vertigo nystagmus approach final .pptx

vertigo nystagmus approach harisson based

1. Approach to Vertigo Mm Moderators Dr. P . Suresh MD,Professor Dr J Aparna MD,Asst Proff Dr Krishna Kumar MD,Asst Proff Dr . K Sai Likhitha PGY 1 st year General Medicine

2. Dizziness Dizziness is a nonspecific term used by patients to describe various perceptions of altered spatial orientation. First pivotal step is to recognize that most patients who complain of dizziness are actually complaining of 1 of 3 distinct symptoms: Vertigo near syncope Dysequilibrium

3. Dizziness What does it feel like when you are dizzy The room is spinning I am about to black Out Walking feels off balance vertigo Near Syncope Dysequillibrium Ask the patient

4. Vestibular Physiology ; Peripheral system Component Function Semicircular Canals Detect angular acceleration (rotation) Utricle Detect horizontal linear acceleration, head tilt Saccule Detect vertical linear acceleration Hair Cells Convert mechanical deflection → nerve signals Endolymph Transmits motion force to sensory structures Vestibular Nerve (CN VIII) Carries signals to brainstem & cerebellum

5. Head Movement (Angular / Linear) Endolymph Displacement Fluid shifts inside semicircular canals / otolith organs Cupula or Otolithic Membrane Deflection Mechanical bending of sensory structures Hair Cell Stereocilia Bending → Toward kinocilium = depolarization (↑ firing) → Away = hyperpolarization (↓ firing) CN VIII (Vestibular Nerve) Carries excitatory & inhibitory signals in push–pull fashion Vestibular Nuclei (Brainstem) Primary integration hub with inputs from vision & proprioception Cerebellar Integration Flocculonodular lobe fine-tunes eye–head coordination & posture Reflex Outputs to VOR and Vestibulo Spinal Pathways Vestibular Physiology

6. Vestibular Physiology ; Central System Components : Vestibulo Cerebellar Pathway Vestibulo Ocular Vestibulo Spinal Vestibulo Reticular Vestibulo Thalamic

7. How does the Central pathways actually work Running to catch a Bus : Vestibular Appartu s : Detects Motion Vestibulo Ocular : Stabilizes the gaze on the bus even while the head is bobbing Lesion leads to Oscillopsia Vestibulo Spinal : Lateral VST ,Activates Extensors of the leg ..stays upright Medial VST, Stabilizes the neck mucles Vestibulo Thalamic Cortex : Spatial Orientation Vestibulo Reticular System : Dampens Autonomic response Lesion leads to Motion Sickness

8. In short Apparatus: Detects motion. VOR: Stabilizes gaze. Vestibulospinal: Keeps posture stable. Thalamic Pathway: Guides spatial orientation. Reticular Connections: Controls autonomic balance.

9. CAUSES OF VERTIGO 1 . Peripheral BPPV b. Labyrinthitis or vestibular neuritis c. Meniere disease 2. Central Cerebrovascular disease (1) VertebroBasilarInsufficiency (2) Cerebellar or brainstem stroke (3) Cerebellar hemorrhage (4) Vertebral artery dissection (VAD) (5) Brainstem aneurysm Cerebellar degeneration Migraine MS

10. Watch out for spontaneous Nystagmus Usually Seen in Peripheral Vertigo Mechanism : Arises from an imbalance of vestibular input between the two labyrinths or vestibular nerves. Tests for Nystagmus

11. Move the Stimulus all the way to the subject left side > 45 degrees and hold it there so that the subjects eye is turned far to the side . Observe for a distinct and sustained jerk nystagmus at maximum deviation for a min of 5 – 10 secs and repeat on the contralateral side. Usually occur in Central Vertigo Mechanism : Results from dysfunction of central gaze-holding or ocular motor pathways (cerebellum, vestibular nuclei, brainstem integrators). Gaze Evoked Nystagmus

12. Feature Peripheral (Vestibular) Central (CNS) Mechanism Vestibular tone imbalance → abnormal VOR Dysfunction of gaze-holding/ocular motor pathways Direction Unidirectional, horizontal with torsion Variable (uni-/bidirectional, vertical, torsional) Fixation Suppressed by visual fixation Not suppressed Alexander’s law Present Associated symptoms Vertigo, nausea, tinnitus, hearing loss Neurological signs (ataxia, diplopia, dysarthria) Common causes Vestibular neuritis, labyrinthitis, Ménière’s disease, BPPV Stroke, MS, cerebellar degeneration, drug intoxication (e.g., anticonvulsants) Peripheral Vs Central Nystagmus

13. ALEXANDER’S LAW It describes the behaviour of Nystagmus in patients with unilateral vestibular lesions. 1. Nystagmus is most intense when the patient looks in the direction of the fast phase .2. Nystagmus decreases in intensity when the patient looks straight ahead. 3. Nystagmus is least intense (sometimes absent) when looking in the direction of the slow phase.

