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225 Cards in this Set

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Where is REM sleep generated?
Major sleep induction nucleus that inhibits wake promoting neurons; *sleep center*
VLPO-Ventrolateral preoptic nucleus
REM-on neurons
REM-off neurons
Neuropeptides that are promoters of wakefulness
Hypocretin/orexin(modulates feeding) acts at lateral hypothalamus-inhibit REM; histamine from tuberomamillary nucleus
Has role in homeotic sleep drive, sleep induction, slow wave sleep (Stage 3 NREM)
Main pacemaker for circadian system
SCN of anterior hypothalamus
Abnormal events that intrude sleep
What is narcolepsy? Tetrad?
dysfunction in regulation of REM sleep, tetrad of daytime sleepiness, cataplexy (sudden loss of muscle tone), sleep paralysis, hypnagogic hallucinations
What substances reduce REM sleep?
Tricyclic antidepressants (TCAs), MAOinhibitors, Amphetamines, Opiods, alcohol
What substances reduce slow wave sleep?
Benzodiazepines, caffeine
What is made in TMN?
Histamine, an imp wake promoting nt
REM sleep characterized by?
EEG similar to wakefulness, muscle atonia, hippocampal THETA activity
EEG for
Stage 2 sleep?
Stage 3 sleep?
REM sleep?
2- sleep spindles, K complex
3-delta waves, high voltage, slow waves
REM- sawtooth waves
What sleep stage is most of the nite spent in?
Stage N2
Caffeine is an example of what?
methyxanthine; adenosine receptor antagonist
What is sleep-wake cycle and two-process model?
Homeostatic drive-sleep dependent, governed by need for sleep; 1st part of nite high (high adenosine)
Circadian rhythm-sleep independent, entrained by light-dark cycle; 2nd part of nite its low
How is REM atonia controlled?
By REM-on cells in PC, via glutamatergic pathways to IVMM and SLD
lesions of SLD, PC would cause what?
loss of REM-on neurons cause loss of REM sleep, atonia, and theta EEG
Main nucleus for sleep?
Main nucleus for wakefulness?

Wakefulness- SCN
What inhibits the SCN (the wakefulness nucleus)/causes drowsiness?
Melatonin; secretion is stimulated in dark
What is the drowsy phase of wakefulness char by on EEG?
alpha waves
stimulates orexin/hypocretin neurons, used in narcolepsy to keep them awake
Hypothalamic nuclei involved in fluid-electrolyte balance
Supraoptic nucleus (SON), Paraventricular nucleus (PVN), Median pre-optic area (MnPO)-all have osmoreceptors
Hypothalamic nuclei involved in feeding behavior
PVN. Ventromedial Nucleus (VMN), Arcuate Nucleus (ARC), Lateral Hypothalamic area (LHA)
Lesion of VMN
INCREASE in body weight, levels off to new basal body wt
Lesion of lateral hypothalamus
DECREASE in body weight, but over time will gain wt to a point lower than pre-lesion body weight
NPY formation? Action?
made in ARC, goes to PVN to INCREASE food intake
Leptin formation? Action?
secreted by fat cells, acts on leptin receptors in hypothalamus to decrease NPY secretion; decrease NPY-->decrease food intake
Ghrelin formation? Action?
secreted by gut, increases NPY, signals hungers and increase food intake
secreted by gut, decreases food intake by signaling satiety
How does hypothalamus control posterior pituitary? (oxytocin, vasopressin) (neurohypophysis)
Neural control via MAGNOcellular (large) neurons in PVN (oxytocin) and SON (ADH); project axons to posterior pituitary to release hormones
How does hypothalamus control anterior pituitary? (adenohypophysis)
Humoral Control via PARVOcellular (small) neurons located thru-out hypothalamus; project axons to median eminence
What does the medial PARVOcellular neurons make?
CRH-(for ACTH), TRH-(for TSH)
Difference in brain of dyslexics?
Planum temporale DOES NOT show left cortical asymmetry that normal ppl do; left temporoparietal cortex deficient functioning on fMRI; Microgyria; larger splenium
Signs of dyslexia
reading, spelling, writing difficulties, spelling reversals and poor spelling
Damage to arcuate fasciculus (aka superior longitudinal fasciculus)
conduction aphasia, auditory comprehension and speech articulation preserved, difficulty repeating heard speech
2 main skills for phonological processing
phonemic awareness-recognition of units of language, decoding-words to sounds of language
3 imp neural systems in reading
1. Anterior system in left inferior frontal (broca's) 2. dorsal parietotemporal (wernicke) 3. ventral occipitotemporal
what is the link betw written forms and auditory forms?
angular gyrus in temporoparietal junction (primary visual-->AG-->Wernickes)
Acquired dyslexia
dyslexia as a result of brain injury
Microgyria sx
impaired processing of rapid acoustic information
Differences in patterns of neural activation of dyslexics
increased activity of right hemisphere, increased activation of frontal areas such as Broca's, decreased activation of temporoparietal cortex (angular gyrus)
Where is working (short-term) memory localized to?
frontal lobe, anterior cingulate and dosolateral prefrontal brain

