Understanding & Managing Vertigo : Dr Vijay Sardana
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Transcript of Understanding & Managing Vertigo : Dr Vijay Sardana
UNDERSTANDING AND MANAGING VERTIGO
Vijay Sardana MD,DM
Professor & Head,Deptt. Of Neurology,
Medical College, Kota
Prevalence of Vertigo and Giddiness
5% of patients visiting the GP
10% of patients visiting the Otorhinolaryngologists
Life time prevalence-30%
3rd most common symptom
Vertigo Defination
Illusion of spinning sensation of self or Surroundings, usually due to disturbance of vestibular system
Vertigo:-Problems
Vertigo patients are nobody’s babyShunting between GPs, Physician, Neurologist, ENT specialist and psychiatrists.With or without investigations-it is vestibular Suppressant.Few dedicated physicians for vertigo.
What causes vertigo ?
Contradictory information from:
Vestibular, Visual & proprioceptive system
Causes of Dizziness
Types of Types of DizzinessDizziness
PatientsPatients
ExperienceExperience
Pathologic CausesPathologic Causes
VertigoVertigo Illusion of movement of Illusion of movement of
patients or Surroundingspatients or Surroundings Disturbance of peripheral or CNS Disturbance of peripheral or CNS pathways of vestibular systempathways of vestibular system
Syncope orSyncope or
PresyncopePresyncope
Impending loss of Impending loss of
consciousnessconsciousness
Cerebral perfusion of brain falls Cerebral perfusion of brain falls below a critical levelbelow a critical level
DisequilibriumDisequilibrium A sense of imbalanceA sense of imbalance Vestibular,Vestibular,
Proprioceptive,Proprioceptive,
Cereballer,VisiualCereballer,Visiual
III defined III defined dizzinessdizziness
EmotionalEmotional
disordersdisorders
Hyperventilation,Hyperventilation,
Anxiety, Depression,Anxiety, Depression,
Conversion reactionConversion reaction
VertigoNeuroanatomical & Neurochemical Basis
Glutamate-Vestibular nerve fibersAcetylcholine muscaranic recepters(m2)- pons & medullaGABA-Vestibular neuronsHistamine-diffusely in vestibular structures. -H1& H2 receptors- Pre & post synaptically on vestibular cells.
Vertigo - Mechanisms
Mechanism Known : -Migraine -Epilepsy -Meniere’s disease -Central causes
In most of case- no convincing scientific evidence of cause & mechanism.
Vertigo
Common “Peripheral Vertigo”
Benign positional vertigoVestibular neuronitisLabyrinthitisMeniers.s diseasePost traumatic vertigo
Vertigo
Central Vertigo
Vestibular portion of 8th nerve Vestibular nuclei within brain stem Central connections of vestibular nuclei- *Cerebellar Floccules *Visual sensory connections *Afferent from joint & tactile receptors
Vertigo Central Vertigo-Characteristics
Less common than peripheral & systemic causes. Vertiginous symptoms usually less common. Additional neurological science usually present. Vertigo as a sole manifestation rare.
Vertigo
Peripheral
Short duration Severe, often paroxysmal Accompanied by auditory symptoms Fatiguilibility. Reproducibility inconsistent
Central
• Chronic/Permanent• Less severe, Continuous• S/S of brain stem/ Cerebellum, Auditory less freq• No fatiguilibility• Reproducibility consistent
Vertigo
Peripheral
Nystagmus - Unidirectional - Horizontal-rotatory, Never vertical - Inhibited by visual fixation - Nystagmus with Vertigo Fall & past pointing- towards side of lesion
Central
Nystagmus - Uni/bidirectional - Horizontal-rotatory, vertical - Not inhibited - Sometimes only Nystagmus, no vertigo
-Veriable
Vertigo
Central Vertigo-Causes
Brainstem ischemia & infarction-VBI, infarction in territory of Int.auditory artery (collegen disorder), subclavian steel phenomenon. Demylinating diseases-MS, postinfection demylination CP angle tumors. Cranial neuropathy(isolated 8th nerv/multiple cranial nerves)-vasculitis, granulomatous dis(sarcoidosis), maningeal carcinomatosis.
Vertigo
Central Vertigo-Causes contd.-
Intrinsic Brainstem lesions. Other posterior fossa lesions- cerebellar infarct, haematoma Seizure disorder-CPS Migraine-Basilar artery migraine, migranous aura Degenerative heridofamilial-SCA-PSP Cervical Vertigo-Neck trauma, irradiation to upper cervical sensory roots, CVJ anomalies.
