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108 Cards in this Set

  • Front
  • Back

four cardinal features of nacrolepsy

1. excessive day time sleepiness with "sleep attacks"


2. cataplexy (sudden loss of tone)


3.sleep paralysis (you wake up and you cant move-- body is still in REM)


4. hypnagogic (hallucinations-- continued dream when you are awake)

what does polysomnogram of narcolepsy show?

short sleep latency with REM onset


(REM sleep occuring during wakefulness)

obstructive sleep apnea


symptoms? risk factors? tx?

obstruction of upper airway during sleep with preservation of respiratory effort



risk factors: age, obesity, ethanol use


symptoms: 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 consoled


last for 10 minutes


onset usually in first cycle of sleep

sleepwalking

common, more frequent in children


no 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 common


cna be caused by pee/poop/cough


carotid sinus hypertesensitivity


can be triggered by noxious stimuli (hearing bad news, seeing blood, strong emotion


its 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 onset


consciousness intact

simple partial sensory seizure

weird vision, smells, numbness in one arm


focal onset


consciousness intact

complex partial seizure

focal onset


involves limbic or cognitive structures


affects 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:


absence


tonic-clonic


infantile spasms


atonic

absence: subtle- kids stare into space, fine afterwards (no postictal confusion)


tonic-clonic: typical seizures you think of


infantile spasms: baby does weird thing with arms, you see if on EEG


atonic: 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 population


seizures only occur with fever (generalized onset seizure)


only in small children

absence epilepsy

looking like a few second staring spell


returns immediately to normal


know its going on bc of EEG

infantile spasms

child has generalized onset


associated with developmental regression


also associated with tuberis sclerosis

lennox-gasteaux syndrome

presents in first decade, associated with developental regression

juvenile myoclonic epilepsy

adolescents


generalized onset seizure, suddenly drop tooth brush, knock over drink


in 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)


or


complex 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 agitated


alpha: physical and mental relaxation (normal)


theta: somnolence with reduced consciousness


delta: 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 memory


patients have no functional impairment and do not meet criteria for dementia


between 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 catheters


elderly: medication, infection, metabolic disturbance


young: drugs, alcohol

what investigations to do you for delirium?

electrolytes, renal function, LFTs, blood count, thyroid, B12, drug levels, urine analysis, CXR, pulse ox


then head CT


then lumbar puncture if meningitis/enceph


EEG if seizures


MRI 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 lobes


occipital 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 processes


and 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 decline


presents between 45-65


personality 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 exam


patho: small microinfarcts or strategic infarcts (ex: affect hippocampus)

tx of vascular dementia

treat hypertension to prevent other end-organ disease


antiplatelet agents can help to reduce further strokes

alcoholic dementia

wernicke-korsakoff syndrome


traumatic 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 deficiency


classic triad: confusion, opthalmoplegia (paralysis of eye movements), and gait ataxia


anatomical 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 preserved


lesions of diencephalon and temporal lobes

creutzfeldt-jakob disease (CJD)

prion disease-- proteinaceous infectious particles with no nucleic acids


sporadic-- middle aged/old people-- causes dementia, myoclonus, ataxia, etc


familial: AD


variant: mad cow disease-- consumption of meat products contaminated by


iatrogenic: contaminated growth hormone cadaver extracts


spongiform encephalopathy

which dementias are potentially reversible?

B12 deficiency, hypothyroidism, HIV, syphilis, normal pressure hydrocephalus, treatable mass (subdural hematoma and benign tumor)q

define concussion


what 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 changes


traumatic 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 cascade


reversible 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 astrocytes


involves cerebral cortex, white matter, deep nuclei, brainstem

what is hippocampus involved in?

memory storage


lesion: poor new learning (anterograde amnesia)

what are mammilary bodies involved in?

memory processing, memory of odors


lesion: anterograde amnesia, wernicke korsakoff syndrome

amygdala

coordination of emotional states, esp anger and aggression, with somatic responses


kluver-bucy syndrome (change in aggression, sexuality, hyperorality)


decresaed conditioned fear response


inability to receognize facial and vocal expression of anger in others

orbitofrontal cortex

front of frontal lobe


defer certain immediate gratifications and suppress certain emotions in order to get long term benefits


control over biologic drives/reward circuit


lesion: disinhibition and inappropriate behavior


poor judgement, lack of inhibition or remorse

lateral prefrontal cortex

choose course of behavior by letting us assess various alternatives mentally


planning for future action


if lesion: decreased motivation and attention, disorientation, mood disturbances

ventromedial cortex

experience emotions and meanings of things


control of movement


lesion: 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 body


happens 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)


coma is un-arousalbe unresponsiveness that is caused by focal lesions that affect both hemispheres or the RAS and diffuse problems affecting the entire brain

what composes the reticular activating system?

locus coeruleus, periaquaductal grey, thalamus

what are the treatable causes of a coma?

hypoglycemia


drug intoxication


meningitis


subarachnoid hemorrhage


status epilepticus


increased 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 preserved


coma is unarousable, where as locked in syndome is arousable


both dont have purposeful movements of limb or face


with coma you dont purposefully move eyes and with LI you can look up on command and blink


coma: 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 working


decerebral 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 exam


pupillary response


eye 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 maneuver


corneal reflex (CN 5 and 7)


gag reflex: CN 9 and 10


check for abnormal respiratory patterns, abnormal brain stem reflexes, motor posturing

what do you do for treatment of coma?

Airway, breathing, ciruclation


give naloxone (opioid overdose)/glucose/thiamine


treat specific cause

definition of brain death

coma of KNOWN cause


no hypothermia, drug intoxication, electrolyte disturbance, acid base disturbance


no motor response or brainstem reflex


apnea

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 CT


if cause still unclear-- LP, EEG, MRI

reactive attachment disorder

"extreme insufficient care"


at least 2 behvarois-- minimal social and emotional reponsiveness to tohers, limited pos. affect, episodes of unexplained irrit, sad, fearful


onset of 9 mo-5 yrs


need to rule out autism


disinhibited social engagement disorder

"extreme insufficient care"


at least 2 behaviors-- will willingly interact with unfamiliar adults or go off with unfamiliar adult, overly familiar social behavior, diminished checking back with caregiver


onset between 9 mo- 5 yr

acute stress disorder

exposure to trauma


3 days-1 month


9 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 legs


laughs and squeals


6 mo milestone

pass objects hand to hand, sit with minimal support


imitates speech sounds, single syllables

9 mo milestone

pincer grasp, sits without support


da/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