TEST #3 Disorders of Equilibrium (Dr. Sachen) Flashcards
General Considerations
Balance and awareness of body position in relation to surroundings requires input from two of the following three systems:
1) VISUAL: to judge distance
2) LABYRINTHINE: to judge Acceleration and Position Change
3) PROPRIOCEPTIVE: to judge posture
* Important of ROMBERG TEST**
Dizziness
VERY COMMON PROBLEM IN ELDERLY:
- THIRD most common outpatient complaint
- Affects 33% of all people over age 40 in one study
- More common in ELDERLY
- More common in those with DIABETES and other chronic illnesses - more common in those taking certain medications
- Greatly INCREASED RISK of Falls and Injury
BUT A VERY VAGUE COMPLAINT:
- A SYMPTOM and not a diagnosis
- A sensation of movement, unsteadiness, faintness, dysequilibrium, etc.
Dizziness means different thing to different people
- Spinning, tilting, listing, rolling, falling
- Unsteadiness, imbalance, falling
- Floating, near fainting, lightheadedness
- Blurry vision, hazy
- Disoriented, confused, spacy, dreamlike
- Anxious, tense
Disorders of Equilibrium
First DEFINE the Symptom
1) VERTIGO: illusion of movement of oneself or objects around self may be VESTIBULAR or neurologic in origin
2) DISEQUILIBRIUM: may be CAUSED BY Vertigo but usually a nonvertiginous state of altered static or dynamic balance due to dysfunction of
CEREBELLUM, DORSAL COLUMNS (sensory), MOTOR SYSTEMS (central or peripheral, basal ganglia
3) PRESYNCOPE: Lightheadedness or impending LOSS OF CONSCIOUSNESS often due to orthostasis, arrhythmia, hyperventilation and aggravated by high temperature, prolonged standing, large meals
Vertigo
- Illusion of movement – rotatory, body tilt, impulsion
- Due to disturbance in vestibular dysfunction (Semicircular Canals/ Otoliths)
- Often accompanied by sweating, nausea
- Sometimes associated with HEARING IMPAIRMENT or TINNITUS
Disequilibrium
Nonvertiginous altered static or dynamic balance:
1) SENSORY: proprioceptive deficit, visual impairment, compensated vestibular disorders, worse in dark and associated with a ROMBERG SIGN.
2) MOTOR: Mechanical (arthritis), Peripheral or Central (motor function), Cerebellar, NO ROMBEG SIGN.
3) CEREBELLAR: NO ROMBERG SIGN (Cannot stand with feet together with eyes open or closed).
Presyncope
Sense of impending LOSS of Consciousness!!!!
- Often associated with Pallor, Sweating, visual dimming or constricted fields, weakness
- ETIOLOGIES: arrythmia, hypotension, vasovagal excess, pulmonary emboli, drugs
- Aggravated by increased temperature, prolonged standing, large meals, deconditioning
Central versus Peripheral
PERIPHERAL:
1) Vertigo:
- Intense
2) Duration of Nystagmus:
- Brief
3) Fatigue of Nystagmus:
- Yes
4) Direction of Nystagmus:
- Fixed
5) Direction of Nystagmus:
- Horizontal/ Diagonal
6) Latency of Nystagmus:
- Several Seconds
7) N and V:
- Intense
8) Hearing Loss:
- Possible
9) Neuro Symptoms:
- NEVER
CENTRAL:
1) Vertigo:
- Mild
2) Duration of Nystagmus:
- Persist
3) Fatigue of Nystagmus:
- No
4) Direction of Nystagmus:
- Changeable
5) Direction of Nystagmus:
- Can be Vertical
6) Latency of Nystagmus:
- None
7) N and V:
- Mild
8) Hearing Loss:
- Rarely
9) Neuro Symptoms:
- Usually
Peripheral Causes of Vertigo
- Benign positional vertigo
- Vestibular neuronitis
- Meziere’s Disease
- Drug induced ototoxicity
Peripheral: Benign Positional Vertigo
- BPV is the MOST COMMON CAUSE of RECURRENT VERTIGO, with a lifetime prevalence of 2.4%.
- ETIOLOGY – idiopathic, trauma (head/barometric), infection
- BPV is a clinical SYNDROME characterized by brief recurrent episodes of vertigo TRIGGERED by CHANGES in HEAD POSITIONwith respect to gravity.
- The Duration, Frequency, and Intensity of symptoms of BPV vary, and spontaneous recovery occurs frequently.