Vertigo
Common drugs producing vertigo Anticonvulsant -Barbiturates -Phenytoin -Carbamazepine Alcohol Salicylates Cinchona alkaloids-quinine Aminoglycosides Alkalyting agents
VERTIGO: Clinical evaluationVERTIGO: Clinical evaluation
Good historyGood history
- - To diagnose – 90% To diagnose – 90%
- bond/ relationship with patient- bond/ relationship with patient
Vertigo
Clinical Evaluation
Complete medical history Complete neurological examination esp. nystagmus 5th nerve including corneal reflux,7th,8th nerves, cerebellar signs & long tract signs Otological examination & related tests CT head/MRI EEG when indicated
Vertigo-Treatment
Specific treatment
Antimigraine drugs Antiepileptic drugs Salt restriction & diuretics in meniere’s disease
I Want…….
Fewer attacks every month When attacks occur they are not as bad as before When attacks occur they do not last long
Vertigo
Symptomatic Treatment-Goals
Elimination of vertigoVestibular supression Enhancement/non compromise of process of vestibular compensation Reduction of accompanying neurovegetative & psycho affective signs(nausea,vomiting,anxiety)Treatment of cause
Vertigo
Vestibular Suppression
Decrease in asymmetry in vestibular tone
Decrease in vestibular function in normal & abnormal side both
Vertigo Vestibular Suppressants Anticholinergics -Homatropine -Scopolamine(Hyoscine) Antihistamines -Diphenhydramine -Cyclizine -Dimenhydrinate -Meclizine -Hydrocyzine -Promethazine -Cinnarizine -Flunarizine Benzodiazepines -Diazepam -Lorazepam -Clonazepam
Vertigo
Vestibular Compensation
Plasticity of the CNS Sensory feedback (Vertigo) required for compensation 2 goals (decrease in vertigo and increase in compensation) often incompatible
Vestibular RehabilitationVestibular Rehabilitation AdaptationAdaptation
a phenomenon which helps a patient with persisting a phenomenon which helps a patient with persisting peripheral dysfunctional state to regain normal balance. peripheral dysfunctional state to regain normal balance.
HabituationHabituation
repeated exposure of the body to “mismatched “ sensory repeated exposure of the body to “mismatched “ sensory input.input.
CompensationCompensationa goal directed process induced by some recognized errors, a goal directed process induced by some recognized errors, directed towards its elimination directed towards its elimination
Norre M E, Crit. Rev. Phy. Rehab. Med., 1990, 2, 2, 101-120, Kirtane MV, Ind. J. Otolaryngol HNS, 1999, 51 (2), 27-36.
Norre M E, Crit. Rev. Phy. Rehab. Med., 1990, 2, 2, 101-120, Kirtane MV, Ind. J. Otolaryngol HNS, 1999, 51 (2), 27-36.
Vestibular compensationVestibular compensationRight labyrinth damagedRight labyrinth damaged Left Labyrinth Left Labyrinth
normal normal
Less electrical dischargeLess electrical discharge Normal electrical Normal electrical dischargedischarge
Imbalance between two sides- VertigoImbalance between two sides- Vertigo
Sensation of unequal inputs from two sides by CNSSensation of unequal inputs from two sides by CNS
Habituation and adaptation to the errorHabituation and adaptation to the error
possible wayspossible ways
increasing elect. discharge fromincreasing elect. discharge from Decreasing electrical discharge fromDecreasing electrical discharge from
damaged labyrinthdamaged labyrinth normal labyrinthnormal labyrinth
Not possibleNot possible Cerebellar Clamp or Vestibular shutdownCerebellar Clamp or Vestibular shutdown
Acute compensation by cerebellar clamp or Acute compensation by cerebellar clamp or vestibular shutdownvestibular shutdown
Cerebellum through connections with Vestibular nuclei induces Cerebellum through connections with Vestibular nuclei induces reduction in resting electrical discharge- cerebellum induced reduction in resting electrical discharge- cerebellum induced vestibular shutdownvestibular shutdown
Reduces inequality between electrical discharge between the two sides Reduces inequality between electrical discharge between the two sides by lowering electrical discharge of normal vestibular labyrinthby lowering electrical discharge of normal vestibular labyrinth
Advantages symptomatic relief of
vertigo in acute case
At rest, no vertigo
Advantages symptomatic relief of
vertigo in acute case
At rest, no vertigo
Disadvantage reduced vestibular sensitivity Inhibited vestibular system fails to
react normally to vestibular assault Sudden head movement leads to
vertigo
Disadvantage reduced vestibular sensitivity Inhibited vestibular system fails to
react normally to vestibular assault Sudden head movement leads to
vertigoChronic compensation is essential . Chronic compensation is essential .
