Neurology Flashcards
Vertigo diagnosis
most important is the history. “When you have dizzy spells, do you feel light headed or do you see the world spin around you?” True vertigo is the room spinning. Also need: neuro exam, head and neck exam, cardiac exam
Chronic dizziness is associated with these conditions
Falls, functional disability, orthostatic hypotension, syncope, strokes, fear of falling, depression, decreased social activities
What you need to dx neuro disorders
good hx, focal exam, a good differential dx to present to neurologists
Dizziness, acute v chronic
Dizziness is a term used to describe various abnormal sensations arising from perceptions of the body’s relationship to space or unsteadiness. Acute is 2 months.
Vertigo definition
Sensation of spinning in which the individual perceives movements of the environment in relation to the body (objective vertigo) or vice verson (subjective vertigo)
Dizziness patho
Sensation of postural instability or imbalance, vestibular system maintains spacial orientation at rest and during acceleration. Infection or congestion could alter this.
Diseases that could alter vestibular system
Menieres disease Benign Paroxysmal Positional Vertigo Recurrent Vestibulopathy Labyrinthitis/Vestibular Neuronitis Acoustic Neuroma Drug Toxicity Age related changes related to hair cells
Disorders of the proprioceptive system
Peripheral neuropathy - b12 deficiency and DM, cervical degenerative disorders. Proprioceptive system consists of mechanoreceptors in the joints, peripheral nerves, and posterior columns and multiple CNS connections. ANY CNS disorder can lead to an imbalance causing dizziness. Bells palsy can have prodromal symptoms of dizziness.
Ocular system and dizziness
Vision provides information about spacial orientation. Disorders of the ocular system: cataracts, macular degen, glaucoma, age related changes - decrease in acuity, dark adaption, contrast sensitivity, and accomodation
CN 1
Olfactory, smell.
CN 2
Optic, vision. Opthalmoscope, visual acuity
CN 3
Oculomotor, raise eyebrows, pupil constriction
CN 4
Trochlear
CN 5
Trigeminal, facial sensation
CN 6
Abducens
CN 7
Facial, smile, puff cheeks, raise eyebrows
CN 8
Acoustic, test hearing, test vertigo
CN 9
Glossopharyngeal, palate elevation and gag reflex
CN 10
Vagus, test articulation
CN 11
Spinal accessory, shrug shoulders,
CN 12
Hypoglossal, stick out tongue
The most common type of dizziness reported by older people
Mixed dizziness - different circumstances of being dizzy
Vertigo results from
disorders of the vestibular system and its connecting pathways
Disequilibrium
Feeling of unsteadiness or imbalance primarily involving lower extremities or trunk rather than the head. Patient usually expressese the feeling that he or she is about to fall. Results from disorders of proprioceptive system, musculoskeletal weakness or cerebellar disease
Pre-syncope
Results from hypoperfusion of the brain, is a feeling of lightheaddedness or impending faintness or the sensation that one is about to pass out. ***cardiovascular causes including vasovagal disorders are common causes in older persons
Multifactoral dizziness
“whirling” “tilting” “floating” and other nonspecific sensations
Menieres Disease
(Endolymphatic hydrops) 2-8 percent of older patients with dizziness. Etiology unknown. Pathology: excess endolymph within the cochlea and labyrinth. Involvement of the inner ear, “fullness”. Unilateral in majority of patients. May have nausea/vomiting/ha during episodes. Classic triad: episodic vertigo, tinnintus, and fluctuating sensory-neural hearing loss. True vertigo can last from 1-24 hours.
