Peripheral Diseases Making Balance Disorders
Benign positional paroxysmal vertigo (most common)
Vestibular neuritis
Meniere or endolymphatic hydrops
Vestibular ototoxicity
otosclerosis
Cogan syndrome
Benign Positional Paroxysmal Vertigo (BPPV)
In many cases, the etiology is unknown.
pathophysiology
Channelolithiasis: it most commonly occurs when it falls into the posterior semicircular canal.
• There are dizziness that occur with head movements and end in 10-20 seconds.
• Posterior semicircular canal BPPV is most common.
Diagnosis
Provocation tests (Dix-Hallpike maneuver, modified Barany test)
• Nystagmus with a latent period (2-3 sec)
• Horizontal rotatory nystagmus
• Nystagmus lasting less than 1 minute (tiring)
• Nystagmus decreases as the test is repeated.
Treatment:
• Reposition maneuvers (Epley maneuver)
Vestibular Neuritis
• History of URTI or gastroenteritis
• Very severe dizziness, nausea, vomiting
• Spontaneous nystagmus, horizonto-rotatory
• Neurological examination and hearing are normal.
• Significant improvement is seen in complaints within the first 48 hours.
• Tinnitus, hearing loss, fullness etc. There are no ear complaints.
Meniere's Disease
• In endolymphatic hydrops; There is excess endolymph secretion or lack of absorption.
NOTE
endolymph
- Stria Vascularis: Production
- Endolymphatic Sac: Absorption
• There are recurrent attacks in 2-3 months.
• It is typical for vertigo to wake the patient from sleep.
• As the patient has an attack, sensorineural hearing loss progresses.
• Sudden falling attacks - Tumarkin crises-typically clinical.
Diagnostic criteria:
vertigo
ear fullness
Hearing loss
tinnitus
• Nystagmus is horizontal; but it is not a diagnostic criterion.
Treatment:
Salt in the diet should be reduced.
Vasodilators, diuretics (acetazolamide) are used.
• Severe cases: Medical (gentamicin in the middle ear) or surgical labyrinthectomy (vestibular nerve cut)
NOTE
Rotatory (torsional) nystagmus: Vestibular disease
Horizontal nystagmus: Vestibular disease
Vertical (pushing upwards or downwards): Fractures involving the cerebellum or foramen magnum
Optokinetic nystagmus: Physiological
Vestibular Ototoxicity
Ototoxic drugs:
• Aminoglycosides, Vancomycin, Erythromycin, Tetracycline, Capreomycin, Loop diuretics, Chemotherapeutic agent (Nitrogen mustard, vincristine), Salicylates, Quinine
Otosclerosis
• Spongy bone formation in the otic capsule (hard bone tissue surrounding the inner ear and labyrinth)
• Usually bilateral, most often it starts from the oval window (fissula ante fenestram).
Etiology:
50% autosomal dominant inheritance
Fluorine-zinc deficiency, puberty, menopause
Pregnancy exacerbates symptoms.
It is common in osteogenesis imperfecta.
MEASES VIRUS
• Those located in the oval window: It starts with conductive hearing loss, and later on, it creates sensory hearing loss.
• Otosclerosis involving (onset) the cochlea: It causes sensorineural hearing loss.
• Paracuzzi: Better hearing in noisy environment, all conduction losses are present.
Diagnosis:
Hearing loss that can be conductive-mixed-sensorineural
The acoustic reflex test is impaired.
Carhart notch: There is a decrease in the bone path at 2000 Hz in audiometry.
The Schwartz sign (pinkness of the membrane) is due to the reflex of the vascularity of the metabolic focus above the promontuar. It happens early.
have a family history
Symmetrical progressive hearing loss
In oval window otosclerosis, a stapedectomy is performed and a prosthesis is placed.
The most feared complication of his surgery is the permanent neural-type hearing lose.
Cogan Syndrome
It develops after URTI due to chlamydia infection.
• It is characterized by interstitial keratitis, sensorineural hearing loss, and episodic vertigo.
