deck_3350254 Flashcards
four cardinal features of nacrolepsy
- excessive day time sleepiness with sleep attacks”
what does polysomnogram of narcolepsy show?
short sleep latency with REM onset(REM sleep occuring during wakefulness)
obstructive sleep apneasymptoms? risk factors? tx?
obstruction of upper airway during sleep with preservation of respiratory effort risk factors: age, obesity, ethanol usesymptoms: excessive daytime sleepiness, snoring, cessation of breathing during night, mornng headaches, cognitive complaints tx: CPAP, weight loss
insomnia
difficulty getting to sleep or staying asleep, or non refreshing sleep at least 1 month
restless leg syndrome
urge to move legs, usually during periods of rest or inactivity, typically in the evening (crawling sensation that gets worse when legs remain still and are relieved by moving them)
what is RLS associated with?
iron deficiency anemia
what is restless leg syndrome treated with?
dopamine agonists
REM sleep behavior disorder
loss of normal skeletal muscle atonia during REM sleep, associated with acting out dreams
night terrors
sudden unexplained bouts of terror/fear occurring in stage 3 or 4 sleep. common amongst chidlren who often can neither be awakened or consoledlast for 10 minutesonset usually in first cycle of sleep
sleepwalking
common, more frequent in childrenno memory of doing it, difficult to arouse
bruxism
common sleep disorder where you grind your teeth, can lead to dental erosion
syncope
transient loss of conscoiusness and postural tone that results from brain hypoperfusion, lasts seconds
pre?syncope
light headedness, visual changes, buckling of knees, cognitive slowing, neck pain, headache
cardiogenic syncope
MI, arrhythmias, valvular outflow obstruction
orthostatic syncope
autononomic failture (SC injury or diabetic neuropathy)volume depletion (blood loss, dehydration)medications (anti?hypertensives and antidepressants)
vasovagal syncope
normal variant, most commoncna be caused by pee/poop/coughcarotid sinus hypertesensitivitycan be triggered by noxious stimuli (hearing bad news, seeing blood, strong emotionits a PARASYMPATHETIC response
which kind of syncope is most common?
vasovagal?? exaggeration of normal reflex
tx of vasovagal syncope
avoidance of triggers
tx of orthostatic syncope
if due to orthostatic hypotension, discontinue BP meds, tight stockings, blocks under head of bed, hydrate, more salt, avoid prolonged standing or fast transitions
seizure
symptom?? pathological discharge of of neurons that results in stereotypical behavior or sensation (the symptoms depend on where seizure is)
epilepsy
chronic condition of recurent UNPROVOKED epileptic seizures? if your seizure happens everytime after a certain stimulus, it is not epilepsy
status epilepticus
rare emergency where someone has seizures for more than 30 minutes?? great morbidity and mortality
simple partial motor seizure
recurrent stereotypic motor event (lift your hand over your head)focal onsetconsciousness intact
simple partial sensory seizure
weird vision, smells, numbness in one armfocal onsetconsciousness intact
complex partial seizure
focal onsetinvolves limbic or cognitive structuresaffects cognition, speech, memory impairment (others notice it, bu you dont remember bc of impaired hippocampus)
can a partial onset seizure become a generalized seizure?
yes, partial onset seizure can secondarily spread and become a generalized tonic clonic seizure
generalized onset seizures:absencetonic?clonicinfantile spasmsatonic
absence: subtle? kids stare into space, fine afterwards (no postictal confusion)tonic?clonic: typical seizures you think ofinfantile spasms: baby does weird thing with arms, you see if on EEGatonic: drop attacks (usually have to wear headaches bc when you fall out you can harm head)
how can you tell if its generalized onset seizure?