Weber Rinne megahertz
512
Benign Paroxysmal Positional Vertigo
Etiology unknown in most cases, although some have a history of head injury or viral labyrinthitis. Pathology: Results from freely moving particulate matter within the posterior semicircular canal. This movement causes alteration in the endolymphatic pressure resulting in vertigo and nystagmus
BPPV s/s
Vertigo, nystagmus, sudden onset, n/v. Precipitated by changes in the position of the head. Classically accompanied by rotational nystagmus. Dx w Dix-hallpike test
Recurrent vestibulopathy
Idiopathic, vertigo lasts from 5minutes until 24 hours. Characterized by recurrent episodes of vertigo without auditory or neurological symptoms or signs. As opposed to Menieres disease, auditory symptoms are absent
Acoustic Neuroma
aka Cerebellopontine Angle Tumor. 1-3% of persons with dizziness. A benign tumor of the 8th CN. Clinical features: tinnitus and progressive UNILATERAL sensourineural hearing loss, particularly for the higher frequencies like phone ring or doorbell. Feel unsteady not true vertigo. Large tumors may have occipiral headache, diplopia, paresthesias in trigeminal or facial nerve distribution and or ataxic gait
CNS Disorders
cerebrovascular disease ranges from 4-70 percent among older people with dizziness. TIA/Stroke c/o dizziness, diplopia, dysarthria, numbness or weakness. Cerebellar infarct, posterior lateral medullary infarction Wallenberg Syndrome
Psych disorders and dizziness
Depressive symptoms are a/w dizziness and vice versa among older persons
Cervical disorders and dizziness
Usually present with vague lightheadedness or vertigo a/w turning the head, most common vascular mechanism of cervical dizziness is an obstruction of the vertebral arteries. degenerative changes in the cervical spine may cause dizziness because of impairment of the cervical proprioceptive mechanoreceptors. May present with radicular pain in the neck upon movement as well as dizziness.
Systemic causes of dizziness
hypothyroidism, anemia, electrolyte imbalance, HTN, CAD, CHF, DM. These can lead to decreased cerebral perfusion or oxygen delivery leading to a sensation of dizziness
Orthostatic hypotension
20/10 drop after standing from supine or sitting.
Postural dizziness
dizziness in standing from supine but no drop in pressure
Postprandial hypotension
A decrease in systolic blood pressure of 20 or more in sitting or standing within 1-2 hours of eating a meal
Meds causing dizziness
Antihypertensives, loop diuretics causing ototoxicity or volume depletion, antiarrhythmics, anticonvulsants, anxiolytics through effect on CNS, tricyclic antidepressents, anithistamines, and cold preparations through anticholinergic properties, antibiotics and nsaids and loops cause through ototoxicity especially with decreased renal function which decreases their clearance
Vestibular dizziness
BPPV, Menieres, Vestibular neuritis, labyrinthitis, cholesteatoma, superior semicircular canal dehiscence, perilymphatic fistula
Neurologic dizziness
Vestibular migraine, posterior fossa tumor, MS, cerebellar stroke, vertebrobasilar insufficiency, wallenberg syndrome, trauma, paraneoplastic cerebellar degeneration, benign intacranial HTN, mal de debarqument syndrome
Cardiovascular dizziness
syncope/presyncope, orthostatic hypotension, autonomic dysregulation
Psych dizziness
psychophysiologic dizziness, psychogenic dizziness
Metabolic dizziness
DM, hypothyroidism
Autoimmune dizziness
RA, SLE, Cogan syndrome, wegener granulomatosis, bahcet disease
Iatrogenic dizziness
post surgical
Infectious dizziness
Lyme, Syphillis, HIV, CMV, HSV1
Sense of rotation or being pushed
Vertigo
Relieved by sitting or lying down
Presyncope or impending faint
Imbalance
Sensation localized to the body relieved by support
Ill-defined lightheadedness
Cerebral sensation of being woozy, visual abnormalities
If dizziness cause is uncertain
Provocative testing to stimulate cephalic ischemia by producing orthostatic hypotension, including valsalva, hyperventilation
Stimulate vestibular dysfunction by
swiveling then rapidly stopping in a chair to induce vertigo that the pt can compare to their symptomatic dizziness
Dizziness/Vertigo tx
Tx underlying cause, educate to reduce anxiety, modify activities that lead to dizziness, avoid harm
Pharm tx of dizziness
Vestibular suppressants for acute episodes only. Antihistamines use with caution as they can cause dizziness. Anticholinergics. Benzos for long term treatment
Referral for dizziness
Consider referral to cardiology, neurology, endocrinology. PT for vestibular rehab consists of sets of exercises using movements of the eyes, head and body to stimulate the vestibbular system