retained briefly, not stored
Episodic vs. Semantic memory
Semantic-facts and information

Both are types of explicit memory which can be consciously demonstrated
implicit memory
task-related memory

Priming (neocortex), conditioning (emotional-amygdala, motor-cerebellum), skills (striatum), habituation
How do we form implicit memory vs. explicit memory?
implicit-via basal ganglia and cerebellum, not affected in amnesics

explicit-via hippocampus
What can provoke generalized absence seizures?
What is believed to be the cause of generalized seizures?
since discharges seen everywhere in the brain, thought to be THALAMO-cortical related
Ictus vs. interictal?
Ictus-point at which pt is striken

Interictal-between seizures
Where do convulsive (tonic-clonic) seizures originate in humans?
in brainstem
What is the cause of PRIMARY convulsive (tonic-clonic) seizures?
due to genetic cause of having seizures
What are SECONDARY convulsive (tonic-clonic) seizures?
crescendo build-up of activity resulting from a focal incident, more likely than primary
Causes of Seizures
Microanatomical abnormalities, changes in excitation/inhibition ratio
Specific microanatomical abnormalities
Enhanced excitation=glutamate thru ionotropic and metabotropic receptors cause inward Na+ and Ca++ current

Loss of inhibition= GABA thru GABA-a(post) and GABA-b (pre) causes inward Cl- and outward K+
Specific changes in exc/inhib ratio
instead of single APs send BURSTS of APs; also, paroxysmal depolarizing shift where a balance shift in thalamic and purkinje neurons firing single and bursts changes
Phase 1 monitoring (Wada Test?)
EEG at scalp, neuroimaging, Wada test is unilaterally inject sodium amytal into internal carotid and asses memory and language in awake atmosphere (for partial seizures)
Phase 2 monitoring
EEG intracranially, language mapping of temporal lobe
When can you do a temporal lobe resection for seizures?
seizures from a single focus (partial seizures) in non-eloquent cortex
When is it good to use Vagal Nerve Stimulation for seizures?
Pts with difficult-to-treat epilepsy such as generalized seizures or partial seizures in an imp. area; control seizures better by stopping or decreasing duration, severity and recovery period
What is intractable epilepsy?
despite adequate pharm therapy, 40% of pts will continue to have seizures
What seizure classification is more effective with Anti-epileptic drugs?
Partial seizures may be more well-controlled than generalized, but types of seizures (absence vs. tonic clonic) does not have any difference in effectiveness
Status epilepticus? Tx?
seizures lasting more than 30 minutes, give benzodiazepines to sedate, phenytoin as treatment
1st generation drugs that block Na+ channels? Side effects?
Phenytoin-gold standard for STATUS EPILEPTICUS; (F)osphenytoin is (f)aster
s/e-gingival hyperplasia, coarsening of facial features, hepatic enzyme INDUCER

(C)arbamazepine-gold std for (C)OMPLEX PARTIAL SEIZURES
s/e-hyponatremia, agranulocytosis
1st generation drugs that promotes GABA channels (increase GABA by increasing Cl- conductance)? Side effects?
Phenobarbital (barbiDURATe); increase DURATION of Cl- channel

