Vertigo and the Dizzy Patient
Definitions:
- Dizziness: imprecise term with many meanings; associated with many clinical
conditions
- Vertigo: sensation of disorientation in space combined with a sensation of motion
Clinical pearl for differentiation:
- Vertigo is never continuous for greater than 2 weeks unless the cause is changing
during that time ie growing tumor. Your CNS will adapt to the unbalances
stimulus
- Head motion will make all types of vertigo worse
Pathophysiology:
-
Integration of visual, proprioceptive, and vestibular systems
o Visual gives info about position of body in space
o Proprioceptors give info about relative position of body parts; neck
proprioceptors are importance for determining position of head vs rest of
body
o Vestibular system helps maintain head position and stabilize head mov’t
-
Vestibular system and CNS pathways
o Tonic discharge of the vestibular system is balanced when the head is still.
With movement, the left and right labyrinths are excited/inhibited leading
to a difference in CN VIII activity. This is recognized as motion
o Info leaves the vestibular system via CNVIII
o Goes to nuclei occulomotor nuclei in brainstem and pons, the spinal cord,
and the cerebellum
o 2 pathways involved in integration info with mov’t of the eyes with
respect to body mov’t
 MLF – responsible for nystagmus
 Vestibulospinal tract – responsible for body movements
-
Autonomic system
o Connections with the vestibular system cause the perspiration, nausea and
vomiting associated with vertigo
Approach:
“Dizzy Patient”
Vertigo
Presyncope, Disequilibrium
Peripheral:
Central:
Systemic:
FB
Hair/cerumen against TM
AOM
Labyrinthitis
BPV
Meniere’s
Vestibular Neuronitis
Perilymphatic Fistula
Trauma
Motion Sickness
Meningitis/enceph/abcess
Vertebral basilar A insufficiency
Subclavian steal
Cerebellar hemorrhage
Cerebellar infarct
Trauma- Temporal bone #
Postconcussive syndrome
Cspine injury – lig/muscle
Temporal lobe epilepsy
Tumor
MS
Hypothyroidism
DM
Central vs Peripheral
Nystagmus:
o Occurs when synchronized vestibular info from both vestibular apparatus
becomes unbalanced. The brain believes that the body/head is moving
 Asymetrical stimulation of the medial and lateral rectus via MLF
 Unopposed or unbalanced stimulation causes a slow movement of
the eyes towards the stimulus regardless of the direction of gaze
 Ie the eye drifts towards the vestibular apparatus that is
hypoactive/diseased
 Cortex then corrects for the movements and rapidly returns the
eyes to midline
o Direction of nystagmus is denoted by the fast phase
 Horizontal/rotary = peripheral cause or central cause
 Vertical = central cause
o Peripheral nystagmus:
 Fast phase is AWAY from the affected side
 Increases with gaze toward the normal ear (ie in the direction of
the fast phase)
o NOTE: up to 3 beats of nystagmus in extremes of gaze is normal
Physical exam:
-
Nystagmus:
o To help determine the effect of visual fixation, first have the person focus
on an object such as a picture on the wall. Observe the resulting
nystagmus. Repeat but this time, have the patient stare into a bright light
from an otoscope/ophthalmoscope. The bright light prevents the patient
from fixating on an object. Because nystagmus from a peripheral cause
will be suppressed by fixation, if there is a difference in the patient’s
nystagmus with fixation, it is from a peripheral cause. If the nystagmus is
the same both times, it is likely due to a central cause.
-
Neuro exam:
o Should do complete exam however there are a few high yield components
that you should pay close attention to:
 CN VII since it runs with CNVIII
 CNV – large brainstem nuclei
 CN III-VI – involved with MLF
 Cerebellar exam
 Gait – if a patient CAN’T walk – central cause
 FTN and HTS
Positional Testing/Maneuvers:
- DixHallpike is for the posterior semicircular canals. There is another
test/maneuver for the horizontal canals
-
Hallpike: WARN PATIENT FIRST!
o Move quickly from upright seated position to supine with head turned 45
degrees to one side and extended 45 degrees downwards
o Observe eyes for nystagmus
o Repeat on other side
o Elicitation of symptoms on one side indicates pathology on that sidedownward ear
-
Epley
o If you have a positive Hallpike you can move right into the Epley
 NOTE: this needs to be repeated several times. Each successive
Epley, the symptoms should be less severe.
o Maintain head in position (45 tilt and 45 down) until the nystagmus
extinguishes
o Turn head 45 degrees to other side and wait for nystagmus extinguishes
o Roll onto side and have patient look directly at the floor – wait for
nystagmus to extinguish
o Sit up and have patient look directly forward
Clinical Presentations:
1. BPPV
- short lived, positional, fatiguable with associated N/V
- can be severe and often these patients will report feeling unwell between episodes
and may be anxious or fearful about future episodes
- can precipitate symptoms at bedside with Dix-Hallpike and reasonable success for
resolution with Epley
- teach family members the maneuvers and then let them do them at home
2. Labyrinthitis
- Serous
o Inflammatory response to nearby infections
o Mild to severe positional vertigo with coexisting or antecedent infection.
Can have some hearing loss. Pt is nontoxic.