14. Components : Input: Semicircular canals + otoliths → vestibular nerve. Processing: Vestibular nuclei + MLF + cerebellum. Output: Oculomotor, trochlear, abducens nuclei → extraocular muscles. Vestibulo Ocular Reflex Head turns to the left → Left horizontal semicircular canal excited, right inhibited. Left vestibular nucleus excites right abducens nucleus → activates right lateral rectus + via MLF activates left medial rectus . Eyes move to the right , compensating for leftward head turn.

15. Ask the patient to fixate on a stationary object in front of them.  Rapidly rotate the patient's head 10 degrees from center and assess their ability to maintain a central gaze.  [5] Repeat the procedure, rotating the patient's head to the contralateral side. Head Impulse Test

16. Inability to maintain central fixation on a stationary target during head rotation  Followed by a corrective shift of the eyes back to the stationary target (correction  saccade )  Abnormal VOR

17. Ask the patient to maintain a fixed central gaze and to keep both eyes open during the examination. Repeatedly cover and uncover alternating eyes, while watching for vertical deviation from the central gaze upon uncovering the  eye .  [5] Skew Deviation

18. Positive HINTS plus exam requires any of the following: Normal head impulse test, direction changing nystagmus, purely vertical nystagmus, positive tests of skew deviation, new hearing loss. Negative HINTS plus exam requires all of the following: Abnormal head impulse test, no direction changing nystagmus, no skew deviation, and no new hearing loss.

19. HINTS+ Sign Peripheral lesion Central lesion Head Impulse Abnormal (catch-up saccade) Normal Nystagmus Unidirectional, horizontal–torsional Direction-changing, vertical/torsional possible Test of Skew Absent (normal) Present (vertical misalignment) Hearing (+) Preserved May be lost (AICA stroke)

20. Ask the patient to sit upright on the examination bed and to keep their eyes open during the procedure. Rotate the head by 45° towards the affected side. Keeping the neck rotated,  quickly  lay the patient in a Supine position   with the neck slightly extended ( approx 20°) and the affected  ear  held down at 45°.  Hold this position for 20–30 seconds. Examine the eyes for nystagmus; if present note latency, direction, and duration of nystagmus Inquire if the patient is experiencing vertigo Wait for resolution of nystagmus and vertigo DIX HALLPIKE

21. Ask the patient to lie in a supine position and to keep their eyes open during the procedure. Position the patient's head in neutral position. Quickly turn the patient's head by 90° to one side and examine for nystagmus. Wait for nystagmus to subside. Reposition the patient's head to neutral position, reassess for nystagmus; allow nystagmus to subside. Repeat steps on the opposite side.  Supine Head Roll test This is done to detect horizontal semicircular canal BPPV

22. How to approach when the patient says I feel like the room is Spinning

23. 1st step is to rule out Central Cause

24. Clinical Evaluation Perform Orthostatic Hypotension to rule out Syncope. Conduct a  neurological examination  that includes: Evaluation of  cerebellar features  and full  cranial nerve examination  including: Evaluation of  nystagmus  (e.g., identify  spontaneous nystagmus  and  gaze-evoked nystagmus ) Examination of gait Identification of any focal neurological deficits. Perform Targeted Maneuvers like HINTS plus tests and Dix Hallpike to ascertain the pathology

25. Dizziness Assessment of Dizziness *—Exacerbation of symptoms with movement does not aid in determining whether the etiology is peripheral vs. central. † —Central causes can also occur with patterns triggered by movement. Patient presents with dizziness or vertigo Is the timing episodic or continuous? Continuous Is it associated with trauma or toxins, or spontaneous? Spontaneous HINTS examination No saccade, nystagmus dominantly vertical, torsional or gaze- evoked bidirectional, abnormal test of skew Central etiology † Stroke or transient ischemic attack Saccade present, unidirectional horizontal nystagmus, normal test of skew Peripheral etiology Vestibular neuritis Episodic Is it triggered or spontaneous? Spontaneous Migraine headache Vestibular migraine Psychiatric symptoms Panic attack, psychiatric condition Hearing loss Meniere disease Positive Benign paroxysmal positional vertigo Negative Assess for orthostatic hypotension Triggered* Dix-Hallpike maneuver Trauma or toxin Barotrauma Medications

26. Thank You