on EEG, all cortical neurons begin to fire simultaneously, and if its focal the abnormal discharges start in one place (and may or may not spread)
febrile seizures
most common?? 4% of populationseizures only occur with fever (generalized onset seizure)only in small children
absence epilepsy
looking like a few second staring spellreturns immediately to normalknow its going on bc of EEG
infantile spasms
child has generalized onsetassociated with developmental regressionalso associated with tuberis sclerosis
lennox?gasteaux syndrome
presents in first decade, associated with developental regression
juvenile myoclonic epilepsy
adolescentsgeneralized onset seizure, suddenly drop tooth brush, knock over drinkin young, healthy people (normal development)threshold lowered by drinking, no sleep, etc
temporal lobe epilepsy
seizures are either simple partial (deja vu, transient sense of fear, unpleasant olfactory experience)orcomplex partial?? above sensations followed by confusion and speech problems that last second to minutes, followed by amnesia of event and post ictal cognitive changes (dont feel great)
where do temporal lobe seizures arise from?
hippocampus or amygdala (medial temporal lobe)can see changes on MRI
who is prone to get temporal lobe epilepsy?
most likely if you had seizures as a kid, hit your head as a kid, had a high fever (usually some factor precedes it)
how is epilpesy evaluated?
on EEG to identify type of epilepsy and then MRI to see if there is an underlying cause
what are normal brain waves?
beta: consciously alert agitatedalpha: physical and mental relaxation (normal)theta: somnolence with reduced consciousnessdelta: unconciousness or deep sleep
what does an abnormal EEG with epileptiform discharges show?
characterizes epilepsy syndrome, guides management with medication
abnormal EEG with diffuse slowing
can confirm presence of encepalopathy
normal EEG?? what does that help with?
does NOT exclude any diagnosis
evoked postentials
derivative of EEG, measure the brain waves teh are evoked by an electrical stimulus in teh limbs?? used for intra?operative monitoring during spine surgery
polysomnograms
derivative of EEG in combo with other meausurements, useful in IDing sleep disorders
mild cognitive impairment
memory loss noted by patient or family in which detailed tesitng shows abnormal memorypatients have no functional impairment and do not meet criteria for dementiabetween normal age related decline in cog and dementia?? higher rate of progression to dementia
delerium
acute mental status disorder characterized by normal and fluctuating attention? disturbance in level of awareness and reduced ability to focus, sustain attention (SYMPTOM, not disease)
where is delerium most common?
post surgical and ICU settings
key features of delerium
acute onset of mental status change, attentional deficits, confusion(also altered level of consciousness, illusion/halluc, disturbed sleep/wake cycle, disorientation, memory impairment, behavioral changes)
predisposing factors to delerium
advanced age, dementia, deyhdration, medical illness, infeciton, polypharmacy, drug/alc abuse, sensory deprivation, depression, surgery, bladder catheterselderly: medication, infection, metabolic disturbanceyoung: drugs, alcohol
what investigations to do you for delirium?
electrolytes, renal function, LFTs, blood count, thyroid, B12, drug levels, urine analysis, CXR, pulse oxthen head CTthen lumbar puncture if meningitis/encephEEG if seizuresMRI if stroke or intracranial lesion
what do you do with delirium?
STOP all meds!avoid restraints and other predisposing factors
dementia
acquired, persistent, usually progressive impairment of intellectual function with compromise in many cognitive domains (usulaly memory)? deficits must be significant decline, must interfere with work or social life
what are 3 neurodegenerative pathologic processes we discussed?
alzheimers, lewy body dementia, fronto?temporal
how are neurodegenerative diseases characterized clinically?
dementia, loss of movement control, paralysis and pathologically defined by loss of neurons?? progressive
what is the most common degenerative disease?
alzheimers (women affected more than men) then parkinsons then ALS, huntingtons, friedrichs ataxia
which lobes are affected in alzheimers?
symmetric atrophy of temporal, parietal, frontal lobesoccipital lobes can be sparedw
hich protein is accumulated in alzheimers?
neuritic plaques are extracellular accumulations of polymerized beta amyloid centrally with a rim of dystrophic neuritic processesand neurofibrillary tangles?? intracytoplasmic accumulation of tau protein
frontotemporal dementia (picks disease)? which lobes are affected??what are the behavioral changes?
neurodegenerative disorder that affects the frontal and temporal lobes (asymmetrically)cause personality change?? apathy, disinhibition, loss of insight and emotional control and globcal cognitive declinepresents between 45?65personality change happens first
which protein accumulates in frontotemporal dementia?