Normal situationNormal situation
Right vestibuleRight vestibule equal Left vestibule equal Left vestibule
Right vestibular nucleiRight vestibular nuclei Left vestibular nuclei Left vestibular nuclei
VertigoVertigo
Right vestibule damagedRight vestibule damaged Left vestibule normal Left vestibule normal
Less electricalLess electrical normal electrical. normal electrical. DischargeDischarge discharge discharge
Right vestibular nucleiRight vestibular nuclei left vestibular nuclei left vestibular nuclei
Chronic compensation for vertigoChronic compensation for vertigo
Biswas A, Neurotological Diseases IN ‘An Introduction to neurotology”, 1998, 85-7.Biswas A, Neurotological Diseases IN ‘An Introduction to neurotology”, 1998, 85-7.
Right vestibule damaged Left vestibul normal
normal electrical discharge
Right vestibular nuclei Left vestibular nuclei
Right vestibule damaged Left vestibul normal
normal electrical discharge
Right vestibular nuclei Left vestibular nuclei
Chronic CompensationChronic Compensation
Chronic compensationChronic compensation
equal synapse equal
brain
equal synapse equal
brain
Chronic compensationChronic compensation
Inhibitory effect of cerebellum on vestibular nuclei is gradually removed Inhibitory effect of cerebellum on vestibular nuclei is gradually removed and requisite anatomical restructuring of central vestibular pathways and requisite anatomical restructuring of central vestibular pathways takes placetakes place
Cerebellum monitors afferent ( sensory) and efferent (motor) inputs Cerebellum monitors afferent ( sensory) and efferent (motor) inputs form the two sidesform the two sides
Vestibular nuclei on damaged vestibular side gets connected Vestibular nuclei on damaged vestibular side gets connected anatomically and functionally to vestibular nuclei on normal vestibular anatomically and functionally to vestibular nuclei on normal vestibular side.side.
Capacity of cerebellum to adapt to the affected or changed vestibular Capacity of cerebellum to adapt to the affected or changed vestibular scenario is called plasticity of CNS.scenario is called plasticity of CNS.
Chronic compensationChronic compensation
Whole compensatory mechanism controlled by CNS , mediated Whole compensatory mechanism controlled by CNS , mediated by cerebellum. Compensatory mechanism ineffective if by cerebellum. Compensatory mechanism ineffective if cerebellum malfunctioning, (Cerebellar degeneration)cerebellum malfunctioning, (Cerebellar degeneration)
If after the above compensatory mechanisms, still errors in If after the above compensatory mechanisms, still errors in vestibular functioning, corrected by other afferent such as vestibular functioning, corrected by other afferent such as propioceptive and visual system. propioceptive and visual system.
Central compensation initiated and enhanced by head movements- Central compensation initiated and enhanced by head movements- adaptation exercises and vestibular habituation therapyadaptation exercises and vestibular habituation therapy
..
Vastibular RehabilitationVastibular Rehabilitation
General PrinciplesGeneral Principles
Decrease centrally sedating or vestibular suppressant drugsDecrease centrally sedating or vestibular suppressant drugs Exercise must provoke vertigoExercise must provoke vertigo Initiate as early as possibleInitiate as early as possible Exercise should simulate real life situationsExercise should simulate real life situations Maintenance exercises to recurrence of symptomsMaintenance exercises to recurrence of symptoms
Vertigo
Agents affecting Vestibular Compensation-
Delayed Compes.- Barbiturates Benzodiazepines Antihistamines Neuroleptics
Accelerated compes.- Betahistines Flunarizine Ginkgo-biloba extract Caffeine
Vertigo-Pharmacological Treatment
Anticholinergics-
Homatropine and Scopolamine(Hyoscine) First drug to be used in Vertigo Non selective blocking all muscarinic receptor subtypes(m1 to m5) Adverse effects-Dry mouth, visual disturbences, constipation, memory disturbances cofusion, dysurea, glaucoma
Vertigo-Pharmacological Treatment
Antihistamines- H1 Blockers Mechanism- Poorly understand ? Antimuscaranic properties Cinnarizine and flunarizine-Ca channel blockers with significant H1 blocking effect H2 blockers- Not used Side effects- Sedation Duration of action- 4 to 12 hrs.
