Syncope and Vertigo for healthcare professionals

Presentation on syncope and vertigo

1. SYNCOPE and VERTIGO

2. DIZZINESS "Dizziness” refers to various abnormal sensations relating to perception of the body's relationship to space. Patients may also use the term for other sensations such as visual distortion, nonspecific disorientation and anxiety. SYMPTOMS DESCRIPTION DURATION ASSOCIATED SYMPTOMS GENERAL MECHANISM LIGHTHEADEDNESS (PRESYNCOPE) Transcient slowed consciousness, faintness, can progress to LOC (syncope) Seconds to minutes Warmth, visual changes Global transient cerebral hypoperfusion Vertigo Illusion of motion while stationary (spinning sensation Seconds to weeks nausea Vestibular pathway disruption

3. Syncope Definition Components of syncope Abrupt, transient loss of consciousness Loss of postural tone Brief duration Complete and spontaneous recovery The mechanism must involve global impairment of cerebral blood flow

4. Prodrome - Presyncope - Constellation of lightheadedness, nausea, Diaphoresis and/or visual disturbance Preceding the loss of consciousness lasting for several seconds to minutes Prodrome without subsequence loss of consciousness

5. Major categories of syncope – Neurally mediated syncope Orthostatic syncope Cardiac syncope

6. Physiology

7. Pathophysiology The transient failure of baroreflex leads to neurally mediated syncope Chronic failure leads to orthostatic Syncope Global cerebral hypoperfusion

8. Syncope represent a failure of cerebral blood flow autoregulatory mechanisms Cerebral blood flow autoregulatory response – Cerebral blood flow ranges from 50 - 60 ml/ min per 100 g of brain tissue Remains constant over perfusion pressure ranging from 50 – 150mmhg Latency period is 5-10 s

9. Loss consciousness – cessation of blood flow for 6-8 s Impairment of consciousness – blood flow less than 25 ml/min per 100 g brain tissue Cerebral blood autoregulation fails and syncope occurs - if systolic blood pressure is less than 50 mmhg EEG changes in syncope subjects – shows 2 patterns Slow - flat - slow pattern Slow pattern Syncopal attacks can have presence of myoclonic jerks during the slow period of EEG but seizure discharges are absent in EEG

10. Classification Neurally mediated syncope – Also called vasovagal syncope or reflex syncope Heterogenous collection of etiologies – dysfunctional response of the autonomic nervous system in response to normal stimuli

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12. Orthostatic Syncope/hypotension Reduction of SBP of at least 20 mmHg or DBP of atleast 10 mmHg after 3 mins of standing or head up tilt on a tilt table Sympathetic vasoconstrictor (autonomic) failure Characteristics: 1. pre syncopal symptoms to sudden postural changes 2. Coat hanger headache – neck pain in the suboccipital, posterior cervical and shoulder region 3. Supine hypertension

13. Orthostatic hypotension/syncope Primary autonomic failure – idiopathic central and peripheral neurodegenerative disease Parkinson’s disease Lewy body dementia Pure autonomic failure Multiple system atrophy Secondary autonomic failure – autonomic peripheral neuropathies Diabetes Amyloidosis – hereditary, primary HIV neuropathy Volume depletion Iatrogenic (alpha blockers, Nitrates, TCA antidepressants) Synucleinopathies – due to aggregation of alpha – synuclein in cytoplasm of neurons

14. Cardiac syncope By arrhythmias and structural heart disease History of complete absence of prodrome symptoms Cardiac syncope Bradyarrhythmias Sinus node dysfunction ( SA block) AV block ( mobitz type 2, complete AV block) Tachyarrhythmias - Ventricular tachycardia Inherited channelopathies Long QT syndrome (k+ channel encoding gene mutation) Brugada syndrome (Na + channel encoding gene mutation) Drug induced QT prolongation (antipsychotics, antidepressants, antiarrhythmics) Structural disease – valvular disease (Aortic stenosis) hypertrophic cardiomyopathy

15. Syncope mimics to be differentiated: Seizure Cerebrovascular syncope – vertebrobasilar insufficiency subclavian steel syndrome Alcohol blackouts Drugs (sedatives and hypnotics) Psychogenic pseudosyncope Hypoglycemia

16. Approach to Syncope History – No. of episodes and duration of episodes Presence of prodrome symptoms Injury sustained during fall Duration of confusion post LOC episode Witness of events

17. Duration of loss of consciousness > 5 mins unlikely syncope Consider: Drug side effects Alcohol blackout OSA related hypersomnolence Were the following features present? Tonic- clonic movements during LOC Bladder/bowel incontinence Post event confusion lasting more than few minutes Yes Probable seizure Probable syncope < 5 mins No

18. Syncope Seizure Preceded by lightheadedness, nausea, diminution of vision Preceded by AURA Movement – if present, myoclonic jerks starts after LOC and lasts < 15 secs Abnormal jerky movements before, lasts more than 15 secs Brief period (secs) of confusion after resolution Post ictal confusion lasts long Absent Associated tongue bite, strenuous breathing and urinary incontinence is present

