• Clinical data 90%
  • Efficacy 80%
  • Security 70%
  • Toxicity 30%

Ginkgo biloba
Folium Ginkgo

Synonyms

Pterophyllus salisburiensis Nelson, Salisburia adiantifolia Smith, Salisburia macrophylla C. Koch.

General appearance

The leaves are green, grey-yellow, brown or blackish; the upper side of a leaf may be somewhat darker than the underside. The leaves are fan-shaped, longpetioled and have two lobes with forked veins radiating from the petiole end.

Major chemical constituents

Folium Ginkgo contains a wide variety of phytochemicals, including alkanes, lipids, sterols, benzenoids, carotenoids, phenylpropanoids, carbohydrates, flavonoids, and terpenoids. The major constituents are flavonoids of which mono-, di-, and tri-glycosides and coumaric acid esters that are based on the flavonols kaempferol and quercetin dominate. Lesser quantities of glycosides are derived from isorhamnetin, myricetin, and 3-methylmyricetin. Nonglycosidic biflavonoids, catechins, and proanthocyanidins are also present. Characteristic constituents of this plant material are the unique diterpene lactones ginkgolides A, B, C, J, and M and the sesquiterpene lactone bilobalide.

Medicinal uses of Ginkgo biloba

Uses supported by clinical data
Extracts as described above (Dosage forms) have been used for symptomatic treatment of mild to moderate cerebrovascular insufficiency (demential syndromes in primary degenerative dementia, vascular dementia, and mixed forms of both) with the following symptoms: memory deficit, disturbance in concentration, depressive emotional condition, dizziness, tinnitus, and headache. Such extracts are also used to improve pain-free walking distance in people with peripheral arterial occlusive disease such as intermittent claudication, Raynaud disease, acrocyanosis, and post-phlebitis syndrome, and to treat inner ear disorders such as tinnitus and vertigo of vascular and involutive origin. Extracts and doses other than those described in Dosage forms and Posology are used for similar but milder indications.
Uses described in pharmacopoeias and in traditional systems of medicine
None.
Uses described in folk medicine, not supported by experimental or clinical data
As a vermifuge, to induce labour, for the treatment of bronchitis, chronic rhinitis, chilblains, arthritis, and oedema.

