Neuro Final Exam

Front 1

Relationship btwn diencephalon and cerebral cortex

Back 1

- extensive reciprocal conections btw the thalamus and cortex - thalamic radiations of the internal capsule - both thalamocortical and corticothalamic projections are glutamatergic (+)

-different thalamic nuclei project to different cortical areas

-general rule (few exceptions) - all info destined to reach the cortex must be relayed through the thalamus

thalamus seems to be a staging area for info sent to the cortex

Front 2

locatioin of diencephalon

Back 2

bottom surface of lateral ventricle

- medial thalamus separated from lateral thalamus by internal medullary lamina - C shaped structures

lateral thalamus seperated from internal capsul by external medullary lamina

- subthaalamus (lat) and hypothalamus (med) are underneath the lateral thalamus
-hypothalamus is lateral sides of 3rd ventricle

massa intermedia - interthalamic adhesion between two medial thalamus

epithalamus - small - on medial side of medial thalamus

Front 3

seven nuclear groups of the thalamus

Back 3

Ventral nuclear group
lateral nuclear group
medial nuclear group
intralaminar nuclear group
anterior nuclear group
reticular nuclear group
metathalamic nuclear group

Front 4

ventral nuclear group

Back 4

located in the ventral part of lateral thalamus

nuclei (rostral to caudal) -
1. ventral anterior
2. ventral lateral
3. ventral posterior = VPL+VPM+ VPI

VA and VL have similar connections and functions and are usually considered together as the "motor thalamus"

Front 5

inputs and outputs of Motor thalamus

Back 5

Ventral anterior and ventral lateral nucleus

- inputs -
1. globus pallidus via ansa lenticularis and lenticular fasciculus which converge to form thalamic fasciculus
2. cerebellum via superior cerebellar peduncle(SCP) - deep nuclei - esp dentate

outputs
1. motor cortex (area 4) mostly from VL
2. premotorcortex (area 6) mostly VA

Front 6

function of motor thalamus

Back 6

integrates inputs from several important motor regions and then influences the activity of pyramidal and extrapyramidal motor areas

allows basal ganglia and cerebellum to influence cortical areas giving rise to the major descending motor tracts (both pyramidal and extrapyramidal

Front 7

lesions of the motor thalamus

Back 7

irritative lesions produce involuntary mvmts on the side opposite the lesion - tremor, chorea, athetosis = extrapyramidal

Front 8

ventral posterior nucleus inputs and outputs

Back 8

inputs - ascending sensory pathways
- medial lemniscus and LST/VST - crossed => VPL -> somatosensory cortex (areas 3,1,2)

Vestibulothalmic tract - bilateral -> VPL -> somatosensory cortex (2,3,1)

Vestibulothalmic tract -bilateral -> VPI -> vestibular cortex (ant. intraparietal sulcus)

vestibulothalamic tract -bilateral-> VPM --> somatosensory cortex (3,2,1)

DTT -biolateral --> VPM --> somatosensory cortex

VTT -crossed -> VPM =>somatosensor cortex

ascending taste pathway - uncrossed -> VPMm --> gustatory cortex (area 43)

outputs - postcentral gyrus and adjacent areas

Front 9

Function of ventral posterior

Back 9

- relay sensory info to cortex - cortical processing is necessary for discriminatory aspectsof these sensory modalities

- crude awareness of certain sensory modalities at the level of VP (pain, crude touch)

Front 10

lesions of ventral posterior nucleus

Back 10

different symptoms depending on whether partial or complete lesion

- complete lesion of entire VP
- loss of sensation from contralateral side of body= contralateral anesthesia
- little loss of touch from face since the dorsal trigeminal thalamic tract contains a bilateral representation of the face - there is a loss of pain and temp contralaterally (VTT has a unilateral representation in the face)

partial lesion of VP - thalamic pain syndrome
- spontaneous severe burning type of pain contralateral
- non-noxious stimuli is perceived as pain - light pin prick or cooling the skin is painful
- tx of thalamic syndrome - surgically lesion VP - eliminates pain but produces contralateral anesthesia

Front 11

metathalamic nuclear group

Back 11

(meta = hindmost)
- located caudal to ventral nuclear group and ventral to pulvinar

two nuclei - lateral and medial geniculate bodies
lateral = visual thalamus
medial = auditory thalamus

Front 12

lateral nuclear group

Back 12

located in the dorsal part of lateral thalamus - most caudal nuc -pulvinar forms most of the caudal thalamus

nuclei -
1. lateral dorsal
2. lateral posterior
3. pulvinar

DM

Front 13

inputs and outputs of lateral nuclear group

Back 13

sensory assoc cortex is btw the three main sensory areas (somatosensory, auditory, and visual) - recieves input from all three areas and is involved w/higher order processing of stimuli - integration, interpretation, and association of sensory info -

sensory associtation cortex - recipricol connections

Front 14

function of the lateral nuclear group

Back 14

works together with the sensory association cortex in high order sensory fn imp for sensory perception and attention

Front 15

lesions of lateral nuclear group

Back 15

little info - attention deficits hav been detected in some pts using sophisticcated testing procedures

Front 16

intralaminar nuclear group

Back 16

nuclei found w/in internal medullary lamina

- main in nucleus - centromedian - largest

consists of nuclei embedded in the internal medullary lamina

Front 17

input and output of intralaminar nuclear group

Back 17

main input - from reticular formation via reticulothalamic tract

output - diffuse projection that reaches all areas of the cortex - the intralaminar nuclei are called non-specific thalamic nuclei bc of the diffuseness of this cortical projection

Front 18

fn of intralaminar nuclear group

Back 18

imp link in ascending reticular activating system (ARAS) - intralaminar nuclei and the rest of the ARAS are involved in cortical activation nec to maintain alertness and arousal

- reticular formation is activated by sensory inputs from all sensory modalities - lateral spinothalamic tract sends somatosensory inputs here

- reticular formation then activates the intralaminar nuclei which in turn activate the cerebral cortex to produce arousal

Front 19

lesions of intralaminar nuclear group

Back 19

drowsiness and lethargic state

Front 20

reticular nuclear group

Back 20

consists of (layer of neurons) nuclei situated btw the internal capsule and external medullary lamina

nuclei form a shell over the lateral aspect of the thalamus

Front 21

input and output of reticular nuclear group

Back 21

input - each poriton recevies inputs from a distinct thalamic nucleus and cortical area the has connections w/that thalamic nuc

it also recieves inputs from reticular formation that may play a role in attention

output - each portion sends output to the same thalamic nuc that provides its thalamic input

Front 22

function of the reticular nuclear group

Back 22

modulates cortical activity indirectly via its projections to thalamus

- activation of thalamic relay nuclei (activation of VPL by sensory inputs) results in activation of the cortex and RN

- RN then provides feedback inhibition of the VPL (via gabaergic mechanism) which transiently stops the firing in VPL

the cortex can the reactivate teh VPL and also the RN

RN then provides feedforward inhibition of the VPL which again transiently stops the firing inVPL

sequences of excitation and inhibition results in rhythmic activity in the VPL which is transmitted to cortex and is reflected in waveform of the EEG and critical for norm cortical fn

malfn of the system in the absence seizures seen in petit mal epilepsy

Front 23

anterior nuclear group

Back 23

located in ant pole of thalamus

relay nuc of limbic system of the forebrain

limbic - part of brain concerrned w/emotion

forms rostral pole of the thalamus
enclosed by rostral bifurcation of the internal medullary lamina

Front 24

medial nuclear group

Back 24

forms the medial thalamus

consists of one large nucleus - the dorsomedial nuc - and smaller midline nuclei that are considered part of nonspecific nuc

Front 25

inputs and outputs of the dorsalmedial nucleus

Back 25

inuputs -
1. other thalamic nuclei - esp laterla nuclei - conveys complex sensory info
2. hypothalamus - prob conveys visceral info to DM
3. amygdala - prob conveys emotional information to DM
4. olfactory cortex - conveys olfactory info to DM

output - prefrontal cortex - via ant. thalamic radiations of ant limb of internal capsule
- prefrontal cortex forms the ant pole and orbital surface of the frontal lobe - highes t order motor assoc cortex and is best dev in primates esp humans p imp for producing complex behavior responses

Front 26

function of dorsalmedial nucleus

Back 26

recieves complex info by way of inputs and integrates this info and then activates the behaviorally imp prefrontal cortex

DM and the prefrontal cortex work tegether and are involved in three main fns
1. emotion and motivation
2. memory and learning
3. planning and foresight

Front 27

lesions of Dorsalmedial nucleus, prefrontal cortex or connecting fibers in anterior thalamic radiations

Back 27

1. memory deficits
2. reduction in emotion (particularly anxiety)
3. loss of motivation
4. loss of social inhibitions

have a relaxing effect

used prior to the dev of psychiatric drugs in the 50's
prefrontal lobotomy - surgical removal of portions of prefrontal cortex
prefrontal leucotomy - surgical cutting of the ant thalamic radiations

Front 28

Main function of the hypothalamus

Back 28

maintain homeostasis - wide variety of physiologic processes:
1. resp
2. circulation
3. digestion
4. metabolism
5. food and water intake
6. sleep
7. repro
8. regulation of body temp

regulates all of these by producing a coordinated response involving 3 components - visceral, endocrine and behavioral
Ex - in response to cold environment HT maintains body temp by generating:
visceral - constriction of peripheral blood vessels to decrease heat loss
- endocrine respinse - increase secretion of thyroid hormone = increase metabolism and increase heat production
behavioral - shivering - inc heat production and seeking warmth and shelter to decrease heat loss

Front 29

general connections of HT

Back 29

limbic system (behavior) - forebrain limbic system - amygdala and hippocampus very imp

pituitary (endocrine

Reticular formation = GVE + SVE for visceral
- visceral centers in the reticular fomration activate visceral motor neurons in the brainstem andspinalcord to produce visceral responses - also direct connections of theHT w/visceral motor neurons

Front 30

location of hypothalamus

Back 30

lateral to third ventricle
caudal to lateral thalamus
medial to subthalamus

Front 31

zones of hypothalamus

Back 31

1. periventricular - contains many fibers
2. medial - contains most of the nuclei
3. lateral - contains MFB

