|Year : 2018 | Volume
| Issue : 3 | Page : 196-200
Role of Ginkgo biloba for controlling residual dizziness after successful treatment of benign paroxysmal positional vertigo: Our experiences at a tertiary care teaching hospital of Eastern India
Santosh Kumar Swain1, Ishwar Chandra Behera2, Mahesh Chandra Sahu3
1 Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India
2 Department of Community Medicine, IMS and SUM Hospital, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India
3 Department of Medical Research Laboratory, IMS and SUM Hospital, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India
|Date of Web Publication||20-Jul-2018|
Prof. Santosh Kumar Swain
Department of Otorhinolaryngology, IMS and SUM hospital, Siksha “O” Anusandhan (Deemed to be University), K8, Kalinganagar, Bhubaneswar-751003, Odisha
Source of Support: None, Conflict of Interest: None
OBJECTIVES: Canalith repositioning therapy (CRP) is usually effective treatment in benign paroxysmal positional vertigo (BPPV). However, still, some patients present residual dizziness after successful and effective repositioning maneuver. The objective of this study was to evaluate the therapeutic effect of Ginkgo biloba extract on residual dizziness after canalith repositioning maneuver in patients of BPPV. G. biloba is a phytomedicine which enhances the blood supply to inner ear and brain.
MATERIALS AND METHODS: Ninety-two patients with BPPV were divided into two treatment groups, Ginkgo biloba group and Non-Ginkgo biloba group. In this prospective study, the Ginkgo biloba group received the similar CRP as the non-Ginkgo biloba group, with addition of G. biloba treatment after CRP. The duration of residual dizziness of Ginkgo biloba group and non-Ginkgo biloba group were compared. The scores of dizziness handicap inventory of these two groups were also compared.
RESULTS: The duration of residual dizziness of Ginkgo biloba group was shorter than non-Ginkgo biloba group. There were no significant differences in the dizziness handicap inventory scores in the 1st week, whereas many significant differences in 2nd, 3rd, 4th, 5th, 6th, 7th, and 8th weeks.
CONCLUSION: This study demonstrates that G. biloba can significantly minimize the residual dizziness after successful therapy with repositioning maneuver in patients of BPPV.
Keywords: Benign paroxysmal positional vertigo, Epley's maneuver, Ginkgo biloba, residual dizziness
|How to cite this article:|
Swain SK, Behera IC, Sahu MC. Role of Ginkgo biloba for controlling residual dizziness after successful treatment of benign paroxysmal positional vertigo: Our experiences at a tertiary care teaching hospital of Eastern India. Int J Health Allied Sci 2018;7:196-200
|How to cite this URL:|
Swain SK, Behera IC, Sahu MC. Role of Ginkgo biloba for controlling residual dizziness after successful treatment of benign paroxysmal positional vertigo: Our experiences at a tertiary care teaching hospital of Eastern India. Int J Health Allied Sci [serial online] 2018 [cited 2019 Jan 18];7:196-200. Available from: http://www.ijhas.in/text.asp?2018/7/3/196/237256
| Introduction|| |
Benign paroxysmal positional vertigo (BPPV) is characterized by brief periods of vertigo triggered by changing head position relative to gravity. It is the most common peripheral vestibular disorder, accounting for one-third of vestibular diagnosis in the population. Its incidence varies between 11 and 64 cases/100,000 populations. It is common in the age between 50 and 55 years in idiopathic cases  It is more commonly seen in older ages because of the degeneration of statoconia, arising from demineralization, shown in histopathology studies. The mechanism for BPPV is that otoconia which are derived from the macula, moves into the endolymph of semicircular canal. Otoconia is the small calcium carbonate particles, which makes a change of the flow of endolymph in the semicircular canal, cause excitability of vestibular receptors. Nystagmus in BPPV may be torsional, vertical, or horizontal and is characterized by findings such as latency, crescendo and decrescendo, transience, reversibility, and fatigability. Although in most cases of BPPV, the posterior canal is affected, BPPV of the horizontal canal, ranging from 5% to 30% and more rarely anterior canal involved. The main diagnostic test for the posterior canal BPPV is the Dix–Hallpike test, which aims to trigger the labyrinthine symptom or sign such as vertigo, nausea, and/or nystagmus. Anterior/superior canal BPPV produces bilaterally positive Dix–Hallpike test. BPPV is often associated with vestibular neuritis, vertebrobasilar insufficiency, chronic otitis media, and following ear surgery. BPPV is often misdiagnosed by clinician and sometimes overinvestigated. BPPV was first described by Barany in the literature in 1921. He attributed this lesion with otolithic organs. Dix and Hallpike in 1952 first performed provocative positional testing which was named in their honor. The main treatment of BPPV is to reposition the otoconia by liberating maneuvers or Brandt–Daroff exercises. Anti-vertigo drugs and antiemetic drugs are useful in acute episode of vertigo; these are not effective for BPPV patients.Ginkgo biloba decrease the blood viscosity, improve the microcirculation, and acts as antioxidant. It also increases the central compensation in experimental animals. This study showed similar efficiency of G. biloba extract EGb 761 as beta-histine for controlling vertigo. Beta-histine increases the quality of life by improving the recovery rate of vertigo by improving the microcirculation to the labyrinth. Although the repositioning maneuvers are effective in improving the vertigo in BPPV, some patients still complain some kind of residual dizziness. The aim of this study was to evaluate the role of G. biloba on residual dizziness after successful particle repositioning treatment in patients of BPPV.
