PDR for Herbal Medicines

(Barré) #1
HERBAL MONOGRAPHS GINKGO/343

arachidonate-independent platelet aggregation. Ginkgolide B
blocks the binding to PAF to its receptor resulting in an
antagonistic effect (Chung, 1987). This effect will inhibit
PAF-induced bconchoconstriction and airway hyperactivity,
along with T-lymphocyte proliferation and cytokine produc-
tion. PAF induces inflammation and changes in vascular
permeability (Braquet, 1989: Delia Loggia, 1993).

Other effects consist of spasmolytic properties through direct
action on alpha-adrenoceptors and smooth muscle relaxing
properties via the signal transduction pathway, intracellular
I cAMP, antagonism of the adrenergic nervous system and
hyperpolarization (Hellegouarch, 1985; Struillon, 1995).


CLINICAL TRIALS
Dementia

A placebo-controlled, double-blind, randomized trial with a
particular extract of Ginkgo biloba (EGb 761) was conducted
to assess the efficacy and safety in Alzheimer's disease and
multi-infarct dementia. Alzheimer's Disease Assessment
Scale-Cognitive subscale (ADAS-Cog), Geriatric Evaluation
by Relative's Rating Instrument (GERRI) and Clinical
Global Impression of Change (CGIC) were used to evaluate
the response in 309 patients over a 52-week period. EGb 120
mg daily was safe and was shown to stabilize or improve
cognitive performance and the social functioning of dement-
ed patients for 6 months to 1 year (Le Bars, 1998).

Peripheral Occlusive Arterial Disease

The clinical efficacy of Ginkgo biloba special extract (EGb
761) was demonstrated in 111 patients with peripheral
occlusive arterial disease (POAD) in Fontaine stage lib and
intermittent claudication. The mean pain-free walking dis-
tances were very similar at the beginning of the treatment
period. After 8, 16 and 24 weeks, the EGb treatment group
was significantly better than the placebo group with maxi-
mum walking distance and relative increases of the pain-free
walking distance. The doppler indices remained nearly
unchanged during the coarse of therapy (Peters, 1998).

Equilibrium Disorders

An open, controlled study consisted of 44 patients complain-
ing of vertigo, dizziness or both, caused by vascular
vestibular disorders. The patients were randomly treated with
extract of Ginkgo biloba (EGb 761) 80 mg twice daily or
with betahistine dihydrochloride (BI) 16 mg twice daily for 3
months. A complete neuro-otologic and equilibrimetric
examination was performed at baseline and after 3 months of
treatment, including an evaluation of clinical findings.
Dizziness and vertigo improved in 64.7% of patients in the
BI treatment group and in 65% of those in the EGb 761
treatment group in the first month of therapy. No significant
changes were observed in cranial scans for patients with a
'central' cranial pattern or with the equilibrium score. EGb
761 induced a slight decrease of saccadic delay and
considerably increased saccadic velocities while BI im-
proved saccadic accuracy but did not modify delay. EGb 761
improved smooth pursuit gain three times more than BI.
Both drugs asymmetrically reduced nystagmus maximum
velocity and improved the sinusoidal vestibulo-ocular reflex.
BI considerably reduced, whereas EGb 761 considerably
improved, visuovestibular ocular reflex (Cesarani, 1998).

INDICATIONS AND USAGE
Approved by Commission E:


  • Symptomatic relief of organic brain dysfunction

  • Intermittent claudication

  • Vertigo (vascular origin)

  • Tinnitus (vascular origin)


The Commission E approvals listed are limited to special
standard extracts of Ginkgo.

Unproven Uses: The drug is used for disturbed brain
functions that result in dizziness and headache with emotion-
al lability and anxiety. Ginkgo has been demonstrated to
improve concentration and memory deficits as a result of
peripheral arterial occlusive disease.

Chinese Medicine: Among traditional Chinese uses for
Ginkgo biloba are asthma, tinnitus, hypertonia and angina
pectoris.

Homeopathic Uses: Homeopathy includes tonsillitis and
cephalgia among the indications for use of Ginkgo.

CONTRAINDICATIONS
The drug is contraindicated in patients knowa to be
hypersensitive to Ginkgo biloba preparations.

Patients with known risk factors for intracranial hemorrhage
(systematic arterial hypertension, diabetes amyloid senile
plaques) should avoid the use of Ginkgo biloba due to a
recent case report of subarachnoid hemorrhage associated
with the herb (Vale, 1998).

Ginkgo biloba exerts ischemic protective and antioxidant
effects through the flavonoids. This occurs through a free
scavenger action and prevention of lipid peroxidation. Lipid
peroxidation is involved in producing tissue and vascular
damage, and neuronal loss, which may lead to dementia
(Dorman, 1992; Koc, 1995; Otamiri, 1989). The herb also
reduces neutrophil infiltration and increases blood flow to
prevent the progression of dementia ischemia. The anti-
oxidant and membrane-stablizing activity increases cerebral
hypoxia tolerance (Koltringer, 1989; Otamiri, 1989).
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