HR block 6 part 2 Flashcards

(452 cards)

1
Q

Lesion to Right PPRF–L/R gaze effect?

A

Left gaze is normalNeither eye can move to the right

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2
Q

Lesion to Left MLF–L/R gaze effect?

A

Left Gaze normalRight Gaze: Left eye unable to move medially; Right eye nystagmus

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3
Q

Left Abducens Lesion and Left MLF–gaze?

A

Left Gaze : Neither eye can moveRight Gaze: Left eye unable to move medially; Right eye nystagmus

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4
Q

Horizontal Gaze Zone

A

4th Ventricle–PPRF

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5
Q

Vertical Gaze Zone

A

Rostral Midbrain Reticular Formation

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6
Q

Horizontal and Vertical Gaze Control Zones connected by?

A

MLF

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7
Q

Ventral Part of Rostral Midbrain Reticular Formation is associated with _____ gaze

A

downward

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8
Q

Dorsal Part of Rostral Midbrain Reticular Formation is associated with _____ gaze

A

upward

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9
Q

Each Superior Colliculus receives input from _____ half of visual field

A

contralateral

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10
Q

______ divides superior colliculus into superficial and deep layers

A

stratum opticum ( retinal axons white matter )

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11
Q

Retinal axons terminate on neurons of _____ layer of superior colliculus

A

superficial

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12
Q

How is cell activity of superior colliculus affected when receiving multiple senses (touch, vision, auditory)? Which layer of S. Colliculus receives this information?

A

Cell activity increases due to additive effectDeep Layer

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13
Q

Which layer of superior colliculus contains premotor nuerons that compute saccades?

A

Deep

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14
Q

Which layer of superior colliculus contain cells that excite motor neurons?

A

Superficial

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15
Q

Relationship of tectospinal tract with MLF

A

tectospinal is ventral to MLF (and dorsal to Medial Lemniscus)

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16
Q

Lesion to superior colliculus will cause _________?

A

Loss (for the most part) of ability to make saccades in contralateral visual fieldSome saccades still form due to presence of fibers from frontal eye field bypassing superior colliculus

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17
Q

Tectospinal Tract Function?

A

Direct head movements to match eye movements

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18
Q

Why does S. Colliculus Lesion not eliminate all saccades

A

Frontal Eye Fieldhas some tracts run through S. Colliculus while others bypass S. Colliculus to serve as compensatory mechanism to produce saccades