Pharmacology

Experimental pharmacology

Cerebrovascular insufficiency and peripheral vascular diseases

In vitro studies. A standardized extract of Ginkgo biloba (100μg/ml) did not produce isometrically recordable contractions in isolated rabbit aorta but did potentiate the contractile effect of norepinephrine. Higher concentrations (EC50  1.0 mg/ml) produced a concentration-dependent contraction that could be antagonized by the α-adrenoceptor-blocking agent phentolamine. Both cocaine and desipramine, inhibitors of catecholamine re-uptake, potentiated the contractile effect of norepinephrine but inhibited the contractile effects of astandardized extract of G. biloba and tyramine. The results of these experiments indicate that the contractile action of G. biloba may be due to the release of catecholamines from endogenous tissue reserves, and this activity may explain some of the therapeutic effects of the drug in humans (e.g. improvement in cerebrovascular and peripheral vascular insufficiency). On the basis of experiments comparing the effects of an extract of G. biloba, phentolamine, propranolol, gallopamil, theophylline, and papaverine on the biphasic contractile response of norepinephrine in isolated rat aorta, researchers concluded that G. biloba had musculotropic action similar to that of papaverine. This activity was previously reported for the flavonoids quercetin, kaempferol, and isorhamnetin, isolated from the leaves of G. biloba. The flavonoids and papaverine both inhibit 3,5-cyclic-GMP phosphodiesterase, which in turn induces endothelium dependent relaxation in isolated rabbit aorta by potentiating the effects of endothelium-derived relaxing factors. In vitro studies have demonstrated that G. biloba extracts scavenge free radicals. Ginkgo biloba extracts have been reported to reduce free radicallipid peroxidation induced by NADPH-Fe3 systems in rat microsomes, and to protect human liver microsomes from lipid peroxidation caused by ciclosporin A. The extract also inhibits the generation of reactive oxygen radicals in human leukocytes treated with phorbol myristate acetate. The antioxidant action of G. biloba extract may prolong the half-life of endotheliumderived relaxing factor by scavenging superoxide anions.
Both the flavonoid and terpenoid constituents of G. biloba appear to aid the free-radical scavenging activity of the drug. Ginkgo biloba extract protected against brain tissue hypoxic damage in vitro.
The ginkgolides and bilobalide were responsible for the antihypoxic activity of the extract. Ginkgolides A and B have been shown to protect rat hippocampal neurons against ischaemic damage, which may be due to their ability to act as antagonists to receptors for platelet-activating factor (PAF).
In vivo studies. Oral administration of G. biloba extract protected rats against induced cerebral ischaemia. Intravenous perfusion of a G. biloba extract prevented the development of multiple cerebral infarction in dogs injected with fragments of an autologous clot into a common carotid artery. These data suggest that G. biloba extract, administered after clot formation, may have some beneficial effects on acute cerebral infarction or ischaemia caused by embolism. Other experiments demonstrated that animals treated with G. biloba extract survived under hypoxic conditions longer than did untreated controls. Longer survival was due not only to significant improvements in cerebral blood flow, but also to an increase in the level of glucose and ATP. Other studies have shown that a G. biloba extract devoid of ginkgolides but containing bilobalide had protective activity when administered intraperitoneally to mice with induced hypobaric hypoxia. Intravenous infusion of G. biloba extract significantly increased pial arteriolar diameter in cats and improved cerebral blood flow in rats. The active constituents of G. biloba responsible for increasing cerebral blood flow appeared to be the non-flavonoid compounds; ginkgolide B may be responsible for this action owing to its PAF-antagonist activity. Furthermore, intravenous administration of a standardized G. biloba extract and ginkgolide B to rats showed that the extract, but not ginkgolide B, decreased the brain’s use of glucose. The constituents of G. biloba responsible for its anti-ischaemic activity remain undefined. The flavonoids, ginkgolides, and bilobalide have all been suggested, but it is possible that other constituents may be responsible. An extract of G. biloba was effective in the in vivo treatment of cerebral oedema, a condition of excessive hydration of neural tissues owing to damage by neurotoxic agents (such as triethyltin) or trauma. Bilobalide appeared to play a significant role in the antioedema effect. Oral or subcutaneous administration of an extract of G. biloba to rats with acute and chronic phases of adriamycin-induced paw inflammation partially reversed the increase in brain water, sodium, and calcium and the decrease in brain potassium associated with sodium arachidonate induced cerebral infarction.
Mice treated with a standardized extract of G. biloba (100 mg/kg, orally for 4–8 weeks) showed improved memory and learning during appetitive operant conditioning.

Vestibular and auditory effects

Ginkgo biloba extract improved the sum of action potentials in the cochlea and acoustic nerve in cases of acoustically produced sound trauma in guinea-pigs. The mechanism reduced the metabolic damage to the cochlea. Oral or parenteral administration of a standardized G. biloba extract to mice (2mg/kg) improved the ultrastructure qualities of vestibular sensory epithelia when the tissue was fixed by vascular perfusion (66). Improvement was due to the effects of the drug on capillary permeability and general microcirculation. Positive effects on vestibular compensation were observed after administration of G. biloba extract (50 mg/kg intraperitoneally) to rats and cats that had undergone unilateral vestibular neurectomy.
Antagonism of platelet-activating factor (PAF) The ginkgolides, and in particular ginkgolide B, are known antagonists of PAF. PAF is a potent inducer of platelet aggregation, neutrophil degranulation, and oxygen radical production leading to increased microvascular permeability and bronchoconstriction. Intravenous injections of PAF induced transient thrombocytopenia in guinea-pigs, which was accompanied by nonhistamine-dependentbronchospasm. Ginkgolide B has been shown to be a potent inhibitor of PAF-induced thrombocytopenia and bronchoconstriction. PAF or ovalbumin-induced bronchoconstriction in sensitized guinea-pigs was inhibited by an intravenous injection of ginkgolide B (1–3mg/kg) 5 minutes prior to challenge.