Pharm mgmt of orthostatic hypotension
Caffeine, Fludrocortisone, Midodrine, Desmopressin, Erythropoeiten
definition of dementia DSM-5
decline in cognition involving at least one or more cognitive domains:
learning and memory
language
executive function (make decisions, balance checkbook)
complex attention* added in dsm5
perceptual- motor (tripping over everything)
social cognition*added in dsm5
- must represent a significant decline from previous level of functioning
- deficits NOT explained by another mental disorder and no not occur exclusively in the context of delirium
number one job pertaining to alzheimer’s
early recognition- history taking is key
new name for dementia according to DSM5
major neurocognitive disorder
criteria for dementia according to DSM 4
A1. Memory impairment A2. At least one of the following: Aphasia Apraxia Agnosia Disturbance in executive functioning B. The cognitive deficits in A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning C. The cognitive deficits do not occur exclusively during the course of delirium
criteria for DSM 5
A. Evidence of significant cognitive decline
from a previous level of performance in one or
more cognitive domains:
Learning
and memory
Language
Executive
function
Complex attention*
Perceptual- motor
Social cognition*
B. The cognitive deficits interfere with
independence in everyday activities. At a
minimum, assistance should be required with
complex instrumental activities of daily living,
such as paying bills or managing medications.
C. The cognitive deficits do not occur
exclusively in the context of a
delirium
D. The cognitive deficits are not better
explained by another mental disorder (eg,
major depressive disorder, schizophrenia)
biggest problem with dementia
insidious nature of the problem, years typically pass before informants come forward (rarely self reported)
mild cognitive impairement (MCI)
generally defined by the presence of memory difficulty
and objective memory impairment but preserved ability to function in daily life.
cause/ differentials for: Gradual onset of short- term memory loss and functional impairment in more than one domain:
I. Executive function (finances,
shopping, cooking, laundry, transportation)
II. Basic activities of daily living (feeding, dressing,
bathing, toileting, transfers)
cause- dementia
differentials: Alzheimer disease, Parkinson
dementia, Lewy body dementia,
Pick’s disease, alcohol-related dementia, Creutzfeld-Jacobs disease
cause/ differentials for: Stepwise, sudden deterioration in
cognition; episodes of confusion, aphasia, slurred speech, focal weakness
cause- Cerebrovascular disease
differentials- Vascular dementia, multi-infarct
dementia, Binswanger’s dementia (subcortical dementia)
cause for: Acute cognitive impairment
with clouded sensorium; difficulty with attention; may have
hypersomnolence
cause- delirium
Complains of memory loss, decreased concentration, impaired judgment, feels worse in morning
and hopeless
cause- depression
differentials- Minor depression, dysthymic disorder, major depression, pathologic grief reaction
examination for dementia patient should include
cognitive, mini mental exam, clinical dementia rating, mini cog, neuropsychological testing, premorbid ability (SEE up to date “Eval of cognitive impairment and dementia” these are explained- one will be on exam)
clinical dementia rating (CDR)
(0, 0.5, 1, 2, 3)
Score only as decline from previous usual level due to cognitive loss, not impaired due to other factors
•increasingly used in clinical decision making as well, such as driving
•In a semi- structured interview with the patient and caregiver
http: //www.biostat.wustl.edu/~adrc/cdrpgm/ind
ex. html (BECOME FAMILIAR WITH THIS)
delirium
Acute confusional state characterized by an alteration of consciousness with reduced ability to focus, sustain, or shift
attention
dx of delirium
multi- layered- 5 key features (need all of them)
1. abrupt disturbances
2. disturbances in attention
3. disturbance in cognition
4. no other explanation of the disturbance
5. disturbance is caused by a medical condition, substance
intoxication or withdrawal, or medication side effect
management of delirium
Avoiding factors known to cause or aggravate delirium, such as multiple medications, dehydration, immobilization, sensory impairment, and sleep disturbance
1. identifying and treating underlying problem
2. providing supportive/ restorative care to prevent further physical and cognitive decline
3. Where appropriate, controlling dangerous and severely
disruptive behaviors using low dose, short acting pharmacologic agents
syncope
is a symptom defined as a transient,
self- limited loss of consciousness, usually leading to falling.