Front 32

nuclei of the HT

Back 32

grouped into 3 main HT regions
ant - chiasmal and infundibular levels
- preoptic nuclei
- suprachiasmatic nucleus
- ant nucleus
- supraoptic and paraventricular nuclei

tuberal HT region
- dorsomedial HT nuc
- ventromedial HT nuc
- arcuage nuc
post ht region
- mammillary nuc
- post hypothalamic nuc

Front 33

preoptic nuclei

Back 33

- located in front of the optic chiasm
-although actually part of the telencephalon the preoptic area is closely related to the HT both structurally and fnally
-important for repro fn
sexually dimorphic
- ant HT region

Front 34

suprachiasmatic nuc

Back 34

located abv the optic chiasm

- recieves fibers from the optic n and consititues the biological clock - reg circadian rhythms

- ant HT region

Front 35

ant nuc

Back 35

heat dissipation center
neurons are sensitive to blood temp
- activates neural mech that result in sweating and vasodilation when blood temp increases

ant HT region

Front 36

supraoptic and paraventricular

Back 36

regulate hormonal release from the posterior pituitary

ant HT region

Front 37

dorsomedial HT nuc

Back 37

exact fn unknown

Front 38

ventromedial HT nuc

Back 38

VMN - satiety center
- its neurons are sensitive to blood glucose levels
- activates neural mechanisms that inhibit eating
- lesions of the VMN in rats results in extreme over - feeding response
- the portion of thelateral HT located just lateral to VMN is callled the "feeding center" - lesions of this region results in inhibition of feeding

Front 39

arcuate nuc

Back 39

modulates hormonal release from theant pituitary

Front 40

mammillary nuc

Back 40

has connections w/the hippocampus
involved in memory

Front 41

post hypothalamic nuc

Back 41

lesions cause narcolepsy
the post hypothalamic region also contains a heat conservation center

Front 42

inputs into hypothalamus

Back 42

1. amygdala - projects to HT via 2 pathways 1. stria terminalis or 2. ventral amydalofugal pathway (VAFP)
- the stria terminalis projects to the medial zone of the HT
- the VAFP projects to the lateral zone of the HT
- generates emo responses by activating HT

2, hippocampal formation = part of limbic system
- connects w/HT via a fiber bundle called the fornix
- the fornix synapses primarily in mammillary bodies
- provides HT w/info concerning memory

3. olfactory cortex, septum, andreticular formation - connect w/ HT via medial forebrain bundle
- medial forebrain bundle runst through the lateral HT and contains both descending fibers from the olfactory cortex and septum conveying olfactory and emo info and ascending fibers from reticular formainton conveying visceral info

fibers in the MFB synapse in both lateral and medial zone of HT

Front 43

output pathways from hypothalamus

Back 43

1. hypothalamotegmental tracts
2. periventricular fiber system
3. mammillothalamic tract

Front 44

hypothalamotegmental tracts

Back 44

fiber pathways that originate in the HT course in the medial forebrain bundle and terminate in the RF - one special component in the tract originates soley in the mammillary bodies - mammillotegemntal tract)
the reticular formatino in turn projects to viscerla nuclei in the BS sand SC to produce visceral response and to somatic motor nuclei to produce bh responses ( reticulospinal tract)

Front 45

periventicular fiber system

Back 45

runs in the walls of the 3rd ventricle
some fibers synapse in the periaquaductal gray to produce bh responses the remaining fibers to produce bh response - the remaining fibers continue caudally and as the dorsal longitudinal fasciucls in the floor of the aqueduct and fourth ventricle
- fibers synapse in visceral nuclei of cranial n

Front 46

mammillothalamic tract

Back 46

originates in mammillary bodies and terminates in the ant thalamic nuc
tractis inp part of the circuitry of the limbic system which is involved in memory, bh, and emo

Front 47

neurohypophysis - hypothalamic control of

Back 47

posterior pituitary
regulated by - hypothalamic regions - supraoptic nuc and paraventricular nuc - magnocellular portion
- these HT neurons syn oxytocin and vasopressin -ADH

pathway - supraopticohypophysial tract
- formed by the axons from SO and PV
- courses through the pit stalk and terminates upon caps in the neurohypophysis

fnal aspects - the activity of SO and PV neurons can be affected by neural inputs and by changes in osmolarity of the blood. Increases in osmolarity, which could be produced by dehydration excite the SO and PV neurons that release vasopressin

- when these cells are excited, action potentials run down their axons (in the supraopticohypophyseal tractA and release oxytocin or vasopressin from the axon terminals in the neurohypophysis
- enter the bloodstream
- vassopressin causes water resorption by the kidneys which in turn decrease blood osm
- oxytocin causes contraction of the smooth mm of the uterus and mammary glands so it is imp for birthing and lactation
itis also involved in the social bonding - maternal -infant - via its actions on portions of the limbic system

Front 48

adenohypophysis - hypothalamic control of

Back 48

hypothalamic regiion- ventromedial and infundibular nuc
[arvocellular poriton of the paraventricular nuc
- neurons syn releasing factors for the hormones of the adenohypophysis
- two part pathway - neuronal and humoral
Tuberoinfundibular tract - this tract isd formed by axons of neuorns in the tuberal hypothalamus and parvocellular portion of the paravetnricular nuc
axons terminate on caps in median eminence - when they are excited by hormones in the circulation or by neural inputts APs travel down and release the hormone releasing factors from axon terminals the releasing factors travel to the adenohypohysis via pit portal system of v

pituitary portal sys - runs from median eminence to ant pit releasing factors cause the release of their respective hormones in to circulation

Front 49

lesions of hypothalamus

Back 49

often produce visual field defects due to close proximity of HT to optic chiasm and optic tract

Front 50

common causes of hypothalamic damage

Back 50

tumors - in the wall of 3rd ventricle or of the pituitary
infections- often spread along base of brain to affect HT
skull fractures - fracture of the base of the skull may involve HT

Front 51

signs and symptoms of HT damage

Back 51

in order of frequency of occurence
1. sexual abnormaities (most common)
- children - precocious puberty - there appears to be a HT mech which inhibits puberty. This may be destroyed by HT lesions

adults - regression of secvondary sexual characteristics due to loss of releasing factors for gonadotrophins

2. diabetes insipidus - increased urine production due to a loss of ADH secretion
- damage- supraoptic nuc, paraventricular nuc, or pituitary stalk containing supraopticohypophysial tract

3. emotional and bh disturbances - range from manina to depression or involve other kidns of inappropriate bh such as excessive rage

4. sleeping disorders - often result in narcoplepsy

5. eating disorders - obesity or emaciation depending on the location of the lesion in respect

6. disorders of thermal regulation - often hyperthermia due to lesion of the heat dissipation center in the ant hypothalamus

7. diencephalic epilepsy - seizure activity - autonomic storms

Front 52

hypothalamic syndromes

Back 52

usually severe HT symptoms occur together as recognizable hypothalamic syndroms
ex - frohhlich's syndrome characterized by obesity combined w/regression of secondary sexual organs it is caused by lesions in the region of the ventromedial hypothalamic nuc - satiety center and source of releasing factors for gonadotropins

Front 53

fnal anatomy of the limbic system

Back 53

limbic sys used to denote a number of forebrain regions that are involved in 2 main fns

1. emotional bh - mainly the amygadala
2. memory formation- mainly the hippocampus

Front 54

broca's grand lobe limbique

Back 54

cortex nearest the inner border of the cortical surface
- it includes the septal area and the cingulate and parahippocampal gyri
- no fn suggested by broca

1878

Front 55

papez circuit

Back 55

1937

stressed interaction of the limbic lobe with hypothalamus and hippocampus in emotional fns
recent studies suggest that papezcircuit is also very imp for memory fn

Front 56

maclean

Back 56

1952 - first to coin the term limbic system

- MacLean noted that the amygdala like the hippocampus had strong interconnections w/the hypothalamus and was imp for emo

suggested that it should be considered part of the same system as the Papez circuit

limbic system - cingulate gyrus parahippocampal gurys, hippocampus, septum (septal area) amydala (and usually the hypothalamus

Front 57

amygdala

Back 57

locationin anteromedial temporal lobe, deep to uncus

Structure - abt15 diff nuclei that can be grouped into 3 major subdiv
1. corticomedial amygdala (CM)
- located along surface of brain adjuacent to uncus
- olfactory connections
basolateral amygdala
- subcortical portion of amydala larger than corticomedial amygdala
-connections w/ limbic assoc. cortex -
- the limbic assoc cortex consist of the ant temporal, ventral insular, orbital frontal, parahippocampal and cigulate cortex. These cortical areas form a continuous zone along the medial inf and lateral cortical surfaces and are concerned w/the most complex activities of the CNS including the formation of sensory perceptions emotionalbehavior and memory storage

central nucleus - subcortical part of the amygdala with connections with the brainstem and limbic assoc cortex

Front 58

amygdala

Back 58

-involved in 3 aspects of emo fn
1. evaluates emo significance of sensory stiumli or events
2. generates emo responses esp fear and anxiety
3. forms emotional memories

Front 59

limbic association cortex

Back 59

aka - paralimbic areas

inputs from the most complex motor and sensory areas of the cortex
- motor association cx
- sensory association cx

fns of the limbic assoc cortex
1. formation of sensory perceptions
2. emo bh
3. memory storage

Front 60

two main fiber tracts connect the amygdala w/subcortical regions

Back 60

1. stria terminalis - exits post aspect of amygdala and takes a c-shaped looping course just medial to the caudate nuc
- at the level of the ant commissure the stria courses downward to enter themedial hypothalamus

2. ventral amygdalofugal pathway (VAFP)
- exits the dorsomedial aspect of the amygdala runs beneath the globus pallidus (adjacent to the ansa lenticularis and nucleus basalis then enteers the lateral hypothalamus
- some of the fibers continue caudally in the medial forebrain bundle of the lateral hpothalamus to innervate visceral nuclei of the brainstem
- VAFP also sends fibers to the ventral striatum and nuc basalis of meynert ( a cholinergic nuc which projects to the cortex and amygdala and which is one of the first brain regions to degernate in alzheimers dx

Front 61

main fns of amygdala

Back 61

evaluate the emo significance of sensory stimuli (objects, events)

to generate appropriate mep responses to emo significant sensory stimuli
- to create memories of emo events

Front 62

emo response of coming across a snake

Back 62

1. visual info processed in primary visual cortex -> higher visual areas in temporal lobe
- amygdala also recieves snesory info from all of the other sensory modalities via limbic assoc areas
- thalamic inputs provide an additional crude representation of sensory stimuli

