; Case 57-1 (Questions 4, 10) generally younger patients start with dopamine agonists, whereas older patients may start with levodopa. 4 Initial therapy with dopamine agonists is associated with a lower risk of developing Case 57-1 (Questions 4, motor complications than with levodopa, but all patients will eventually require 10–15) levodopa. 5 Advanced PD is characterized by motor fluctuations including a gradual decline in Case 57-1 (Questions on time, and the development of troubling dopaminergic-induced dyskinesias. 15–18), Case 57-2 Dopamine agonists, monoamine oxidase type B (MAO-B) inhibitors, and (Question 1), Case 57-3 catechol-O-methyltransferase (COMT) inhibitors can reduce motor fluctuations; (Questions 1, 2) amantadine can improve dyskinesias. Deep brain stimulation of the globus pallidus interna or subthalamic nucleus may benefit patients with advanced PD. 6 It is controversial whether any therapies for PD are truly disease-modifying or Case 57-2 (Question 1) neuroprotective. 7 Comprehensive therapy for patients should include attention to the many Case 57-4 (Questions 1, 2) progressive complications of PD, including neuropsychiatric disturbances and autonomic dysfunction. RESTLESS LEG SYNDROME 1 Dopamine agonists are first-line treatments for restless leg syndrome (RLS). They Case 57-5 (Question 3) are preferred because they are longer acting than levodopa, and reduce symptoms throughout the entire night. Other effective therapies include carbidopa/levodopa, gabapentin, benzodiazepines, and opiates. 2 A common problem with long-term use of dopaminergic agents in RLS, particularly Case 57-5 (Question 4) levodopa, is an augmentation effect. This refers to a gradual dosage intensification that occurs in response to a progressive worsening of symptoms after an initial period of improvement. Gradual withdrawal of therapy and substitution with other agents should be performed, rather than continued dopaminergic dose escalation. continued 1 P1: Trim: 8.375in × 10.875in Top: 0.373in Gutter: 0.664in LWBK915-57 LWW-KodaKimble-educational September 17, 2011 2:31 2 CHAPTER CASES ESSENTIAL TREMOR 1 Essential tremor should be distinguished clinically from tremor associated with PD Case 57-6 (Question 1) or other causes. 2 Treatments of choice for essential tremor include propranolol or primidone. In Case 57-6 (Question 2) refractory cases, targeted botulinum toxin A injections can be useful. PARKINSON DISEASE research, please view the episode “My Father, My Brother, and Me” from the Public Broadcasting System program Frontline at Section 13 http://www.pbs.org/wgbh/pages/frontline/parkinsons/). Incidence, Prevalence, The relative contributions of environment and genetics to the and Epidemiology occurrence of PD remains controversial; rural living, pesticide exposure, and consumption of well water have consistently been Parkinson disease (PD) is a chronic, progressive movement dis- associated with increased lifetime risk of PD, whereas cigarette order in which drug therapy plays a central role. Since its original smoking and caffeine ingestion appear protective.9 Mutations in description in 1817 by Dr. James Parkinson, the term parkinson- Neurologic Disorders several genes, including α-synuclein (SNCA), leucine-rich repeat ism has come to refer to any disorder associated with two or more 1 kinase-2 (LRRK2), parkin, PTEN-induced kinase-1 (PINK1), and features of tremor, rigidity,bradykinesia, or postural instability. DJ-1,havebeenobservedinrarefamilialinheritedcasesofPD,but Most cases of PD are of unknown cause, and referred to as idio- thesegeneslacktypicalMendelianpatternsofinheritance,anddo pathic parkinsonism; however, viral encephalitis, cerebrovascular not account for the threefold increased risk of developing PD for disease, and hydrocephalus have symptoms similar to PD as part 1 individuals who have a first-degree relative affected with sporadic of their clinical presentation. Unless otherwise stated, all refer- PD.10 Recent advances in molecular genetics and genome-wide ences to PD in this chapter refer to the idiopathic type. association studies have revealed other novel risk genes; however, The age at onset of PD is variable, usually between 50 and 2 the exact linkage between genetics, environment, and clinical 80 years, with a mean onset of 55 years. Both the