Treatment Options

111: treatment of patients with MSA is a clinical challenge. There is a significant lack of controlled clinical
trials and a relative abundance of anecdotal reports. Most treatment protocols are ‘borrowed’ from
treatment protocols for PD and autonomic disorders.

5$

There is no effective medical treatment for ataxia and gait and balance disturbances. Most patients with
prominent parkinsonism demonstrate some response to levodopa, but hardly any to dopamine agonists.
Levodopa is tolerated relatively well, but can unmask or exacerbate orthostatic hypotension. Dyskinesias
do occur but not as frequently as in PD. The symptomatic effect sometimes appears to be transient, but
often, when levodopa is reduced or stopped, it deteriorates after withdrawal. One should try levodopa
up to 250 mg qid. Excessive daytime sleepiness has been reported after an acute challenge of 250 mg
levodopa, so titration seems advisable (60). There is no evidence that levodopa is toxic in MSA (61).
Responsiveness to levodopa is related to the extent of the lesion in the dorsal striatum (62). Paroxetine
up to 30 mg tid has been tried to alleviate motor symptoms. In a small, double-blind, placebo-controlled
trial involving 20 patients for a period of only two weeks, a modest improvement ofmotor functions of
the upper limbs and speech was found, without any improvement of mood (63). Further trials are
needed. Specific motor symptoms include focal dystonia, where botulinum toxin should be considered,
and dysphagia, dysarthria, and stridor, where speech therapy and physical therapy can play a role.
Sometimes percutaneous endoscopic gastrostomy and tracheostomy arc Options. For the prevention of
111 and related fi'actures, an early use ofwalking dc and a wheelchair is recommended.

I i Dysft 1

The treatment of urinary symptoms is empirical. Neurogenic bladder symptoms can be treated with
anticholinergics like oxybutinin chloride, tolterodine tartrate, or trospium chloride. The risk of possible
cognitive deterioration seems hypothetical. Trials are lacking, however. The postmicturation residue
should be measured since a large residue can lead to incontinence. prresent, clean, intermittent self-
catheterization is an option, but with progression of the disease, an indwelling, suprapubic catheter is
usually needed (I 3,14).

rt ostatic Hypotension
For the treatment of orthostatic hypotension, the blood pressure is less relevant than the symptoms the
patient experiences. Often non-pharmacologic treatments suHice: sufficient fluid intake, sufficient salt
intake, smaller and more frequent meals to prevent postprandial hypotension, and individualized elastic
body garments. Fludrocortisone 0.1-0.3 mg per day leads to sodium retention and thus to an increase of
the intravascular volume. Head-up tilt during sleeping also leads to an increase of the intravascular
volume and improves early morning hypotension. Desmopressine (0.2-0.4 mg) can improve morning
postural hypotension and additionally nocturnal polyuria.

eMo fit ion

Growth hormone has been used in an attempt to modify the disease progression in a placebo-controlled
trial in 43 patients. There was a trend to less worsening as measured by the UMSARS in the growth
hormone-treated group. The treatment was well tolerated. Further studies in more patients and perhaps
with higher doses have to be done before any definite conclusions on its effect can be drawn (64).

There have been some reports on the effect of deep brain stimulation of the subthalamic nucleus and of
the internal pallidum (65), but results so far have been poor, and on the basis of the limited data
available, deep brain stimulation is not recommended for MSA (66).