| Materials and Methods|| |
This is a prospective study, and it was a parallel-group, open-label, clinical trial, comparing a patient group treated with G. biloba extract with an untreated control group. It was carried out at a tertiary care hospital of Eastern India. This study was approved by Institutional ethics committee in December 2012. A total of 92 patients were participated during this study period and all are followed up by December 2017. All 92 patients were randomized into two groups, Ginkgo biloba group and non-Ginkgo biloba group, each group comprising 46 patients. The Ginkgo biloba group treated with same canalith repositioning therapy (CRP) as non-Ginkgo biloba group. The G. biloba therapy was started after CRP. In Ginkgo biloba group, G. biloba (leaf extract available as tablet form) was given orally in the dose of 40 mg thrice daily for 3 weeks (Micro Labs, manufactures of Ginkoba Tablet were used). All patients of BPPV were followed up till complete resolution of dizziness which was known by interviews at the outpatient department of vertigo clinic or by telephonic conversation. In addition to above smoking and alcohol were strictly avoided by the patients during our study period.
Inclusion and exclusion criteria
Inclusion criteria in our study were first diagnosis of BPPV, healthy person with no history of vestibular disorder and vertigo, unilateral posterior semicircular canal BPPV, time interval between onset of vertigo to treatment of <1 week, residual dizziness after proper and successful repositioning treatment, and patient should not have any systemic diseases such as diabetes, hyperlipidemia, and cerebrovascular diseases. The exclusion criteria were past history of any vertigo; history of migraine; history of head trauma; history of vascular diseases; history of concomitant treatment with anti-vertigo drugs, antiplatelet drugs, diuretics, corticosteroids, benzodiazepines; and patients with central nervous diseases or terminal conditions.
The detail clinical history and physical examinations were done among all patients and Dix–Hallpike test was also done for confirming the diagnosis. In this study, only canalolithiasis type of BPPV and posterior canal type were included. The diagnosis of BPPV was based on symptoms such as transient attacks of rotational vertigo induced by changing head position without any hearing loss or tinnitus; positional vertigo and nystagmus induced by Dix–Hallpike maneuver. The Epley's maneuver was performed only one time and in those vertigo and nystagmus disappeared were selected in this study. After Epley's maneuver, all patients were requested to avoid sudden head movement to affected side. Statistical analysis was conducted using software SPSS 20 version (IBM, Armonk, New York, United States) with help of Student's t-test and Chi-square test for comparing the data.
The steps of Dix–Hallpike test are depicted in [Figure 1]. They are described as follows: patient sits upright on an examination table and head is turned to one side by 45° and then briskly taking head backward and down with head hanging position at 30° on the back of the table. If patient is using spectacles, it should be removed before starting maneuver. Patient is advised not to close the eyes during procedure and examiner should wait approximately 20–30 s for seeing the nystagmus. If there was no nystagmus, the patient will sit up and similar procedure is repeated with head turned to opposite side by 45°.
