Disorders Of Equilibrium (Sachen) Flashcards

1
Q

Balance and awareness of body position in relation to surroundings require input from two of the following three symptoms?

A

Visual: to judge distance
Labyrinthine: to judge acceleration and position change
Proprioceptive: to judge posture
(Importance of Romberg test)

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2
Q

Describe dizziness as a common clinical problem

A

3rd most common outpatient complaint
Affects 33% of all people over age 40
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 injry

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3
Q

What can dizziness mean to different people?

A
Spinning, tilting, listing, rolling, falling
Unsteadiness, imbalance, falling
Floating, near fainting, lightheadedness
Blurry vision, hazy
Disoriented, confused, spacy, dreamlike
Anxious, tense
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4
Q

Define vertigo

A

Illusion of movement of oneself (rotary, body tilt, impulsion) or objects around self
May be vestibular (semicircular canals/otoliths) or neurologic origin
Often accompanied by sweating, nausea
Sometimes associated with hearing impairment or tinnitus

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5
Q

Define disequilibrium

A

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

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6
Q

Define presyncope

A

Lightheadedness or impending loss of consciousness
Often associated with pallor, sweating, visual dimming or constricted fields, weakness
Etiologies: orthostasis, arrhythmia, hyperventilation, hypotension, vasovagal excess, pulmonary emobli, drugs
Aggravated by high temperature, prolonged standing, large meals, deconditioning

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7
Q

Describe sensory disequilibrium

A
Proprioceptive deficit
Visual impairment
Compensated vestibular disorders
*Worse in dark*
Associated with Romberg sign
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8
Q

Describe motor disequilibrium

A

Mechanical (arthritis)
Peripheral or central (motor function)
Cerebellar
No Romberg sign

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9
Q

Describe cerebellar disequilibrium

A

No Romberg sign (cannot stand with feet together with eyes open or closed)

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10
Q

Compare peripheral vs central disorders of equilibrium

A
Peripheral:
Intense vertigo
Brief, fixed, horizontal/diagonal nystagmus with several seconds of latency and fatigue of nystagmus
Intense nausea and vomiting
Possible hearing loss
Never any neuro symptoms
Central:
Mild vertigo
Persistent, changeable direction, can be vertical nystagmus with no latency and no fatigue of nystagmus
Mild nausea and vomiting
Rarely hearing loss
Usually neuro symptoms
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11
Q

What are peripheral causes of vertigo?

A

Benign positional vertigo
Vestibular neuronitis
Meniere’s disease
Drug induced ototoxicity

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12
Q

What is Benign Positional Vertigo (BPV)?

A

Most common cause of recurrent vertigo, with 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 position with respect to gravity
Duration, frequency, and intensity of symptoms of BPV vary, and spontaneous recovery occurs frequently
Thought due to debris floating in endolymph of any of semicircular canals (posterior most common)

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13
Q

Describe posterior BPV

A

81-89% frequency
Provacative manuever: Dix Hallpike with affected ear down
Nystagmus: Torsional

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14
Q

Describe horizontal BPV

A

8-17% frequency
Provacative maneuver: Supine roll test (Pagnini-McClure)
Nystagmus: horizontal direction changing

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15
Q

Describe anterior BPV

A

1-3% frequency
Provocative manuever: Dix Hallpike with affected ear up
Nystagmus: Downbeat, torsional
Requires careful assessment to rule out brainstem or cerebellar lesions

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16
Q

Describe diagnosis of benign positional vertigo

A

Can be made on clinical grounds in patient with postural vertigo
Confirmed by Dix Hallpike position testing

17
Q

Describe treatment of benign positional vertigo

A

Positional exercises often helpful

Medications:
Vestibular suppressants: meclizine, scopolamine, valium
Antiemetis: Phnergan, Compazine
Anxiolytics

Physical therapy: vestibular rehabilitation (balance therapy)

18
Q

Describe Vestibular Neuronitis

A

Peripheral equilibrium disorder
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 weeks
Not characteristically positional

19
Q

Describe Meniere’s disease

A

Peripheral equilibrium disorder
Onset between 20-50 yrs of age (rarely older)
M:F = 3:1

Thought to be due to an increase in volumen of labyrinthine endolymph because of poor absorption (endolymphatic hydrops)

Recurrent episodes of spontaneous vertigo

  • Lasting more than 20 minutes, typically hours, but less than 24 hr
  • subsequent disequilibrium could last several days
  • audiometrically documented low frequency of hearing loss
  • Tinnitus
  • Aural fullness
20
Q

What drugs cause drug induced equilibrium?