Clinical pharmacology

Cerebral insufficiency

Cerebral insufficiency is an inexact term to describe a collection of symptoms associated with dementia. In dementia owing to degeneration with neuronal loss and impaired neurotransmission, decline of intellectual function is associated with disturbances in the supply of oxygen and glucose. In clinical studies G. biloba effectively managed symptoms of cerebral insufficiency including difficulty in concentration and memory, absent-mindedness, confusion, lack of energy, tiredness, decreased physical performance, depressive mood, anxiety, dizziness, tinnitus, and headache. Several mechanisms of action of G. biloba have been described: effects on blood circulation such as the vasoregulating activity of arteries, capillaries, veins (increased blood flow); rheological effects (decreased viscosity, by PAF-receptor antagonism); metabolic changes such as increased tolerance to anoxia; beneficial influence on neurotransmitter disturbances; and prevention of damage to membranes by free radicals. Treatment of humans with G. biloba extract has been shown to improve global and local cerebral blood flow and microcirculation, to protect against hypoxia, to improve blood rheology, including inhibition of platelet aggregation, to improve tissue metabolism, and to reduce capillary permeability. A critical review of 40 published clinical trials (up to the end of 1990) using an orally administered G. biloba extract in the treatment of cerebral insufficiency concluded that only eight of the studies were well performed. Almost all trials reported at least a partially positive response at dosages of 120–160mg a day (standardized extract) and treatment for at least 4–6 weeks. In a comparison of G. biloba with published trials using co-dergocrine (dihydroergotoxine), a mixture of ergoloid mesilates used for the same purpose, both G. biloba extract and co-dergocrine showed similar efficacy. A direct comparison of 120mg of G. biloba standardized extract and 4.5mg codergocrine showed similar improvements in both groups after 6 weeks. A meta analysis of 11 placebo-controlled, randomized double-blind studies in elderly patients given G. biloba extract (150 mg orally per day) for cerebral insufficiency concluded that eight studies were well performed. Significant differences were found for all analysed single symptoms, indicating the superiority of the drug in comparison with the placebo. Analysis of the total score of clinical symptoms indicated that seven studies confirmed the effectiveness of G. biloba extract, while one study was inconclusive.

Peripheral arterial occlusive disease

The effectiveness of G. biloba extract in the treatment of intermittent claudication (peripheral arterial occlusive disease Fontaine stage II), as compared with a placebo, was demonstrated in placebo-controlled, double-blind clinical trials by a statistically significant increase in walking distance. Sixty patients with peripheral arterial occlusive disease in Fontaine stage IIb who were treated with the drug (120–160mg for 24 weeks) and underwent physical training also clearly increased their walking distance. Out of 15 controlled trials (up to the end of 1990) only two (23, 24) were of  acceptable quality. The results of both studies were positive and showed an increase in walking distance in patients with intermittent claudication after 6 months, and an improvement of pain at rest in patients treated with 200 mg of G. biloba extract for 8 weeks. After meta-analysis of five placebo-controlled clinical trials (up to the end of 1991) of G. biloba extract in patients with peripheral arterial disease, investigators concluded that the extract exerted a highly significant therapeutic effect.