Regardless of the etiology, the underlying mechanism
responsible for syncope is ?
a drop in cerebral oxygen delivery below the threshold for consciousness also known as transient cerebral hypoperfusion
pathophys behind syncope- The “blunted baroreflex sensitivity” with aging is
manifested as
a reduction in the heart rate response to hypotensive stimuli
pathophys behind syncope- Older adults are prone to reduced blood volume:
a decline in plasma renin and aldosterone, which
causes excessive salt wasting by the kidney, a rise
in atrial natriuretic peptide, and concurrent diuretic therapy
orthostatic hypotension
Is arbitrarily defined as either a 20 mmHg fall in systolic blood pressure or a 10 mmHg fall in diastolic blood pressure on assuming an upright posture from a supine
position
possible causes of orthostatic hypotension
Aging, HTN, medications, myocarditis, atrial myxoma, aortic stenosis, constrictive pericarditis, hemorrhage, diarrhea, vomiting, ileostomy, burns, hemodialysis, salt losing nephropathy, diabetes insipidus, adrenal insufficiency, fever, extensive varicose veins, primary autonomic failure syndromes, secondary autonomic dysfunction and volume depletion
orthostatic hypotension- Precipitating factors
speed of positional change, prolonged recumbency, warm
environment, raised intrathoracic pressure (coughing, defecation, micturition), physical exertion, and vasoactive drugs.
Carotid Sinus Syndrome & Carotid Sinus Hypersensitivity pathophys
–Characterized by episodic bradycardia and/or
hypotension resulting from exaggerated baroreceptor
mediated reflexes or carotid sinus hypersensitivity
–Is diagnosed in persons with otherwise unexplained
recurrent syncope who have carotid sinus
hypersensitivity
–Is considered present if carotid sinus massage
produces asystole exceeding 3 seconds
(cardioinhibitory), or a fall in systolic blood pressure
exceeding 50 mmHg in the absence of cardioinhibition (vasodepressor), or a combination of the two (mixed).
Carotid Sinus Syndrome: Presentation
The syncopal symptoms are usually precipitated by mechanical stimulation of the carotid sinus such as head turning, tight neckwear, neck pathology, and by vagal stimuli such as prolonged standing. In a significant number of patients no triggering event can be identified
carotid sinus syndrome- possible triggers
postprandial state, straining, looking or stretching
upward, exertion, defecation, and micturition
normal response to orthostasis
an ↑ in heart rate, rise in peripheral vascular resistance (↑ in diastolic blood pressure), and minimal ↓ in systolic blood pressure, to maintain an adequate cardiac output
pathophys of vasovagal syncope
The possible mechanism involves a sudden fall in venous return to the heart, rapid fall in ventricular volume, and virtual collapse of the ventricle because of vigorous ventricular contraction → stimulation of ventricular mechano-receptors and activation of Bezold–
Jarisch reflex leading to peripheral vasodilatation (hypotension) and bradycardia.
more pathophys of vasovagal syncope
Possible central sympathetic inhibition due to several neurotransmitters: serotonin, endorphins, and arginine vasopressin
older persons susceptible to vasovagal syncope because?
Hypertension, atherosclerotic cerebrovascular disease, cardiovascular medications, and impaired baroreflex sensitivity can cause dysautonomic responses during prolonged orthostasis (in which blood pressure and
heart decline steadily over time) and render older persons susceptible to vasovagal syncope. also Diuretic use further increase the risk of vasovagal syncope bc they cause you to become hypovolemic.
presentation of vasovagal syncope
The hallmark is hypotension and/or bradycardia sufficiently
profound to produce cerebral ischemia and loss of neural
function
Usually there is a precipitating factor/situation to cause vasovagal syncope such as?
