Neuro Lect 5

  1. Accounts for 1% of visits to US office based physicians. Of patients older than 60 yrs, 20% have experiences this enough to affect their daily lives. Can be a sensation a pt interprets as abnormal with no pathological and localizable value.
  2. Dizziness is a general term that describes a variety of feelings to include what sensations?
    • vertigo
    • disequilibrium
    • light headedness
  3. What are the three categories dizziness is broken into?
    • faintness/syncope
    • vertigo
    • miscellaneous head sensation
  4. What are semantically appropriate definitions people use to describe dizziness?
    • lightheaded
    • faint
    • spinning
    • giddiness
  5. What are potentially misleading definitions people use to describe dizziness?
    • mental confusion
    • blurred vision
    • HA
    • tingling
  6. A sense of rotational motion. Indicates a dysfunction with the vestibular pathways.
  7. A term used to describe the feeling of being "unsteady" or about to fall, and is often associated with some type of abnormal gait.
  8. The sensation that one is about to faint.
  9. A term used to describe a transient cerebral hypoperfusion (orthostatic).
    presyncope (often prodrome to true syncopal event)
  10. Mild lightheadedness, impaired sensation in feet, poor vision, affects elderly when walking. Also known as benign disequilibruim of aging.
    multiple sensory defect dizziness
  11. Transient loss of consciousness and postural tone from other vasopressor or cardiogenic causes that ultimately results in brain hypo perfusion. Characterized by sudden loss of consciousness, and postural collapse with spontaneous recovery.
    • syncope (fainting)
    • experienced by 30% of adult populations, accounts for 3% of ER visits
  12. What are the vascular tone disorders that can cause syncope?
    • vasovagal (neurocardiogenic)
    • postural
    • carotid sinus hypersensitivity
    • situational
    • glossopharyngeal neuralgia
  13. Vascular tone disorder that causes syncope associated with sympathetic withdrawal (vasodilation), increased parasympathetic activity (bradycardia), and sympathetic withdrawal (difference from vasovagal). Referred to as the common faint and accounts for nearly half of all syncopal episodes. Is recurrent, often present with a prodrome (secs to mins before). Rare occurrence in supine patients. Pts will be pale, duration and responsiveness varies, clonic jerks may occur. Sphincter control is maintained.
    vasodepressor (neurocardiogenic)
  14. Vascular tone disorder that causes syncope found in pts with a chronic defect in vasomotor reflexes which causes a systemic fall in arterial blood flow when a person stands upright. Is always associated with changes in position, is found to occur in about 30% of elderly (polypharmacy & antidepressants may contribute). Often associated with autonomic nervous system abnormalities (sweating, impotence, sphincter control).
    postural (orthostatic) hypotension
  15. What are common causes for postural (orthostatic hypotension)? What are the less common causes?
    • DM
    • nutritional deficiencies
    • amyloid polyneuropathy
    • physical deconditioning
    • -------------------------
    • Shy-Dager syndrome
    • straitonigral degeneration
    • guillain-barre variant
  16. Vascular tone disorder that causes syncope by increased pressure on carotid baroreceptors. Typically occurs after shaving, wearing a tight collar or simply turning the head to one side which can cause afferent nerve fibers to activate the efferent sympathetic nerve fibers in the heart and blood vessels. Usually occurs in men >50yrs.
    carotid sinus hypersensitivity
  17. What can carotid sinus hypersensitivity cause?
    • sinus arrest
    • atrioventricular block
    • vasodilatation
    • mixed response
  18. Vascular tone disorder that causes syncope with cough, deglutition, micturition, defecation due to an abnormal autonomic control involving cardioinhibitory, vasodepressor (or both) responses.
    situational syncope
  19. Vascular disorder that causes syncope that is often preceded by pain in the oropharynx, tonsillar fossa or tongue. LOC is more likely associated with asystole. MOA is likely to involve activation of afferent impulses in the glossopharyngeal nerve that terminate in the nucleus solitaries of the medulla which then activate the dorsal motor nucleus of the vagus nerve.