Vertigo-Pharmacological Treatment
Histaminergic Medication-
Betahistine
Mode of action
Betahistine Vascular EffectsVascular Effects
(in inner ear & brain)(in inner ear & brain)
Neurological EffectNeurological Effect
(in brain)(in brain)
Betahistine-Vascular Effects
H3 autoreceptor H3 autoreceptor AntagonistAntagonist
Inhibits autoregulationInhibits autoregulation
of histamine releaseof histamine release
Improve cochlear micro circulationImprove cochlear micro circulation
Improve cerebral/vertibrobasilar blood flowImprove cerebral/vertibrobasilar blood flow
H1 AgonistH1 Agonist
Betahistine-Neurological Effects
Regulates firing activity of Regulates firing activity of
Vestibular NucleiVestibular Nuclei
Blocks H3 ReceptorsBlocks H3 Receptors
Betahistine : Pharmacokinetics
Oral administration Rapid and complete absorption Mean plasma half-life : 3 to 4 hrs Complete excretion via urine in 24 hrs Very low plasma protein binding 2 inactive metabolites namely – Pyridylacetic acid & 2-(2-aminoethyl) pyridine have been found
Betahistine : Tolerability
minimal side effects No sedation Low level of gastric side effects No anticholinergic effcts No extrapyrimidal side effects
Betahistine : Contraindication
Hypersensitivity to Betahistine Pheochromocytoma
Betahistine : Special Precautions
Use with antihistamines Patients with bronchial asthma Patients with peptic ulcers
Vertigo-Pharmacologic treatment
Acetylleucine
Mechanisms -? Precursors of neuromediator- peptidic- Activation of vestibular afferent -? Anti calcium properties May enhance compensation IV / Oral
Vertigo-Pharmacologic treatment
Antidopaminergic Drug
Block dopaminergic receptors in area postrema of the brainstem,has anticholinergic and antihistaminic(H1) activity Neuroleptics neurovegetative symptoms psychoeffective symptoms
- Phenothiazine derivatives - Butyrophenones - Benzamides Domperidone & Metochlopramide
Adverse effects- Ortho.hypotension, Somnolence,Extrapyramidal syndrome,
anticholinergic side effects; NMS
Vertigo-Pharmacologic treatment
Benzodiazepines
GABA modulators – act centrally to suppress vestibular response May impair vestibular compensation Anxiolytic effect
Vertigo-Pharmacologic treatment
Calcium Antagonist
Cinnaizine(1966) Cinnaizine(1966) Flunarizine(1985) Flunarizine(1985)
MechanismMechanism
? ? Vestibular hair cells Vestibular hair cells endowed with ca endowed with ca channelschannels
--H1 antihistamnic propertiesH1 antihistamnic properties
-Sedative-Sedative
-Antidoaminergic action-Antidoaminergic action
Adverse effects : Short term-Sedation,Weight gain Long term-Depression,Parkinsonism
Vertigo-Pharmacologic treatment
Miscellaneous
Ginkgo biloba Piribidil- Dopaminergic agent Ondansatron 5 HT3 antagonist
To treat Vertigo A Physician needs a drug which…….
Has Effect on cochlear & cerebral blood flow Regulates vestibular nuclei firing Offers symptomatic & prophylactic therapy Does not interfere with compensation mechanism Does not cause drowsiness
Vertigo-Pharmacologic treatment
Worldwide trends-
US – Benzodiazepines Meclizine France – Acetylleucine Flunarazine India - Cinnarizine Betahistine
Vertigo- Treatment
General Comments
It is difficult to set out rational & well documented rules for administration of drugs.
Clinical pharmacology of anti vertigo drugs complex. Clinical trials reliability? Spontaneous recovery-Placebo control trials
When to refer a Specialist
Serious vertigo which is disabling Vertigo lasting longer then 4 weeks Hearing loss CNS or psychological disorder
Vertigo- Treatment
General Guidelines
Acute disabling vertigo should be treated Mild vertigo may be left alone “Omnious” vertigo should be investigated Treatment period should be shortest possible Lengthy confusing prescriptions should be avoidedVestibular rehabilitation should be used early
Vertigo
Concluding Remarks-
Our habits of ant vertigo prescription are empirical and insufficiently evaluated
Improvement in practice of clinical pharmacology for vertigo is needed
New treatment may emerge from research in receptor subtypes, neuromodulators and agents affecting central compensation.
Vestibular rehab. Is underutilized
Thanks