The steps of Epley's maneuver are depicted in [Figure 2]. They are described as follows: position 1: Patient sits on the examination couch and head turned toward affected ear by 45° and then patient rapidly brought downward in head hanging position. Then, nystagmus appears after 20–30 s which is called as latent period. Head will stay in this position till the nystagmus disappears; position 2: Head is turned to unaffected side and keep for 2 min in this position; position 3: The whole body and head are turned away from the affected ear to a lateral recumbent position and wait for 2 min; position 4: Patient is come to the sitting position with head turned away from the affected side by 45° and wait for 2 min; position 5: In sitting position, patient brings his face forward with chin 20° downward and wait for 2 min.
| Results|| |
All the patients of BPPV included in this study strictly obeyed the inclusion and exclusion criteria. Residual dizziness: after successful canalith repositioning maneuver, residual dizziness occur which is characterized by vertigo or lightheadedness or unsteadiness. Basic characteristic of two groups (Ginkgo biloba and non-Ginkgo biloba) such as age and gender showed no significant differences [Table 1]. The duration of residual dizziness after successful repositioning maneuver were quantified. It showed that there were much significant differences in the duration of residual vertigo between Ginkgo biloba group (10.11 days) and non-Ginkgo biloba group (28.32 days). The duration of residual dizziness of Ginkgo biloba group was shorter than non-Ginkgo biloba group (P = 0.0001). The details of duration of residual dizziness of above two groups are given in [Table 2]. The dizziness handicap inventory of two groups was also compared [Table 3]. It showed that there were no significant differences in the scores of dizziness handicap inventory in first 7 days of two groups. There were significant differences in the 2nd, 3rd, 4th, 5th, and 6th weeks. The result showed that G. biloba improves the residual dizziness after successful CRP in patients with BPPV.
| Discussion|| |
The patients treated in the study with G. biloba extract recovered faster than those of the non-Ginkgo biloba group. BPPV is the most common etiology for peripheral vertigo, characterized by short repeated episodes of mild-to-severe vertigo induced by changing the head position and accompanied with imbalance and nausea. Often BPPV is idiopathic in nature, but it may also result from head trauma, vertebrobasilar insufficiency, vestibular neuritis, otological surgery, endolymphatic hydrops, or middle ear pathology. The clinical manifestations in BPPV are due to undue presence of calcium carbonate particles in the labyrinth, which are statoconia arising from the utricle, which is the etiological explanation when particles adhere to the cupula of the semicircular canal, whereas canalithiasis is the explanation when free-floating particles are present in the semicircular canal, rather than fixed to the cupula. Cupulolithiasis describes the otoconia particles adherent to the cupula of semicircular canal. Patients of BPPV shows impaired balance system and damaged vestibule. The damaged vestibule is the etiopathology for causing residual dizziness after successful Epley's maneuver. There are different explanations for residual dizziness after successful maneuver as follows: the remaining otolithic debris is inadequate to deflect the cupula to sufficient amount for provoking vertigo and nystagmus; otolithic dysfunction, which is the cause of BPPV, might account for transient episodes dizziness; some hidden vestibular lesions which are not diagnosed from history may coexist with BPPV; and central adaptation after canalith repositioning maneuver may need longer time for resolution. Dix–Hallpike maneuver is considered as gold standard for the diagnosis of BPPV. There are different treatment modalities for BPPV. These are vestibular habituation exercises, vestibular sedative drugs, surgical ablation of the posterior semicircular canal, and repositioning maneuvers. The canalith repositioning maneuvers which is more commonly adopted for treating BPPV. The most commonly known maneuver for treatment of BPPV is Epley's maneuver which gives rise to improvement of vertigo. Epley's maneuver is also called as canalith repositioning maneuver which involves a five position cycle where the patient's head is moved in such a way to displace any loose materials inside the posterior semicircular canal into the utricle of the labyrinth. After successful repositioning maneuver, the vertigo and nystagmus of patients with posterior canal BPPV are disappeared, but postural instability persists. The oxidative degeneration is the basic pathophysiology