    glossopharyngeal neuralgia
  20. What are the cardiovascular disorders that can cause syncope?
    • brady arrhythmias: sinus, sinoatrial block, sinus arrest, sick sinus syndrome, atrioventricular block
    • tachy arrhythmias: SVT with structural cardia disease, afib with WPW syndrome, a-flutter (1:1), ventricular tachy
  21. What are the cardiopulmonary etiologies that can cause syncope besides arrhythmias?
    • PE
    • pulmonary HTN
    • atrial myoxoma
    • myocardial disease (massive MI)
    • left vent myocardial restriction of constriction
    • pericardial tamponade
    • aortic outflow tract obstruction (stenosis)
    • hypertrophic obstructive cardiomyopathy
  22. Syncope with what disorders can occur from a mechanical or arrhythmic abnormality with no prodrome (falling/sudden drops common), is usually associated with conduction of exertion/post exertion and can occur with patient in a recumbent position.
    cardiovascular disorders
  23. What cerebrovascular diseases can cause syncope?
    • vertebrobasilar insufficiency
    • basilar artery migraine
  24. What disorders rarely cause syncopal events but can lower the threshold for them?
    • vertebrobasilar insufficiency/basilar artery migraine
    • Note: brainstem is responsible for maintaining consciousness, the vertebrobasilar arteries supply the brainstem; basilar artery migraine is rare and causes syncope in ADOLESCENTS
  25. What are cerebral causes for syncope other than vertebrobasilar insufficiency or basilar artery migraines?
    • basilar artery TIA
    • subclavian steal syndrome
    • migraine (up to 10% of pts)
    • carotid sinus syncope
  26. What are some common ddx for syncope?
    • anxiety attacks
    • hyperventilation syndrome
    • seizures
    • hypoglycemia
    • acute hemorrhage
    • hysterical fainting
  27. Cause of syncope usually related to postural changes, emotional stress, pain, straining and is typically precede by pallor, sweating, nausea, and malaise. Recovery is rapid with laying down. Pt may have "seizure-like" motor movement but is not a post-octal state.
    vasovagal (simple faint)
  28. What are the diagnostic tests used for syncope?
    • ECG: look at sinus node function and AV conduction, reveals cause in 20-50%
    • autonomic testing: check orthostatic vital signs, consider carotid massage if no stenosis/head up tilt table test to determine if vasovagal
    • exercise testing: when sxs are exercise related
  29. What testing should you do first when diagnosing a reason for syncope? How is it done?
    • autonomic testing (head-up table testing)
    • passively tilt at 70 degrees for 10-40 mins with isoproterenol infusion
  30. Syncope characterized by LOC along with tachycardia becoming bradycardia, pt appears ashen-grey and may have some clonic jerks of the face or hands. Pulse is typically thready and depth of unconsciousness will vary.
    • vasovagal
    • Note: consciousness regained rapidly, residual sxs may persist a few minute, confusion should be brief (30 secs)
  31. How is vasovagal syncope treated?
    • place pt in supine position with feet slightly elevated
    • feel improved pulse
    • tx any underlying causes
  32. What are the historical features that differentiate seizures from syncope?
    • seizure: "aura" symptoms (olfactory, visual, auditory or taste hallucinations), post-ictal state (brief/prolonged)
    • syncope: prodromal lightheadedness (brain hypoperfusion), clear thinking upon recovery
    • Note: may have features for several hours or a few seconds
  33. Sense of rotational motion or hallucination of movement (pt vs environment) associated with impulsion and oscillopsia, N/V, and gait ataxia. Most often caused by an acute asymmetry or imbalance of neural activity between left and right vestibular systems. Must differentiate central/peripheral cause.
