Vestibular Pathology Flashcards by PT Student

-Benign paroxysmal positional vertigo
-Hypofunctioning conditions: unilateral/bilateral
-Menier’s disease
-Perilymphatic fistula

Peripheral nervous system conditions

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-Vestibular migraine
-Persistent postural perceptual dizziness
-Head trauma
-Brainstem stroke/vertebrobasilar insufficiency (VBI)
-Cerebellar disorders, multiple sclerosis
-Cervicogenic dizziness

Central nervous system disorders

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Otoconia in utricle become loose and fall of macular and drop most often into the posterior semicircular canal

Pathology of BPPV

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Most common cause of vertigo due to peripheral disorder especially in individuals > 50 y/o

BPPV

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Does BPPV involve hearing loss, aural fullness, or tinnitus

Generally no

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Symptom trigger for BPPV

Positional ie. Supine -> sitting, rolling in bed, bending over, looking up
- Typically lasts for 30 sec - 2 min

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Otoconia in endolymph
- Symptoms and (geotropic) nystagmus transient

Canalithiasis

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Otoconia stuck in cupula
- Symptoms and (ageotropic) nystagmus persistent

Cupulolithiasis

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-Nystagmus will have both a vertical and torsional component
-Short duration typically <1 min

Clinical presentation for posterior canal BPPV

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Canal repositioning maneuver

Treatment for posterior canal BPPV

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-Horizontal nystagmus that shoulder either be ageotropic and long lasting (cupulolithiasis) or geotropic and short duration (canalithiasis)

Horizontal canal BPPV

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360 or 270 degree BBQ roll maneuver

Treatment for canalithiasis

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Side is one with more robust symptoms

Positive side for canalithiasis

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Cassani maneuver

Treatment for cupulolithiasis

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Side usually opposite of most symptomatic side

Positive side for cupulolithiasis

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Second most common peripheral vertigo

Unilateral hypofunctioning: vestibular neuritis

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Typically viral, or d/t trauma, surgical transection
-Inflammation from infection (or other insult) results in hypofunctioning of vestibular nerve
-Can also involve cochlear branch of CN 8

Etiology of vestibular neuritis

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Involvement of cochlear branch of CN 8 -> impacts hearing

Labyrinthitis

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Asymmetry in resting vestibular tone typically manifests as vertigo, nausea, and spontaneous nystagmus

Acute/initial pathophysiology of vestibular neuritis

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Spontaneous rebalancing of resting firing rate of the tonic vestibular system results in reduction of nystagmus, vertigo, and nausea, usually within 14 days via cerebellum adjusting gain

Pathophysiology of vestibular neuritis occurring days-weeks post insult

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-Reports of room spinning dizziness lasting around 3-4 days associated with imbalance and nausea
-Spontaneous nystagmus and gaze holding nystagmus can be seen acutely and will follow Alexander’s law (will beat towards the more neuronally active ear/away from affected ear)

Clinical manifestations of vestibular neuritis

Head impulse test, dynamic visual acuity test

Testing for vestibular neuritis

Recurring vertigo episodes thought to occur due to abnormally large amounts of endolymph collecting in the inner ear
-Most commonly in individuals 40-60 years

Meniere’s disease

Stress, fatigue, emotional distress, atmospheric pressure changes, certain foods (high sodium)

Triggers for Meniere’s disease

Largely unclear, theories: circulation problems, viral infection, allergies, autoimmune reaction, migraine, genetic component

Etiology of Ménière’s disease

-Episodic vertigo lasting min-hours, fluctuating hearing loss, ear fullness, or tinnitus -Nystagmus presents spontaneously during an attack and beats towards the affected ear

Clinical presentation of Ménière’s disease

Episodic, spontaneous, and intense vertigo lasting minutes to hours typically not more than 24 hours

Early stages of Ménière’s

Develop imbalance due to peripheral vestibular dysfunction, progression of hearing loss to permanent

Chronic stages of Ménière’s

No specific diagnostic test available made clinically

Testing for Ménière’s disease

Low sodium diet -> diuretics -> steroid injection -> gentamycin injection -> nerve section or labryrinthectomy