19. Neurally mediated syncope Orthostatic syncope Cardiogenic syncope Precipitants Clearly identifiable triggers Precipitated by moving from lying/ sitting to standing position Precipitated by exertion Prodrome Present Present Present or absent Injury during fall Uncommon Uncommon Common Age of onset Typically younger Typically older Typically older Notable risk factors None Parkinson’s disease, diabetes, alcoholism, Heart failure, CAD, family history of sudden cardiac death Relevant examination None Orthostatic hypotension Pathological murmur ECG findings none none Current arrhythmias, evidence of ischemia or CAD, evidence of proarrhythmia (e.g. long QT syndrome

20. Diagnostic next step: Neurally mediated syncope Orthostatic syncope Cardiogenic syncope If vasovagal or situational, Testing unnecessary, But Ambulatory ECG monitoring can be considered Carotid hypersensitivity can be confirmed by carotid sinus massage Complete cardiovascular exam Ambulatory ECG monitoring Echocardiogram Electrophysiological study IV fluid expansion with fluids drug withdrawal of alpha antagonists, Nitrates, TCA antidepressants if taken Tilt table testing CT brain indicated if associated head injury h/o MRI brain

21. Vertigo A sense of spinning or other motion that may be Physiological – after a sustained head rotation Pathological due to vestibular dysfunction Lesion may be In labyrinth, vestibular nerve, nucleus and connections

22. Pathophysiology : Asymmetric labyrinthine discharge – imbalance in inputs from 2 labyrinths Bilateral lesions – no vertigo but imbalance and instability of vision is present when head moves (oscillopsia)

23. Approach : true vertigo or not history : Spinning sensation Falling to one side Aggravated by head movements Associated nausea, auditory symptoms, brainstem symptoms Timing and duration of episodes: Single or recurrent episodes Lasting for Seconds, mins, hours, days Triggers : Spontaneous Triggers – position change, Head motion, aural or visual triggers Associated symptoms: Hearing loss, tinnitus – meniere disease Headache, photophobia Present or prior neurological symptoms – multiple sclerosis, stroke Imbalance > vertigo – bilateral vestibular dysfunction

24. Peripheral vertigo Central vertigo Timing, duration and triggers Recurrent, transient, position induced Single, prolonged, spontaneous, persistent symptoms Associated symptoms Vomitting +, tinnitus ( Menierse’s disease, hearing loss (labyrinthitis) Brain stem signs and symptoms – unsteadiness, Ataxia, Diplopia, Dysarthria, weakness, dysphagia Nystagmus Unidirectional horizontal nystagmus Suppressed by visual fixation Fatigability present Downbeat nystagmus – vertical with downward fast phases Gaze evoked nystagmus – horizontal nystagmus that changes direction with gaze Not suppressed by visual fixation Pursuit and saccades Pursuit is intact; Saccades are accurate Poor pursuit and dysmetric saccades Peripheral or central vertigo

25. saccades

26. History Vitals Focused physical exam Ear exam Neurological examination HINTS exam (head impulse, Nystagmus, test of skew) Dix- hallpike maneuver

27. HINTS exam Vestibulo – ocular reflex: VOR keeps the image of the object on the fovea irrespective of head movement Head impulse test is a bedside test to test vestibular function Examiners hand placed on either side of pts head Small amplitudes rapid head movement applied, pt fixated on a target Suitable for pts with h/o long duration continuous vertigo

28. Deficient VOR – rotation is followed by a catch up saccade in the opposite direction. Abnormal head impulse test – implicated in peripheral vertigo Acute prolonged vertigo with spontaneous nystagmus and normal Head impulse test indicates a central pathology

29. Vestibulo spinal reflex – maintains balance Vestibular nuclei projection to anti gravity muscles to maintain posture Rhombergs test done – positive if patient is stable with eyes open and sways with eyes closed Indicates dorsal column dysfunction Also in unilateral labyrinthine or vestibular lesion – sway to the side of lesion In B/L vestibulopathy – sway to wither direction In cerebellar dysfunction – postural imbalance both with eyes open and closed

30. Test of skew: Vestibular tone imbalance resulting in vestibular ocular misalignment in absence of oculomotor muscle weakness Suspected if vertical diplopia symptoms is present Presence of a corrective vertical movement which becomes obvious with cover test

31. Dix- hallpike maneuver - Suitable for pts with h/o episodic vertigo

32. Peripheral vertigo Labyrinth Vestibulocochlear nerve Benign paroxysmal positional vertigo Meniere disease Perilymphatic fistula Vestibular neuritis Vestibular swannoma Bilateral vestibular hypofunction

33. Central vertigo vascular Non – Vascular Stroke / transient ischemic attack Lateral medullary syndrome Cerebellar infarct or hemorrhage Multiple sclerosis

34. References : Harrison principles of internal medicine 21 st edition Strong medicine Textbook of physiology – Guyton Diseases of EAR, NOSE & THROAT - P. L. Dhingra

35. Thank you