Diazepam (FREnzodiazepine); increase FREQUENCY of Cl- channel, used for detoxification

s/e-sedation, tolerance, dependence, *Cyt P-450 induction w/Phenobarbital
1st generation drug that blocks Na+ channels, blocks Ca++ channels, and increases GABA? Side effects?
Valproate-gold standard for primary (idiopathic) generalized seizures, also used for migraines

s/e-MANY ADVERSE, weight gain, tremor, hair loss, fatal hepatotoxicity
What is the gold standard for primary (idiopathic) generalized seizures? Why?
Valproate; because it does everything! blocks Na+ channels, blocks Ca++channels, promotes GABA
3 common mechanism by which AEDs work
Block Na+ channels, enhance GABA receptor, block T-type Ca++ channels
What AED is used to treat absence seizures?
Ethosuximide; blockade of T-type calcium channels
What increases GABA release?
Gabapentin, off-label use
Lamotrigine- use, mech, side effects?
partial seizures; blocks Na+ channels; most favorable cognitive profile BUT major s/e: STEVEN's Johnson Syndrome, fatal, ulcerations of all mucosal surfaces
What two drugs should you never combine?
Lamotrigine and Valproate-causes SJS!!!
2nd generation Ca++ blocker used for add-on therapy of partial epilepsy
Levitiracetam, few side effects
What type of pt is a ketogenic diet effective?
children who have failed numerous drug trials, but many side effects
unequal pupillary size
Papilledema; what does it indicate
swelling of the optic disc, indicates increase intracranial pressure
difficulty with language
slurred speech
Global aphasia vs. Receptive aphasia vs. Expressive aphasia
Global-unable to understand or speak
Receptive-can't understand, able to speak
Expressive-able to understand, can't speak
Dementia vs. delirium
Dementia-impaired cognition
Delirium-impaired attention that produces disorientation

Both have normal awareness
repeating the same behavior
stiffness of the meninges, but various signs such as stiff neck that occur with irritation of the meninges
sudden (seconds or less)
Conversion disorder vs. Factitious disorder
Conversion: we know the pt caused this but the pt (really) doesnt know it

Factitious:the pt chose to cause the physical finding bc they are mentally disturbed
Mydriasis; what does unilateral dilated pupil w/worst headache of life suggest? Bilateral?
dilated pupils
Unilateral: possible SAH, compression via PCA aneurysm
Bilateral: very rare, eyedrops
Diplopia. Intermittent?
w/worst headache and diabetes? w/worsening headaches and bradycardic?
w/sudden onset R sided headache?
Intermittent? neuromuscular prob (myasthenia graivs)

Worst headache + diabetes? microvascular infarct of 3rd nerve, pupils normal bc fibers lie on surface

Worsening headaches+bradycardic?
tumor w/increasing intracranial pressure

Sudden onset R sided headache? retinal detachment
What is the formula for Cerebral perfusion pressure? When does ischemia occur?
Mean arterial pressure-Intracranial pressure
Occurs when ICP > MAP
Ways to reduce ICP
1. if a tumor, remove it
2. diuretics such as mannitol
3. steroids for inflammatory edema
4. hyperventilation to reduce CO2 causing vasoconstriction
5. give phenobarbital to reduce metabolism causing vasoconstriction
Glasgow coma scale
used to assess if surgery is worthwhile, score<9(/15) will NOT get surgery
Paresis? w/decreased reflex in left leg? w/both legs and arms reflexes decreased? w/left calf/shin pain, foot drop after exercise? w/both legs and sensory loss to mid-abdomen?
w/decreased reflex in left leg? SCIATICA
w/both legs and arms reflexes decreased?
w/left calf/shin pain, foot drop after exercise?
anterior compartment syndrome
w/both legs and sensory loss to mid-abdomen?
cord compression from tumor
Lethargic child that is difficult to arouse. @2am? after sporting accident? poorly behaved and recent falls?
@2am?ask if cough medicine taken

