JC100 (ENT) - Vertigo Flashcards
Inputs, integration and effectors to maintain balance
3 sensation inputs:
- Vision – 70%
- Proprioception – 15%
- Vestibular input – 15%
Integrated at central (brainstem, cerebellum)
Effector = motor system (lower limbs, core muscles) = postural support adjustment
Anatomical components of the peripheral and central vestibular system
Peripheral:
Semicircular canals - rotatory movement
Vestibule (saccule, utricle) - linear movement
Vestibular nerve
Central: Vestibular nuclei Brainstem Cerebellum Vestibular cortex Spinal cord
Anatomical components of the Labyrinth
Bony labyrinth surrounds membranous labyrinth containing perilymph and endolymph:
Semicircular canals (3 on each side) Otolithic organs: utricle and saccule
Semicircular canals
- Orientation and anatomical locations
- Connection to other structures in labyrinth
- physiological activation of vestibular nerve
Semicircular canals at the superior part of labyrinth:
3 canals perpendicular to each other: horizontal (aka lateral), posterior, superior (aka anterior)
Open into the utricle, with dilation ampulla at anterior end
Activation:
- A gelatinous mass called cupula cover the sensory epithelium (hair cells)
- Flow of endolymphatic fluid relative to cupula cause shearing of hair cell cilia:
Stereocilia bent towards kinocilium increase firing rate of vestibular nerve
Stereocilia deflected away from kinocilium decrease firing rate (inhibition)
Describe the pairing of semicircular canals for vestibular nerve firing
The semicircular canals are paired:
Horizontal canals
Right superior / left posterior (in same plane)
Left superior / right posterior
When head turns to the left, endolymph does not follow due to inertia:
o Left canal is excitatory
o Right canal is inhibitory
Brain interpret the difference in discharge as movement
Otolithic organs
- Function
- Anatomical positions
- Components for vestibular nerve firing
Otolithic organs: Sense linear acceleration
Located at the macula in utricle and saccule:
Macula of utricle lies in the horizontal plane
Macula of saccule lies in the vertical position
Embedded in gelatinous layer are:
Cilia from hair cells
Otoconia (consists of CaCO3 or calcite crystals)
Physiological activation of otolith organs
Trace the neural pathway from otolith organs to execute vestibular reflexes
Translational head movement in any particular direction will displace hair bundle
- Increase excitability of (depolarize) a subgroup of hair cells»_space;release transmitter to vestibular nerve
- Decrease excitability of (hyperpolarize) another subgroup on the same otolith organ
Pathway:
- Hair cell (in semicircular canals, otolith organs)-
vestibular nerve-
Scarpa’s ganglion-
vestibular nucleus (superior, lateral, inferior, medial)-
spinal/ocular motor neuron-
vestibular reflexes - Modulated by cerebellar Purkinje cells (innervate neurons in the vestibular nucleus)
Vestibular ocular reflex
- Function
During rapid impulsive head movement, produce an equal but opposite amount of eye movement to stabilize images on the retina
Maintain visual acuity on object of interest during acute head movement
Nystagmus
- ## Clinical definition
involuntary, rhythmic, oscillating movement of the eyes
Especially for saccadic eye movement (fast corrective movement to pick up next target)
Define the COWS reflex test for nystagmus
Cold-opposite:
Irrigated with COLD water: Eyes deviate to ipsilateral ear and the nystagmus beats away to the OPPOSITE ear.
Warm-same:
Irrigated with WARM water: Eyes deviate to contralateral ear and the nystagmus beats towards to the SAME ear.
4 main types of dizziness
Differentiate the 4 types’ description
- Nonspecific lightheadedness (無法分辨) = most common
- Vague, doesn’t fall - Pre-syncope (快昏倒了)
- Impeding faint/ LOC +/- generalised weakness
- Postural change
- Worse in morning - Disequilibrium (走路不穩)
- Impaired balance and gait
- No abnormal head sensation/ no illusion or movement or faintness - Vertigo (天旋地轉)
- Hallucination of movement
- Typically rotatory
Ddx non-specific light-headedness
Hyperventilation Hypoglycaemia Anaemia Head trauma Associated with psychogenic disorders (e.g. depression, anxiety, phobia)
Ddx pre-syncope
Orthostatic hypotension
Autonomic dysfunction
- secondary to diabetes, cardiovascular diseases (e.g. arrhythmias, myocardial infarction, carotid artery stenosis)
Medications (esp elderly on multiple medication), e.g. anti-
hypertensive, anti-arrhythmic drugs
Ddx of disequilibrium
Ageing (most common) - multisensory deficits
- Deficit in vision, proprioception, vestibular organs, neural pathway…etc
Peripheral neuropathy
Musculoskeletal disorder
Gait disorder
Parkinson’s disease
Peripheral vs central vertigo
- Triggered by which type of movement
- Triggered by gaze or not
Peripheral
- Horizontal or torsional (mixture of up or down with horizontal), never vertical
- Same direction in all gazes
- Looking in the direction of nystagmus makes nystagmus more obvious
Central:
- Can be vertical or other direction
- May change direction with change in gaze
Peripheral vs central vertigo
- Compare onset and duration
- Fatigability
- Effect of gaze on vertigo
- Associated symptoms
Peripheral = Acute onset and short duration, subsides in days
- Visual fixation helps suppress vertigo
- Fatigable vertigo: gets better after repeated episodes
- Severe nausea and vomiting
- Otological symptoms *** e.g. labyrinthitis
- Mild instability only
Central = Subacute/ slow onset with long duration, persistent
- Visual fixation does not suppress vertigo
- Not-fatigable: persistently same severity
- Variable nausea and vomiting
- Neurological symptoms ***
- Severe instability *** (can’t stand)
Causes of peripheral vertigo
In semicircular canals and vestibule:
1) Benign paroxysmal positional vertigo (BPPV) = commonest
2) Meniere’s Disease
3) Perilymph fistula
4) Labyrinthitis
5) Superior canal dehiscence
6) Vestibular insufficiency
7) Ototoxicity
8) Trauma (fracture temporal bone / vestibular concussion)
In vestibular nerve:
1) Vestibular neuritis/ neuronitis
2) Vestibular paroxysmia (vascular loop compression of CN VIII)
Causes of central vertigo
a) Central-vestibular vertigo (lesion of brainstem/ cerebellum, e.g. CVA/ tumour)
b) Migrainous vertigo
c) Cerebellar ataxia (e.g. infarction, Wilson’s disease, congenital)
d) Metabolic (dysthyroid, anaemia, electrolyte, hypoglycemia)
e) Medication (e.g. phenytoin overdose)
BPPV - Benign paroxysmal postural vertigo
- Pathogenesis
Most commonly affects posterior semicircular canal
Etiology – canalolithiasis:
Particulate from otoconia (for saccule or utricle) is
dislodged (after head injury/ idiopathic) then stuck in
posterior semicircular canal
Inertia of crystal continues to stimulate the ampulla by a plunger effect (piston-effect) >> continues to move the endolymph when head is still
BPPV
- Clinical presentation
- Duration of episodes
True vertigo provoked by turning over to particular position in bed or when reaching up
No hearing symptom (cochlea not affected; no infection)
Usually lasts for ~3 weeks