• It can be confused with Meniere's syndrome.
Vestibular neuritis
Meniere or endolymphatic hydrops
Vestibular ototoxicity
otosclerosis
Cogan syndrome
Benign Positional Paroxysmal Vertigo (BPPV)
In many cases, the etiology is unknown.
pathophysiology
Channelolithiasis: it most commonly occurs when it falls into the posterior semicircular canal.
• There are dizziness that occur with head movements and end in 10-20 seconds.
• Posterior semicircular canal BPPV is most common.
Diagnosis
Provocation tests (Dix-Hallpike maneuver, modified Barany test)
• Nystagmus with a latent period (2-3 sec)
• Horizontal rotatory nystagmus
• Nystagmus lasting less than 1 minute (tiring)
• Nystagmus decreases as the test is repeated.
Treatment:
• Reposition maneuvers (Epley maneuver)
Vestibular Neuritis
• History of URTI or gastroenteritis
• Very severe dizziness, nausea, vomiting
• Spontaneous nystagmus, horizonto-rotatory
• Neurological examination and hearing are normal.
• Significant improvement is seen in complaints within the first 48 hours.
• Tinnitus, hearing loss, fullness etc. There are no ear complaints.
Meniere's Disease
• In endolymphatic hydrops; There is excess endolymph secretion or lack of absorption.
NOTE
endolymph
- Stria Vascularis: Production
- Endolymphatic Sac: Absorption
• There are recurrent attacks in 2-3 months.
• It is typical for vertigo to wake the patient from sleep.
• As the patient has an attack, sensorineural hearing loss progresses.
• Sudden falling attacks - Tumarkin crises-typically clinical.
Diagnostic criteria:
vertigo
ear fullness
Hearing loss
tinnitus
• Nystagmus is horizontal; but it is not a diagnostic criterion.
Treatment:
Salt in the diet should be reduced.
Vasodilators, diuretics (acetazolamide) are used.
• Severe cases: Medical (gentamicin in the middle ear) or surgical labyrinthectomy (vestibular nerve cut)
NOTE
Rotatory (torsional) nystagmus: Vestibular disease
Horizontal nystagmus: Vestibular disease
Vertical (pushing upwards or downwards): Fractures involving the cerebellum or foramen magnum
Optokinetic nystagmus: Physiological
Vestibular Ototoxicity
Ototoxic drugs:
• Aminoglycosides, Vancomycin, Erythromycin, Tetracycline, Capreomycin, Loop diuretics, Chemotherapeutic agent (Nitrogen mustard, vincristine), Salicylates, Quinine
Otosclerosis
• Spongy bone formation in the otic capsule (hard bone tissue surrounding the inner ear and labyrinth)
• Usually bilateral, most often it starts from the oval window (fissula ante fenestram).
Etiology:
50% autosomal dominant inheritance
Fluorine-zinc deficiency, puberty, menopause
Pregnancy exacerbates symptoms.
It is common in osteogenesis imperfecta.
MEASES VIRUS
• Those located in the oval window: It starts with conductive hearing loss, and later on, it creates sensory hearing loss.
• Otosclerosis involving (onset) the cochlea: It causes sensorineural hearing loss.
• Paracuzzi: Better hearing in noisy environment, all conduction losses are present.
Diagnosis:
Hearing loss that can be conductive-mixed-sensorineural
The acoustic reflex test is impaired.
Carhart notch: There is a decrease in the bone path at 2000 Hz in audiometry.
The Schwartz sign (pinkness of the membrane) is due to the reflex of the vascularity of the metabolic focus above the promontuar. It happens early.
have a family history
Symmetrical progressive hearing loss
In oval window otosclerosis, a stapedectomy is performed and a prosthesis is placed.
The most feared complication of his surgery is the permanent neural-type hearing lose.
Cogan Syndrome
It develops after URTI due to chlamydia infection.
• It is characterized by interstitial keratitis, sensorineural hearing loss, and episodic vertigo.
• It can be confused with Meniere's syndrome.