pick bodies (tau?ositive spherical intracytoplasmic nuronal inclusions)
lewy body dementia
dementia with lewy bodies is the second most common cause for dementia?cog impairment, parkinsonism, prominent visual hallucinations, other psych symptoms (sleep disorders too)?? brain has lewy bodies in neocortex, limbic system, and brainstem?? synuclein proteinopathy
what are the non?degenerative pathologies that are progressive?
vascular, alcoholic, CJD
describe features of vascular dementia
stepwise decline in cognitive function with focal neuro symptoms and signs on exampatho: small microinfarcts or strategic infarcts (ex: affect hippocampus)
tx of vascular dementia
treat hypertension to prevent other end?organ diseaseantiplatelet agents can help to reduce further strokes
alcoholic dementia
wernicke?korsakoff syndrometraumatic lesions including chronic subdurals (inc risk of falls and trauma in alcoholism)can have alzheimers pathology, vascular disease like vascular dementia
wernicke?korsakoff
due to thiamine deficiencyclassic triad: confusion, opthalmoplegia (paralysis of eye movements), and gait ataxiaanatomical distribution: mamillary bodies, hypothalamus, thalamus, periaquaductal gray matter, colliculi, floor of 4th ventricle
what is administered to patients at risk for wern?korsakoff?
glucose given with thiamine bc acute thiamine deficiency can be precipitated by IV glucose admin or carb loading(administering thiamine causes rapid reversal of opthalmoplegia within hours, recovery from ataxia and confusion is slower)
korsakoff syndrome
follows repeated bouts of encepalopathy?? as it subsides, patient has amnestic disorder?? ANTEROGRADE and RETROGRADE amnesia (cant make new memories?? makes them up (confabulation)altertness, attention, social behavior and cog function are preservedlesions of diencephalon and temporal lobes
creutzfeldt?jakob disease (CJD)
prion disease?? proteinaceous infectious particles with no nucleic acidssporadic?? middle aged/old people?? causes dementia, myoclonus, ataxia, etcfamilial: ADvariant: mad cow disease?? consumption of meat products contaminated byiatrogenic: contaminated growth hormone cadaver extractsspongiform encephalopathy
which dementias are potentially reversible?
B12 deficiency, hypothyroidism, HIV, syphilis, normal pressure hydrocephalus, treatable mass (subdural hematoma and benign tumor)q
define concussionwhat is it called when you get repeated concussions?
continuum of brain injury raising from mild cases where you are dazed to persistant neurological abnromalities and structural changestraumatic encepalopathy
pathologically, what happens in a concussion?
loss of neuro function due to axonal dysfunction (axonal distortion or stretching?? eflux of K into extracellular space, influx of Ca, release of glutamade?? excitotoxic cascadereversible neuronal depression to permanent diffuse axonal damage
chronic traumatic encepalopathy?? brain changes?
atrophy, dilatation of lateral and 3rd ventricles, thinning of corpus callosum, neuronal loss and tau deposition (neurofibrillary tangles) and in astrocytesinvolves cerebral cortex, white matter, deep nuclei, brainstem
what is hippocampus involved in?
memory storagelesion: poor new learning (anterograde amnesia)
what are mammilary bodies involved in?