after sporting accident? epidural hematoma; emergent CT

poorly behaved and recent falls? child abuse; emergent CT
How to deal with suicidal or homicidal thoughts
Follow-up, the more detailed response, the higher the risk
Neck stiffness w/cough, fever, difficult to arouse. Child's neck NOT stiff? Man's neck is stiff? HIV w/stiff neck? man w/stiff neck but painting related?
Child's neck NOT stiff? still give LP
Man's neck is stiff? LP + antibiotics
HIV w/stiff neck? brain abscess, risk of herniation so CT before LP

man w/stiff neck but painting related? Meningismus if stiffness in anterior-posterior directions only
65 w/confusion/wandering. severe in evening, but alert and follows commands? unable to follow commands, easily distracted? thinks you are evil, refuses to follow commands?
evening, but alert and follows commands?dementia *sundowning*
unable to follow commands, easily distracted? delirium
thinks you are evil, refuses to follow commands? psychotic or delirious
65yr old man talking in bed constantly. w/nonsensical speech, and R stimulation deficift? w/constant noises and right hand twitching?
w/nonsensical speech, and R stimulation deficift? fluent speech stroke in MCA affecting wernicke's area

w/constant noises and right hand twitching?complex partial status epilepticus, does not regain consciousness in between; risk of drying from excessive brain activity. Tx-intravenous anticonvulsant
54 yr old woman blackout. w/feeling hot, spinning, vision going gray, twitching movts of legs? w/warm feeling in her stomach/bad smells and amnesia abt event?
w/feeling hot, spinning, vision going gray, twitching movts of legs? hypotensive episode w/ myoclonus

w/warm feeling in her stomach on and off and amnesia abt event? seizure w/aura
For headaches, what is the nerve responsible for pain referred to the eyes, temple, forehead?
referred to the back of the head?
Opthalmic division of trigeminal nerve

upper cervical spinal nerves
Pain expression system in headaches?
Pain transmission system?
trigeminal nerve, upper cervical roots

2nd order neurons which sit in trigeminal nucleus-->thalamus

3rd order neurons of thalamus-->sensory/limbic cortex
What does the 1st branch of the trigeminal nerve innervate?
meningeal artery and vein in dura mater
For most primary headache disorders (migraines), what is the pain sensitive afferent?
Trigeminal nerve
Causes of secondary headache? (0.18% pts)
Systemic or Secondary risk factors-fever, wt loss, HIV, cancer
Neurologic symptoms-deficits, confusion
Onset-sudden or abrupt
Older- over 50
Previous history or Progressive headache
Categories of primary headaches and features
Short duration-cluster headaches <4hrs

Recurrent long duration- migraines, tension-type; >4hrs, <15days/month

Chronic Daily-chronic migraine or chronic tension, continua, daily; >4hrs, >15days/month
Cluster headaches
unilateral short-lived headaches that occur in closely spaced intervals followed by relatively long pain free remissions
Migraine w/o aura
unilateral, pulsating, severe intensity, aggravation w/exercise

NAUSEA, photophobia, phonophobia

Leading headache that causes ppl to seek treatment
Tension type headache
bilateral, non-pulsating, mild to moderate intensity

most common primary headache
Aura? proposed mechanism? Difference in seizures and migraine
focal neurologic deficits preceding h/a onset by hours or days

cortical spreading depression; wave of excitation followed by wave of inhibition, vascular changes follow

Aura causes migraine, aura is a pre-symptom in seizure
4 phases of migraine attacks
Prodrome, aura, headache, postdrome
Familial hemiplegic migraine?
Difference betw. type 1 and type 2.
migraine w/aura that causes hemiparalysis; genetic disorder that leads to brain hyperexcitability via glutamate increase
1:gof, increase Ca++influx
2:lof, glia less able to take in glut.
CNS activation during migraine.
Pain perception?
Migraine generator?

