There are no sensory findings, but a wide variety of paresthetic and other sensory complaints and discomforts are common. These affect mainly the calves and abdomen and are among the most distressing of the nonmotor symptoms. Drooling is troublesome; an excess flow of saliva has been assumed, but actually the problem is probably one of failure to swallow with normal frequency. Seborrhea and excessive sweating are claimed to be secondary as well, the former due to failure to cleanse the face sufficiently, the latter to the effects of the constant motor activity but this explanation seems lacking to us; an autonomic disturbance is more plausible. Other nonmotor features are mostly in the category of autonomic disturbances and include most prominently, constipation, abdominal or back pains and cramps, erectile dysfunction, joint aches, and various other sensory experiences that may be difficult for the patient to describe. There is a tendency in some patients to have orthostatic hypotension and sometimes syncope; this has been attributed by Rajput and Rozdilsky to cell loss in the sympathetic ganglia. However, these features, as well as REM sleep behavior disorder (Chap 18) are not as frequent as in multiple system atrophy (Shy-Drager syndrome) or in Lewy body dementia. Several of our younger Parkinson patients with recurrent syncope proved to have cardiac arrhythmias; hence, other causes of fainting must be considered. Any relationship to cardiac denervation, which is detectable by special testing, is not clear.
Postural instability is a core feature of the advancing illness; it can be elicited by tugging at the patient’s shoulders from behind and noting the lack of a small step backward to maintain balance often with a fall or the initiation of backward festination. The tendon reflexes vary, as they do in normal individuals from being barely elicitable to brisk. Even when parkinsonian symptoms are confined to one side of the body, the reflexes are usually equal on the 2 sides, and the plantar responses are flexor. Exceptionally, the reflexes on the affected side are slightly brisker, which raises the question of corticospinal involvement, but the plantar reflex remains flexor. In these respects, the clinical picture differs from that of corticobasal ganglionic degeneration, in which rigidity, hyperactive tendon reflexes, and Babinski signs are combined with apraxia (see further on).
As mentioned earlier, Parkinson disease may be complicated by dementia, a feature described by Charcot. The reported frequency of this combination varies considerably based on the selection of patients and type of testing. An estimate of 10 to 15 percent (Mayeux et al) is the generally accepted figure and matches our experience but it has been higher in some series. The incidence increases with advancing age and duration of disease, approaching 65 percent in Parkinson patients older than 80 years of age, but mental decline may become apparent in patients in their late fifties. The pathologic basis of the dementia is discussed below.
The overall course of the disease is quite variable. In the majority of patients, the mean period of time from inception of the disease to a chairbound state is 7.5 years, but with a wide range (Hoehn and Yahr; Martilla and Rinne). As much as 10 percent of cases remain relatively mild and only very gradually progressive, and such patients may remain almost stable for 10 years or more. These trajectories have been altered by modern therapies.