NHB FINAL

Describe the James-Lange theory 1887

Cannon- Bard theory 1929

Schachter's cognitive theory 1975

What represents "afferent feeback" and influences cognitive processes in decision making

Limbic lobe components

Papez Circuit

Sham rage

No "Sham rage"

Uvea components

Aqueous Humor contents

Aq. humour secretion

Open Angle Glaucoma

Closed Angle Glaucoma

Drugs to decrease production of Aq. humour

Drugs to increase outflow of Aq. Humour

Beta Blocker for Glaucoma

Alpha Agonist for Glaucoma

Prostaglandin analogues for Glaucoma

Carbonic annhydrase inhibitor

Cholinergics for Glaucoma

Foveola- center of fovea

Most common cause of blindness
Degenerative process involving choroid-retina interface
(Basal laminar deposits, atrophy of RPE, loss of photoreceptors, Neovascularity)

RPE
Rods, cones
OLM
ONL
OPL
INL
IPL
GCL
NFL
ILM

Name the 4 types of photoreceptors

11-cis retinal to all-trans-retinal to Activated G protein which activates cGMP phosphodiesterase which hydrolyzes cGMP, diminishing it and closing NA channels, hyperpolazing membrane

Dark effects on rods

Degeneration of photoceptors
Waxy pallor, arteriolar attenuation, bony spicules

part of blood-retinal barrier
phagocytoses junk from photoceptors
stores vit A
absorbs light minimizing scattering
Connects to photoceptors

•Jelly like substance
•Made of collagen II
•Mostly water
•Salts, sugars, and GAG (HA)
•Only attaches to two areas
–ON
-Ora Serrata

•Magnocellular layers 1&2

–Responds to contrast & mvmt

–Responds to color, form, & detail

•Parvocellular layers 3-6

•Projections are either ipsi or contra

–1,4, & 6 are contra

–Composed of 1.2 million nerve fibers
–Diameter of 1.5 mm
–Runs through of Annulus of Zinn (origin of rectus muscle) and enters optic canal

•Optic nerve

–10 mm above pituitary gland
–55% of fibers decussation

•Optic chiasm

–Part of thalamus
–Crossed & uncrossed synapse
–Magnocellular neurons
•Motion detection, stereoacuity, and contrast sensitivity
–Parvocellular neurons
•Spatial resolution, color vision
–Koniocellular neurons

•Lateral geniculate body

–Connects LGB to cortex
–Meyer’s loop (inf ret fibers) travel around vent. system in temporal lobe à ”PIE in SKY”
–Superior retinal fibers go through parietal cortex à “PIE in FLOOR”

–Brodmann’s area 17
–Divided horizontally by calcarine fissure (Superior retinal fibers go inferiorly and vice versa)
–Macula fibers are on posterior VC
–Peripheral VF are ANT VC
–Temporal crescent on VF (55-100 degrees)

Nerve à Chiasm à Optic tract
Posterior 1/3 of optic tract
Travel in brachium of superior colliculus to midbrain (pretectal nucleus)
Synapse
2 Edinger-Westphal nucleus

Edinger-Westphal nucleus
Pregang parasymp fiber travel with inferior division of CN III
Ciliary ganglion synapse
Sympathetic & Sensory pass
Postgang parasym fibers (short ciliary nerves) enter globe Innervate sphincter & ciliary m.

•Disruption in CNS
•Light-Near Dissociation
•If one sided
–Limited direct response
–Good consensual response
–Normal near response
•Reason:
–Fibers for near response approach EW from ventral position bypass affected midbrain area.Frontal eye fields & efferent system intact

•Sympathetic pathway
•Interruption = Horner
•Hypothalamus (IMLCC)
•Ciliospinal center of SC
•Superior cervical ganglion
•Postgang via ICA
•Cavernous sinus
•Travel with V1 into orbit
–Ciliary ganglion – Short to choroidal blood vessel
–Long to iris dilator and ciliary muscle

–SCG to Iris dilator muscle
–Etiology: ICA Dissection

–Spinal cord to SCG
–Etiology: Mediastinal or Apical lung tumors
–Most common: Neuroblastoma, Pancoast tumors

–Hypothalamus to spinal cord
–Etiology: Brainstem lesions (MB, Pons, Med)
–Most common: Strokes like PICA (AKA?)