2. temporal visual areas including the temporal pole ( part of the limbic assoc cortex) id the object as a snake
3. temporal cortex then transmits this complex sensory info to the amygdala on the basis of previous experience the amygdala ids the object asdangerous evokes a conscious sensation of fear
4. amygdala activates the apprpriate subcortical areas including hypothalamus, brain stem, and striatum to generate appropriate behavior response to the snake - increase hr, bp resp, and mm tension and ultimately an escape respionse - bh response to othe r stimuli would be diff and could include aggression, feeding/drinking or social/sexual bh

Front 63

limbic association cortex, olfactory system and certain thalamic nuclei connection to amygdala

Back 63

fns - provides amygdala w/info abt external world
- role of the amygdala is to produce appropriate rresponses to bh - significant to stimuli

Front 64

hypothalamus brain stem and striatum connection to amygdala

Back 64

via stria terminalis and ventral amygdalofugal pathway (VAFP)

-fn - by way of these connections to subcortical areas the amygdala can produce visceral endocrine and bh response esp bh related to emo and basic biol drives - fighting fleeing feeding repro and social bh) these bh are closely assoc w/emo responses

Front 65

Nucleus basalis of meynert connection to amygdala

Back 65

reciprocal connections via VAFP

fn - formation of emo memories - neurons of the nuc basalis utilize acetylcholine as a nt and project to the amygdala and cerebral cortex

their degeneration in alzheimers dx may contribute to memory losses in these pts - nuc also imp for attention

Front 66

hippocampal formation and parahippocampal gyrus connection to amygdala

Back 66

recipricol conection
fn - formation of emotional memories

Front 67

catecholamine DA, NE and serotonin containing bs nuclei - project to the amygdala

Back 67

these projections to the amygdala are imp for det mood and fro emo memory fns
amygdala is one of the main sites of action for psychiatricc drugs including antipsychotics (DA receptor antagoinsist) and antidepressants (serotonin and NE uptake inhibitors

Front 68

dorsomedial (mediodorsal) thalamic nucleus connection to amydala

Back 68

recieves projections from amydala

fn- formation of emo memories

Front 69

Kluver-Bucy

Back 69

lesions of the amygdala

- first produced in monkeys by lesioning the medial temporal lobe - esp amygdala - occasionally seen in humans w/bilateral ant temporal lobe lesions - temporal lobe encephalitis

1. loss of appropriate emo and social bh
- a loss of fear and aggressiveness in caged monkeys
- inappropriate social interactions in free ranging monkeys
- some pts w/amygdalar lesions (urbachh0wiethe dx in which amygdala is selectively calcified may not experience fear

2. oral tendencies 0 inedible objects are mouthed - ccan't id food

3. hypersexuality - attempted to mate w/ inaminate objects - can't id appropriate sexual partners

Front 70

hippocampal formation (hippocampus)
location

Back 70

dorsomedial temporal lobe behind amygdala deep to parahippocampal gyrus

Front 71

structure of hippocampus

Back 71

series of interconnected critical zones that extedn the rostrocaudal extent of the hippocampal formation
1. dentate gyrus - located in dorsomedial hippocampus adjacent to fibria of the fornix

2. cornu ammonis (four subfields Ca2, CA3, CA4, CA1)
- cont w/dentate gyrus
- C-shaped shape of a rams horm( when seen in cross section
- CA3 and CA1 are the most prominent subfields

3. subiculum - located btw cornu ammonis and parahippocampal gyrus
- source of most of the outputs of the hippocampal formation

Front 72

intrinsic circuitry of the hippocampal formaiton

Back 72

formation of memories by hippocampus depends o nthe sequence of intrinsic connections (often called the "trisynaptic circuit")
all connections use glutamate + ad a nt)
1. neocortex - any nonlimbic assoc cortex to entorhinal cortex of ant parahippocampal gyrus - provides info to be remembered
2. entorhinal cortex to dentate gyrus via perforant path first synapse of TSC
3. dentate gyrus to CA3 via mossy fibers - second synapse of TSC
4. CA3 -CA1 third synapse of TSC
5. subiculum to
a. entorhinal cortex (continues revereration of the circuit
b. neocortex (where memories are stored
c. septum and mammillary bodies via fornix

Front 73

fornix

Back 73

fiber bundle connecting to hippocampal formation to subcortical regions such as hypothalamus

begins adjacent to dentate gyrus as a thin ribboncalled fimbria of the fornix
takes a C shapped looping course parraleling the parahippocampal andcingulate gyrus sepearted from cingulate by corpus callosum

approaches the ant commissure where it divides into a sml precommissural fornix which passes in front of the AC to reach theseptum and a larger postcommisural fornix which passes behind the AC to reach the mamillary bodies

Front 74

extrinsic connections of the hippocampal formation

Back 74

1. limbic assoc cortex - parahippocampal gyrus (entorhinal cx) projects to hippocampus via perforant pathway - the hippocampal formation ( subiculum) then projects back to the parahippocampla gyrus

2. mammillary bodies via postcommissural fornix - output pathway of HF

3. septal area via precommisural fornix - reciprocal

4. amygdala - reciprocal imp for the formation of emo memories

Front 75

main fn of hippocampus

Back 75

memory and learning
bilateral damage to hippocampal formaiton results in the inability to form new memories - anterograde amnesia

Front 76

Wernicke-Korsakoffs syndrome

Back 76

diencephalic amnesia

1. signs - anterograde amnesia - can't form new memories - plus variable amts of retrograde amnesia
- confabulation (make up studies when asked to recall memories)
2. lesions - mammillary body - dorsomedial thalamus
3. cause - thiamine deficiency due to malnutrition (often assoc w/alcholism)

Front 77

temporal lobe epilepsy

Back 77

hippocampus and amygdalaare prone to seizures

Front 78

alzheimer's dx

Back 78

assoc w/severe neuronal degeneration in severe limbic areas including the nucleus basalis of meynert, amygdala, hippocampus, and cerebral cortex (especially the limbic assoc areas) are all structures that recieve stronge cholinergic innervation

a progressive demential characterized by loss of several higher cognitive fns including memory loss, difficulty in thinking and emo problems

Front 79

psychosurgery

Back 79

surgical operations that lesion limbic andlimbic assoc areas in order to alleviate psychiatric symptoms
still preformed occasional y in certain pts who don't respond to psychiatric drugs

Front 80

prefrontal lobotomy and leucotomy

Back 80

used in past to alleviate anxiety, depression, and OCD
-leucotomies still used occasionaly but utilize electrodes or gamma knife radio surger to make lesions of the ant thalamic radiatiosn which connect the prefrontal corgex with subcortical areas such as the dorsomedial thalamic nuc

- ant capsulotomy - lesioning the ant thalamic radiations in the ant limb of the internal capsule

subcaudate tractotomy - lesioning the ant thalamic radiations that course below the head of the caudate

Front 81

cingulotomy

Back 81

lesioning the cingulum bundle and or the ant cingulate cortex - used to treat pain, anxiety and depression or OCD

Front 82

hypothalamic syndrome

Back 82

1. diabetes insipidus results from loss of vasopression (ADH) secretion leading to thirst and high urinary output
2. endocrine imbalance
3. impaired thermoregulation
4. sleep disturbances
5. emo/behavioral changes

Front 83

sx= wt gain, listless, episodic fever w/o apparemt cause, ceased menstruating, drank copious amts of water passed excessive amts of urine, fell asleep freq during the day, had reversed sleep wake cycles and occasionaly erupted into a violent state of rage w/o provocation

Back 83

craniopharyngioma. Due to the close proximity of the hypothalamus and pituitary to the optic chiasm, tumors in this region may also cause visual deficits such as bitemporal hemianopsia.

led to hypothalamic syndrome

Front 84

homeostasis

Back 84

a relatively stable state of equilibrium or a tendency toward such a state btw the diff but interdepedent elements or groups of elements of an organism, pop or group

integrated regulation of several variables endcrine,autonomic, neurochem, to achieve opimal phys fn
- req that central regions involved in homeostasis be responsive to signals from from periphery and be connected to effector mechanisms (oarts of nervous system and peripheral organs that directly control physiological phenomena like heart rate, vasodilation, hormone secretion

Front 85

homeostatic challenge

Back 85

homeostatic challenge to elicit Hypothalamus response
1. temp
2. hunger
3. sleep
4. emo
5. thirst
6. stress
7. CV/resp

physiological response - endocrine and visceral components
- pit and brainstem
- stop-gap

behavioral response
- affective, motivational, cognitive components
- limbic system

Front 86

hypothalamic control of body wt

Back 86

energy imbalance det body wt changes

assume 25lb wt gain from age 25-65
total food intake over the 40 year period ismore than 18 metric tons
- error in food intake over energy expenditure produceds wt gain is less than "0.03%"

individual variability
-bh, endocrine, and neural components
- HT is the primary CNS node metabolic reguation
ther regions involved in bh and cognitive components of energy balance
- cortical regions involved in olfaction (orbitofrontal, inferior temporal and insular cortices) taaste (frontoparietal operculum and ant insula and bh inhibition (prefrontal cortex

subcortical regions involved in motivated bh and reward (nuc accumbens)

Front 87

hypothalamus and E balance

Back 87

LH - Feeding center
- stimulation elicits feeding
-lesions reduce feeding
VMH - satiety center
- stimulation reduces feeding
- lesions increase feeding
- case studies have described hyperphagia accompanied by rage and dementia in patients with VMH lesions
- Revised/Current view: Both LH and VMH play role in feeding and metabolism. In long term, more important for body weight regulation than feeding.
-

Front 88

sset point hypothesis

Back 88

the hypothalamus encodes a set point for body weight and will defend against substantial deviations by regulation food intakeand or caloric expenditure

Front 89

multiple peripheral factors regulate food intake

Back 89

hormones from the periphery regulate feeding
ghrelin- gut
insulin- pancreas
leptin - adipose

plasma levels in humans vary systmatically across circadian cycle and in relation to feeding
- Influence feeding primarily via CNS feedback loops that involve the hypothalamus
Wren et al. (2001) found i.v. ghrelin ↑’d food intake by 28% in healthy adults exposed to free buffet
Many other hormones and peptides influence hunger, satiety and metabolism

The point here is that the hypothalamus responds to a number of peripheral cues that signal metabolic status. The hypothalamus does not do its thing in a vacuum

