Marys Medicine

Rational medical therapy of vertigo

Dr Anirban Biswas
-neurotologist
Kolkata, India

 Cinnarizine??  Betahistine??  Prochlorperazine??  Dimenhydrinate??  Ginkgobiloba??  None of the above??  Psychotropic drugs??  Reassurance?? Anirban Biswas, neurotologist

 Provide symptomatic relief – taking care of the
inherent ill-effects of anti-vertigo drugs  Diagnose the cause of the vertigo and treat the cause
of the vertigo rather than merely suppress &
camouflage the symptom of vertigo

 Restore the deranged balance function
 Try to improve the neuronal metabolism, improve
cognition & correct any concomitant psychological /
cognitive disorder
Anirban Biswas, neurotologist

 Vertigo / imbalance is just a symptom or manifestation
of an underlying disorder; the causative pathology needs to be known for treatment  Symptomatic treatment with anti-vertigo drugs may relieve symptoms but will not cure the causative
disorder
 Objective of management is to correct the cause, (not
merely suppress the symptom) and to promote vestibular compensation  Sensory epithelium is non-mitotic; dead vestibular cells do not regenerate once damaged
Anirban Biswas, neurotologist
 Restoration of deranged balance function after the
vestibular labyrinth is damaged is possible only by
vestibular compensation which is a natural process
 Drugs that depress the CNS jeopardise the central compensatory mechanism and inhibit vestibular
 Peripheral vestibular disorders are usually self-limiting and
do not require perpetual /eternal drug therapy with vest
 Central disorders usually present with imbalance;
suppressing vestibular sensitivity by vestibular sedatives will aggravate the imbalance as CNS gets deprived of normal
vestibular input Anirban Biswas, neurotologist
• Vertigo / imbalance and psychogenic disorders are co-morbid conditions; the psychogenic part needs
effective management • Neurotropic agents / antioxidants / cognition enhancing drugs have a positive role in the
management of balance disorders Prolonged use of antivertigo drugs is hazardous and detrimental to the balance system; current recommendation for duration of therapy with antivertigo drugs is 3-5 days maximum 7 days Anirban Biswas, neurotologist
 BPPV  Vestibular neuritis  Migraine related vertigo Specific therapies exist for all of
 Phobic postural/ psychogenic vertigo  Labyrinthi and none require long
 Meniere's disease  Vestibu contd lar siez
non-ures
specific therapy with
 Sensory ataxia /posterior column lesions  Ototox vertigo drugs
 Central vertigo due to oculomotor or other CNS diseases like extrapyramidal disorders  …………… Anirban Biswas, neurotologist
Balance disorder patients are not just
---they have a lot of other problems
like irrational behaviour, poor concentration, forgetfulness
They have COGNITIVE deficits and show poor cognitive skills in the
domains of:-
- memory,
- concentration,
- arithmetic and reading
they also have psychological and emotional disorders
VERTIGO or IMBALANCE are just one of their many problems
A HOLISTIC MANAGEMENT is NEEDED
Vestibular sedatives -do they help or harm? Increasing cerebral & inner ear blood flow -does it really help in all patients? Exercises for vestibular compensation -does it have any role? Neurotropic agents and antioxidants - are they helpful ? Psychotropic drugs - any role to play? Anirban Biswas, neurotologist
-PROCLORPERAZINE -DIAZEPAM How do these drugs provide symptomatic relief ? - receptor blockage in cholinergic pathways - inhibiting vestibular nuclei - decreasing discharge rate in the vest nuclei - sedating the CNS All these processes INHIBIT the central vestibular compensatory mechanism sensory conflicts that increase vertiginous symptom enhances compensation
Anirban Biswas, neurotologist
Vestibular nuclei
Input from left and right vestibular system remains of
similar intensity (e.g. of size ‘50') under normal conditions
Anirban Biswas, neurotologist
Vestibular nuclei
More the difference between the 2 sides, more is the sensory conflict ; More the sensory conflict, more is the vertigo and better is the vestibular compensation Anirban Biswas, neurotologist
vestibular nuclei
Vestibular suppressants depress labyrinthine i.e. peripheral vestibular function bilaterally
Anirban Biswas, neurotologist
vestibular nuclei
Bilateral suppression reduces the difference between the intensity level of input between
the two sides(30 6) thereby providing temporary relief from vertigo.
However this reduces the sensitivity of the balance system and
inhibits compensation both of which are undesirable. Anirban Biswas, neurotologist
Providing symptomatic relief for the first few days suffices in most cases as these
peripheral vestibular disorders are self-limiting conditions; anti-vertigo drugs MUST be
discontinued after acute symptoms subside
and not continued eternally
The deranged balance function is naturally restored by the process of central vestibular compensation that can be enhanced and expedited by vestibular rehabilitation
Anirban Biswas, neurotologist
Advantages:- - ameliorates patient's physical distress of vertigo - & nausea/vomiting - relieves patient from severe mental distress & anxiety that accompanies the vertigo Disadvantages:- - camouflages the underlying disease which remains - jeopardises the natural process of VESTIBULAR COMPENSATION ingrained in our systems Anirban Biswas, neurotologist
 Is cerebral hypoxia the only cause of vertigo?? If not, then why use drugs to enhance cerebral blood supply in every pt. of vertigo ?? Do we need to increase cerebral / inner blood flow in a 30 yr old patient who has presented with acute vertigo and no other symptom ?? Anirban Biswas, neurotologist
only when  there is other evidence of cerebral hypoperfusion like dysarthria, dysphagia, other lower cranial nerve deficits as isolated acute vertigo is practically never
caused by vertebrobasilar insufficiency
 cerebral hypoxia may be the expected cause in aged vasculopathic subjects suffering from chronic vertigo along with other symptoms like dementia Excessive vasodilatation e.g., with Ca+ channel blockers causes dizziness, hypotension, headache, flushing, nausea etc …pg 836 Goodman &Gillman Anirban Biswas, neurotologist
 VESTIBULAR COMPENSATION is the mainstay of therapy in peripheral vestibular lesions  VESTIBULAR COMPENSATION is enhanced and facilitated by VESTIBULAR REHABILITATION THERAPY (VRT) which are exercises consisting of HEAD / BODY / EYE movements to increase sensory conflicts.  Recurrence of symptoms are often due to decompensation and not due to recurrence of disease, hence re-initiation of exercises is the recommended protocol for recurrence of symptoms  Even if drugs for symptomatic relief are used, only such drugs are to be chosen that do not inhibit vestibular compensation i.e., do not cause sedation / CNS depression -Cawthrone Cooksey exercises :- -Yogic asanas :- -Taichi exercises :- Anirban Biswas, neurotologist
1. PYRITINOL 200mg BD - enhances uptake & utilisation of glucose and O2 in CNS, -enhances cholinergic transmission & cerebral microcirculation 2. PIRACETAM 2.4gm daily. - improves microcirculation, - prevents neuronal hypoxia, - enhances neurotransmission -enhances cognition 3. ANTIOXIDANTS (ginkgobiloba), 120 mg daily -prevents oxidative damage in inner ear and brain tissues 1. Psychologic symptoms & psychiatric disorders are
common in patients of vertigo/imbalance - COMORBIDITY. 2. Vertigo/imbalance & psychiatric disorders co-exist as a result of neurological links between vestibular & autonomic systems- NEUROANATOMIC
3. Uncertainty of severity/timing of the attack & inefficiency of diagnosis/treatment leads to anxiety, helplessness,
panic disorders, agoraphobia,
somatisation, depression.
5. Vestibular disorder patients have very high incidence
of abnormality in psychometric test.