•First Order = Central Horner’s

•Nucleus in midbrain
•Red nucleus and CST in cerebral peduncles
•Passes through SCA & PCA
•Then lateral to Post comm artery – IMP !
•Enters cavernous sinus
•Receives sympathetics from ICA
•Passes through SOF and divides into sup & inf
•Innervates all EOM EXCEPT SO & LR

•Nucleus in caudal mesencephalon
•Passes between PCA and SCA
•Lateral wall of cavernous sinus
•Enters orbit via superior orbital fissure outside annulus of Zinn
•Innervates SO muscleONLY nerve that leaves dorsal aspect of CNS

•Nucleus in dorsal pons
•Medial to CN VII
•Through pyramidal tract
•Exit lower pons
•Climbs over the clivus over petrous ridge along skull base
•Enters cavernous sinus
•SOFSupplies LR

•CN III
•CN IV
•CN V1
•CN V2
•CN VI
•So whenever multiple cranial nerves, ALWAYS rule out CS lesion

•Right MLF turns eyes to right
•Left MLF turns eyes to left
•Lesion of MLF = ipsilateral INO

–Nasal fibers = Temporal loss
–Infero-nasal & Infero-temporal fibers = Ipsi Temporal lobe = Contra Pie in sky
–Supero-nasal & Supero-temporal = Ipsi Parietal lobe = Contra Pie in floor
–Optic tract = Contra homonymous hemianopsia
–Occipital lobe = Contra homonymous hemianopsia with macular sparing

CN 3,4, V1, V2, 6

•9th leading cause all ages
•3rd leading cause age 15 -24
•30,000/year, 12/100,000 in US
•1 million word wide

•1 : 23
•1 : 200 female adolescents
•1 : 4 persons over age 64
•50% had a prior attempt
•1:100 will complete, 10% die in 10 years

mental illness + psychosocial stressor + (intoxication + impulsivity + means) =

Depressed people have higher risk of suicide when?

Schizophrenia have high risk of suicide when?

Decreased serotonin metabolite 5-HIAA in what areas of suicide victims?

Frontal cortex of suicide victims has

Decreased 5-HIAA in what pts?

Increased NE (4-hydroxyphenylglycol), causes

Dopamine aka homovanillic acid levels in suicide

• serum cholesterol
•Abnormalities in urine breakdown products
• 5 HT 2 platelet receptors

Methods of Suicide

•55-60% Firearms

Common Method for suicide in General Hospital

Common method in Psych ward

•60% told spouse
•50% told relatives
•18% told therapist

•Responsibility to family
(minors at home)
•Fear of killing oneself
•Fear of the unknown
•Religious beliefs
•Future plans
•Help seeking

•How bad do you feel?
•Do you wish you were dead?
•Thoughts of ending your life?
•Thoughts about a particular way to end your life?
•How close have you come in doing anything?

Assessing Suicide Attempts from Pt

•Isolation and timing

Pts report of Attempted suicide

•Alleged purpose of the attempt

•False sense of security
•Significant if refused
•No research support
•More than ½ of inpatient suicides had them in place

papez circuit + amygdala
+ dorsomedial thalamus, + basal forebrain nuclei
+ prefrontal cortex (orbital and medial)

Placidity- emotional blunting
Psychic blindness- prosopagnosia
Hypersexuality
Hyperorality
Cause- lesions of medial temporal lobe structures, requires lesion of amygdala

basal forebrain components

Medial temporal lobe parts

Limbic Cortex parts

cholinergic neurons
“pleasure center”