Front 90

leptin

Back 90

- released from adipose tis
- activates anorexigenic neuropeptide system (POMC; CART) - decrease food intake
- inhibits orexigenic neuropeptide systems(AGRP; NPY; orexin MCH) - increase food intake
- expression of orexigenic peptides in increased in response to fasting

- first order neurons located primarily in arcuate nucleus of hypotalamus and serve as the major first responders to peripheral cues indicative of E balance
- act on second orderhypothalamic neurons that coordinate the appropriate bh and physiological responses
many of these neurons are als o sensitive to other circulating factors that indicate metabolic status - insulin and glucose (orexin inhibited by high glucose)

leptin resistance - could be a contributor to obesity
leptin plays a role and is illustrative of the role of peripheral factors regulating complex physiological and bh phenomena of food intake and metabolism

Front 91

Hypothalamus and fluid homeostasis

Back 91

body 2/3 water
lose significant but varying amt every day through urination, respiration, perspiration, evaporation
- dehydration if severe can lead to irreversible damage to crucial organs - kidneys and brain
- physiological basis of thirst
- multifactorial (cell dehydration, extracellular dehydration; blood hypertonicity, dry mouth plays minor role
- interplay btw fluid intake and sodium appetite
- infusion of hypertonic saline into rostral hypothalamus stimulates drinking bh in animals
- baroreceptors in aortic arch, venous return and lungs facilitate autonomic responses to dehydartaion

Front 92

thirstb drinking physiological response

Back 92

physiological factors - physiological response
- signals from periphery
- may be detected driectly- osmolarity
- may be transduced - barroreceptor convey info via vagus to NTS then HT
leads to
Subjective experience - thirst
- subjective, conscious experience has cognitive emo, motivvational components that contribute to appetitive phase
- involvement of ant cingulate and insular cortices
leads to
behavioral response - drinking
- coordinated motor output that mediates consummatory phase

Front 93

organum vasculosum of the lamina terminalis (OVLT)

Back 93

hypothalamic sensor
osmosensitive
- circumventricular area - part of the CNS where the blood-brain- barrier is compromised so there is increased access to ions/prot/toxins/etc contained w/in the vasculature

neurons are sensitive to smalldeviations from setpoint osmolarity
- regulate activity of the magnocellular neurosecretory cells (MCNs) in supraoptic and paraventricular nuclei
- vasopressin and oxytocin modulate diruresis and naturesis (oxytocin inc naturesis) ADH increases antiduresis

Front 94

supraoptic nucleus

Back 94

hypothalamic 'effector'

magnocellular VP and oxytocin neurons project to post pituitary

Front 95

vasopressin and oxytocin cell activity in response to hypertonic chalange

Back 95

firing rate directly increased byhypertonic conditions
greater reelase of VP and oxytocinfor greater salt changes
pulsitile at first then increasing for VP
but for oxytocin little change and then sudden rise

Front 96

mean osmotic threshold

Back 96

284 mosm/L - av which VP is released

Front 97

HT and fluid homeostasis
what affects what

Back 97

dehydrated state =
- increased serum osm=
- osmosensitive hypothalamic neurons
- inc the release of VP from SON into post pit
- inc water resorption from kidneys
- causes vsoconstriction/vasodilation BP
- increases thirst

hydrated state =
- decreased serum osm
- decreased activity of osmosensitive hypothalamic neurons (lining 3rdventricle)
- inhibits release of VP from SON into post pit

Front 98

HT and thermoregulation

Back 98

unlike poikilothermic animals (amphibians and reptiles) - active across a wide range of temps
- prolonged substantial deviations in direction from norm body temp can result in organ and tissue damage or death

- precise reg of body temp is crucial
- ALL neurons are temp sensitive in a general sense
- enzymatic and biophysical processes that govern neuronal fn are temp-sensitive

- PRECISE detection of sml changes in Temp and ability to enact approp reg mech to deal w/challenges is a hypothalamic fn

- ant hypothalamus includingmedial preoptic area contains "temp reduction center
- increases blood temp (less than 1 degree increase) activates warm-sensitive neurons to facilitate phys and bh cooling mech
- lesions disrupt fine set point regulation
- crude form of temp reg is preserved

post hypothalamus contains heat conservation center
- decreases in blood temp activate this area to facilitate physiological and bhral warming mech
- pro-inflammatory cytokines (IL) inc temp "set-point" resulting in fever - also promote sick bh - increased sleep decreased appetite etc
- causes immune response
- causes liver and metabolic response - acute-phase response

Front 99

central regulation of febrile response

Back 99

cytokines acceess the brain at the OVLT a circumventricular organ
- cyclooxygenase in these cells catalyzes prostaglandin formation (PGE-2)
- acts on ant.. hypothalamus/preoptic area to inc temp set point

Front 100

hypothalamus and stress

Back 100

- reg of ant pit is imp for stress responses
-HT regulates cortisol secretion from the adrenals
- cortisool is the prototypical "stress hormone"
- adaptive in short term - maladaptive chronically
CRH->ACTH-> cortisol

CRH made by paraventricular nuc project to the median eminence and release CRH into pit portal system
CRH acts oncells of ant pit that make adrenocorticotropin hormone (ACTH) which travels through the bloodstream to adrenals where it stimulates release of cortisol

Front 101

HPA axis

Back 101

hypothalamic-pit-adrenal axis - mediates stress interactions btw brain and periphery

- amygdala can stimulate HPA axis
- hippocampus is rich in glucocorticoid receptors
- cortisol facilitates hippocampal fn (memory formation
- chronic cortisol elevations are deleterious to hippocampal fn
and inhibit cortisol release at the parvocellular CRH producing neurons of HT

Front 102

stresshormone dysregulation in depression

Back 102

dexamethasone mimics the effects of cortisol - tricking the body into thinking cortisol levels areelevated - recruiting reg mech that supress cortisol release
- ppl w/depression show "escape from this suppression of cortisol
-initialsuppresion but then cortisol levels rebound to abn high levels

depressed ppl have higher than norm levels of cortisol chronically

Front 103

duchenne

Back 103

french neuroloist pioneered use of trascutaneous electrical stimulation to activate small groups of mm of facial expression
noted difference btw smile evoked by electrical activation of zygomaticus major and the natural smile

Front 104

limbic system

Back 104

neural substrates of emotion
- wide range of aversive or pleasant states mediated by diff neural substrates
- assoc w/visceral motor responses, somatic bh and powerful subjective feelings
- emo has expressive, experiential and physiological componets
- experiential aspects of emo is crucial for survival - protects individual from dangerous situations
- expressive - component of emo is crucial for social fning -

Front 105

emotional expression

Back 105

damage to right motor cortex impairs voluntary smile but leaves spontaneous smile intact

damage to left forebrain region providing extrapyramidal innervation of facial nuc preserves voluntary smile but impairs spontaneous smile

corticobulbar input to the lower face part of the nuc of VII is contralateral

"duchenne smile" is which can only be elicated naturally- response to humor or pleasure

Front 106

Sham rage

Back 106

decorticate when descending projections from post hypothalamus were left intact - no obvious target of rage

- subjective experience of emo req limbic and cortical involvement = basiccircuitry for expression of organized behaviors accompanying emotions is in the diencephalon and the brain stem structures connecting it
- other limbic structures (amygdala) also provide descending regulation of emo behavior output

Front 107

amygdala and fear response

Back 107

sensory info arrives in basolateral cortex. the central nuc is the major output center of the amygdalar complex w/projections to brainstem, hypothalamic and forebrain regions that coordinate autonomic behavioral and endocrine response to emotionaly-salient stimuli

anxiolytic drugs (benzodiazepines) act primarily on amygdala to inhibit responses

stimuli -> sense organ-> thalamus-> sensory cortex -> hippocampus
thalamus sensory cortex and thalamus -> amygdala lat nuc which projects to basolatera, accessory basal and central nuc.
accessory basal and basolateral nuc of amygdala projects to central nuc

central nuc outputs to central gray, lateral hypothalamus, bed nuc of stria terminalis
central gray -> emo behavior
lateral hypothalamus -> autonomic response
bed nuc of stria terminalis -> hormonal response

Front 108

classical fear conditioning

Back 108

neural sensory input -> conditioned stimulus
primary reinforcer -> unconditioned stimulus
dependent on amygdala
requires prot syn
model of post traumatic stress disorder?
extinction is also a form of learning requiring prot syn and may have therapeutic potential

amygdala has been implicated not just in PTSD but panic disorder as well - unlike pTSD where etiology is linked to a discrete experience and the manifestation is linked to discrete stimuli, panic disorder tends to be a non-specific

Front 109

associative learning in amygdala

Back 109

coincident activation of strong sensory inputs (primary reinforcers (taste, touch, pain) w/ neutral sensory inputs (visual, auditory stimuli related to an object) strengthens the weak inputt in the Hebbian like manner
putputs - orbital and medial prefrontal cortex0 implicit motor actions, explicit conscious processing to obtain rewards, avoid punishers, and implement long-term plan
hypothalamus and brain stem - visceral motor effector system to prepare body for action

blocked by NMDA glutamate antagonist which also prevetns LTP

Front 110

Urbach- Wiethe dx

Back 110

rare congenital disorder
bilateral calcification and atrophy of ant-medial temporal lobe structures (including amygdala)
-hippocampus largely spared

impaired recognition of facial expressions of fear
- impaired conditioned autonomic/visceral responses to fearful stsimuli
- preserved declarative recall of CS/US pairings
Rare autosomal recessive condition

Front 111

hippocampal circuitry

Back 111

limbic association cortex -> parahippocampal gyrus --1-> dentate gyrus --2-> CA3 --3->CA1 --> subiculum --> limbic assoc ctx/entorhinal ctx/mammillary
1+2+3 trisynaptic pathway
step 1 - called perforant path b/c fibers penetrate through cortext to dentate gyrus

2 - mossy fibers
3- schaeffer collaterals axons from CA3 projects to the contralateral hippocampus project to CA1

input structure of hippocampal formation - dentate gyrus
output structure = subiculum

Front 112

long term potentiation

Back 112

represent anatomical/physiological substrate underlying the formation of many types of memories

unimodal and polymodal assoc areas (frontal,temporal, and parietaly lobes) reciprocating fibers w/ parahippocampal cortex + perirhinal cortex
both have reciprocating fibers with entorhinal cortex which projects to all dentrate gyrus, hippocampus CA3 and CA1 and subiculum
subiculum projects back to entorhinal cortex