6. Better clinical outcome provided when psychotropic
drugs are combined with vestibular drugs in many
patients of vertigo.
7. Neuroanatomical connections have been established between vestibular and autonomic nervous systems.
Anirban Biswas, neurotologist
1. Psychologic responses to dizziness can RETARD recovery and start a Vicious circle of persistent dizziness and psychological disturbance each helping to perpetuate the 2. Dizziness becomes chronic in patients who react negatively 3. Anxiety & panic caused by the vertigo increases autonomic symptoms one of which is dizziness. Dizziness augments the autonomic symptoms. Anirban Biswas, neurotologist
Diazepam
4. Promethazine
5.
Cinnarizine
6. Betahistine
7.
Meclizine
8. Ginkgo biloba
 belongs to the phenothiazine group of antipsychotics – known to induce extrapyramidal disorders like PARKINSONISM, chorea, acute dystonia with oculogyric crisis, opisthotonus, torticollis etc.  pharmacologically recommended use is as an  has antihistaminic(H1), anticholinergic (muscurinic M1), antidopaminergic(D2) effects.  best drug for providing symptomatic relief in acute  vegetative features that accompany acute vertigo like nausea, vomiting are greatly relieved.  by blocking D2 receptors inhibits cortical arousal alertness level is reduced drowsiness ensues.  Because of its CNS depressant effects patient has to start vestibular exercises immediately such that inhibition of vestibular compensation can be counteracted by expediting compensatory mechanism through rehabilitation exercises.  Best avoided in patients presenting with INSTABILITY  Available as 5 mg tablets and 12.5mg/ml injection  A sublingual preparation is available .  If oral preparation can not be used because of severe nausea, a single injection of 12.5mg usually suffices.  A single oral dose of 5 to 10 mg is reasonably effective. If vomiting persists then 5mg TDS for 1 to 3 days (max-5days) may be used.  Extrapyramidal effects like acute dystonic reactions, oculogyric crises, pseudo parkinsonism and akathisia are the major drawbacks - more common in children and adolescents.  can also cause a life threatening condition called neuroleptic malignant syndrome  sublingual preparation sometimes causes local erosive cheilitis of lips and tongue (patient can swallow the tablet in such situation)  Hypotension, esp orthostatic hypotension can occur  anticholinergic effects are often distressing for the pt  Very effective/ best drug for symptomatic relief  Relieves both vertigo as well as nausea-vomiting  CNS depressant- hence very likely to inhibit vest. comp.  Significant side-effects: e.g. extrapyramidal reactions, hypotension, anticholinergic effects  Best used for a very short course to relieve acute
symptoms