-
-
Suppurative
o Severe vertigo with associated severe hearing loss, N/V. Will see a
coexisting exudative AOM. Pt is febrile and toxic.
Toxic
o Typically gradual onset of symptoms (vestibulotoxic meds) but severe
hearing loss +/- tinnitus and associated N/V. Can see ataxia in these
patients if they are in the chronic phase of illness.
3. Vestibular Neuritis
o Sudden onset of severe vertigo that increases for hours and then subsides
over days. Associated N/V. NO hearing loss. +/-Spontaneous nystagmus
towards involved ear
o Can have residual positional vertigo
4. Meniere’s
o Abrupt onset of severe rotational vertigo that lasts hours with
N/V/tinnitus. NO nystagmus.
o Permanent hearing loss.
5. Vestibular Schwannoma
o Considered peripheral and moves centrally
o Gradual onset and increase in severity of vertigo with associated unilateral
hearing loss and tinnitus.
o As tumor enlarges, get focal neuro signs and headaches
6. Vascular Causes
a. Wallenberg’s syndrome – Lateral Medullary Infarct
 PICA
 Vertigo plus:
 Ipsilateral loss of facial pain/temp (CN V tract)
 Contralateral loss of body pain/temp (Spinothalamic tract)
 Ipsilateral horner’s syndrome (sympathetic fibres)
 Ipsilateral pharyngeal and laryngeal paralysis (CN X
nucleus and nerve)
 Ipsilateral cerebellar signs: nystagmus, dysarthria, limb
ataxia (cerebellum)
b. Cerebellar hemisphere infarct
 Sudden onset of severe vertigo, nausea + other cerebellar signs.
May have isolated nausea as well.
c. Cerebellar hemorrhage
 Sudden onset of severe vertigo, N/V and headache. This patient
looks sick with dysmetria, true ataxia. If increased ICP, may see
ipsilateral CN VI palsy
d. Vertebrobasilar insufficiency
 Brief initial episode may be only seconds to minutes and
associated with headache and +/-other cerebellar symptoms
(dysarthria, ataxia, diplopia) plus motor/sensory complaints
e. Subclavian steal
 classic is syncope with exercise but can be more subtle.
Associated symptoms may include N/V, ataxia, hoarse voice,
pain/temp loss, vertigo
7. Vertebrobasilar Migraine
o Vertigo flowed by headache associated with dysarthria, visual, and
parasthesias
o Similar episodes in the past with no residual deficits
8. Diving and Vertigo
- Causes:
o Middle ear, inner ear, alternobaric vertigo
o Decompression sickness Type II (DCS II)
o Air gas embolism (AGE)
Decompression Sickness
- Def’n: spectrum due to nitrogen bubbles and severity depends on amount, size,
and location of bubbles
- Risk Factors: male, age, abesity, fatigue, dehydration, exertion, cold temp, high
altitude diving, timing of flying, presence of PFO. ??alcohol and nicotine
- Type 2
o CNS:
 Spinal DCS: MC in upper lumbar area giving sensory and motor
findings plus back and abdo pain
 Starts as distal prickly sensation that advances proximally
and then turns into motor/sensory findings
 Can also see bladder, bowl and priapism
 Brain
 h/a, blurred vision, diplopia, dysarthria, fatigue,
inappropriate behaviour, sense of detachment
 NO LOC
o Lung: “the chokes”
 Symptoms depend on number and volume of bubbles
 Progressive dyspnea, cough, and CP
 Signs: cyanosis, hypotension, increased CVP, Rheart strain,
decreased ET CO2
o Ear: “the staggers”
 Nausea, dizziness, vertigo, nystagmus
Arterial Gas Embolism
- Clincal picture: any diver who has breathed compressed air at any depth and has
cerebral, cardiac, or pulmonary symptoms should be preseumed to have AGE
o Typically dramatic, sudden symptoms (CVS, Resp, CNS)
-
Cerebral
o ALOC, LOC, h/a, dizziness, s/z, CN, motor, sensory, cerebellar findings
9. Toxicology and Vertigo
o Medication with Direct Vestibulotoxicity:
 aminoglycosides
 anticonvulsants
 alcohols
 quinine
 quinidine
 minocycline
 Caffeine and nicotine can make vestibular symptoms worse
Pearls:
1. BPPV vs Meniere’s vs Vestibular Neuritis:
- 30s - BPPV
- 30 min – Meniere’s
- 30 hours – Vestibular neuritis
2. Vestibular Neuritis vs Cerebellar Infarct
- Is a very important distinction since vestibular neuritis is relatively benign and a
cerebellar infarct can be life threatening.
- In young otherwise healthy patients with acute severe vertigo, no neuro signs, and
features consistent with a peripheral cause (ie nystagmus is suppressed with visual
fixation, horizontorotational nystagmus and falling and nystagmus are in opposite
directions) there is no need to get further imaging.
- Imaging is indicated if the exam isn’t entirely consistent with a peripheral lesion
- Helpful clinical exam tips:
o Stroke: fall towards the side of the lesion AND nystagmus is more
pronounced on the side of the lesion
o Vestibular neuritis: falls towards the side of the lesions BUT nystagmus is
away from the lesion