Front 113

hippocampal fn

Back 113

essential for the formation of new long-term declarative memories
- semantic - categorical (what a bicycle looks like)
- episodic = narrative (what i did this morning)
- long-term potentiation (LTP) w/in trisynaptic pathway (especially schaeffer collateral projections CA3 to CA1) a possible physiological correlate of memory consolidation

- hippocampal atrophy a prominent neuropathological hallmark of AD - cell loss or developmental abn have also been assoc w/a number of other neuropsychological disorders TLE schizophrenia, autism
- specific spatial

Front 114

HM surgery for temporal lobe epilepsy

Back 114

removed most of medial temporal lobes bilateral
IQ norm > high unaffected but unable to form new-long term declarative memories

severe anterograde amnesia

workign and procedural memory intact( circuitry involving prefrontal cortex and striatum, working- dependent on the dorsolateral prefrontal cortex
memories from before damage largely intact

still likes shows, doing crosswords and watching tv - can't make friends, cannot remember a person for longer than ten minutes
he thinks truman is still present, news of mother's deat evokes same painful grief for a short period of time, doesn't know how old, shocked by looking in the mirror

Front 115

hippocampys and aging

Back 115

medial temporal lobe structures may be paritculary affected by atrophy - consistent anatomical correlate of age -related cognitive decline and AD (less than a year to several years

Front 116

Alzheimer's dx

Back 116

one in 7 americans over 71 has some type of dementia

- mild cognitive impairment precedes AD assoc w/ subtle cognitive deficits
-first brain regions to show neurodegeneration in AD include hippocampys and assoc parts of temporal lobe cortex

moderate-to-severe AD assoc w/ widespread cortical involvement

prototypical age -related memory disorder

Front 117

diffuse neuromodulatory transmitter systems

Back 117

Ach - from basal forebrain
Dopamine - from ventral midbrain (including ventral tegmental area)
serotonin - from raphe nuclei
NE - from locus cer

diffuse project widely to many if not all limbic regions often by poorly defined pathways

neuromodulatory - dont drive limbic circuitry modulate interactions w/ing limbic circuitry
- involved in numerous neuropsychiatric disorders
- drugs used to treat these disorders as well as drugs abuse act on these symptooms
- emotion, learning, and memory; motivation)

Front 118

Acetylcholine

Back 118

cholinergic neurons in basal forebrain project hippocampys, amygdala, and neocortex
basal forebrain includes nucleus basalis

ACH is imp for cognitivefn (attention, learning and memory)
- cholinergic neurons are lost in alzheimers dx (earliest and most consistently observed neurotransmitter deficit)
- cholinergic systems target of some cognitive enhancerse used to treat AD (donepizil
5 drugs approved to treat AD - 4 are acetylcholinesterase inhibitors mild-to-moderate, mild to severe in Donepizil)
5th is an NMDA glutamate antagonists (moterate to severe )

Front 119

Dopamine

Back 119

neurons in ventral midbrain project to limbic and cortical regions

ventral tegmental area source of DA inputs to limbic and cortical regions including the nucleus accumbens (part of ventral striatum), amygdala, and prefrontal cortex

VTA is mdial to substantial nigra

DA important for motivated behavior and reward

implicated in reinforcing and additive properties of psychostimulant drugs

implicated in certain neuropsychiatric disorders (schizophrenia)

Front 120

serotonin

Back 120

5-hydroxytryptamine

neurons in the brainstem raphe nuclei project to almost all limbic and cortical regions

- involved in modulating mood and affect
- implicated in depression, anxiety and OCD
-selective serotonin reuptake inhibitors (SSRIs Prozac) used to treat these disorders

Front 121

Norepinephrine

Back 121

noradrenalin

NE neurons in brainstem locus coeruleus and lateral tegmentum) send widespread projections to cortical and limbic regions

- part of ascending reticular activating system, involved in arousal, wakefulness, attention,
- targe of some psychostimulant drugs (amphetamine, cocaine) may mediate some of the activating properties of these drugs but not their rewarding and reinforcing properties
- implicated in mood disorders; older antidepressants elevate NE levels by blocking reuptake (tricyclic antidepressantsO or preventing extracellular enzymatic degradation (MAO inhibitors

Front 122

primary cortical areas

Back 122

comprise a sml percentage of total cerebral cortex

Front 123

cortical fn

Back 123

1. assimilates and interprets sensory information
2. anatomical substrate for the highest forms of human fn ( language, art, music, math, fine motor skills, etc)
3. one of the mot accessible parts of the brain (imaging, surgery, etc)
4. often the target of neuropathical conditions such as tumors, strokes, infections, and epileptic seizures

Front 124

cortical development across life span

Back 124

by week 5 the 5 major subdivisions of the brain are identifiable

1. Telecephalon - cerebral hemispheres (including cerebral cortex) and basal ganglia
2. diencephalon
3. mesencephalon
4. metencephalon
5. myelencephalon

cerebral cortex accounts for 45% of the vol of the adult brai

age/ brain wt
newborn - 400 g
1 yr - 800g
6 yr - 1200g
adult - 1400g

Front 125

cortical volume - quantitative

Back 125

male
right hemisphere 300 cc
left hemisphere 295 cc
female
right hemisphere 267 cc
left hemisphere 264 cc

male vs female statistically significant even after correcting differences in body wt
-

Front 126

cortical atrophy in age

Back 126

some loss of cortical vol occurs w/aging 4% overall reduction by 75
- 12% loss of frontal cortical vol
substantial variability but most pronounced in lateral prefrontal cortex - imp for reg certain aspects of bh and cognition - working memory

normal aging - mild decline in cortical vol
AD - dramatic cortical atrophy, beginning in limbic cortical areas and then, in later stages,expanding to entire cortex

Front 127

cortical dimensions

Back 127

abt 0.2 m squared

only abt 1/3 visible on the external surface

thickness varies from 1..5 -4.5 mm depending on cortical region
- thinnest - primary visual cortex
- thickest - primary motor cortex

Front 128

cortical dysgenesis

Back 128

at least 25 syndromes have been described that disrupt norm dev of the cortex

- improper development generally signals a failure of normal cell proliferation or migration

Front 129

Lissencephaly

Back 129

smooth brain
- general term used to describe disrupted gyral and sulcal paterning

type of cortical dysgenesis
- typically accompanied by epileptic seizures and profound mental retardation

Front 130

general histological features of the cortex

Back 130

mature cerebral cortex contains abt 20 bil neurons
number of neurons only not glial cells

cortical neurons can be grouped into 2 major classifications
1. spiny neurons
2. aspiny neurons

Front 131

spiny neurons

Back 131

"spines" are dendritic specializations for receiving of synaptic input

comprise abt 75% of cortical neurons

excitatory

use AA glutamate as nt

include
a. pyramidal neurons
b. cstellate cells

Front 132

pyramidal neurons

Back 132

majority of cortical spiny neurons - contribute axons to large fiber bundles such as the corpus callosum and corticospinal tract- that allow the cortex to influence activity of other cortical, bs, and sc areas

major output neuron of cerebral cortex

spine is a site of extraordinary plasticity - not static structures during early dev or even adulthood
- morphological and physiological properties of these structures can be altered by a variety of experience-dependent phenomena - both pathological and non-pathological

Front 133

spines and cortical fn

Back 133

b/c tremendous density of spines a single cortical pyramidal neuron may receive input from thousands of other neurons

post mortem histological studies have demonstrated reductions in cortical pyramidal neuron spine density in several neuropsychiatric condtions includign various dementias, chronic alcoholism, schizophrenia and trisomy 21

full complement(10-15 bil) cortical neurons is present byapprox 18 weeks of embryonic dev - thus the rapidpostnatal inc in cortical mass is largely due to myelination and dendritic sprouting - including increase in spine density

Front 134

aspiny neurons

Back 134

aka spine-sparse neurons

- few if any dendritic spines
- abt 25% cortical neurons
- interneurons - make synaptic connections w/nearby pyramidal cells - axonal process does not leave its nucleus of origin. (cortical area of origin)
- modulate neighboring pyramidal cells which in turn project to other cortical and subcortical areas

inhibitory use the aa = gamma aminobutryic acid (GABA) as a transmitter
- conductors/traffic cops
CHANDELIER CELLS-
loss of or reductions in chandelier cells have been reported in epileptic pts in epileptic foci
- make contacts near axon hillock they serve as the final break on AP generation -
- post-mortem schizophrenic pt - alterations in chandelier cell number and or morphology
Double BOUQET CELL
-synaptic contact w/apical dendrite - reg how singals arive at pryamidal cell

LARGE BASKET CELL
- synaptic contact w/basilar dendrites

Front 135

organization of the cerebral cortex

Back 135

laminar organization- based on superficial to deep variations in histological features

columnar organization - based on superficial to deep commonalities in fnal properties

Front 136

weigert stain

Back 136

reveals myeloarchitecture - pattern of myelinated fibers that course through an area

allow for delineation of cortical areas according to a number of histological critera

Front 137

Nissle and golgi stains

Back 137

reveal different aspects of cytoarchitecture

nissl - good for demonstrating cell packing density as well as size and morphology of cell bodies - not much abt axonal or dendritic processess

golgi - only stains a representative subset of neurons - cells that are stained show much more detail in terms of dendritic arborization and axonal processes than is seen w/nissl staining

allow for delineation of cortical areas according to a number of histological critera

Front 138

cortical layers

Back 138

most regions have 6 layers = isocortex = "same" cortex - abt 90% of total cortical area - aka neocortex -motor and visual cortex

other cortical regions have 3-5 layers allocortex - other cortex - aka archicortex(4) /palocortex (3)
- hippocampus and olfactory cortex

Front 139

isocortex layers

Back 139

1. molecular - rich in fibersbut few neurons

2.external granular - densely paced small cells

3. external pyramidal - medium sized pramidal cells - recieves extensive input from other cortical areas - large in primary motor cortex

4. internal granular - small pyramidal and stellate cells -large in visual cortex

5. internal pyramidal - many large pyramidal cells

6. multiform - mixture of pyramidal cells and irregularly shapped cells

Front 140

cytoarchitectonic differences

Back 140

1. overall thickness of cortex
2. relative thickness and density of different layers
3. size and shape of neurons