Where does sumatriptan act?
Pain perception? anterior cingulate cortex; sumatriptan decreases pain

Migraine generator? raphe nuclei, locus coerulus, periaqueductal gray
Primary pain producing process in migraine?
Trigeminal vascular jx releases mediators such as CGRP that activate meningeal BV causing pain
Triptans? Targets of triptans?
selective 5HT1D/1b AGONISTS, serotonin receptors on presynaptic terminal 5HT1D and blood vessel 5HT1B; reduce pain inducing vasodilation
Allodynia w/migraine
normal stimuli are considered painful, 2/3 of migraine sufferers, predicts better pain free response if allodynia absent
Modifiable Yellow flags for chronic daily headache
attack frequency, obesity, med overuse, stress, sleep disturbance
Pathway to stimulate reward centers (such as in addiction)
VTA to nucleus accumbens using dopamine
What is dopamine assoc. with?
euphoria as well as attention and learning
Opioid antagonist used in opiate overdose
Treatment for alcohol withdrawal/detoxification
Opioid agonist therapy to prevent heroin relapse
Methadone; pts exhibit tolerance and withdrawal phenomena but do not fit criteria for dependence; good b/c cross tolerant with heroin to ease withdrawal
Conditioned place preference
prefer place that was assoc with drug intake
Withdrawal induced conditioned place aversion
prefer place where no withdrawal symptoms occurred
Sites of action of Stimulants
Nucleus Accumbens and Ventral Pallidum (terminal portion of mesocorticolimbic pathway)
Sites of action of Opiates
VTA and periaqueductal gray (origins of mesocorticolimbic pathway)
Where do most addictive substances act?
Mesocorticolimbic pathway
Target and mech of Nicotine
bind to nicotinic receptor located on CELL body of VTA neuron --> DA release in NA
Target and mech of Cocaine
binds to dopamine TRANSPORTER located on terminal axon of dopamine neuron in VTA -->prevents DA reuptake --> more DA in synapse of NA
Target and mech of Morphine
binds to u-opiate receptor on GABA neuron to inhibit GABA release --> more DA release in NA
What can cause a PHYSICAL withdrawal?
u-opiate receptor antagonist at Locus Coeruleus and Periaqueductal Gray
What can cause a MOTIVATIONAL withdrawal?
u-opiate receptor antagonist at Amygdal, VTA, NA, PeriAqGray
What drugs use Gi signalling to inhibit GABA firing and increase DA in synapse? receptors?
Opiates via opiate receptor and
Cannabinoids via CB1 receptor
What drugs use Gs signalling to inhibit dopamine re-uptake and stimulate DA release, respectively? receptors?
Cocaine via dopamine reuptake transporter
Addictive substances may acutally improve psychological performance in these pts
Wernicke-Korsakoffs Syndrome
acute form of encephalopathy due to thiamine deficiency; vision changes, ataxia, and impaired memory
Central Pontine myelinolysis
locked-in syndrome, spastic quadriplegia, demyelination of pons
Marchiafaua-Bignami Syndrome
demyelination of corpus callosum, stupor, coma, seen in middle aged to elderly alcoholics
blocks opioid receptors, reduces relapse rate
IMP! make sure pt is opioid free for 7-10 days before starting meds b/c can induce withdrawal
acts to inhibit GABA and increase glutamate, reduces symptoms of protracted abstinence

s/e diarrhea and somnolence
interferes with degradation of alcohol (blocks acetaldehyde dehydrogenase)
given for opioid overdose for respiratory support and counteract CNS depression *different from naltexone-opioid receptor antagonist in making alcohol unrewarding*
Alternative opioid detox treatment? Mech? Benefits?
Buprenorphine-partial opiate agonist at low does, antagonist at high does, low risk of overdose/abuse, available in combination wtih naloxone (antagonist)
preferable for pts who want to avoid clinic daily settings of methadone maint.
Where should you go to if impaired?
Committee for Physician Health (CPH)- anonymous, confidential, for substance use and psychiatric disorders

OPMC is bad. lose license.
intentional behavior
consciousness that enables ppl to be aware of their personal past and future
3 big causes of coma
cerebrovascular disease
Levels of Consciousness

Confusion-clouding of sensorium (dif. from delirium which includes hallucinations and agitation)