Vertigo and tinnitus

Ginkgo biloba extracts have been used clinically in the treatment of inner ear disorders such as hearing loss, vertigo, and tinnitus. In a placebo-controlled, double-blind study of 68 patients with vertiginous syndrome of recent onset, treatment with G. biloba extract (120–160mg daily, for 4–12 weeks) produced a statistically significant improvement as compared with the placebo group.
The results of clinical studies on the treatment of tinnitus have been contradictory. At least six clinical studies have assessed the effectiveness of G. biloba extract for the treatment of tinnitus. Three studies reported positive results. One multicentre, randomized, double-blind, 13-month study of 103 patients with tinnitus showed that all patients improved, irrespective of the prognostic factor, when treated with G. biloba extract (160mg/day for 3 months). Three other clinical trials reported negative outcomes. Statistical analysis of an open study (80 patients) without placebo, coupled with a double-blind, placebo-controlled part (21 patients), demonstrated that a concentrated G. biloba extract (29.2 mg/day for 2 weeks) had no effect on tinnitus.

Contraindications

Hypersensitivity to G. biloba preparations.

Warnings

No information available.

News and Journals

References
1. DeFeudis FV. Ginkgo biloba extract (egb 761): pharmacological activities and clinical
applications. Paris, Elsevier, Editions Scientifiques, 1991:1187.
2. Hänsel R et al., eds. Hagers Handbuch der pharmazeutischen Praxis, Vol. 6, 5th ed.
Berlin, Springer-Verlag, 1994.
3. Squires R. Ginkgo biloba. Australian traditional medicine society (ATOMS), 1995:9–14.
4. Huh H, Staba EJ. The botany and chemistry of Ginkgo biloba L. Journal of herbs, spices
and medicinal plants, 1992, 1:91–124.
5. Farnsworth NR, ed. NAPRALERT database. University of Illinois at Chicago, IL,
August 8, 1995 production (an on-line database available directly through the
University of Illinois at Chicago or through the Scientific and Technical Network
(STN) of Chemical Abstracts Services).
6. Keys JD. Chinese herbs, their botany, chemistry and pharmacodynamics. Rutland,
VT, CE Tuttle, 1976:30–31.
7. Pharmacopoeia of the People’s Republic of China (English ed.). Guangzhou, Guangdong
Science and Technology Press, 1992:64.
8. Melzheimer V. Ginkgo biloba L. aus Sicht der systematischen und angewandten
Botanik. Pharmazie in unserer Zeit, 1992, 21:206–214.
9. Van Beek TA, Lelyveld GP. Thin layer chromatography of bilobalide and ginkgolides
A, B, C and J on sodium acetate impregnated silica gel. Phytochemical analysis, 1993,
4:109–114.
10. Hasler A, Meier B, Sticher O. Identification and determination of the flavonoids from
Ginkgo biloba by HPLC. Journal of chromatography, 1992, 605:41–48.
11. Hasler A, Meier B. Determination of terpenes from Ginkgo biloba by GLC. Pharmacy
and pharmacology letters, 1992, 2:187–190.
12. Quality control methods for medicinal plant materials. Geneva, World Health Organization,
1998.
13. Deutsches Arzneibuch 1996. Vol. 2. Methoden der Biologie. Stuttgart, Deutscher
Apotheker Verlag, 1996.
14. European pharmacopoeia, 3rd ed. Strasbourg, Council of Europe, 1997.
15. Sticher O. Biochemical, pharmaceutical and medical perspectives of Ginkgo preparations.
In: New Drug Development from Herbal Medicines in Neuropsychopharmacology.