for vestibular diseases such as ototoxicity, acoustic trauma, and endolymphatic hydrops. This oxidative damage may also the cause for vestibular lesion like BPPV. There is a consensuses that beta-histine dihydrochloride is useful in the treatment for controlling vertigo of BPPV patients. Beta-histine has an affinity for histamine H1 and H2 receptors. Histamine increases the spike discharge of the afferent neural fibers of semicircular canal. Histamine receptors are located in the vestibule which regulates the intracellular Ca+. Beta-histine dihydrochloride cause significant reduction of excitation due to histamine and decrease the spike discharge of vestibular hair cells. Beta-histine also increases the microcirculation and relieve endolymphatic fluid pressure. The G. biloba is a phytomedicine having antioxidant property and enhances the microcirculation to the inner ear and brain. There are two active pharmacological components present in the G. biloba leaf extract: flavonoids and terpenoids. Flavonoids in the G. biloba leaf are flavonols, flavones, tannins, biflavones, and associated glycosides of quercitin and kaempferol. These active components act as antioxidants or free radicals scavengers, enzyme inhibitors, and cation chelators. There are two types of terpenoids present in the G. biloba extract: Ginkgolides and bilobalide. Ginkgolides are diterpenes with five types A, B, C, J, and M, where type A, B, and C are around of 3.1% of the total G. biloba leaf extract. Bilobalide accounts for rest 2.9% of the total G. biloba extracts (EGb 761).G. biloba extract (EGb 761) increase the vestibular and cerebral blood flow by lowering the blood viscosity. It also enhances the neuronal plasticity as well as mitochondrial functions and energy metabolism prevents from the oxidative damage of neurons. The efficiency of G. biloba extract (EGb 761) for treating vestibular and nonvestibular vertigo have been proven by randomized, placebo-controlled trials and effective as most commonly prescribed drug like beta-histine. Our study demonstrated that G. biloba enhanced the recovery from residual dizziness after successful treatment with repositioning maneuver. This property may be due to antioxidant activity and enhanced microcirculation to the inner ear and brain. In routine clinical practice, clinician or health-care providers should know the BPPV and its management. They often misdiagnosis the disease and delay the treatment. The health-care providers always remember BPPV is the most frequent cause of dizziness which occur during changing head position and should be treated with repositioning maneuver and advised to give G. biloba for preventing recurrence.
| Conclusion|| |
BPPV is the most common cause for peripheral vertigo. These patients are frequently encountered in Vertigo Clinic. In this study, it was revealed that significant differences in the duration of residual vertigo between Ginkgo biloba group (10.11 days) and non-Ginkgo biloba group (28.32 days). The main constituents of G. biloba are flavonoids and terpenoids. The improvement of microcirculation and antioxidant property of the G. biloba may be the cause to control residual dizziness after c repositioning maneuver in BPPV patients. It cannot be concluded from the results of this study that the findings also apply to other Ginkgo extracts.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Helminski JO, Zee DS, Janssen I, Hain TC. Effectiveness of particle repositioning maneuvers in the treatment of benign paroxysmal positional vertigo: A systematic review. Phys Ther 2010;90:663-78.
von Brevern M, Radtke A, Lezius F, Feldmann M, Ziese T, Lempert T, et al.
Epidemiology of benign paroxysmal positional vertigo: A population based study. J Neurol Neurosurg Psychiatry 2007;78:710-5.
Maia RA, Diniz FL, Carlesse A. Manobras de reposicionamento no tratamento da vertigem paroxística posicional benigna. Rev Bras Otorrinolaringol 2001;67:612-6.
Alvarenga GA, Barbosa MA, Porto CC. Benign paroxysmal positional vertigo without nystagmus: Diagnosis and treatment. Braz J Otorhinolaryngol 2011;77:799-804.
Walther LE, Westhofen M. Presbyvertigo-aging of otoconia and vestibular sensory cells. J Vestib Res 2007;17:89-92.
Korres SG, Balatsouras DG. Diagnostic, pathophysiologic, and therapeutic aspects of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 2004;131:438-44.
De Stefano A, Dispenza F, Suarez H, Perez-Fernandez N, Manrique-Huarte R, Ban JH, et al.
A multicenter observational study on the role of comorbidities in the recurrent episodes of benign paroxysmal positional vertigo. Auris Nasus Larynx 2014;41:31-6.
Uno A, Moriwaki K, Kato T, Nagai M, Sakata Y. Clinical features of benign paroxysmal positional vertigo. Nihon Jibiinkoka Gakkai Kaiho 2001;104:9-16.