Drowsiness and Stupor-sleepy state

Stages of memory

Consolidation-short to long info

Storage-dist of memories

Retrieval-calling up memory from storage
Where is short term memory converted to long term memory?
What region of the brain is responsible for memory of OBJECTS?
Parahippocampal and entorrhinal areas
What region of the brain is responsible for SPATIAL memory?
Right hippocampus
What region of the brain is responsible for memory of WORDS, PEOPLE?
Left hippocampus
What area of the brain shows increased activity when thinking about FUTURE events?
anterior portion of the superior frontal gyrus
How is synaptic strength increased
more efficient synapse
change in diameter of spine
location of synapse
NMDA synchrony
addition of new synapses
AMPA receptors NOT static, traffic continuously
Factors that consolidate memory
Transmitters (ACh, dopamine...)
Stress/Emotions (adrenaline, NE)
Sleep (REM sleep critical for learning)
Up-regulation of AMPA receptors is most likely to result in what to memory?
Increased memory
ACh; what reduces memory?
What improves memory?
what reduces memory? decrease ACh
What improves memory? increase ACh
What is the major nucleus that controls executive function and is the major projection nucleus to the prefrontal cortex (makes us human)
Medial Dorsal Nucleus
What part of the brain has an amazing ability for face recognition?
Inferior Temporal Region
When does it present?
Duration of illness?
alteration of perception, thinking, speaking, emotions, movts and behavior with DELUSIONS and HALLUCINATIONS (auditory)

onset in late teens
lifelong illness
What is an illness that has no clear disctinction from schizophrenia?
Bipolar disorder
Risk factors for schizophrenia
Family Hx

Genes- COMT gene, change in gray matter density (cannabis susceptib)
Neuroregulin gene, psychosis

Paternal Age>50, immigrants, northern latitude, RUBELLA
Describe course of schizophrenia
RELAPSE- pt normal, multiple times
Neurobiological changes in schizophrenia
reduced gray matter and loss of gyrification

INCREASED activity in Brocas, hippocampus, cingulate gyrus (cause hallucinations, positive symptoms, delusions)

Abnormal EEG

REDUCED GAD7, Reelin, precursors of phospholipids
What do you give to schizophrenia pts?

How do they work?
Anti-psychotics (haloperidol)
dopamine (D2) antagonist-block D2 dopamine receptors
What are the first generation anti-psychotics?

Used for?

Haloperidol, D2 receptor antagonist


Extra-pyramidal symptoms: parkinsonism, dystonia, tardive dyskinesia
What are the second generation anti-psychotics?

serotonin receptor antagonism

prevents Extrapyramidal symptoms typical of D2 receptor antagonists by selective dopamine stimulation of nigro-striatal pathway
How long does meds help in schizophrenia?

Relapse rate?
10-20 yrs

relapse rate is 80% in 5 yrs
Serotonin hypothesis of Schizophrenia
LSD (5HT2a agonist)--causes vivid hallucinations and psychosis
Pure serotonin antagonists drugs are not anti-psychotic
NMDA hypothesis of Schizophrenia
PCP blocks ion channel gated by NMDA glutamate receptor-->similar positive, negative and cognitive symptoms
Dopamine hypothesis of Schizophrenia
Positive symptoms due to increased meso-LIMBIC activity (hyperdopaminergia)
Negative symptoms due to decreased meso-CORTICAL activity (hypodopaminergia)
Does not account for cognitive symptoms
Anterior cingulate and Schizophrenia
Decreased activity-->thought disorder and attention deficits
Hippocampus and Schizophrenia
Increased activity-->Responsible for positive symptoms
Neurodevelopmental hypothesis of Schizophrenia
Early insults-->pathological neuron circuits
Multiple hits-->schizophrenia
Need genes
Deficiency in phenylalanine hydroxylase-->prevents phenylalanine to tyrosine conversion
Rate limiting enzyme in sythesis of dopamine
Tyrosine Hydroxylase
What drugs cause dopamine release and prevents reuptake?
Cocaine and amphetamine
What is an antidepressant that is a DA and NE reuptake inhibitor?
What are dopamine agonists that are approved for use in Parkinsons and RLS?
PramipexOLE and RopinorOLE
Which dopamine system is responsible for the amenorrhea and galactorrhea seen with some antipsychotic meds?
What is happening when someone has ADHD? What can you take?
dopamine is deficient in mesocortical system, take a dopamine agonist
Of the 4 dopamine systems, what are the two involved in schizophrenia and what symptoms are they responsible for?
Mesolimbic-increased DA resp for positive symptoms of schizophrenia, such as hallucinations, delusions

