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:
FB
Hair/cerumen against TM
AOM
Labyrinthitis
BPV
Meniere’s
Vestibular Neuronitis
Perilymphatic Fistula
Trauma
Motion Sickness
Central vs Peripheral
Central:
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
Systemic:
Hypothyroidism
DM
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 side- downward 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
- 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)
- Cerebellar hemisphere infarct
§ Sudden onset of severe vertigo, nausea + other cerebellar signs. May have isolated nausea as well.
- 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
- 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
- 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