Nucleus Accumbens
Ventral pallidum

Nucleus Basalis of Meynert

Fornix pathway

MTT pathway

Cingulum pathway

Stria terminalis

Ventral Amygdaloid Pathway

MFB projections include

Regions of the hypothalamus

Preoptic Nuclei

Suprachiasmatic nucleus

Supraoptic and paraventricular (magnocellular neurons)

Arcuate and paraventricular (parvocellular neurons)

Arcuate

medial tuberal

lateral tuberal

Hypothalamus -Autonomic control
Input?
To what hypothalamic nuclei?

Hypothalamic Autonomic Control (Output) Efferent projections

Increased HR--Baroreceptor afferents--solitary tract nucleus--VM and PV

Hypothalamus (PV and Lateral Nuc) to Nucleus ambiguus and Dorsal motor nucleus of X, which are parasympathetic and slow HR, also IML gets inhibited to decrease sympathetics

PV and Arcuate nuclei (parvocellular) releasing factors to portal vein- to ant. pituitary hormones to general circulation

PV and SO (magnocellular) release Hormones with go down Supraoptic hypophyseal tract to post pituitary to general circulation

•Memory impairment (anterograde memory deficit)
•Disruption of Papez circuit:
hippocampus ® fornix ® MB ® MTT ® anterior thal. ® cingulate cortex
•Also: gait ataxia (vermis) and problems with gaze (III)
Bilateral lesions of MB / MTT can lead to

Miosis small pupil (partial constriction)
Ptosis drooping eyelid
Anhydrosis flushing and lack of sweating
in ipsilateral skin of the face
(red, dry skin i.l. face)
Enophthalmus recession of eyeball

nInterface between limbic system and neocortex
ÞCognitive and memory functions
nMajor role in memory formation: consolidation (transfer of information from short-term to long-term memory)
nInvolved mainly in explicit (declarative) and contextual and spatial memory processes
nDysfunctions-disorders:
qTemporal lobe epilepsy
qAmnesia (anterograde)
qAlzheimer’s disease
qSchizophrenia

•Molecular layer
• Granule cell layer
• Polymorphic layer

• Molecular layer
• Pyramidal cell layer
• Polymorphic layer

Transition zone from 3-layered cortex of hippocampus proper to 6-layered neocortex

q“psychomotor epilepsy” Complex partial seizures (seizure spreads to involve both temporal lobes) Hippocampal sclerosis (cell loss in CA1, CA3 and dentate) is the most common pathologic finding

•Bilateral medial temporal lobe resection for untreatable temporal lobe seizures (1953)
•Anterograde amnesia (inability to form new memories)
•Impaired memory consolidation (> minutes)
•Intact working memory (seconds)
•Intact long-term memory (childhood, adolescence)
•Partial retrograde amnesia (few years before surgery)
•Intact learning of motor skills (procedural memory)

qGeneral brain atrophy (atrophic gyri and widened sulci)
particularly prominent in the limbic cortex
qNeurofibrillary tangles and senile plaques
predominantly in the parahippocampal gyrus:
hippocampus and amygdala

qDementia
qMemory loss (starting with short-term memory)
qLoss of judgment; disorientation
qEmotional changes (depression and/or aggressiveness)

nAttaching emotional significance to a stimulus
nEmotional (associative) learning and (implicit) memory
nTriggering emotional responses (emotional behavior)Reward mechanisms

Urbach-Wiethe syndrome

Areas of increased blood flow (PET scan) in the left amygdala and the prefrontal cortex of patients with ? relative to normal control patients.

qConscious experience of emotions
qCognitive interpretation of emotional situations
qAttention
qAnticipation of an upcoming (aversive) stimulus (e.g., pain)
(this may involve other areas of the medial prefrontal cortex)