Front 141

giant pyramidal cells of betz

Back 141

characteristic of layer 5 in primary motor cortex - esp imp for anti-gravity mm (75% of them occur in the leg region of the motor homunculus) and are disproportionately impacted in aging

Front 142

brodmann's map

Back 142

systematic cytoarchitectonic analysis of entire cortex

described 52 distinct areas

subsequent electrical stimulation sstudies in humans have shown high degree of correlation btw cytoarchitectonic boundaries and fnal boundaries

Front 143

connections of cortical layers

Back 143

layers II and II
- origin of commissural and association fibers that connect different cortical regions
a. commissural fibers - connect homologous cortical regions btw hemispheres (primary motor cortex) run in corpus callosum(most) and ant commisure
b. association fibers - connect heterologous coritcal regions w/in same hemisphere- run in large fiber bundls such as sup longitudinal fasciculus

layer IV
- recieves most afferent input from thalamus
- best developed in primary sensor y cortices
- projects to other corticallayers

Layers V and VI
- origin of projection fibers to subcortical regions (striatum, thalamus, spinalcord)
- layer V particularly well-developed in primary motor cortex (giant pyramidal cells of Betz)

Front 144

commissural fiber bundles

Back 144

largely concerned w/connecting homologous cortical regions in diff hemispheres

anterior commisure (olfactory)
and corpus callosum

Front 145

association fiber bundles

Back 145

superior longitudinal fascidulus
and cingulum bundle

largely concerned w/conecting heterologous cortical regions in the same hemisphere = presumably allows for elaboration and integration of sensory information

Front 146

major cortical afferents

Back 146

1. other cortical areas
2. dorsal thalamus
3. basal forebrain/brainstem neuromodulator systems
- Nucleus basalis of Meynert (Ach)
- part of basal forebrain cholinergic system
- degenerates in AD
- Locus coeruleus (norepi)
- Raphe nuclei (serotonin)
- Ventral tegmental area (dopamine)
- adjacent to substantia nigra
- targeted predominantly at frontal cortex

Front 147

columnar organization of the cortex

Back 147

vertically oriented columns sspan the entire thickness of the cortex. contain thousands of neurons interconnected in vertical plane

200-500micrometer wide
basic fnal units of cortical activity

electrode insterted vertically w/in a fnal column, all neurons encountered respond to the same stimulation the same way
- but if it is placed in obliquely it will eventually extend beyond the initial fnal column and extend into an adjacent different functional column - respond to different stimulus

Front 148

all regions of cortex broken into 3 categories

Back 148

1. primary sensory areas
2. primary motor areas
3. association areas

Front 149

primary areas

Back 149

1. primary motor cortex = lowest threshold for eliciting mvmt by electrical stimulation (area 4)

2. primary sensory cortex - first cortical regions to recieve modality- specific info ( primary somatosensory cortex areas 3,1,2)

3. primary auditory cortex (area 41 and 42)
4. primary visual cortex (area 17)
5. primary vestibular cortex (parietal lobe)
6. primary gustatory cortex (fronto-parietal operculum)
7. primary olfactory cortical areas

Front 150

two main categories of association cortices

Back 150

1. sensory association areas
- areas of parietal, occipital, and temporal cortex that receive input from primary sensory areas
- integrate info from diff modalities
2. motor association areas
- located in the frontal lobe
- project to primary motor cortex
- provide dense input to subcortical regions involved w/mvmt generation (basal ganglia)
- involved in execution and temporal sequencing of complex mvmts

Front 151

cerebral lateralization

Back 151

many complex brain fns are more dependent on one hemisphere than the other

clearest ex -
1. L-R segregation of primary motor and sensory fn
2. language
-det dominant hemisphere
- L hemisphere for large majority of ppl of either handedness (95% of righties and 75% of lefties)

- mm ability
- attention
-math

Left -
1. analysis of R visual field
2. stereognosis
3. lexical and syntactic language
4. writing
5. speech

Right hemisphere
1. analysis of L visual field
2. stereognosis
3. emo coloring of language
4. spatial abilities
5. rudimentary speech

Front 152

aphasia

Back 152

w/o speech
several related disorders w/ common feature being loss of language expression and/or comprehension

Front 153

agnosia

Back 153

w/o knowledge - deficit in recognizing the meaning of sensory stimuli
- primary sensory fn intact

Front 154

apraxia

Back 154

w/o capability

inability to carry out skilled or purposeful mvmt
- no frank paralysis

Front 155

occipital lobe boundaries

Back 155

parieto-ccipital sulcus, to preoccipital notch

surface features - cuneaus and lingual gyrus

Front 156

fnal regions of the occipital lobe

Back 156

1. primary visual cortex - brdmann's area 17
- aka V1 (first visual area) and striate cortex
2. occiptital visual association cortex - broadmans areas 18 (parastriate cortex) and 19 *peristraite cortex)

Front 157

striate cortex

Back 157

brodmann's area 17

striate = striped
high density of thalamic innervation in layer 4

myelinated fibers from the LGN arrive in such high density that they form a visible white stripe in the primary visual cortex - making layer 4 greatly expanded allowing it to be subdivided into layers 4A, 4B, and 4C (noted by 18th century italian med student)

Front 158

fnal organization of primary visual cortex

Back 158

cells responding to similar stimuli (edges of a certain orientation are aligned w/in columns

columns alternate between left and right eye (occular dominance)
- demonstrated by injecting radiolabeled tracer into one eye - tracer is transynaptically transported back to the primary visual cortex layer IV where it can be seen as the white lines in the picture - a stripe or column corresponding to input from the injected eye alternates w/dark stripe column which corresponds to input from the non-injected eye - density of the input is roughly equal
- not in the presence of monocular deprivation during crucial dev period early inlife - input from non-deprived eye = white columns has almost completely overtaken the area previously devoted to input from deprived eye, indicating that normal dev of the primary visual cortex is activity dependent

pediatric amblyopia and strabismus - where patch

Front 159

pediatric strabismus

Back 159

causes misalignment of the eyes resulting in double vision
30,000 babies each year
typically stop using one of their eyes to avoid dbl vision
results in deprived sensory input to the cortical area devoted to that eye = results in improper dev of the primary visual cortex and fnaly monocular vision

while treatable with surgery, exercises, or an eye patch

Front 160

visual association cortex

Back 160

location - areas 18 and 19

major inputs - area 17
- pulvinar of thalamus via "extrageniculate pathway" - the pulvinar occupies much of the post portion of the dorsal thalamus

Front 161

extrageniculate pathway

Back 161

projections from pulvinar to visual association areas in temporal and parietal lobes (varieties of 'blindsight' have been reported in some pts w/widespread occipital lobe damage

visual assoc areas of ocipital lobe can recieve visual input from extrageniculate pathway in addition to the more highly processed input from the LGN via the primary visual cortex

retina -> brachium sup colliculus -> sup colliculus -> pulvinar <-> visual association cortex (areas 18 and 19)

Front 162

blindsight

Back 162

trans-cranial magnet stimulation used to transiently inactivate the post occipital cortex (primary visual cortex) = alows for visuo-spatail testing to be performed and reveals the phenomenon known as 'blindsight;
- with primary visual cortex "off-line" subjects claim no conscious awareness of visual stimulus presented on computer screen but when forced to gues at the location of the stimulus they perform at better than chance levels, suggesting some subconscious awareness of spatial aspects of the stimulus

clinically seen in pts following damage to primary visua cortex (area 17)

input from pulvinar to visual association areas remains intact mediates the subconscious spatial awareness of visual stimulus

Front 163

fn of visual association cortex

Back 163

1. higher level visual property recognition, including color and shape - further processing of inputs from area 17

2. localization of objects in space, indlucing direction of mvmt - further processing inputs from pulvinar

3. tracking eye mvmts - also dependent on input from pulvinar - occur after the eyes have fixated on a moving target
- not searching - mediated by frontal eye fields
what and where pathways

Front 164

outputs of visual association cortex

Back 164

1. dorsal stream - projections to inf and sup parietal lobules; imp for localization of objects in space (both hemispheres) and for reading (dominant hemispheres
- where?

2. ventral stream - projections to middle and inf temporal gyri; imp for conscious awareness and recognition of visual stimuli

Front 165

damage to visual association cortex

Back 165

loss of color awareness
- cortical color blindnes
- cannot name, point to, or match colors presented visually - but can name the appropriate color for an object described verbally
- cerebral achromatopsia

loss of tracking eye mvmts
- inability to visually lock on to and follow a moving object

visual agnosia - inability to name or recognize the significance of a visual stimulus although conscious awareness of the object is preserved
- appreciative agnosia - difficulty w/color discrimination and be unable to copy a drawn figure

bilateral lesions of superior parts of area 19 = visual disorientation and inability to execute visually guided hand mvmts - ex- stroke pts

Front 166

temporal lobe boundaries

Back 166

boundaries
1. lateral sulcus
2. line from parietooccipital sulcus to preoccipital notch

Front 167

major fnal regions of temporal lobe

Back 167

1. primary auditary cortex
2. auditory assocaiton cortex
3. visual association cortex

Front 168

auditory association cortex location, input, output,

Back 168

location - sup temporal gyrus ( brodmann's areas 42 and 22)

major input - primary auditory cortex (area 41)

major outputs -
1. inf parietal lobule
-imp for language fn (particularly reading)
2. to limbic structures (hippocampus and amygdala)
- imp for memorial and emo aspects of auditory experiences

Front 169

auditory association cortex fn

Back 169

more elaborate perception and processing of auditory info

identification of sounds

storage of auditory memories

Front 170

damage to auditory association cortex

Back 170

dominant hemisphere
- word deafness
- damage to post portion of area 22 in dominant hemisphere (Wernicke's area) results in a "fluent" aphasia

nondominant hemisphere
- disturbances in the appreciation of music "amusia"

Front 171

visual association areas

Back 171

temporal cortex
location ;
- middle temporal gyrus (area 21)
- inferior temporal and fusiform gyri-aka occipitotemporal gyrus (area 20)

Front 172

pts w/ lesions of visual assoc areas of temporal lobe

Back 172

retain ability to copy images
visual acuity and object awareness are intact

deficit is selective for object recognition
associative agnosia

Front 173

how do you test visual acuity?