A

Peripheral
Alcohol
Salicylates
Anti-epileptics: phenytoin, carbamazepine
Quinine compounds: quinidine, plaquenil
Antibiotics: aminoglycosides, tetracycline, vancomycin
Diuretics: furosemide, bumetanide
Chemotherapeutic: cisplatin, methotrexate, vincristine

21
Q

What are central causes of vertigo/disequilibrium?

A
Vascular: ischemic TIA/stroke, hemorrhage (Cerebellar)
Trauma
Developmental: Chiari
Neoplastic/paraneoplastic
Infectious: meningitis
Vestibular migraine
Inflammatory
Metabolic
Degenerative: Parkinson's
Drugs/toxins
Hereditary
Multiple sclerosis
22
Q

Describe vascular (ischemic) disequilibrium

A

Central
More common in elderly
Abrupt onset
Ischemia of labyrinth, brainstem, or both (unclear at times)
Vertigo associated with other neuron symptoms (N&V, diplopia, dysarthria, hiccups, weakness, and/or sensory loss)
Repeated episodes of isolated vertigo without other neurological symptoms should always suggest nonneurological cause

23
Q

Describe cerebellopontine angle tumor

A

Central: neoplastic/paraneoplastic
Acoustic neuroma (Schwannoma), meningioma, and cholesteatomas
Generally involves CN V, VII, VIII
1st symptom = hearing loss
1st sign = absent corneal reflex
Acoustic neuromas often associated with neurofibromatosis types I an especially II
Hearing loss, tinnitus, vertigo (uncommon), facial pain or sensory loss, facial weakness, and perhaps long tract signs

24
Q

Describe paraneoplastic cerebellar degeneration

A

Central
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 cancer diagnosis
May improve with treatment of cancer

25
Q

What are the requirements for diagnosis of vestibular migraine?

A

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:
-headache (unilateral, pulsatile, moderate to severe intensity)
-photophobia, phonophobia, nausea
-visual aura
Unaccounted for by other diagnosis

26
Q

Describe infectious causes of central disequilibrium

A

Viral: EBV, HSV, HIV, PML
Rickettsial: RMSF, Lyme’s disease
Bacterial: meningococcal, pneumococcal, H. Flu
Fungal: cryptococcal, histoplasma

27
Q

What are metabolic causes of central disequilibrium?

A

Deficiencies: Vitamin B1, B12, E

Hypothyroid

  • affects cerebellum
  • slowly evolves
  • replacement improves function

Wilson’s disease (copper metabolism)

  • dysarthria, movement disorder, Kayser-Fleisher rings
  • low serum ceruloplasmin, high 24 hr Cu
28
Q

What toxins cause central disequilibrium?

A

Toxins: heavy metals, CO, glue (toluene), organic solvents

Ethanol

  • Acute
  • chronic: affects cerebellar vermis causing truncal and lower extremity ataxia, irreversible

Medications: DPH, anticonvulsants, 5-FU, Li, Mtx

29
Q

Describe Parkinson’s disease and disequilibrium

A

Degenerative
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 deficiency of dopamine production in substantia nigra

30
Q

Describe spinocerebellar ataxia

A

Hereditary
Heterogeneous (32 of them): are all trinucleotide repeat disorders, mostly autosomal dominant, some recessive
SCA1 (olivopontocerebellar) and SCA3 (Machado-Joseph) are most common
Slowly progressive cerebellar ataxia of limbs combined with brainstem signs (dysarthria, oculomotor disturbance, spasticity) and peripheral neuropathy
Affects gait early and severely, leading to bed confinement
Treatment is supportive: death is often outcome

31
Q

What are the obligatory features of Friedrich’s ataxia?

A

Autosomal recessive disorder due to mutation on chr 9
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

32
Q

What are the secondary features of Friedrich’s ataxia?

A
Extensor plantar responses
Pes cavus
Scoliosis
Cardiomyopathy (often cause of death)
\+/- optic atrophy, nystagmus
33
Q

What is the prognosis of Friedrich’s ataxia?

A

No treatment available
Neurologic dysfunction typically results in 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

34
Q

Describe Ataxia-telangiectasia

A

Autosomal recessive: chr 11 mutation

Progressive pancerebellar degeneration involving nystagmus dysarthria, and gait, limb, & trunk ataxia which begins in infancy (

35
Q

Describe oculocutaneous telangiectasia, immunologic impairment, and other clinical findings in ataxia-telangiectasia

A

Oculocutaneous telangiectasia usually appears in teen years
-bulbar conjunctivae are typically affected first, followed by sun-exposed areas of skin, including ears, nose, face, and antecubial 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 pts

Other common clinical findings are progeric changes of skin and hair, hypogonadism, and insulin resistance