Emotional stress(fight/flight response), anxiety, mental anguish, trauma, physical pain or anticipation of physical pain (e.g., anticipation of venesection), warm environment, air travel, and prolonged standing
vasovagal syncope classified into 3 types:
Cardioinhibitory (bradycardia), vasodepressor (hypotension), and mixed (both)
vasovagal syncope- Manifestations occur in 3 phases:
A prodrome (aura- ie taste in your mouth, smell, vision change), loss of consciousness, and postsyncopal phase
*The most common triggers of vasovagal syncope in older patients:
*prolonged standing and vasodilator medications
Prodromal symptoms include: (elderly patients may not remember prodromal sx)
Extreme fatigue, weakness, diaphoresis, nausea, visual defects, visual and auditory hallucinations, dizziness, vertigo, headache, abdominal discomfort, dysarthria, and paresthesias
vasovagal syncope may mimic what? why?
seizure since during syncopal period some patients develop involuntary movements usually myoclonic jerks, but tonic– clonic movements also occur
Recovery for vasovagal syncope
Usually rapid, but older patients can experience protracted symptoms such as confusion, disorientation, nausea, headache, dizziness, and a general sense of ill health.
postprandial hypotension**
In healthy older patients, systolic blood pressure falls by
11 to 16 mmHg, and heart rate rises by 5 to 7 beats/min
60 minutes after meals of varying compositions and
energy content
postprandial hypotension*
***In older persons with hypertension, orthostatic
hypotension, and autonomic failure, the postprandial
blood pressure fall is much greater and without the
corresponding rise in heart rate. (heart rate can’t go up in older patients sometimes bc of meds)
postprandial hypotension: Postprandial Physiologic
Changes
Increased splenic and superior mesenteric artery blood flow at the expense of peripheral circulation and a rise in plasma insulin levels without corresponding rises in
sympathetic nervous system activity.
–
Vasodilator effects of insulin and other gut peptides, including neurotensin and VIP contribute
to hypotension.
possible reasons for syncope dx- neuro
Neurally mediated Orthostatic hypotension Acute vertibrovascularstroke Migraine Seizure
possible reasons for syncope dx- endocrine
hypoglycemia, addison’s disease
possible reasons for syncope dx- psych
psychogenic pseudosyncope
possible reasons for syncope dx- cardi
Acute coronary syndrome Ventricular arrhythmias A – V block ☼☼Wolff –Parkinson White syndrome Cardiac temponade Aortic dissection PE Ruptured AAA Acute A-Fib Heart failure Volume depletion Sinus node dysfunction Long QT syndrome Aortic Stenosis Hypertrophic cardiomyopathy Mitral Stenosis Atrial myxoma Subclavian steal syndrome
syncope dx most important step
*most important tool is a careful history! It will suggest the correct cause and exclude other potential indicators. Hx should be focused on nature of events prior, during, and after syncope (i.e. supine position indicates probable cause of arrhythmia or seizure)
syncope dx- what should be ordered?
tests should be guided by h & p. Important to get SBP (supine and upright). Lab tests- serum electrolytes, glucose, hematocrit, blood and urine tox screening (to r/o drugs and etoh), cardiac enzymes (to r/o MI) and EKG should be done on all patients bc it could provide a clue to cause of syncope (e.g. prolongation or bundle branch block may indicate bradyarryhthmias)
if cardiac cause for syncope is suspected order?
step 1. echo, halter, stress test, lunh scan
step 2. EP study
step 3. carotid sinus message (CSM), upright tilt table test
step 4. Loop ECG
if neurally mediated is suspected for syncope order?
step1. CSM, tilt test
step2. echo, halter
step3. EP study (if heart disease)
if cerebrovascular or psychiatric cause is suspected for syncope order?
step1. psych eval
step2. EEG if seizures suspected
step3. doppler ultrasound of the carotid and vertebrobasilar systems
step4. MRI of cerebral vasculature