Balatsouras DG, Koukoutsis G, Ganelis P, Korres GS, Kaberos A. Diagnosis of single- or multiple-canal benign paroxysmal positional vertigo according to the type of nystagmus. Int J Otolaryngol 2011;2011:483965.
Barany R. Diagnose von Krankheitserscheinungen im bereiche des otolithenapparates. Acta Otolaryngol 1921;2:434-7.
Patangay KK, Ansari R. Benign paroxysmal positional vertigo: Our experience. Indian J Otolaryngol Head Neck Surg 2016;68:39-41.
Bhattacharyya N, Gubbels SP, Schwartz SR, Edlow JA, El-Kashlan H, Fife T, et al.
Clinical practice guideline: Benign paroxysmal positional vertigo (Update). Otolaryngol Head Neck Surg 2017;156:S1-47.
Luo Y. Alzheimer's disease, the nematode Caenorhabditis elegans
, and Ginkgo biloba
leaf extract. Life Sci 2006;78:2066-72.
Hamann KF. Special ginkgo extract in cases of vertigo: A systematic review of randomised, double-blind, placebo controlled clinical examinations. HNO 2007;55:258-63.
Soto E, Chávez H, Valli P, Benvenuti C, Vega R. Betahistine produces post-synaptic inhibition of the excitability of the primary afferent neurons in the vestibular endorgans. Acta Otolaryngol Suppl 2001;545:19-24.
Seok JI, Lee HM, Yoo JH, Lee DK. Residual dizziness after successful repositioning treatment in patients with benign paroxysmal positional vertigo. J Clin Neurol 2008;4:107-10.
Bhattacharyya N, Baugh RF, Orvidas L, Barrs D, Bronston LJ, Cass S, et al
. linical practice guideline: benign paroxysmal positional vertigo. Otolaryngology-Head and Neck Surgery 2008;139 suppl 5:47-81.
Caldas MA, Ganança CF, Ganança FF, Ganança MM, Caovilla HH. Clinical features of benign paroxysmal positional vertigo. Braz J Otorhinolaryngol 2009;75:502-6.
Di Girolamo S, Ottaviani F, Scarano E, Picciotti P, Di Nardo W. Postural control in horizontal benign paroxysmal positional vertigo. Eur Arch Otorhinolaryngol 2000;257:372-5.
von Brevern M, Schmidt T, Schönfeld U, Lempert T, Clarke AH. Utricular dysfunction in patients with benign paroxysmal positional vertigo. Otol Neurotol 2006;27:92-6.
Stambolieva K, Angov G. Postural stability in patients with different durations of benign paroxysmal positional vertigo. Eur Arch Otorhinolaryngol 2006;263:118-22.
Watanabe K, Inai S, Hess A, Michel O, Yagi T. Acoustic stimulation promotes the expression of inducible nitric oxide synthase in the vestibule of guinea pigs. Acta Otolaryngol Suppl 2004;553:54-7.
Maslovara S, Soldo SB, Puksec M, Balaban B, Penavic IP. Benign paroxysmal positional vertigo (BPPV): Influence of pharmacotherapy and rehabilitation therapy on patients' recovery rate and life quality. NeuroRehabilitation 2012;31:435-41.
Laurikainen E, Miller JF, Pyykkö I. Betahistine effects on cochlear blood flow: From the laboratory to the clinic. Acta Otolaryngol Suppl 2000;544:5-7.
DeFeudis FV, Drieu K. Stress-alleviating and vigilance-enhancing actions of Ginkgo biloba
extract (EGb 761). Drug Dev Res 2004;62:1-25.
Smith JV, Luo Y. Studies on molecular mechanisms of Ginkgo biloba
extract. Appl Microbiol Biotechnol 2004;64:465-72.
Huang S, Jeng C, Kao S, Yu JJ, Liu D. Improved haemorrheological properties by Ginkgo biloba
extract (Egb 761) in type 2 diabetes mellitus complicated with retinopathy. Dtsch Arztebl Int 2004;23:615-21.
Abdel-Wahab BA, Abd El-Aziz SM. Ginkgo biloba
protects against intermittent hypoxia-induced memory deficits and hippocampal DNA damage in rats. Phytomedicine 2012;19:444-50.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3]