memory processing, memory of odorslesion: anterograde amnesia, wernicke korsakoff syndrome
amygdala
coordination of emotional states, esp anger and aggression, with somatic responseskluver?bucy syndrome (change in aggression, sexuality, hyperorality)decresaed conditioned fear responseinability to receognize facial and vocal expression of anger in others
orbitofrontal cortex
front of frontal lobedefer certain immediate gratifications and suppress certain emotions in order to get long term benefitscontrol over biologic drives/reward circuitlesion: disinhibition and inappropriate behaviorpoor judgement, lack of inhibition or remorse
lateral prefrontal cortex
choose course of behavior by letting us assess various alternatives mentallyplanning for future actionif lesion: decreased motivation and attention, disorientation, mood disturbances
ventromedial cortex
experience emotions and meanings of thingscontrol of movementlesion: apathy, decreased spontaneous movmement, gait disturbance, incontinence
global aphasia
cant be fluent, comprehend, or repeat
mixed transcortical aphasia
cant be fluent or comprehend, but can repeat
transcortical motor aphasia
cannot be fluent, but can comprehend and repeat (like brocas but you can repeat words)
transcortical sensory aphasia
like wernickes but can repeat(so they are fluent, cannot comprehend, but can repeat)
conduction aphasia
can comprehend, and be fluent, but cannot repeat
anomic aphasia
only have trouble naming
hemineglect
most often with right parietal or frontal lobe infarcts/lesions?? neglect of contralateral half of world and bodyhappens more often on LEFT side of view bc left world only has 1 hemisphere paying attention to it (language takes up a lot of space in left brain) and right world has 2?? so if you have lesion on right, left will not compensate)
what do you need for consciousness?what causes coma?
one of your two cerebral hemispheres AND the reticular activating system (turns on” the brain)
what composes the reticular activating system?
locus coeruleus, periaquaductal grey, thalamus
what are the treatable causes of a coma?
hypoglycemiadrug intoxicationmeningitissubarachnoid hemorrhagestatus epilepticusincreased ICP (hyperventilation, mannitol, decompressive surgery)
what are the top culprits for coma?
drug poisoning, hypoxia after arrest and resuscitation, trauma, non?traumatic bleeding, stroke
compare coma and locked in syndrome
in locked in: pt appears unresponsive, but cognition is preservedcoma is unarousable, where as locked in syndome is arousableboth dont have purposeful movements of limb or facewith coma you dont purposefully move eyes and with LI you can look up on command and blinkcoma: no sleep cycle LI: normal sleep cycle
what causes locked in syndrome?
lesion of bilateral ventral pons taking out the bilateral cortical spinal and cortical bulbar tracts, but not RAS
what does the glasgow coma scale measure? what is the range?
measures eye opening, verbal response, and motor response
decorticate? decerebrate?
decorticate is flexion?? less dreadful bc rubrospinal tracts are workingdecerebral is extension?? it means the lesion is below red nucleus
how do you check cranial nerves in person with coma?what other things do you check?
funduscopic exampupillary responseeye deviation: left hemipheric lesion affects frontal eye fields, left pontine lesion affects CN 6 and descending corticospinal tract (midline gaze)vestibular ocular reflex: dolls head maneuvercorneal reflex (CN 5 and 7)gag reflex: CN 9 and 10check for abnormal respiratory patterns, abnormal brain stem reflexes, motor posturing
what do you do for treatment of coma?
Airway, breathing, ciruclationgive naloxone (opioid overdose)/glucose/thiaminetreat specific cause
definition of brain death
coma of KNOWN causeno hypothermia, drug intoxication, electrolyte disturbance, acid base disturbanceno motor response or brainstem reflexapnea
how is peristant vegetative state different than a coma?
in PVS, you have sleep/wake cycles, withdrawal from noxcious stimuli and non?purposeful movement you respond to startle auditory and visual(whereas in coma you have only reflex and postural motor function, no auditory or visual function),
what evaluation is done for coma?
PE and history, basic labs, head CTif cause still unclear?? LP, EEG, MRI
reactive attachment disorder
extreme insufficient care”
disinhibited social engagement disorder
extreme insufficient care”
acute stress disorder
exposure to trauma3 days?1 month9 symptoms across 5 categories: intrusion, negative mood, dissociative, avoidance, arousal
milestone for 2 month old?? motor and speech
hold head up 45 degree and smiles
4 month milestone
grasp objects (pull hear, earrings), bear weight on legslaughs and squeals
6 mo milestone
pass objects hand to hand, sit with minimal supportimitates speech sounds, single syllables
9 mo milestone
pincer grasp, sits without supportda/ma/ba jabbers(also stranger anxiety around here)
12 mo milestone
stand alone, dada/mama specific, responds to name
15 months milestone
walk alone, follow simple commands such as STOP
18 months milestone
walks up steps, 6 word vocab
24 months milestone
runs, combines words
