Parkinson disease (PD) has highly characteristic neuropathologic findings and a clinical presentation, including motor deficits and, in some cases, mental deterioration.
Two hallmark features in the substantia nigra pars compacta are loss of neurons and presence of Lewy bodies. The degree of nigrostriatal dopamine loss correlates positively with severity of motor symptoms.
Reduced activation of dopamine1 and dopamine2 receptors results in greater inhibition of the thalamus and reduced activation of the motor cortex. Clinical improvement may be tied to restoring activity more at the dopamine2 receptor than at the dopamine1 receptor.
PD develops insidiously and progresses slowly over many years.
Initial symptoms may be sensory, but as the disease progresses, one or more classic primary features present (eg, resting tremor, rigidity, bradykinesia, and postural instability that may lead to falls).
Resting tremor is often the sole presenting complaint. However, only two thirds of PD patients have tremor on diagnosis, and some never develop this sign. Tremor is present most commonly in the hands, often begins unilaterally, and sometimes has a characteristic “pill-rolling” quality. Resting tremor is usually abolished by volitional movement and is absent during sleep.
Muscular rigidity involves increased muscular resistance to passive range of motion and can be cogwheel in nature. It commonly affects both upper and lower extremities; neck and facial muscles may be affected.
Intellectual deterioration is not inevitable, but some patients deteriorate in a manner indistinguishable from Alzheimer disease.
Nonmotor symptoms are common and must be identified, treated, and monitored (Table 56–1).
TABLE 56–1Nonmotor Symptoms and Possible Treatments |Favorite Table|Download (.pdf) TABLE 56–1 Nonmotor Symptoms and Possible Treatments
|Symptom ||Possible Treatments |
|Anxiety ||Cognitive behavioral therapy, selective serotonin reuptake inhibitors, venlafaxine, minimize “off” times. |
|Cognitive impairment ||Eliminate anticholinergic agents. Add cholinesterase inhibitor. |
|Constipation ||Fiber, hydration, exercise, laxatives, stool softeners. |
|Daytime sleepiness ||Proper night time sleep hygiene, reduce dose of dopamine agonist, referral to sleep specialist to rule out apnea and sleep disorders. |
|Depression ||Selective serotonin reuptake inhibitor, newer-generation serotonin norepinephrine reuptake inhibitor, cognitive behavioral therapy. |
|Drooling ||Local injection of botulinum toxin, atropine sublingual drop, glycopyrrolate, ipratropium sublingual spray. |
|Dysphagia ||Referral to speech therapist, dysphagia diet, avoid anticholinergic medications, manage dry mouth. |
|Fatigue ||Caffeine, armodafinil, modafinil, proper night time sleep hygiene, referral to sleep specialist to rule out sleep disorder. |
|Falling ||Referral to physical therapy; assistance with ambulation, minimize risk for bone fractures, treat osteoporosis. |
|Hallucinations/psychosis ||Eliminate adjunctive medications, especially anticholinergic agents and dopamine agonists. Add clozapine, quetiapine, pimavanserin. |
|Impulse control disorder ||Discontinue dopamine agonist or add clozapine, quetiapine, or naltrexone |
|Insomnia ||Nonbenzodiazepine GABAA agonists, trazodone. |
|Orthostatic hypotension ||Reduce dose of alpha-blockers, dopamine agonist, diuretics, vasodilators. Abdominal compression, add salt and water to diet, water boluses, fludrocortisone, midodrine, droxidopa, pyridostigmine. |
|Overactive bladder ||Behavioral therapies (eg, bladder training, fluid management, pelvic floor muscle exercises), ...|
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