Bilateral radiofrequency cingulotomy lesion for the treatment of chronic pain

nExecutive functions
nConscious experience - subjective feelings
nCognitive component of emotions (evaluation)
nEmotion-driven and reward-based decision-making
nCognitive control of limbic functions (emotions)
qSham rage experiment:
Decortication precipitates emotional behavior
qPhineas Gage case Emotional instabilityFear and fear extinction

Case of Phineas Gage

Orbital and medial

Prefrontal control of emotions

•bipolar sensory neurons
• with G-protein coupled receptors
• unmyelinated axons collect into olfactory fila
• form olfactory nerve CN I
• penetrate cribriform plate
• terminate in glomeruli
• synapse on dendrites of mitral cells

nBenign tumor; does not invade brain tissue
nGrows along the olfactory tract
nPrincipal symptoms:
qLoss of smell (anosmia)
qHeadache (DD frontal sinusitis, migraine and neuralgia)
nOther symptoms:
qCompression of the optic nerve(s)
ØVisual deficits (visual field deficits or even blindness if tumor grows large enough)
nCan grow to a large size prior to being diagnosed because changes in the sense of smell are difficult to detect routinelyTx: Surgical excision only if symptomatic or enlarging

nManifestation of temporal lobe epilepsy
nOriginate in the vicinity of the uncus
nBegin with “olfactory” hallucinations (illusion of smell or taste) along with chewing movements of lips and tongue
n“Uncus”:
qmedial protuberance from the anterior end of the parahippocampal gyrus caused by the underlying amygdala
qsite of the primary olfactory cortex
nPrimary olfactory cortex includes:
qpiriform cortex
qperiamygdaloid cortex
q(anterior) entorhinal cortex

Deccorticate shame rage
Korsakoff's syndrome

Horner syndrome

Memory loss (amnesia)

Alzheimers Disease structures involved

Temporal lobe epilepsy "limbic seizures"

Kluver-Bucy sundrome
Urbach-Wiethe syndrome

Fear-Anxiety
Depression

Schizophrenia

Reward-addiction

Acquired disorder, isolated loss of spoken or written language, different types

Defect in articulation with intact mental function, comprehension and word memory

Dysarthria

Aphonia

Wernicke's area

Area 44,45
Motor function of speech

non-fluent aphasia, expressive, motor- loss of fluency, some improvement from time of initial insult- not much recovery after 4-6 months

Fluent aphasia, receptive, sensory,

disconnection b/w Wernickes and Brocas areas, --disturbed repitition

transcortical disturbance

Global loss of languag functions

Anterior lesions cause loss of ?

Lesions b/w Wernickes and Brocas cause loss of ?

Posterior lesions cause loss of ?

Crossed Wernickes Aphasia

Input from visual cortices converges on angular gyrus which projects to Wernickes area, output from Wernickes area reaches Brocas area through the arcuate fasciculus, output from Broca's projects to the laryngeal representation in the primary motor cortex

Input from primary auditory cortex reaches Wernickes, output from Wernickes reaches Brocas area by means of arcuate fasciculus, brocas area projects to laryngeal representation in the primary motor cortex.

Classic type of M.S.

Neuomyelitic optica

Acute fulminant type of MS

Concentric rings of demyelinated/myelinated white matter, variant form of MS

Large, usually symmetric, hemispheric plaques, MS variant

Chromosome 22

Oligodendrogliomas genetic basis

NF1 genetic basis

Hemangioblastoma genetic basis

Best Verbal Response

Best Motor Response 1-6

Eye Opening 1-4

GCS- 50% mortality when?

Over 9 GCS

Causes of Coma

Lateral 2/3s of RF

Medial 1/3 of Rf

Vegetative state

Akinetic mutism

Cheyne-Stokes respiration

Central neurogenic hyperventilation

Apneusis

Cluster breathing

Ataxic breathing

Dural Venous Sinus Pressue + (CSF fromation X Resistance for CSF Absorption) = ?