Symposium of the XIXth CINP Congress, Washington, DC, June 27–July 1, 1994.
16. Guidelines for predicting dietary intake of pesticide residues, 2nd rev. ed. Geneva,
World Health Organization, 1997 (unpublished document WHO/FSF/FOS/97.7;
available from Food Safety, WHO, 1211 Geneva 27, Switzerland).
17. Sticher O. Quality of Ginkgo preparations. Planta medica, 1993, 59:2–11.
18. Van Beek TA et al. Determination of ginkgolides and bilobalide in Ginkgo biloba
leaves and phytochemicals. Journal of chromatography, 1991, 543:375–387.
19. Hasler A et al. Complex flavonol glycosides from the leaves of Ginkgo biloba.
Phytochemistry, 1992, 31:1391.
20. German Commission E monograph, Trockenextrakt (35–67: 1) aus Ginkgo-biloba-
Blättern Extrakt mit Aceton-Wasser. Bundesanzeiger, 1994, 46:7361–7362.
21. Kleijnen J, Knipschild P. Ginkgo biloba. Lancet, 1992, 340:1136–1139.
22. Kleijnen J, Knipschild P. Ginkgo biloba for cerebral insufficiency. British journal of
clinical pharmacology, 1992, 34:352–358.
23. Bauer U. Six month double-blind randomized clinical trial of Ginkgo biloba extract
versus placebo in two parallel groups in patients suffering from peripheral arterial
insufficiency. Arzneimittel-Forschung, 1984, 34:716–720.
24. Saudreau F, Serise JM, Pillet J. Efficacité de l’extrait de Ginkgo biloba dans le
traitement des artériopathies obliterantes chroniques des membres inferieurs au
stade III de la classification de Fontaine. Journal malade vasculare, 1989, 14:177–
182.
25. Blume J et al. Placebokontrollierte Doppelblindstudie zur Wirksamkeit von Ginkgo
biloba-Spezialextrakt EGb 761 bei austrainierten Patienten mit Claudicatio
intermittens. VASA, 1996, 2:1–11.
26. Schneider B. Ginkgo biloba Extrakt bei peripheren arteriellen Verschlußkrankheiten.
Arzneimittel-Forschung, 1992, 42:428–436.
27. Haguenauer JP et al. Traitement des troubles de l’equilibre par l’extrait de Ginkgo
biloba. Presse medicale, 1986, 15:1569–1572.
28. Coeur et circulation, 02.97.0 Troubles de l’artériosclérose. IKS monthly bulletin, 1994,
6:532–533.
29. Kade F, Miller W. Dose-dependent effects of Ginkgo biloba extraction on cerebral,
mental and physical efficiency: a placebo controlled double blind study. British
journal of clinical research, 1993, 4:97–103.
30. Auguet M, DeFeudis FV, Clostre F. Effects of Ginkgo biloba on arterial smooth muscle
responses to vasoactive stimuli. General pharmacology, 1982, 13:169–171, 225–
230.
31. Auguet M, Clostre F. Effects of an extract of Ginkgo biloba and diverse substances on
the phasic and tonic components of the contraction of an isolated rabbit aorta.
General pharmacology, 1983, 14:277–280.
32. Peter H, Fisel J, Weisser W. Zur Pharmakologie der Wirkstoffe aus Ginkgo biloba.
Arzneimittel-Forschung, 1966, 16:719–725.
33. Pincemail J et al. In: Farkas L, Gabor M, Kallay F, eds. Flavonoids and bioflavonoids.
Szeged, Hungary, 1985:423.
34. Barth SA et al. Influences of Ginkgo biloba on cyclosporin induced lipid peroxidation
in human liver microsomes in comparison to vitamin E, glutathione and Nacetylcysteine.
Biochemical pharmacology, 1991, 41:1521–1526.
35. Pincemail J et al. Ginkgo biloba extract inhibits oxygen species production generated by phorbol myristate acetate stimulated human leukocytes. Experientia, 1987,
43:181–184.
36. Pincemail J, Dupuis M, Nasr C. Superoxide anion scavenging effect and