  34. What are the three systems that vertigo can arise from?
    • vestibular apparatus
    • visual system
    • somatosensory system (info from skin, joint, muscles/tendons)
  35. How is pre syncope distinguished from vertigo?
    • presyncope: about to pass out, sxs after prolonged recumbency, improved by sitting/lying down
    • vertigo: spinning, rotating, moving, brought on by change in head position, additional neuro sxs (hear loss/ringing, nystagmus, ataxia)
  36. What is the location of vertigo associated with intense, short lived episodes of dizziness, typically affected by head position with nystagmus always present (horizontal, NOT vertical), inner ear symptoms and acoustic symptoms?
    peripheral vertigo
  37. What is the location of vertigo associated with long episodes of unchanging dizziness, is not affected by head position or movement, may or may not have nystagmus (vertical or horizontal), and has additional nervous system findings?
    central vertigo
  38. What are the additional nervous system findings present in central vertigo?
    • motor/sensory deficits
    • hyperreflexia
    • extensor plantar responses
    • ataxia dysarthria
  39. What kind of vertigo occurs in normal individuals in certain situations due to intersensory mismatch (car sickness), involves the vestibular system being subjected to unfamiliar head movements (sea sickness), unusual head/neck position (painting a ceiling) or following a spin?
    physiologic vertigo
  40. What kind of vertigo occurs due a lesion arising in one of the stabilizing sensory systems, or incorrect optical Rx, peripheral neuropathy, or vestibular dysfunction (most common)?
  41. What are common causes of peripheral vertigo?
    • benign paroxysmal positional vertigo (BPPV/viral)
    • acute/chronic peripheral vestibulopathy
    • Meniere's disease
    • acoustic neuroma
    • gentamycin ototoxicity
  42. What are common causes for central vertigo?
    • alcohol intoxication
    • Wernicke's encephalopathy
    • MS
    • alcoholic cerebellar degeneration
    • TIA/stroke
    • cerebellar ataxias
  43. Severe vertigo with a latency of 2-40 seconds with fatigability and habituation describe the features of what affected location?
    • peripheral (vertigo)
    • Note: produces significant distress, no neurologic findings on exam
  44. Mild vertigo with no latency period, fatigability or habituation describe the features of what affected location?
    central (vertigo)
  45. What are the causes for central vertigo?
    • vascular: infarct, AVM
    • chronic: MS, ETOH induced, hypothyroid, congenital
    • tumor
  46. What is included/found in the examination on a patient with central vertigo?
    • orthostatic VS
    • nystagmus
    • buits
    • cerebellar signs: romberg, gaits (wide), intention tremor, finger to nose/heel to shin/RAM
    • abnormal Weber and/or Rinne: weber lateralizes away from side of lesion, Rinne has diminished AC and BC
    • positive Barany maneuver
  47. The main radiations of which nerve go to the nuclei of CN III, IV, VI, spinal cord, cerebral cortex, and cerebellum?
    • CN VIII (vestibular portion)
    • Note: vestibular ocular reflex (VOR) maintains visual stability during movement
  48. What are the three factors that maintain balance and are tested for using the Romberg test?
    • visual system
    • proprioception
    • vestibular system
    • Note: taks 2/3 of these to maintain balance, closing the eyes makes pt with proprioceptive loss run off of 1 system which is why they fall over with Romberg test
  49. How is nystagmus characterized?
    • position of gaze
    • amplitude
    • direction
  50. What are the terms for fast and slow eye movements of nystagmus?
    • saccades: fast
    • pursuit: slow
  51. With peripheral vestibular disorders, what eye position causes maximal nystagmus?
    when gaze is AWAY from the affected side
  52. What are the ocular disorders associated with central lesions?
    • gaze pareses
    • defective saccades/pursuits
    • nystagmus in any or all directions
    • ocular dysmetria (overshoot of visual target during saccadic movement)
  53. What type of nystagmus is a visual impairment that begins in infancy?
    pendular nystagmus
  54. What are the results of the Weber test in a patient with unilateral conduction deafness?
    vibration is heard in the DISEASED ear
  55. What are the results of the Weber test in a patient with unilateral partial nerve deafness?
    vibration is heard in the NORMAL ear
  56. What are the results of the Rinne test in a patient with unilateral conduction deafness?
    fails to hear air vibration after bone conduction
  57. What are the results of the Rinne test in a patient with unilateral partial nerve deafness?
    hears vibration in the air after bone conduction is gone
  58. What maneuver stimulates the semicircular canal by having the patient in a sitting position, rotating the head to one side and helping the patient lie down with the head off the table? What is evaluated with this test?
