Ancillary treatments In the management of the patient with Parkinson disease, one must not neglect the maintenance of general health and neuromuscular efficiency by a program of exercise, activity, and rest. Physical therapy and exercises such as those performed in yoga may be of help in achieving these ends. Sleep may be aided by soporific antidepressants. Postural imbalance and falls can be greatly mitigated by the use of a cane or walking frame. A number of excellent exercise programs have been devised specifically for patients with Parkinson disease, and measures such as massage and yoga have their advocates. Among therapies that have been studied systematically, tai chi has been found to improve balance and reduce falls as measured by objective criteria (Li et al), indicating that these approaches are of substantial value. Several of our patients have taken up dancing and report that their balance in daily circumstances is improved. Our position has been that any activity that keeps the patient moving and committed is of great value. Speech exercises help the motivated patient.
Hypotensive episodes respond to fludrocortisone, droxidopa, pyridostigmine, or midodrine given each morning. Compression stockings and increased water and salt intake have also been recommended but have not been not well studied. The subject is reviewed by Wu and Hohler. Focal dystonias of the foot are partially treatable with local injections of botulinum toxin. In addition, the patient often needs emotional support in dealing with the stress of the illness, with the anxiety that seems to be an integral part of the disease in some patients, in comprehending the future, and in carrying on courageously in spite of it.
Multiple System Atrophy (Striatonigral Degeneration, Shy-Drager Syndrome, Olivopontocerebellar Degeneration)
As the name multiple system atrophy indicates, this depicts a group of disorders characterized by neuronal degeneration mainly in the substantia nigra, striatum, autonomic nervous system, and cerebellum. Following a report in 1964 by Adams and colleagues of what was then called striatonigral degeneration, many patients were recognized in whom the changes of striatonigral and olivopontocerebellar degeneration were combined and who had symptoms and signs of cerebellar ataxia and parkinsonian manifestations. The pathologic changes were found by chance in 4 middle-aged patients, in 3 of whom a parkinsonian syndrome had been described clinically, none with a family history of similar disease. Rigidity, stiffness, and akinesia had begun on one side of the body, then spread to the other, and progressed over a 5-year period but with minimal characteristic tremor of idiopathic Parkinson disease. A flexed posture of the trunk and limbs, slowness of all movements, poor balance, mumbling speech, and a tendency to faint when standing were other elements. There was an early-onset cerebellar ataxia in the fourth patient that was later obscured by a Parkinson syndrome.
The postmortem examinations disclosed extensive loss of neurons in the zona compacta of the substantia nigra, but notably, there were no Lewy bodies or neurofibrillary tangles in the remaining cells. Even more striking were the degenerative changes in the putamina and to a lesser extent in the caudate. Secondary pallidal atrophy (loss of striatopallidal fibers) was present. In the patient with ataxia there was, in addition, advanced degeneration of the pons, olives, and cerebellum (see below). Bannister and Oppenheimer astutely named the broad syndrome “multiple system atrophy.”
Recognizing that the clinical and pathologic features of striatonigral degeneration, with or without autonomic failure, can coexist with olivopontocerebellar atrophy,