 Provides good symptomatic relief  Increases blood supply to the brain and inner ear  Not known to have any teratogenic effect  Too many side-effects Anirban Biswas, neurotologist
 Anticholinergic- competitive antagonsit of histamine at H1 receptors and blocks cholinergic transmission not only in higher vest pathways but also other pathways  Antidopaminergic – blocks D2 receptors and block the release of dopamine  Ca- channel blocker- prevents entry of Ca-ions in the labyrinthine cells and in the smooth muscles of blood vessels  Anti-5HT properties – antagonises 5HT or serotonin which regulates GI motility and provides sense of wellbeing CINNARIZINE – mech of action Action of cinnarizine for relief of vertigo is exerted 1. CNS depression 2. Inhibition of vestibular labyrinth (thereby reducing sensory conflict) 3. Receptor blockage in histaminergic and cholinergic 4. Decreasing the discharge rate in vestibular nuclei + increases blood supply to the inner ear and brain, hence
helpful if vertigo is caused by hypoxia of brain/inner ear
 Available as 25 mg and 75 mg tablets  75 to 225mg tds for 5-7 days  Long continued use can induce undesirable Due to anticholinergic properties-
1 Xerostomia 2 Dry sore throat 3 Warm,blotchy,red skin due to decreased epidermal thermal dissipation 4. Increased body temperature 5. Mydriasis,photophobia 6. Cycloplegia-loss of accomodation 7. Diplopia 8. Increased intraocular pressure 9.Loss of coordination 10.Tremors 11.Tendency to be easily startled 12.Tachycardia 13.Urinary retention 14.Diminished bowel movement-sometimes paralytic ileus(via vagus) Due to anti-dopaminergic properties (due to
prevention of MgATP dependent production of electrochemical gradient-lowered level of dopamine in basal ganglia neurons) 1 ) Depresssion 2) Tremor 3) Muscle rigidity 4) Akathisia 5) Tardive dyskinesia 6) Drug induced Parkinsonism-due to its affinity for the D2 receptors in the stratum of brain Due to Ca channel blocking properties-affect
depolarization in SA and AV node and also affect AV conduction -a negative inotropic effect is produced in the cardiac cells. Pedal edema occurs as smooth muscles in vascular wall are prevented to contract Throbbing headaches occur commonly  labyrinthine sedative effect ; hence provides reasonably good symptomatic relief.  anti-vasoconstrictive effect  reduces slugging phenomenon of blood in narrow  stabilises vascular endothelium  Anticholinergic drug hence induces CNS depression  Side effects like pedal oedema, drowsiness, extrapyramidal symptoms like Parkinsonism/ tremor anticholinergic effects,  Provides symptomatic relief
 Increases blood flow to brain and inner ear
 Does not depress the CNS
 Only non-sedative antivertigo drug without any
anticholinergic and antidopaminergic effects