Mesocortical-increased DA resp for negative symptoms of apathy, affective flattening, anergy; also mediates focus, conc, attn of frontal lobes *4As*
Of the 4 dopamine systems, what are the two that experience negative anti-dopaminergic effects for schizophrenia treatment and what symptoms are they responsible for?
Nigrostriatal- D2 blockade can cause parkinson's symptoms

Tuberoinfundibular- HPA axis, hyperprolactinemia; can give Bromocriptine, a dopamine agonist for these symptoms
What post-synaptic enzymes breakdown DA?
If your pt has hyper prolactinemia from a dopamine antagonist, what can you give them?
Bromocriptine, a dopamine agonist
What drugs can interact with tyramines (cheeses, wine) and cause HTNsive crisis?
How do TCAs work?
What are TCAs good for?
name one
5-HT/serotonin reuptake inhibition, NE reuptake inhibition, serotonin antagonist

treating SEVERE depression

How do SSRIs work?
What are SSRIs good for?
name one
5-HT reuptake inhibition

Anti-depressant, anti-anxiety


s/e-sex dysfunction
How do MAOIs work?
What are MAOIs good for?
name one
inhibit MAO, increase NE

Anti-depressant (ATYPICAL)


avoid TYRAMINE!!!
Advantage to SARIs over SSRIs?
less sexual dysfunction
What herbal can cause serotonin syndrome if paired with an SSRI or MAOI?
St. john's wart
What cell body is NE made
locus ceruleus
What cell body is Serotonin (5HT) made?
Raphe nuclei
What is found to be low in pts who have committed violent suicide? What is it?
5-HIAA, metabolite of serotonin
How do 2nd gen SNRIs work?
What are 2nd gen SNRIs good for?
name one
increase 5HT (+) *increase NE*!

Anti-depressant, anti-anxiety (+) CHRONIC PAIN

s/e sex dysfunction
How do 2nd gen NaSSAs work?
What are 2nd gen NaSSAs good for?
(Advantage of NaSSAs)
universal blocker, tricks brain into thinking its catecholamine poor, increases 5HT activity

favorable s/e profile
Serotonin syndrome
Altered mental status, autonomic dysfunction, tremor, ataxia, myoclonus, anxiety, agitation, hyperkineasia, hyperreflexia
From overstimulation of 5-HT receptors by SSRIs, TCAs, MAOIs
Dysthymic Disorder
chronic, unremitting, low lying depression
Poorer prognosis (personality based)
Interstitail nucleus of anterior hypothalamus
Present in males, hard to define in females
No significant difference between heterosexual and homosexual men
SDN-POA neurons
At birth, women shown to have a large drop in cell numbers
Estrogen (aromatized from testosterone) in men reduces programmed cell death
Amygdala processing differences
Right-associated with memory for central information (big picture)=greater in men
Left-associated with memory for details=greater in women
Males vs. Females Prevalence for Personality Disorders
Males: schizoid, antisocial, OCD
Females: dependent, histrionic, borderline
Personality Disorder Clusters
A-"Weird"--schizotypal, paranoid, schizoid; first degree relatives
B-"Wild"--Borderline, Antisocial, Narcissistic, Histrionic; in families
C-"Worried"--Avoidant, Dependent, OCD; in families