superoxide dismutase activity of Ginkgo biloba extract. Experientia, 1989, 45:708–
712.
37. Robak J, Gryglewski RJ. Flavonoids are scavengers of superoxide anions. Biochemical
pharmacology, 1988, 37:837–841.
38. Oberpichler H et al. Effects of Ginkgo biloba constituents related to protection against
brain damage caused by hypoxia. Pharmacological research communications, 1988,
20:349–352.
39. Krieglstein J. Neuroprotective effects of Ginkgo biloba constituents. European journal of
pharmaceutical sciences, 1995, 3:39–48.
40. Braquet P. The ginkgolides: potent platelet-activating factor antagonists isolated
from Ginkgo biloba L.: chemistry, pharmacology and clinical application. Drugs of the
future, 1987, 12:643–648.
41. Oberpichler H. PAF-antagonist ginkgolide B reduces postischemic neuronal damage
in rat brain hippocampus. Journal of cerebral blood flow and metabolism, 1990, 10:133–
135.
42. Prehn JHM, Krieglstein J. Platelet-activating factor antagonists reduce excitotoxic
damage in cultured neurons from embryonic chick telencephalon and protect the rat
hippocampus and neocortex from ischemic injury in vivo. Journal of neuroscience
research, 1993, 34:179–188.
43. Larssen RG, Dupeyron JP, Boulu RG. Modèles d’ischémie cérébrale expérimentale
par microsphères chez le rat. Étude de l’effet de deux extraits de Ginkgo biloba et du
naftidrofuryl. Thérapie, 1978, 33:651–660.
44. Rapin JR, Le Poncin-Lafitte M. Consommation cérébrale du glucose. Effet de l’extrait
de Ginkgo biloba. Presse medica, 1986, 15:1494–1497.
45. Le Poncin-Lafitte MC, Rapin J, Rapin JR. Effects of Ginkgo biloba on changes induced
by quantitative cerebral microembolization in rats. Archives of international
pharmacodynamics, 1980, 243:236–244.
46. Cahn J. Effects of Ginkgo biloba extract (GBE) on the acute phase of cerebral
ischaemia due to embolisms. In: Agnoli A et al., eds. Effects of Ginkgo biloba extract on
organic cerebral impairment. London, John Libbey, 1985:43–49.
47. Chatterjee SS. Effects of Ginkgo biloba extract on cerebral metabolic processes. In:
Agnoli A et al., eds. Effects of Ginkgo biloba extract on organic cerebral impairment.
London, John Libby, 1985:5–14.
48. Karcher L, Zagermann P, Krieglstein J. Effect of an extract of Ginkgo biloba on rat
brain energy metabolism in hypoxia. Naunyn-Schmiedeberg’s archives of pharmacology,
1984, 327:31–35.
49. Le Poncin-Lafitte M et al. Ischémie cérébrale après ligature non simultanèe des
artères carotides chez le rat: effet de l’extrait de Ginkgo biloba. Semaine hopitale Paris,
1982, 58:403–406.
50. Iliff LD, Auer LM. The effect of intravenous infusion of Tebonin (Ginkgo biloba) on
pial arteries in cats. Journal of neurosurgical science, 1982, 27:227–231.
51. Duverger D. Anoxie hypobare chez la souris avec les différents extraits de Ginkgo
biloba. Le Plessis Robinson, France, Institut Henri-Beaufour, 1989 (Report no. 1116/
89/DD/HK).
52. Duverger D. Anoxie hypobare chez la souris avec l’un des constituants de l’EGB:le
HE 134. Le Plessis Robinson, France, Institut Henri-Beaufour, 1990 (Report no. 1182/
90/DD/HK).
53. Krieglstein J, Beck T, Seibert A. Influence of an extract of Ginkgo biloba on cerebral
blood flow and metabolism. Life sciences, 1986, 39:2327–2334.
54. Beck T et al. Comparative study on the effects of two extract fractions of Ginkgo