 Mechanism of action not very clear  Controversies in dosage (24-900mg/day) Anirban Biswas, neurotologist
Structural analogue of histamine Agonistic action on H1 receptors Antagonistic action on H3 receptors 1. Inhibition of labyrinth reducing sensory conflict 2. Decreasing discharge rate in vestibular nuclei 3. Increasing blood flow; esp in stria vascularis of inner ear which may have an effect in reducing endolymphatic hydrops 4. Claimed to enhance arousal and also expedite vestibular compensation Anirban Biswas, neurotologist
• The increased blood flow is due to its action both on H1 and H3 receptors • The much hyped H1 agonistic action is pretty weak-this action was observed only at levels which were 100 fold higher than therapeutic. • Moreover this action is negated by the antihistaminic group of drugs • However due to its H3 antagonistic effect ?some increase in vestibulo-cochlear blood flow may be possible  Betahistine has been shown to enhance vestibular compensation and facilitate recovery of balance function in a 1995 study by Tighilit et al  But this study was on cats and not a human study and dose used was 100 times the recommended therapeutic dose for humans. Anirban Biswas, neurotologist
 It has been claimed that betahistine enhances restoraton of vestibular function through central adaptation by activating central histaminergic system through a vestibular-hypothalamus-vestibular loop.  It induces excitatory effects on the neuronal activity at cortical and subcortical levels by activating H1 receptors. -Betahistine available as 1. Dihydrochloride. 2. Mesilate -Dose is controversial :-Therapeutic recommendation 32-72mg/day but some centers promote 600-900 mg/day in Meniere's disease. 5-7 days at 72mg/day for symptom control 2-3 mths at 96- ?? mg/day for confirmed MD  Different allergic and skin related side effects and hypersensitivity reactions like tingling, numbness, burning sensation, resp.distress can occur due to increased histamine level  To be used with caution in asthmatics and peptic ulcer pts as it is a mild H2 agonist and can enhance gastric secretion  Systemic administration causes peripheral vasodilatation and a fall in systemic blood pressure-so use of very high dose should be avoided.  Competitively antagonizes the actions of histamine at H1 receptors  Anticholinergic effects are lesser compared to other conventional antihistaminics  Sedation induced is minimal.  Anti emetic and antivertigo effects are as good as that of dimenhydrinate  Approved as OTC product by FDA hence safety profile is very good  No teratogenic effect.  Adverse effects are due to both anticholinergic and antihistaminic properties though very mild in nature.  Available as25 to 50 mg tablets.  Specially useful for various forms of motion sickness-has to be taken before undertaking the journey.  Reasonably good vestibular sedative with antiemetic properties  CNS depressant, likely to depress Vest. Comp mech  Does not increase cerebral / inner ear blood flow  Less pronounced anticholinergic activity hence much less side effects though as effective as other antihistamine anti vertigo drugs  Best used for symptomatic relief for 3-5 days
 Conventional antihistaminic with high anti-cholinergic activity.  Mechanism of action: inhibits spread of hyperactive vestibular input via MLF to centers for vegetative regulation in medulla -e.g-centers for heart rate, respiration, vomitting, sweating etc.  Thus very effective in acute vertigo with pronounced vegetative symptoms  Absence of extrapyramidal features is the biggest advantage of this antiemetic.  ADVERSE EFFECTS: Highly sedative-impairs psychomotor skill.Concomittant use of alcohol or other CNS depressant should thus be discouraged.  Best avoided in breastfeeding mothers  Better avoided in patients having enlarged prostate, glaucoma, emphysema, chronic bronchitis. – applies to other anticholinergics too  At very high doses it can affect colour discrimination, night vision, visual reaction time, stereopsis.  Available as 50 mg tablets  50-100 mg 3 to 4 times daily is the dose which should best not be exceeded.  3 to 5 days is usually sufficient for an optimal  A combination of Cinnarizine 20 mg and Dimenhydrinate 40 mg per tablet is now available- an effective and well tolerated treatment option.  CNS depressant, hence best discontinued as
soon as acute symptoms subside (3-5 days)

 antiemetic effect not associated with extra
pyramidal features

 very effective in acute vertigo with
pronounced vegetative symptoms

 tranquilising & anxiolytic effects  decreases resting activity of vestibular nuclei ; hence provides symptomatic relief  acts upon the reticular formation and limbic systems in the brain hence reduces concomitant anxiety  dramatic effects in psychogenic vertigo  CNS depressant – hence best avoided  Just one or two doses to control symptoms in very  Improves health of endothelium in blood vessels and hence increases transport through blood brain barrier  Improves arterial / venous tone in hypoxic areas  Decreases platelet agglutination  Inhibits oxygenated free radicals  Has to be continued for a minimum of three months  Does not provide relief in acute vertigo, but has been shown to
be effective in aged vasculopathic patients suffering from
chronic vertigo and instability due to central degenerative
-RESTRICT use of symptom relieving anti-vertigo drugs -TREAT the CAUSE of the vertigo which is just a symptom of some underlying disorder -EXPEDITE vestibular compensation through physical therapy as this is the only way to restore balance -TREAT the concomitant PSYCHOLOGICAL and COGNITIVE impairment for a complete recovery Anirban Biswas, neurotologist
Dr. Anirban Biswas Neurotologist Bellevue Clinic Kolkata Vertigo & Deafness Clinic Salt lake Kolkata http://www.dranirbanbiswas.com

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