Cluster B and C are highly comorbid
Panic Attack
Period of intense fear/discomfort with rapid onset and short duration accompanied by a feeling of impending doom
Characteristic autonomic findings (sweating, nausea, dizziness)
Voluntary and intention production of symptoms created to achieve secondary gain (avoidance of punishment, financial compensation/drugs, retaliate for legal penalty/job loss)
Body Dysmorphic Disorder
Preoccupation with imagined physical defect
Major depression, delusinoal disorder, OCD, social phobias
females, Adolescence
Treat with SSRI
Preoccupation with having or contracting a serious illness
Persists in spite of negative medical work-up
Belief not delusional
Cluster C DIsorders
"Worried" personality type
High degree of comorbidity with cluster B
Reduction in dopaminergic activity and increased serotonergic activity
Narcissistic Personality Disorder
inflated self esteem, sense of self importance, grandiosity and entitlement; unempathic, fragile self esteem
Interpersonal exploitation
Coexists with other cluster Bs
Intolerant of criticism
Devalue others
Idealization and omnipotence
Antisocial Personality Disorder
Disregard for social norms, violation of other's rights, lack of remorse
Lack anxiety in stressful situations
Appear pleasant or charming
Criminal activity common
Associated with ADHD
Receitful, remorseless and aggressive
**Cannot be diagnosed before the age of 18**
EEGs abnormal--reduction in prefrontal grey
Obsessive Compulsive Personality Disorder
Perfectionism, inflexibility, emotional constriction, indecisiveness
Preoccupation with rules and perfectionism
Hoard worthless objects
What Personality disorder is associated with increased levels of HVA? what is it?
Schizotypal; dopamine metabolite
Schizotypal vs. paranoid vs. schizoid
Schizotypal: ODDBALL


schizoid: NO EMOTION
fears of having a serious illness

GI and cardiac complaints most common
Conversion disorder
loss of sensor or motor function suggesting a neurological deficit
Common sx seen in pain disorder?

What should you give?
unremitting pain that does not fluctuate in intensity or with changes in emotion;

Analgesics NOT Helpful
Antidepressants drugs of choice
Posttraumatic Stres Disorder
Direct cause implied
Symptoms experienced after exposure to a traumatic event in which the event involved death or threat of death or serious injury followed by the response of fear/helplessness or horror
Re-experience the event
Overreactivity to cues or reminders
Avoidance behaviors, detachment and decreased interest
Children--foreshortened future
Not necessarily appear immediately after the actual trauma
For all anxiety disorders, you should give SSRIs as first line treatment, except for what disorder? What drug should you give?
PTST; give MAO Inhibitors
Grades 1-2
ening form of diffuse infiltrating astrocytic neoplasia
Tumor progresses to more malignant form
Hits cerebral hemispheres
Survival >5 years
Anaplastic astrocytoma
Grade 3: Malignant form
M > F
Cerebral hemispheres
No necrosis
Survival 2-3 years
Glioblastoma multiforme
Grade 4: most malignant form--80% from previous existing astrocytoma
Amplification of growth factor receptors and p53 mutation
M > F, aged 50+
Necrosis with pseudopalisading and vascular proliferation
Survival 8-10 months
Tumor of arachnoid cells (from villi)
F > M
Excellent prognosis if completely resected
Tumor of undifferentiated blasts
Exclusively in cerebellum of children
5 year survival 75%
Pilocytic astrocytoma
A tumor of children
Isolation Aphasia
Variety of fluent aphasia
Can ONLY repeat--repeat everythign that is said
Infarction in watershed area
Develop demential, cortical blindness, hemiparesis
Cannot name objects, cannot follow requests-->general cognitive impairment
Conduction Aphasia
Variant of fluent aphasia
Lesion in arcuate fasciculus between Wernicke's and Broca's area
Can hear, speak, follow commands, name objections
Fluent Aphasia
Wernicke's aphasia
Inability to express oneself, problem with content of words or phrasing
Can be substitutes and neologisms
**Paraphasias-individual abnormal words**
Temporal or parietal damage-trauma, tumor (usually structural)
No cognitive or physical deficit
Contralateral homonomous hemianopsia (cannot see right visual field-->damage of optic radiations)
Non-fluent aphasia
Broca's aphasia
Non-verbal, <50 WPM, dysarthric (area near motor strip--weakness of arm and lower face), speak only when spoken to, nouns and verbs, no demential, normal emotion
Left middle cerebral artery