- Thought due to DEBRIS FLOATING IN ENDOLYMPH of any of the semicircular canals (posterior most common).
Diagnosis of Peripheral: Benign Positional Vertigo
- Can be made on clinical grounds in a patient with positional vertigo.
- Confirmed by DIX- HALLPIKE position testing.
Treatment of Peripheral: Benign Positional Vertigo
1) Positional exercises often helpful
2) MEDICATIONS:
a) Vestibular suppressants – meclizine, scopolamine, valium
b) Antiemetics – Phenergan, Compazine, etc.
c) Anxiolytics
3) Physical therapy – vestibular rehabilitation (balance therapy)
BPV by Canal Type
POSTERIOR:
1) Estimated Frequency:
- 81-89%
2) Provocative Maneuver:
- Dix Hallpike*
3) Nystagmus:
- Torsional
HORIZONTAL:
1) Estimated Frequency:
- 8-17%
2) Provocative Maneuver:
- Supine Roll Test (Pagnini- McClure)
3) Nystagmus:
- Horizontal Direction Changing
ANTERIOR:
1) Estimated Frequency:
- 1-3%
2) Provocative Maneuver:
- Dix Hallpike*
3) Nystagmus:
- Downbeat**, Torsional
- In posterior canal benign positional vertigo, nystagmus is provoked following Dix Hallpike positioning with the affected ear down. In anterior canal benign positional vertigo, nystagmus is provoked following Dix Hallpike positioning with the affected ear up.
** The observation of vertical positional nystagmus requires CAREFUL assessment to rule out brainstem or cerebellar lesions.
Peripheral: Vestibular Neuronitis
- Spontaneous attack of vertigo that does not involve hearing loss or tinnitus and resolves spontaneously.
- Characterized by vertigo, nausea, and vomiting of acute onset, typically lasting up to 2 wk.
- Not characteristically positional
Peripheral: Meziere’s Disease
– Described by Meniere in 1861
– Onset between 20-50 years of age (rarely older)
– M:F = 1:3
– Thought due to an increase in the volume of labyrinthine endolymph because of poor absorption (endolymphatic hydrops)
Peripheral: Meziere’s Disease Cont
1) Recurrent episodes of spontaneous vertigo
– lasting more than 20 minutes, typically hours, but less
than 24
– subsequent disequilibrium could last several days
2) Audiometrically documented low frequency hearing loss
3) Tinnitus
4) Aural fullness
Peripheral: Drug Induced
1) Alcohol
2) Salicylates
3) Anti epileptics – phenytoin, carbamazepine
4) Quinine compounds – quinidine, plaque nil
5) Antibiotics – aminoglycosides, tetracycline, vancomycin
6) Diuretics – furosemide, bumetanide
7) Chemotherapeutic – cisplatin, methotrexate, vincristine
Central causes of Vertigo/ Disequilibrium
- Vascular – ischemic TIA/stroke
- Vascular – hemorrhage (cerebellar)
- Trauma
- Developmental - Chiari
- Neoplastic/paraneoplastic
- Infectious – meningitis
- Vestibular migraine
- Inflammatory
- Metabolic
- Degenerative – Parkinson’s
- Drugs/Toxins
- Hereditary
- Multiple sclerosis
Central: Vascular (Ischemic)
- More common in the ELDERLY
- ABRUPT ONSET!!!!!!!
- Ischemia of labyrinth, brainstem or both (may be unclear at times)
- Vertigo associated with other neuro symptoms (N&V, diplopia, dysarthria, hiccups, weakness and/or sensory loss)
- REPEATED EPISODES OF ISOLATED VERTIGO WITHOUT OTHER NEUROLOGICAL SYMPTOMS SHOULD ALWAYS SUGGEST A NON-NEUROLOGICAL CAUSE!!!!!!
Central: Neoplastic/ Paraneoplastic
CEREBELLOPONTINE ANGLE TUMOR
• ACOUSTIC NEUROMA (Schwannoma), meningioma, and cholesteatomas.
• Generally involves CN’s V, VII,VIII.
(1st SYMPTOM = HEARING LOSS; 1st SIGN = absent CORNEAL REFLEX)**
- Acoustic neuromas often associated with Neurofibromatosis types I and ESPECIALLY II.
- Hearing loss, tinnitus, vertigo (uncommon), facial pain or sensory loss, facial weakness and perhaps long tract signs.