Back 173

ask pt to reproduce a drawing of a visual stimulus or provide a detailed verbal description

Front 174

temporal visual association areas major connections

Back 174

major connections
input - occipital visual association regions (area 18 and 19)
output - limbic areas, particularly amygdala and hippocamus
- amygdala and hippocampus have reciprocal connections w/ auditory areas 42 and 22 and visual areas 20 and 21 association areas of temporal cortex imp for visual and auditory memory formation - particularly for memories w/strong emotional content

Front 175

temporal visual association areas fn

Back 175

1. storage of visual memories
2. whole object recognition -recognition of complex visual patterns

Front 176

ventral stream damage

Back 176

visual agnosia
associative agnosia sometimes referred to as a true visual agnosia b/c visual perception is fully intact

visual agnosia- inability to recognize objects by sight

most commonseen after left hemisphere damage
- visual acuity intact but object identification impaired

pure visual agnosia = ability to identify using other sensory modalities is intact - pt unable to visual id something but correctly id the object in response to an auditory cue

Front 177

prosopagnosia

Back 177

mos well studied manifestation of agnosia

inability to recognize faces
associated w/bilateral damage to areas 20/21

acquired and developmental forems
type of category-specific agnosia

Front 178

temporal lobe epilepsy

Back 178

10% of pop will experience a seizure
1% of pop will be diagnosed w/epilepsy
temporal lobe most common seizure focus

pathological event resulting from hyperexcitation of cortical and subcortical (amygdala and hippocampus) temporal lobe structures

may be preceded by an
aura - general feeling of unease, fear of deja vu accompanied by a sensory illusion (usually a foul odor or taste)

may be accompanied by automatisms (lip smacking, chewing, and swallowing)

causes vivid, experiential memories or dream like experiences w/ strong emotional component

in cases nonresponsive to drug tx, may require ablation of epileptic focus or removal of portions of temporal lobes

Front 179

surgical tx of temporal lobe epilepsy

Back 179

electrodes may be placed to monitor seizure activity and determine epileptic focus

determine if pt is a good canidate

effective in eliminating or dramatically reducing seizures severity and frequency in 70-90% of pts

Front 180

parietal lobe boundaries

Back 180

central sulcus - seperates parietal from frontal lobe

lateral sulcus - separates parietal from temporal lobe

line from parieto-occipital sulcus to preoccipital notch seperates it from parietal lobe

Front 181

3 major fnal regions of the parietal lobe

Back 181

1. primary somatosensory cortex
2. somatosensory association cortex
3. post parietal cortex

primary vestibular area is also found here near the jnct of the intraparietal sulcus and the postcentral gyrus

Front 182

parietal lobe fn

Back 182

conscious awareness of discriminative aspects of somatic sensation - some general aspects of pain and temp sensation reach consciousness at the thalamic level

- electrical stimulation elicits modified forms of tactile sensation (tingling)

- high intensity stimulation can elicit motor response on contralateral side of body - contributes fibers to the corticospinal tract

Front 183

somatosensory cortex and damage

Back 183

can reorganize in response to damage occuring at any step along ascending pathways (plasticity: - an ability to reorganize in an experience driving manner)

amputation - central reorganization following peripheral insult

stroke recovery of fn - central reorganization following a central insult

may be altered by non-pathlogical events- musicians who play stringed instruments and braile readers

Front 184

somatosensory association cortex
location, input, and output

Back 184

location - ant part of the sup parietal lobule (broadmann's areas 5 and 7a)

major input - primary somatosensory cortex

majr output - post parietal cortex

Front 185

fns of the somatosensory association cortex

Back 185

integration of somatosensory info

imp for use of tactile and proprioceptive info in building a comprehensive mental picture of an unseen stimulus "stereogenosis"

Front 186

lesions of the somatosensory association cortex

Back 186

tactile agnosia (astereognosia) - inability to correlate the surface texture, shape, size, weight, etc. of an object or to correlate somatosensory input with previous expeirence

primary somatosensory fn and object concepts are intact - inability to id common hand held objects based on somatosensory input

anomia- tactile agnosia - pt can describe object but can't name it

true tactile agnosia- inability to id the object does not result from a deficit in fine motor skills nec to perform a tactile analysis of the object (that would be damage to the premotor cortex)

Front 187

posterior parietal cortex location

Back 187

mostly in the inf pareital lobule including
BA 40 - supramarginal gyrus - caps off the post termination of the lateral sulcus

BA 39 - angular gyrus - immediately behind supramarginal gyrus capping off the parietal termination of the sup temporal sulcus

BA 7b = posterior part of sup parietal lobule

Front 188

Posterior parietal cortex major connections

Back 188

reciprocal
1. sensory assoc areas
- somatosensory association cortex (5 and 7a)
- visual association cortex (areas 18 and 19)
- auditory association cortex (area 42 and 22)

2. pulvinar and lateral nuc group from thalamus

3. frontal cortical regions
- prefrontal cortex (imp for modulating bh)
- premotor cortex (temporal and spatial coordination of cortex mvmt patterns)
- ant cingulate cortex and frontal eye fields imp for attention

crucial for attention

what sensory stimuli are salient (i.e. relevant/deserving of attention) right now? The sound of the lecturer or the sound of people talking out in the hall? The sight of the slides or the sight of the clock on the wall?

Front 189

Posterior parietal cortex fns

Back 189

highest order assoc cortex w/many varied imp fns
fns are hemispherically lateralized

dominant hemisphere - 3 Rs
- language fn, particularly reading and writing, mathematical ability

Non-dominant hemisphere - spatial representations of stimuli
- focusing attention on sensory input

Front 190

Posterior parietal cortex frontal interactions and attention

Back 190

bottom up attentional processes, attention is captured by an unignorable sensory stimulus like sudden loud noise
- PPC registers the sensory event andrecruitsthe frontal cortex to coordinate appropriate response (directing gaze toward stimulus) ARAS-strongly modulated by
- PPC recruits frontal attention networs
- automatic
- exogenous attention

Top down attentional processe
- frontal areas recruit PPC
- effortful
- endogenous attention
- driven by rules and some sort of mental representation (working memory dependent on dorsolateral PFC) and actual sensory experience represented

Front 191

PPC damage dominant hemisphere

Back 191

lesions in dominant hemisphere give rise to Gerstmann's syndrome

characterized by:
1. Finger agnosia - inability to id fingers
2. left-right confusion
3. acalculia - impaired ability to perform even basic mathematical calcs
4. agraphia - impaired ability to write

1 and 2 tested by touch your right ear w/your left thumb

if large enough could include wernicke's area or the arcuate fasciculs the resulting language deficit makes the neurological exam more challenging

Front 192

PPC dambage to non-dominant hemisphere

Back 192

result in:
1. impairments in understanding spatial relationships - difficulty in drawing and reading maps

2. anosognaosia - denial of or failure to acknowledge disability - when large stroke affects primary motor cortex

3. contralateral neglect
- failure to acknowledge stimuli in contralateral sensory field
- lack of attention to contralateral side of body
- tested by copying drawing - neglect detail of left side

nonsensical confabulations

Front 193

lateralization of attention on posterior parietal cortex

Back 193

attention to stimuli in right sensory fields is mediated via both hemispheres whereas attention to stimuli in the left sensory field is mediated only via the right hemisphere

damage to dominant (left) PPC can be compensated for in terms of attention by intact right PPC

both hemispheres activated in response to visual stimulys in right visual field but only the right is activated in response to visual stimulus presented to the left visual field

Front 194

PPC damage bilateral

Back 194

simultagnosia - inability to simultaneously visually perceive multiple objects
core featue in Balint's syndrome

attention to a single visual stimulus negates conscious perception of any other stimulus in the visual field

Front 195

insular lobe location

Back 195

depths of lateral sulcus
brodmann's areas 13-16

Front 196

insular cortex

Back 196

usually 3 short and 2 long syri separated by the central insular sulcus
circular sulcus outside long gyrus near outside of insula

blood supply - Sylvian branch of middle cerebral a covers insula

Front 197

major connections of the insula

Back 197

input from some somatosensory cortical regions (esp smatosensory association cortex)

input from thalamic nuclei that play a role in vestibular and visceral sensation (VPi - relay for vestibular and visceral sensation; centromedian - major intralaminal nuc imp for visceral pain)

- reciprocal connections w/ amygdala

Front 198

fns of the insula

Back 198

1. visceral sensory and autonomic fns
- insula, via connections with limbic regions probably imp for emotional component of visceral pain
- electrical stimulation produces chewing mvmts, visceral sensations and autonomic responses

gustation
- integration of olfaction and taste (flavor)
- primary gustatory cortex extends into ant dorsal insula

vestibular sensation
- post insula involved in vestibular processing

interoception
- subjective sense of physiological condition
- req integration of sensory and emo components
-post portion of dorsal insula
- perhaps lateralized to right (non-dominant) hemisphere

Front 199

insula and nicotinic addiction

Back 199

loss of smoking addiction - damage of insula in

damage to insula - pts may not register the powerful autonomic and visceral correlates of withdrawl that contribute to relapse

Front 200

frontal lobe boundaries and size

Back 200

boundaries
- central sulcus
- lateral sulcus

size > 1/3 of entire cerebral cortex

Front 201

frontal lobe major fnal areas

Back 201

1. primary motor cortex
2. premotor cortex
3. frontal eye fields
4. prefrontal cortex
5. broca's motor speech area

Front 202

premotor cortex location

Back 202

ant and parallel to primary motor cortex extends on the medial surface of the frontal lobe just ant to the paracentral lobule
- supplementary motor area
- corresponds to BA6

Front 203

premotor cortex major inputs and outputs

Back 203

inputs
1. motor thalamus - VA
2. parietal association areas - reciprocal
3. prefrontal cortex

major outputs -
1. primary motor cortex
2. also contributes to descending motor pathways
3. putamen

Front 204

premotor cortex fn

Back 204

involved in sensory guidance of mvmt and controls the more prox mm and trunk mm of the body
- helps to orient the body before moving

planning and coordination of the complex patterns of motor output

electrical stimulation can elicit mvmts
- requires a greateer intensity of stimulation and involves larger groups of mm than primary motor cortex
- frontal aversive field - e-stim may cause rotation of eyes, trunk and head to opposite side

supplementary motor area has rostral (pre-SMA) and caudal (SMA) proper components

pre-SMA involved in awuasition of new motor sequences

SmA involved with execution of automatic/well-rehearsed motor patterns

Front 205

lesions of premotor cortex

Back 205

most commonly obsserved deficit is motor apraxia - impaired ability to carry out purposeful, complex, voluntary mvmts in absence of paralysis

may also be seen folllowing damage to parietal association area (extensively interconnected w/premotor cortex

ant. (premotor) apraxia can be differentiated from post(parietal) apraxia
-both do poorly n motor tests only post do poorly on analogous perceptual tests

other deficits following lesions to premotor cortex include clumsiness in writing and drawing

grasp reflex may return

alien hand sign may be present - feeling on the part of the pt that hand is foreign and acting of its own volition. - more commonw when damage is relatively selective for the supplementary motor