incidence expression of disease remains uncertain.11 and prevalence of PD are age-dependent, with annual incidence estimates ranging from 10 cases per 100,000 (age 50–59 years) to 100 cases per 100,000 (age 80–89 years), and an estimated preva- Pathophysiology lence of 1% of the population older than 65 years of age.3,4 Men PD affects the portion of the extrapyramidal system of the brain are affected slightly more frequently than women.5 Despite the involving the basal ganglia, an area composed of the substan- availability of effective symptomatic treatments to improve both tia nigra, neostriatum, and globus pallidus. Together, they are quality of life and life expectancy,no cure exists. The symptoms of involved with maintaining posture and muscle tone and reg- PD are progressive, and within 10 to 20 years, significant immo- ulating voluntary smooth motor activity. The pigmented neu- bility results for most patients.6 More rapid rates of symptom rons within the substantia nigra have dopaminergic fibers that progression and motor disability have been observed in patients project into the neostriatum and globus pallidus, and in PD, these who are older at the onset of clinically recognizable disease.7 PD dopamine-producing neurons are progressively depigmented. itself does not cause death; however, patients often succumb to complications related to impaired mobility and function (e.g., aspiration pneumonia, thromboembolism) and overall frailty.6 For an image of the areas of the brain affected For a supplemental table listing contact by PD, go to http://thepoint.lww.com/ information for organizations that can serve AT10e. as a resource to persons with PD (as well as other movement disorders) and their families, Postmortem pathologic examination of the basal ganglia go to http://thepoint.lww.com/AT10e. reveals the presence of Lewy bodies within the remaining dopaminergic cells of the substantia nigra.12 These abnormal intraneuronal protein aggregates are considered pathognomonic Etiology for the disease. Lewy body pathology appears to ascend the brain The etiology of PD is poorly understood. Most evidence sug- in a predictable manner in PD, beginning in the medulla oblon- gests it is multifactorial, and attributable to a complex interplay gata in preclinical stages (which may explain observations of between age-related changes in the nigrostriatal tract, underly- anxiety, depression, and olfactory disturbance), ascending to the ing genetic risks, and environmental triggers. Support for this midbrain (motor dysfunction), and spreading eventually to the hypothesis can be found in several historic observations, most cortex (cognitive and behavioral changes).13 notably the postviral parkinsonian symptoms occurring after The exact pathological sequence leading to neurodegener- epidemics of encephalitis in the early 1900s, and the discovery ation is unclear, but free radicals formed as by-products of that ingestion of a meperidine analog, 1-methyl-4-phenyl-1,2,3,6- dopamine auto-oxidation have been implicated. The oxidative tetrahydropyridine (MPTP), by heroin addicts in northern stress imparted by these events may provide the stimulus for California during the early 1980s caused a rapid and irreversible inflammation and cellular apoptosis, thereby initiating the cas- parkinsonism.8 (For an excellent in-depth discussion of the cade of neurodegeneration. The finding that a critical threshold importance of the MPTP discovery and its influence on PD of neuronal loss (at least 70%–80%) occurs before PD becomes P1: Trim: 8.375in × 10.875in Top: 0.373in Gutter: 0.664in LWBK915-57 LWW-KodaKimble-educational September 17, 2011 2:31 clinically apparent suggests that adaptive mechanisms (e.g., 3 lack of normal changes in facial expression and speaks in a upregulation of dopamine synthesis or downregulation of synap- soft, monotone voice. A strong body odor is noted. Exami- tic dopamine reuptake) may somehow influence disease progres- nation of his extremities reveals a slight ratchetlike rigidity sion during the preclinical stages. in both arms and legs, and a mild resting tremor is present in his right hand. His gait is slow but otherwise normal, Overview of Drug Therapy with a slightly bent posture. His balance is determined to be normal,
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