biloba on local cerebral blood flow and on brain energy metabolism in the rat under hypoxia. In: Krieglstein J, ed. Pharmacology of cerebral ischemia. Amsterdam, Elsevier,
1986:345–350.
55. Krieglstein J, Oberpichler H. Ginkgo biloba und Hirnleistungsstörungen.
Pharmazeutische Zeitung, 1989, 13:2279–2289.
56. Oberpichler H et al. Effects of Ginkgo biloba constituents related to protection against
brain damage caused by hypoxia. Pharmacology research communications, 1988, 20:349–
352.
57. Lamor Y et al. Effects of ginkgolide B and Ginkgo biloba extract on local cerebral
glucose utilization in the awake adult rat. Drug development research, 1991, 23:219–
225.
58. Chatterjee SS, Gabard B. Effect of an extract of Ginkgo biloba on experimental
neurotoxicity. Archives of pharmacology, 1984, 325(Suppl.), Abstr. 327.
59. Otani M et al. Effect of an extract of Ginkgo biloba on triethyltin-induced cerebral
oedema. Acta neuropathology, 1986, 69:54–65.
60. Borzeix MG. Effects of Ginkgo biloba extract on two types of cerebral oedema. In:
Agnoli A et al., eds. Effects of Ginkgo biloba extract on organic cerebral impairment.
London, John Libbey, 1985:51–56.
61. Chatterjee SS, Gabard BL, Jaggy HEW. Pharmaceutical compositions containing
bilobalide for the treatment of neuropathies. US Patent no. 4,571,407 (Feb 18, 1986).
62. Sancesario G, Kreutzberg GW. Stimulation of astrocytes affects cytotoxic brain
oedema. Acta neuropathology, 1986, 72:3–14.
63. DeFeudis FV et al. Some in vitro and in vivo actions of an extract of Ginkgo biloba (GBE
761). In: Agnoli A et al., eds. Effects of Ginkgo biloba extract on organic cerebral impairment.
London, John Libbey, 1985:17–29.
64. Winter E. Effects of an extract of Ginkgo biloba on learning and memory in mice.
Pharmacology, biochemistry and behavior, 1991, 38:109–114.
65. Stange VG et al. Adaptationsverhalten peripherer und zentraler akustischer
Reizantworten des Meerschweinchens unter dem Einfluss verschiedener Fraktionen
eines Extraktes aus Ginkgo biloba. Arzneimittel-Forschung, 1976, 26:367–374.
66. Raymond J. Effets de l’extrait de Ginkgo biloba sur la préservation morphologique des
épithéliums sensoriels vestibulaires chez la souris. Presse médicale, 1986, 15:1484–
1487.
67. Denise P, Bustany P. The effect of Ginkgo biloba (EGb 761) on central compensation
of a total unilateral peripheral vestibular deficit in the rat. In: Lacour M et al., eds.
Vestibular compensation: facts, theories and clinical perspectives. Paris, Elsevier, 1989:201–
208.
68. Lacour M, Ez-Zaher L, Raymond J. Plasticity mechanisms in vestibular compensation
in the cat are improved by an extract of Ginkgo biloba (EGb 761). Pharmacology,
biochemistry and behavior, 1991, 40:367–379.
69. Vargaftig BB et al. Platelet-activating factor induces a platelet-dependent
bronchoconstriction unrelated to the formation of prostaglandin derivatives.
European journal of pharmacology, 1982, 65:185–192.
70. Vargaftig BB, Benveniste J. Platelet-activating factor today. Trends in pharmacological
sciences, 1983, 4:341–343.
71. Desquand S et al. Interference of BN 52021 (ginkgolide B) with the bronchopulmonary
effects of PAF-acether in the guinea-pig. European journal of pharmacology,
1986, 127:83–95.
72. Desquand S, Vargaftig BB. Interference of the PAF-acether antagonist BN 52021 in
bronchopulmonary anaphylaxis. Can a case be made for a role for PAF-acether in