Central: Neoplastic/ Paraneoplastic
PARANEOPLASTIC CEREBELLAR DEGENERATION
- Can occur as a remote effect of systemic cancer
- Most commonly associated with cancer of breast, ovary, lung
- Pathogenesis involves antibodies to tumor cell antigens that CROSS-REACT with CEREBELLAR PURKINJE CELLS
- Can APPEAR AT ANY TIME – may even precede the cancer diagnosis
- May improve with treatment of the cancer
Central: Vestibular Migraine
REQUIREMENTS FOR DIAGNOSIS
- AT LEAST 5 EPISODES of moderate/severe vestibular symptoms lasting 5 minutes to 72 hours.
- Current or previous history of migraine with/without aura.
- One or more migraine features with at least 50% of episodes
a) Headache – unilateral, pulsatile, moderate to severe intensity
b) Photophobia, phonophobia, nausea
c) Visual aura - Unaccounted for by other diagnosis.
Central: Infections
1) VIRAL – EBV, HSV, HIV, PML, etc, etc
2) RICKETTSIAL – RMSF, Lyme’s disease
3) BACTERIAL – meningococcal, pneumococcal, H. flu
4) FUNGAL – cryptococcal, histoplasma
Central: Metabolic
1) DEFICIENCES – Vitamin B1, B12, E
2) HYPOTHYROID
- affects cerebellum
- slowly evolves
- replacement improves function
3) WILSON’S DISEASE (copper metabolism)
- dysarthria, movement disorder, KAYSER-FLEISHER RINGS
- LOW serum CERULOPLASMIN, HIGH 24 hr. Cu
Central: Toxins
1) TOXINS – heavy metals, CO, glue (toluene), organic solvents
2) ETHANOL
a) Acute
b) Chronic: Affects Cerebellar VERMIS causing TRUNCAL and LOWER EXTREMITY ATAXIA: IRREVERSIBLE!!!!!
3) MEDICATIONS: DPH, Anticonvulsants, 5-FU, Li, Mtx
Parkinson’s Disease
- CHARACTERISTIC FEATURES: rest tremor, rigidity, bradykinesia.
- SUBTLE FEATURES: Decreased Blink FREQUENCY, hypomimia, poor upgaze, hoarse muffled voice.
- GAIT FEATURES: festination, short shuffling steps, pulsion (forward or backward), en bloc turns.
- Due to a deficiency of dopamine production in SUBSTANTIA NIGRA.
Hereditary: Spinocerebellar Ataxias
A) HETEROGENEOUS (32 of them) - are all trinucleotide repeat disorders, mostly autosomal dominant, some recessive.
B) SCA 1 (olivopontocerebellar) and SCA 3 (Machado-Joseph) are MOST COMMON!!!!
C) Slowly progressive cerebellar ataxia of limbs combined with brainstem signs (dysarthria, oculomotor disturbance, spasticity) and peripheral neuropathy.
D) Effects gait early and severely leading to bed confinement. Treatment is supportive – DEATH is often the outcome.
Hereditary: Friedrich’s Ataxia
A) AUTOSOMAL RECESSIVE disorder due to a mutation on Chromosome 9.
B) Obligatory Features (present 100% of time)
- Onset before age 20
- Gait ataxia
- Progression of ataxia to involve all 4 limbs
- Dysarthria
- Impaired position/vibratory sense in legs
- Muscle weakness
- Absent tendon reflexes in legs
Secondary Features of Friedrich’s Ataxia
- Extensor plantar responses
- Pes cavas
- Scoliosis
- CARDIOMYOPATHY (often cause of death)
- +/- optic atrophy, nystagmus
Prognosis fo Friedrich’s Ataxia
- No treatment available.
- Neurologic dysfunction typically results in the inability to walk unaided within 5 years after onset of symptoms and in bedridden state within 10-20 years.
- Mean age of death – 35 years
Hereditary: Ataxia- Telangiectasia
a) AUTOSOMAL RECESSIVE – Chromosome 11 mutation
b) Progressive PANCEREBELLAR Degeneration involving nystagmus, dysarthria, and gait, limb and trunk ataxia which begins in infancy (
Hereditary: Ataxia- Telangiectasia Cont
• Oculocutaneous telangiectasia usually appears in the TEEN YEARS.
- BULBAR Conjunctivae are typically affected first, followed by sun-exposed areas of the skin, including the ears, nose, face, and antecubital and popliteal space.
- Immunological IMPAIRMENT (DECREASED IgA and IgE) usually becomes evident later in childhood and is manifested by recurrent sinopulmonary infections in >80% of patients.
- Other common clinical findings are progeric changes of the skin and hair, hypogonadism, and insulin resistance
