Do statins induce Parkinsons?
The following study and letter in response was
published in the German
medical journal Der Nervenarzt.
~~~~~~~~~~~~~~~~~~~~
Study on statin myopathy:

Der Nervenarzt
Publisher: Springer-Verlag Heidelberg
ISSN: 0028-2804 (Paper) 1433-0407 (Online)
DOI: 10.1007/s00115-002-1445-6
Issue: Volume 74, Number 2
Date: February 2003
Pages: 115 - 122
Fibrat-/Statin-Myopathie


~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Letter in response with case study of
statin-unmasked Parkinsons

"To the excellent review about the development
of myopathies following long-term medication of
cholesterol level decreasing fibrates and statins, there
should be considered additional differential diagnostic
possibilities.

Because of the similar clinical symptomatology
with muscle aches and increased stiffness, the
diagnosis of statin-> induced aggravated
Parkinson Disease Syndrome should be
discussed. The development of such muscular
side effects is seen more with statins than with
fibrates.

The case report in Table 1 indicates the
history of a 60 year old patient with statin-induced
Parkinson Syndrome occurring over a long time.

On the other hand, with central effective
statins, a possible neuro-protective effect in
neuro-degenerative diseases has been considered,
especially in dementia. But long term use of statins,
especially Lovastatin, leads to the reduction of
coenzyme Q10 and can cause damage of the
mitochondrial breathing chain. Co Q-10 is an electron
receptor in the mitochondrial complexes 1 and 2 and
very effective absorber of radicals. This antigen
substance increases the complex 1 activity.
Co-Q10 shows a certain therapeutic effect with
encephalomyopathy where there is a lack of
various enzyme functions of the breathing chain.

Dysfunction of various parts of the mitochondrial
breathing chain is also considered in the
pathophysiological mechaism of idiopathic
Parkinson's disease.

Treatment with Co-Q10 in patients who are not
treated with Dopamine for Parkinson patients,
caused less disease symptomatology and
progression than patients treated with
placebo, though placebo treatment can cause
stimulation of dopaminergic neurotransmission.
Therefore, the long-term treatment with Co-Q10
possibly is neuroprotective in idiopathic morbid
Parkinson, though new evidence shows it
appears to cause mild symptomatic effect.

Under these circumstances treatment with
prophylactic medication of Co-Q10 which has
been well tolerated in doses up to 1200mgm in
patients with neurodegenerative diseases should
be considered for statin myopathy or statin-
induced Parkinson syndrome in addition to
discontinuation of the cholesterol decreasing
medication.

The Table 1 summarizes a patient with Parkinson
syndrome.

1995: start of therapy with Fluvastatin 40 mg.

1997: increasing weakness with shoulder and hip
pain on the right

1999: diagnosis of right sided Parkinson
syndrome of akinetic dominance type.
Careful induction of Pergolid with daily doses
of 3 mg and Salagen 7.5 mgm

2000: complaints about increasing edema
development in legs, loss of hair, start of a
potas.sium sparing diuretic and increasing
of Pergolid medication from 4.5 mg
in June 2000 to 6 mgm in December.

March 2001: discontinuation of Fluvastatin,
continuation of Pergolid 6 mg

June 2001: reduction of Pergolid to 4 mgm

Sept 2001 Pergolid 3 mgm. Improvement of edema

December 2001 discontinuation of Pergolid and
diuretics

March, 2002 discontinuation of Salagen"

Dr. Th. T. Muller