Front 206

frontal eye fields location

Back 206

location - ant to premotor cortex
post parts of medial frontal gyrus (primary FEF)
dorsal part of inf frontal gyrus (secondary FEF)
includes parts of BA 6, 8, 9

Front 207

frontal eye fields major inputs and outputs

Back 207

inputs
1. post parietal cortex
2. ant cingulate cortex
- these are areas imp for attention

major outputs
1. sup colliculus
2. brain stem gaze center in reticular formation
- activates brainstem nuclei of cranial n involved in eye mvmts

secondary eye fields contain a mirror image of primary fields involved in relaxation of antagonistic mm during voluntary eye deviations

Front 208

FEF and saccadic eye mvmts

Back 208

willful decision to direct visual attention to the left would be initiated in the right FEF

descending projections to paramediant pontine reticular formation mediate activation of the lateral rectus and via MLF connections w/contralateral oculomotor nuc - coordinated contraction of the right medial recuts resulting in deviation of the eyes to the left

Front 209

functions of FEF

Back 209

controls voluntary conjucate eye mvmts

electrical stim causes eye deviation to opposite side
- may also cause other patterns of eye mvmt
- unilateral stimulation may cause bilateral opening or closing of eyelids

Front 210

lesions of FEF

Back 210

cause deviation of eyes toward side of lesion and impairment of voluntary conjugate eye mvmt toward opposite side

convergence and involuntary tracking/smooth pursuit mvmt of eyes remain intact - mediated by occipital areas

saccades - searching eye mvmts

Front 211

prefrontal cortex location

Back 211

frontal pole and orbit regions of frontal lobe

includes parts of several brodmann's areas

last cortical area to fully mature

Front 212

connections of Prefrontal cortex

Back 212

major inputs
1. mediodorsal nuc of thalamus
2. amygdala
3. parietal and temporal association areas
recieves info from high order asosc areas and limbic regions of the thalamus and temporal lobe and uses this info to exert control over those brain areas which are involved in behavior output

PFC-> caudate -> GP -> VA -> premotor cortex -> bh
PFC-> premotor cortex -> bh
major outputs
1. premotor cortex
2. caudate (PFC can influence premotor cortex directly or indirectly via basal nuclei

Front 213

Prefrontal cortex fns

Back 213

- highest order motor assoc area
- planning; attention; foresight; astract thought
- working memory
- use of previous experience and emotional status to promote behavioral responses appropriate to current situation
- many of the fns whose subtle individual variations give rise to "personality"

determint proper or appropriate bh output req integration of sensory info, context, physiological and emo status

Front 214

working memory

Back 214

ability to hold a fact or concept in mind to bridge the temporal gap between acquisition of that info and executing bh appropriate to that info

Front 215

execcutive fn

Back 215

set of cognitive abilites that control and regulate other abilities and behaviors.

nec for goal-directed bh
they include the ability to initiate and sotp actions to monitor and change behavior as needed and to plan future bh when faced with novel tasks and situations

allow us to anticipate outcomes and adapt to changing situations

the ability to form concepts and think abstractly are often considered components of executive fn

Front 216

lesions of PFC

Back 216

tumors; strokes; head inj
1. dificulty in planning and executing complex bh
2. personality changes
3. socially inappropriate bh
4. inability to understand cosequences of action
5. loss of aversive aspect of pain even though sensory experience of pain is intact
5. alleviation of anxiety and depression

Front 217

language areas of the brain

Back 217

language fns are largerly lateralized and determine the dominant hemisphere

language has both receptive and expressive components

language incorporates visual auditory and motor fn

tremendous variety of acquired deficits in language abilitiesl classified as aphasias

Front 218

broca's motor speech area location, input and output

Back 218

location - opercular and triangular parts of inf frontal gyrus in dominant hemisphere

brodmann's areas 44 and 45

recieves major input from wernicke's area area 22 and sends its major output to primary motor cortex area 4 specifically to tounge lips and laryngeal representations

Front 219

fns of broca's area

Back 219

1. speech production
2. coordinates complex mvmts of tounge, lips, and larynx nec for normal speech

subservesa general language productino fn not just speech vocalization

Front 220

lesions of broca's area

Back 220

result in broca's aphasia
aka expressive or non-fluent aphasia
paucity of speech, tremendous difficulty in speech production
no paralysis of mm of speech
language comprehension largely intact but may show some sublte deficits in extracting appropriate meaning from sentences in which word order is not straight forward

apraxia of speech

Front 221

Wernicke's area location and input and output

Back 221

location - post part of sup temporal gyrus in dominant hemisphere
area 22

recieves input from primary auditory cortex (41) and projects to brocas 44/45 via arcuate fasciculus

Front 222

fn of wernicke's area

Back 222

language comprehensioin

Front 223

lesions of wernicke's area

Back 223

aka receptive or fluent aphasia

1. normal rate, rhythm and intonation of speech
2. language may be excessive (logorrhea or press of speech)
3. speech includes made up words (neologisms)
4. failure to convey a coherent message ( empty speech)
5. pt lack insight into their language deficits

Front 224

conduction aphasia

Back 224

arcuate fasciculus part of sup longitudinal fasciculus connects language comprehension center in temporal lobe w/language production center in frontal lobe

- a lesion here "disconnects" Wernicke's and broca's area resulting in a condicution aphasia

- fluency and comprehension good
- reading aloud impaired; silent reading with comprehension is intact
- writing and naming are impaired
- consistently observed deficit - inability to repeat individual nonsense words or unrelated sequences of common words

Front 225

what is the fn of homologous regions of brocas and wernickes areas in non-dominant hemisphere

Back 225

may be imp for non-verbal aspects of speech such as prosody, intonation, spontaneous gestering

area 44/45 - expressive aspects of these features
area 22 - receptive aspects of these features

damage to areas 44/45 of the nondominant hemisphere may show normala speech production w/appropriate ocntent but might speak w/o varying pitch, speed and gesturing in a way that would normally lend emotional color to speech

pt w/ damage to area 22 in non-dominant hemisphere would prob presumably recognize the explicit meaning of speech, but might have difficulty in picking up on the emo tones that norm modulate our understanding of what the speaker is truely trying to convey

Front 226

frontotemporal lobar degeneration

Back 226

aka pick dx

amnestic aphasia and frontotemporal atrophy

tauopathy- class of neurodegenerative cond characterized by pathological aggregation of tau protein insie neurons. Tau is a major component of neurofibrillary tangles assoc w/ alzheimers dx but FTLD doesn't have all the other features of AD such as extracellular amyloid plques

at least 3 subtypes
1. frontotemoraldementia
2. primary progressive aphasia
3. semantic dementia

early changes in emo and social fning
language impairments

Front 227

source of meningitis

Back 227

1. hematogenous - from pneumonia, ottitis media, skin inection

2. contiguouos spread of sinusitis, mastoiditis, nasopharyngitis

3.penetrating - head inj

4. congenital dural defect

Front 228

meningitis

Back 228

entry of organisms into the subarachnoid space is facilitated by
- disruption of the blood-CSF barrier by trauma
- circulating endotoxin
- initial infection of the meninges

clinical symptoms caused - infection, exudate, and vasculitis

can damage cranial n III,IV, VI, VII

Front 229

infections of meningitis

Back 229

- pure pia-arachnoiditis - headache, stiff neck, kernig and brudzinski signs

- subpial encephalopathy -
- confusion, stupor, coma and convulsion
- the tis beneath the pia is not penetrated by bacteria; hence the change is probably toxic

ependymitis - ventriculitis

Front 230

exudation - meningitis

Back 230

exudation purulent exudate - large numbers of neutrophils, scattered macrophages, fibrin, and necrotic cellular debris) in the subarachnoid space

organized exudate obstruct basal cistern leading to hydrocephalus

Front 231

meningitis vasculitis

Back 231

secondary to inflammation around vessels, resulting in thrombosis and infarction of brain (seizure, and focal neurological deficits)

Front 232

bacterial meningitis

Back 232

fever, headache, meningismus, and altered mental status

less common sx- cranial n palsies/ focal signs
-seizure

bacterial meningitis -
Haemophilus influenza - kids, and babys
Streptococcus pneumoniae - adult, kids,
Neisseria meningitidis - adult, kidds
Escherichia coli
staphylococcus aureus
listeria moncytogenes - stupid

Front 233

meningitis signs

Back 233

fever, headache, and neck stiffness

Front 234

diagnosis

Back 234

- sx and sympt
- brain images MRI or CT - to rule out abscess or other mass lesion
- lumbur puncture - CSF study is diagnostic
- searching for source of infection
- monitoring for possible complications

Front 235

CSF study

Back 235

- elevated opening pressure in menningitis
- elevated protein> 100mg/100ml
glucose<60%
predominant polymorphonuclear cells
bacterial smear
Ag
cultures

Front 236

meningococcal meningitis

Back 236

- the meningococcus resides in the nasopharynx, and airborn transmission in crowded places (schools or barracks) causes "epidemic meningitis"

initially bacteremia causes fever malaise and petechial rash

intravascularc coagulopathy may cause lethal adrenal hemorrhage (waterhouse-friderichsen syndrome)
- untreated meningococcal bacteremia is prone to initiate an acute fulminat meningitis
- tx - penicillin
- prevention - vaccine

Front 237

cyptococcal meningitis

Back 237

chronic, subacute, or rarely acute CNS infection by Cyptococcus neoformans

isolated worldwide from soil, fruits, and matter contaminated by pigeon excreta. the organism enters the body through the lungs, from which it may disseminate to all organs

meningitis - is most common form of cryptococcosis mostly an opportunistic infection in immunocompromised persons

usually chronic or subacute onset of headache, nausea, irritability, somnolence

cranial n involvement

CSF - indian ink preparation
- culture - Ag