    • barany maneuver AKA hall-pike maneuver
    • nystagmus (whichever down side produces it is the "affected" side)
  59. Most common cause of acute peripheral vertigo, is due to otolithic crystals in the semicircular canal (probably) causing brief, sudden episodes of severe vertigo often with N/V. Can occur with any change in head position. Lasts for a couple of weeks with spontaneous resolution, has no hearing loss, and always presents with positional nystagmus (delayed onset, resolves in secs to mins).
    benign paroxysmal positional vertigo (BPPV)
  60. How is BPPV managed?
    • epley repositioning: dislodges otolith from canal
    • pharmacotherapy: meclizine 25mg po q4-6hrs, valium 5mg TID, scopolamine patch
  61. What is Meniere's disease triad?
    • fluctuating hearing loss: sensorineural (as it worse vertigo gets better)
    • episodic vertigo: typically lasts mins to days
    • low freq tinnitus: ringing in ears
  62. What is the suspected pathology behind Meniere's disease?
    too much endolymph
  63. What are the treatments for Meniere's disease?
    • diuretics (HCTZ/tramterine, aka Maxzide)
    • meclizine
    • scopolomine
    • valium
    • rehab
    • hearing aid
    • Meniett device
    • surgery
  64. What general term refers to spontaneous attacks of vertigo of no apparent cause with spontaneous resolution, nystagmus, no hearing loss, and no CNS dysfunction?
    acute peripheral vestibulopathies
  65. What are the causes of acute peripheral vestibulopathies and how is it treated?
    • acute labrynthitis, vestibular neuritis
    • supportive care
  66. Benign tumor arising from the sheath of CN VIII in the internal auditory canal causing insidious onset of hearing loss (unilateral sensorineural), tinnitus, HA, vertigo, and facial weakness.
    acoustic neuroma AKA acoustic schwannoma
  67. What is the best test and treatment for an acoustic neuroma?
    • MRI with contrast
    • surgical excision by translabyrinthine, craniectomy or combined approach (good prognosis)
  68. What are the drugs that cause toxic vestibulopathies and what do they do?
    • gentamycin: concentrates in endolymph, is ototoxic to sensory hair cells
    • alcohol: makes vestibular system unusually sensitive to gravity and position (peripheral), vertigo starts within 2 hrs, vertigo & nystagmus accentuated with eyes closed
    • salicylates: chronic high doses affect sensory hair cells
    • quinine: similar to aspirin
    • cis platinum: ototoxic chemo agent
  69. What is the classic triad of Wernicke's encephalopathy?
    • gait ataxia
    • ophthalmoplegia
    • confusion
  70. Caused by thiamine deficiency (esp alcoholics) which inhibits metabolism in brain regions with high metabolic requirements.
    Wernicke's encephalopathy
  71. What is the treatment for Wernicke's encephalopathy? What are some adverse affects of this disease?
    • 100mg IV thiamine for 5 consecutive days (for practical purposes all pts with undx altered mental status, oculomotor d/o or ataxia should get thiamine)
    • ataxia may not be fully reversible, and deficits in learning and memory may follow
  72. Caused by years of alcohol abuse leading to degeneration of Purkinje cells. Evolves gradually, causing gait ataxia and tremor. Nystagmus is usually absent, cognition remains intact. Is irreversible, even with abstinence from alcohol.
    alcoholic cerebellar degeneration
  73. What are the hallmarks of alcoholic cerebellar degeneration (ACD)?
    • midline cerebellar lesions w/ predominant involvement of lower extremities
    • chronic course
    • irreversibility after ETOH cessation
  74. Occlusion of the cerebellar artery that may cause SUDDEN onset of dizziness or vertigo along with some CN palsies (possibly). May result in cerebellar infarction, is best imaged with CT/MRI and requires a high index of suspicion.
    vertebrobasilar TIA (stroke)
Card Set
Neuro Lect 5
neuro lect 5