report of statin induced Parkinsonism

eml · medicine forum Guru Wannabe Joined: 12 Jun 2005 Posts: 135

the following is from a german medical journal. This is the english
translation:

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

J. Finsterer A1

A1 Neurologische Abteilung,KA Rudolfstiftung,Wien
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.

1996: 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

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