0-5lymphocytes/ul, 45-85 glucose mg/dl, 15-45 proteins mg/dl, 70-180mmH2O

Neonates 0-2 mo acute meningitis organisms

3 mo- 50 years

> 50 years

Similarities of major agents in acute meningitis

Increased Pressure, Increased WBC (esp nuetrophils), Decreased Glucose, Increased Protein

Chronic meningitis- TB

Meningeal infiltrate on basilar surface
Granuloma and few mycobacteria in immunocompetent, but sheets of macrophages and lots of mycobacteria in immunocompromised
Arteritis in what artery?

Hyponatremia in blood
CSF- increased lymphocytes, increased protein, decreased glucose
Definitive test?

Decreased glucose, increased protien, mildly increased lymphocytes, yeast in gram stain prep india ink or mucin stain prep
soap bubbles in perivascular spaces

Acute presentation in AIDs
Subacute/chronic in immunocompetent
papilledema in 1/3, nerve palsies in 1/5
Pulminary infx often clears before meningitis shows.
brain abscess also common

EEG- periodic high voltage discharges in one or both temporal lobes in a background of general slowing

CT/MRI findings in HSV-1 encephalitis

Increased Protein, Slightly elevated lymphocytes, normal glucose
CSF

False negatives first couple days or after 10-14 days, takes 6-8 hrs, procedure of choice for definitive diagnosis of HSV-1 encephalties

1) Spread along olfactory nerve fibers
2) Reactivation of latent virus in trigeminal ganglion and axonal spread to fibers innervating dura

Acyclovir treatment = 20% mortality, with 50% experiencing sequelae
Basal/medial temporal lobe often shows hemorrhagic necrosis
see viral inclusion bodies histologically

Agents that cause Brain Abscess

50%- spread from infection (otitis media, dental/facial abscess)
25%- hematogenous spread (endocarditis)
Cryptogenic (20%)
Penetrating trauma

Stages of Abscess formation (4)
Once abscess is walled off, have to have surgery

Delta- slow wave sleep 0-3Hz
Theta- drowsiness, arousal 4-7Hz
Alpha- relaxed wakefulness 8-13 Hz
Beta- intense mental activity > 14 Hz

Part of hypothalamus controlling circadian rhythm and temperature, melatonin, and cortisol levels

SCN projects to?

Time givers synchronizing agents

-promotes wakefulness
-receives light via retinohypothalmic tract
-receives non-photic info via serotonergic pathway from dorsal raphe nucleus
-regulates indirect pathwy from sup cervical ganglion to pineal gland

VLPO

Stage 4 sleep

Stage 3 Sleep

Low voltage 2-7 hz activity mixed with rapid eye movements and reduced chin activity

Less than 20% delta activity with K complexes and spindles

less than 50% alpha and then 50% 2-7 Hz mixed activity

Greater than 50% is alpha activity 8-13 hz or low voltage 2-7 Hz mixed activity

(ARAS), the midbrain reticular formation (ACh), posterior hypothalamus (histamine),Lateral Hypothalamus(Hypocretin/orexin) and the nucleus basalis of Meynert (ACh).

bind to GABA-A receptors; decrease sleep latency and the number of awakenings, while improving sleep duration and sleep quality; dependency

newer hypnotics; non-BZD structure but act similar to GABA agonist, binding to the BZD site; relatively low side effects (growing concern about this) and risk of dependency

Melatonin agonist acting at melatonin receptors in SCN. Good for sleep initiation (short half-life), low abuse potential, minimal side effects

Orexin A and Orexin B are Nt's released by lateral thalamus that stabilize wakefulness and inhibit REM sleep. They increase transmission of LC and Raphe Nuclei, tuberomammillary nucleus.

stimulants (Modafinil; pemoline, amphetamines, e.g. Adderall) for sleepiness
REM suppressors (tricyclic antidepressants or MAOIs) for cataplexy. Not entirely adequate; some have serious side effects (e.g., pemoline/liver).