bronchopulmonary anaphylaxis in the guinea-pig? In: Braquet P, ed. Ginkgolides, Vol.
1. Barcelona, JR Prous, 1988:271–281.
73. Braquet P et al. Involvement of platelet activating factor in respiratory anaphylaxis,
demonstrated by PAF-acether inhibitor BN 52021. Lancet, 1985, i:1501.
74. Költringer P et al. Die Mikrozirkulation und Viskoelastizität des Vollblutes unter Ginkgo biloba extrakt. Eine plazebokontrollierte, randomisierte Doppelblind-Studie.
Perfusion, 1989, 1:28–30.
75. Költringer P et al. Mikrozirkulation unter parenteraler Ginkgo biloba Extrakt-
Therapie. Wiener Medizinische Wochenschrift, 1989, 101:198–200.
76. Jung F et al. Effect of Ginkgo biloba on fluidity of blood and peripheral microcirculation
in volunteers. Arzneimittel-Forschung, 1990, 40:589–593.
77. Schaffler K, Reeh PW. Doppelblindstudie zur hypoxieprotektiven Wirkung eines
standardisierten Ginkgo-biloba-Präparates nach Mehrfachverabreichung an gesunden
Probanden. Arzneimittel-Forschung, 1985, 35:1283–1286.
78. Hofferberth B. Simultanerfassung elektrophysiologischer, psychometrischer und
rheologischer Parameter bei Patienten mit hirnorganischem Psychosyndrom und
erhöhtem Gefässrisiko—Eine Placebo-kontrollierte Doppelblindstudie mit Ginkgo
biloba-Extrakt EGB 761. In: Stodtmeister R, Pillunat LE, eds. Mikrozirkulation in Gehirn
und Sinnesorganen. Stuttgart, Ferdinand Enke, 1991:64–74.
79. Witte S. Therapeutical aspects of Ginkgo biloba flavone glucosides in the context of
increased blood viscosity. Clinical hemorheology, 1989, 9:323–326.
80. Artmann GM, Schikarski C. Ginkgo biloba extract (EGb 761) protects red blood cells
from oxidative damage. Clinical hemorheology, 1993, 13:529–539.
81. Ernst E, Marshall M. Der Effekt von Ginkgo-biloba-Spezialextrakt EGb 761 auf die
Leukozytenfilterabilität—Eine Pilotstudie. Perfusion, 1992, 8:241–244.
82. Rudofsky G. Wirkung von Ginkgo-biloba-extrakt bei arterieller Verschlusskrankheit.
Fortschritte der Medizin, 1987, 105:397–400.
83. Lagrue G, et al. Oedèmes cycliques idiopathiques. Rôle de l’hyperperméabilité
capillaire et correction par l’extrait de Ginkgo biloba. Presse médicale, 1986, 15:1550–
1553.
84. Gerhardt G, Rogalla K, Jaeger J. Medikamentöse Therapie von Hirnleistungsstörungen.
Randomisierte Vergleichsstudie mit Dihydroergotoxin und Ginkgo biloba-
Extrakt. Fortschritte der Medizin, 1990, 108:384–388.
85. Hopfenmüller W. Nachweis der therapeutischen Wirksamkeit eines Ginkgo biloba
Spezialextraktes. Arzneimittel-Forschung, 1994, 44:1005–1013.
86. Meyer B. Etude multicentrique randomisée a double insu face au placebo du
traitement des acouphènes par l’extrait de Ginkgo biloba. Presse medicale, 1986,
15:1562–1564.
87. Sprenger FH. Gute Therapieergebnisse mit Ginkgo biloba. Ärztliche Praxis, 1986,
12:938–940.
88. Witt U. Low power laser und Ginkgo-Extrakte als Kombinationstherapie. Hamburg,
Germany (unpublished document; available through NAPRALERT, see reference 5).
89. Coles RRA. Trial of an extract of Ginkgo biloba (EGB) for tinnitus and hearing loss.
Clinical otolaryngology, 1988, 13:501–504.
90. Fucci JM et al. Effects of Ginkgo biloba extract on tinnitus: a double blind study. St.
Petersberg, FL, Association for Research in Otolaryngology, 1991.
91. Holgers KM, Axelson A, Pringle I. Ginkgo biloba extract for the treatment of tinnitus.
Audiology, 1994, 33:85–92.