Treatment (medical) for Ménière’s disease

Loss of separation between middle and inner ear due to fistula developing at round and oval windows of the middle ear (breakdown in bony canal, fluid can leak out making inner ear more susceptible to pressure changes in environment -> overstimulation of system)

Perilymphatic fistula

Blow to the head or surgical intervention (popping sound heard)

Etiology of Perilymphatic fistula

Imbalance, positional vertigo, nystagmus and hearing loss, worse with strain/valsalva

Symptoms associated with Perilymphatic fistula

Bed rest, no straining which would cause Perilymph leakage, goal = fistula to heal/close - May require surgery

Treatment for Perilymphatic fistula

Physical therapy for Perilymphatic fistula

CONTRAINDICATED

Exposure to ototoxic chemicals/medications, advanced Ménière’s disease, autoimmune ear conditions

Etiology of bilateral vestibular disorders

-May or may not experience hearing loss or vertigo -Complain of imbalance** worse is dark environments, oscillopsia (d/t loss of gaze stabilization provided by VOR)

Clinical presentation associated with bilateral vestibular dysfunction

-Self-spinning (internal vertigo, swaying) > room spinning vertigo lasting usually < 3days -Nausea -Migraine symptoms; unilateral head pain, photo/phono-sensitivity, +/- aura

Symptoms associated with vestibular migraine

-Possibly spontaneous -Change in head/body position, visual stimulation -Hormonal fluctuation, barometric pressure changes, poor sleep, stress, dietary

Triggers for vestibular migraine

5 minutes to 72 hours

Symptom duration for vestibular migraine pts

- Chemicals involved in trigemino-vascular system also present within central vestibular centers -TVS and vestibular nuclei also connected to nociceptive center within brainstem -Evidence of hyperactivity increases vestibular sensitivity in pts with migraine, also altered sensory processing within thalamocortical networks

Pathophysiology of vestibular migraine

-Sensitive to oculomotor/vestibular exam (hypersensitivity) and demonstrate imbalance sensory processing/integration -Positional nystagmus - not in typical BPPV pattern, longer duration and/or different nystagmus direction -Treating as BPPV may exacerbate symptoms d/t overstimulation

Clinical findings associated with vestibular migraine

Two vertebral arteries joint together to form basilar artery that supplies brainstem/cerebellum

Vertebral artery

-Dizziness/vertigo -Headache -Neck pain

Symptoms associated with vertebral artery dissection

-Anterior inferior cerebellar artery -Posterior inferior cerebellar artery -Superior cerebellar artery (Come from basilar artery)

Three major arteries supplying cerebellum

-Vertigo -Nausea -Hoarseness -Difficulty swallowing (dysphagia)

Symptoms associated with stroke in the posterior inferior cerebellar artery aka Wallenburgs syndrome

Chronic dysfunction of the vestibular system associated with long-term maladaptation to vestibular dysfunction, medical or psychological event that triggered vestibular symptoms

Persistent postural perceptual dizziness (3PD)

-Non-spinning vertigo or self-motion, swaying, rocking -Imbalance/unsteadiness -Lightheadedness/wooziness -Mild dissociated (floating, spaced-out)

Symptoms associated with 3PD

- Patient education - Vestibular rehabilitation - Serotonergic medications - Cognitive-behavioral therapy

Treatment for 3PD

Non-specific sensation of altered orientation in space and disequilibrium originating from abnormal afferent activity from the neck

Cervicogenic dizziness

-Imbalance/unsetadiness -Dizziness “in my head”, disorientation -Neck pain (at rest, with movement, or to palpation), limited ROM, headache

Symptoms associated with cervicogenic dizziness

-Abnormal cervical proprioception -Sensory mismatch between c-spine afferent and other sources of equilibrium (eyes, ears) -Disruption of the normal afferent signals from upper cervical proprioceptors to vestibular nucleus -Results in inaccurate depiction of head and neck orientation in space

Pathophysiology of cervicogenic dizziness