Repeated interruptions in breathing (for more than 10 s at a time) during a PSG (both REM and NREM); >5 interruptions/hour

vObesity
vMale sex
vAge
vAdenotonsillar hypertrophy, particularly in children and young adults
vAlcohol use
vCraniofacial skeletal abnormalities, particularly in nonobese adults and children
vFamily history: Risk increases with each additional close family relative with OSAHS

diaphragm does not contract
due to CNS abnormality.

collapsed upper airway (usually obese people).

Mixed Apnea

Best treatments for Cataplexy Now

association b/w two stimuli

association b/w stimuli and behavior

Apply a positive stimulus = strengthen behavior

Apply a negative stimulus = decrease behavior

Remove a Negative stimulus = increase behavior

Remove a positive stimulus = decrease behavior

Social Cognitive Theory
-Bandura
-motivational factors involved in behavior
Imitated learning requires

Birth to 2
learn through motor and reflexes
thought from sensation, movement
learns she is seperate from environment

language to 7 years
assumes everyone sees things like them
oriented to present, but can think about things not immed present
thinking influenced by fantasy
can use symbols to represent objects

7 to early adolescence
can think abstractly and make rational judgements about concrete phenomena w/o manipulating physically

Adolescence
can make rational judgments, no longer a req to have concrete objectscan take another's views
can hypothetical and deductively reason

id-
ego-
superego-

Unconscious
Defense mechanisms
Hypnosis
Talking dialog for therapy

Prefrontal cortex
ex. hearing sequence of numbers and repeating them
Required to encode and recall explicit memory

Visuospatial sketchpad

Articulatory loop

Implicit memory structures

Explicit memory structures

Emotional memories

Automatic recall

Active recall

Non associative learning

habituation

Sensitization

Amygdala lesions

Hippocampus is important for acquisition of spatial memory in rats, but not its storage

Perforant pathway

Mossy fiber pathway

Schaffer collateral pathway

Snail gill withdrawal reflex

Stronger 5-HT input causes long term changes -

^{? phosphorylates K channels closing them, decreasing thershold and increasing excitability of membrane}

disturbance of consciousness
reduced ability in attention
change in cognition, not from preexisting condition
Acute
quiet or loud
prevalent in hospitals 10-25%, 3 month mortality rate

delirium risk factors

Haloperidol (anti-psychotic), treats?

memory impairment + decline in executive functioning + 4 A's? = what disease

Workup for treatable causes of Dementia

Statins and Alzheimers DZ

Treats Amyloid toxicity in Alzheimers by preventing its deposition, delay nursing care for 1 yr

Cholinesterase inhibitors for tx of Alz DZ

Tx inflammatory process in Alz, but usefulness does not offset GI bleeding risks

Free radical toxicity tx for Alz

Treats glutamate toxicity in Alz dz. An NMDA receptor antagonist

Treats nerve growth deficiency in Alz Dz. Mimics a naturally occuring growth factor, helps to generate new cells, may prevent death

Other Alz tx possibilities

1) tight junctions between Müller cells and inner segments of photoreceptors

Nuclei/cell bodies of photoreceptors

synapses b/w bipolar cells and photoreceptors (includes horizontal cells)

bipolar, horizontal, amacrine cell nuclei

bipolar and amacrine synapses with ganglion cells

Axons from ganglion cells form optic nerve

thin basal lamina

At foveal pit, these layers are pushed aside to minimize number of layers light has to penetrate to get to photoreceptors

Retina à Optic nerve à Optic chiasm à Optic tract à
Lateral Geniculate Nucleus of the thalamus à Optic radiation
à Primary visual cortex

magnocellular, form the
M channel and are responsible for movement
and contrast

· are parvocellular, form the P channel and are responsible for color and form

o Pupillary constriction to change the depth of focus
o Prevents diverging light rays from hitting the periphery of the retina and resulting in a blurred image
o Requires cerebral cortex participation

·





Area 19





Magnocellular Projection
(movement, stereopsis)
Deficit in this area leads to loss of movement so moving cars look frozen





Parvocellular Projection
(inferotemporal Ctx, form& color)
Deficit in this area would result in a black&white worldMagnocellular projection (movement, stereopsis – depth perception)
· Parvocellular projection in inferotemporal ctx (form, color)
· Damage in these areas results in odd deficits, such as loss
of form but not color, or being unable to see movement.

1) entire left field loss with macular sparing

1) left upper quadrantanopsia (upper, outer quadrant).

Medications to treat alcholism

Medications to treat opiate addiction

Medications to treat Nicotine addiction

Methohexitol

SIG E CAPS = Major depressive episode

Manic Episode= DIG FAST

Unacceptable feelings and thoughts are expressed through actions
(Immature)
ex: tantrums

Temporary, drastic changes in personality, memory, consciousness, or motor behavior to avoid emotional stress.
Ex: multiple personality disorder

Avoidance of awareness of some painful reality.
Ex: common in newly diagnosed AIDs patients

Partially remaining on a more childish level of development
ex: men fixating on sports games

Modeling behavior after another person who is more powerful (although not necessarily admired)
ex: abused child identifies himself as abuser

An unacceptable internal impusle is attributed to an external source
ex: man who wants another woman thinks his wife is cheating.

process where a warded-off idea or feeling is replaced by an (unconsciously derived) emphasis on its opposite
ex: a patient with immoral thoughts enters monastery

Turning back the maturational clock and going back to earlier modes of dealing with the world
ex. children under stress bedwet

involuntary withholding of an idea or feeling from conscious awareness
ex: not remembering a traumatic experience

People are all good or all bad due to intolerance to ambiguity.

guilty feelings alleviated by unsolicited generosity toward others

Appreciating the amusing nature of an anxiety-provoking situation

Process whereby one replaces an unacceptable wish with a course of action that is similar to the wish but does not conflict with ones values.

voluntary withholding of an idea or feeling from conscious awareness
choosing not to think about car wreck till after big exam

Mature women wear a SASH

ADHD brain structures involved

In ADHD, name effect on frontostriatal regions

decreased sleep
decreased appetite
tics

Amphetamines and Methylphenidate MOA

ADHD with tiny laser drilled hole so efficacy for 12 hours

Alpha 2 agonists for treatment of ADHD

good for control of impulsivity and inattention, debatable for hyperactivity.Watch for BP drops, sedative

Antidepressants to treat ADHD

Anger associated with what 3 brain structures

PET study of murderers found NGRI showed reduced glucose metabolism in what structures, and saw assymetric activity in what structures

Nuerological findings in aggressive people

In 10 IED subjects had abnormal response to facial expressions

Low serotonin in CNS and aggression

GABA and aggression

Low NE and aggression

ACH and aggression

Reduced serotonin
Increased dopamine, NE

Reduced GABA
Increased glutamate and ACH

MAOA-L volume reduced in what structures

MAO-L males show increased volume in what structures compated to MAO-H males

5-HTTLPR (Serotonin Transport Linked Promoter Region plymorphism in rhesus monkeys

No-Go experiment

NO-GO anteriro cingulae gyrus

psychostimulants, hallucinogens, sedative hypnotics, opiates, anticholinergics, steroids

Top-down regulation on aggression

Bottom-up "drive" on aggression
signal,trigger

Tx for aggression by decreasing limbic activation, increasing prefrontal control. Esp for organic impairment or psychotic thought processes

Tx for acutely aggressive, Helps calm patients. In some can cause disinhibition, increasing aggression

Tx for those with compulsive aggression.

Tx for aggression, esp in those iwth organic impairment of MR. Requries large doses

Not as helpful as initially hoped in tx aggression

Improves aggression in ADHD patients.

Primary olfactory cortex
(uncus) components