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19
Q

______ and _______ arteries if stretched can compress Cranial Nerve 3

A

Posterior Cerebral ArterySuperior Cerebellar Artery

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20
Q

Anterior Cerebral Arteries supply _____ surface of cortex

A

median

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21
Q

Middle Cerebral Arteries supply _____ surface of cerebral cortex

A

Lateral

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22
Q

Posterior Cerebral Arteries supply ______ surface of cerebral hemisphere

A

caudoventral

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23
Q

Attractive cues stimulate G-actin to be incorporated into ______

A

F-actin

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24
Q

Repulsive Cues support G-actin towards _______

A

lamellipodium

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25
actin and tubulin regulate assembly and disassembly of subunits; however changes in _____ also influence this process
intracellular Calcium 
26
_____ are involved with axon growth and serve as both the ligand and receptor on growing axons
CAM
27
Function of Netrins? What molecule works in opposition?
Present at midline to facilitate axons that are crossing over to opposite hemisphere Slit- stops growth across midline to counteract Netrin
28
Purpose of Semaphorins
Stop Axonal Growth
29
Where are Ephrins mostly located? Function?
Hippocampus to aid in development related to plasticity
30
Name some Chemorepellant molecules. Function?
Slit; Semaphorin Change trajectory or avoid inappropriate target
31
Neurons depend on a minimum amount of ______ for survival and growth
trophic factor (NGF) 
32
T/F NTFs (specific neurotrophic factor) has the same effect on all neuronal populations
False-- NTFs have a range of effect determined by type of neuron
33
GDNF (glial derived growth factor) promotes _____ types of cells
Dopamine
35
Alterations in NTFs have been associated with which diseases? How does this occur?
Parkinson's ; Alzheimer's ; ALSIncrease in p75 receptors which promote cell death and a decrease in Trk receptors which promote cell survival. NTFs bind to both of these types of receptors; in old age there is an increase in p75 receptors
36
How is Baby talk is important for language development?
Axonal guidance to language centers during critical time frame
37
How is the effect different for a cat whose eye was sutured shut from two months to month 36 compared to one that was sutured shut from 12 months to 36 months and then re-opened?
First case will not have vision in that eye due to lack of light exposure during critical time periodSecond case will have some vision in the previously sutured eye; however, it will be diminished. This indicating that deprivations at later stages in life are not as detrimental as deprivation during childhood or critical time for development.
38
Hebb's Postulate
Synapses in one (L) eye will increase if synapses are removed from opposite (R) eye 
39
Sprouting with respect to Parkinson's
cells that remain producing Dopamine will grow in an attempt to provide enough Dopamine to the system 
40
Activity Dependent Plasticity
Ca Influx into cell induces transcription and translation of things such as growth factor to promote neuronal development and axonal development
41
Types of Repair in PNS
Regrowth of axons - recreation of myelin and regrowth via growth coneRestoration of damaged nerve cells - (glial scarring)Wholesale Genesis of new neurons to replace lost neurons
42
Types of peripheral nerve regeneration
1. severed axon- axon segment distal to site of cut degenerates 2. crush axon- damaged distal segments provide a guide for regenerating proximal axons3. completely severed axons- Schwann cells in distal stump of nerve stimulate and guide axon growth via NTFs
43
Describe pathway of apoptosis in CNS
Excses glutamate disregulates Bcl-2 (anti-apoptotic) ; therefore apoptosis is activated via caspase 3
44
Where in CNS can neurogenesis take place?
Olfactory ReceptorsTaste Receptors Hippocampus
45
Describe neurogenesis process.
1. Subventricular Zone generates new neurons (PROLIFERATION)2. Translocation to desired area3. Differentiation for desired axonal development
46
Future of Parkinson's Treatment?
Fetal Tissue transferred to PD patient and does not reject fetal dopamine cells
47
Explain cytokine function in axonal regeneration
glial cells capable of releasing pro and anti inflammatory cytokines. If pro inflammatory are released this will lead to further damage and cell death. 
48
Where is the hypothalmus located?
Floor of the 3rd ventricle ; most ventral diencephalon
49
Boundaries surrounding Hypothalmus
Laterally - optic nervesVentral - tuber cinerum (midline of tuber cinerum is median eminence)Posteriorly- coronal plane between mammilary body and posterior commissure
50
Location and function of median eminence?
midline of tuber cinerum neuroendocrine control of pituitary
51
Nuclei of anterior Hypothalmus
Preoptic Supraoptic Suprachiasmatic
52
Nuclei of posterior Hypothalmus
posterior, mammillary, tuberomammillary, dorsal
53
Nuclei of middle Hypothalmus
paraventriculardorsomediallateralperiventricularventromedialarcuate
54
Name functions of hypothalmus (8) and nuclei that contribute
1. water/ electrolyte balance - supraoptic (ADH) and paraventricular (oxytocin)2. synthesis and secretion of hypothalmic releasing/inhibiting factors that control anterior pituitary3. temperature regulation - anterior and posterior hypothalmic nuclei4. activate sympathetic and adrenal medulla - ant/post hypothalmic areas5. thirst/regulation of drinking - lateral hypothalmus 6. hunger/satiety - lateral / ventromedial hypothalmus 7. regulation of gonadal / sexual fxn - anterior/ preoptic area and arcuate8. regulation of circadian rhythm - suprachiasmatic
55
What is anterior and posterior pituitary made from? 
anterior - ectodermal tissueposterior- neural tissue 
56
Pituitary gland lies in _______
sella turcica
57
Vascular supply of pituitary (ant/post)
anterior pituitary - no significant direct arterial blood supply -- supplied by hypophyseal portal systemposterior pituitary- long/short portal vessels - superior and inferior hypophyseal A. 
58
______ forms anastomoses between Superior and Inferior hypophyseal A.
trabecular A.
59
5 cell types of anterior pituitary and product
1. somatotrophs - growth hormone2. mammotrophs/lactotrophs - prolactin3. thyrotrophs - TSH 4. corticotrophs - ACTH (and other products of POMC)5. gonadotrophs- LH / FSH
60
7 neurohormones from hypothalmus and target pituitary hormones
1. thyrotropin RH - Thyrotropin / Prolactin2. GnRH - LH / FSH3. CRH - ACTH (B-LPH / B-endorphins)4. GH RH - growth hormones5. Somatostain [GH inhibiting hormone] - Inhibit release of GH / thyrotropin6. Dopamine [Prolactin inhibiting factor] - Inhibit prolactin release7. Prolactin releasing factor - Prolactin
61
Long loop vs short loop feedback in hypothalmus
long loop - from target gland hormone [more important]short loop - pituitary topic hormones inhibit secretion of hypothalmus 
62
Precursor for ACTH? By products when producing ACTH?
POMC ; by products: B-LPH (equimolar to ACTH) ; N-terminal fragmentACTH can be broken down to form Melanocyte Stimulating hormone
63
Function of MSH? 
increase skin darkness (pigmentation)
64
Receptor for ACTH in adrenal cortex
MC2R
65
Major regulator of ACTH / POMC
CRH (corticotropin releasing hormone)
66
Describe ACTH secretion pattern
released in response to stressreleased mostly in early AM hours
67
Structural similarities and differences between TSH, LH, FSH
all have same alpha subunit but beta chain is different for each
68
T3
triiodothyronine
69
T4
thyroxine
70
Growth Hormone function
post natal growth -- bones and musclesalso functions in carbohydrate metabolism
71
______ , secreted by _____ and _____ , binds to _____ to provide (predominant) tonic inhibition of prolactin
dopamine, TIDA neurons, tuberohypophyseal dopaminergic neurons, D2 receptor
72
Prolactinoma can cause what?
galactorrhea gonadal dysfunction impotence in men
73
Hypothalmic tumors in kids can cause?
advanced pubertyaltered growth rate
74
Loss of all hormones of anterior pituitary is known as? can be treated by?
panhypopituitarismreplacement therapy 
75
Aldosterone produced in?
Zona glomerulosa
76
Primary glucocorticoid
cortisol
77
Precursors for aldosterone are?
Doc ; corticosterone 
78
sex steroid production occurs in?
zona reticularis
79
How is cholesterol taken into cell?
(Primary) via LDL receptors and endocytosisMay also be made de novo via acetyl CoA
80
Enzyme which converts cortisone (inactive) to cortisol
11-hydroxysteroid dehydrogenase I (HSD-1)
81
_____ is the inactive form of cortisol (examples include cortisone and prednisone)
11-keto
82
Major control of cortisol biosynthesis
ACTH
83
Process of how ACTH increases cortisol
ACTH binds MC2RStimulates LDL uptakecholesterol transferred by StAr (StAr synthesis is also promoted by ACTH)conversion of cholesterol to pregnenolone via desmolasecortisol synthesis
84
Atrophy of ______ and _____ can occur in the absence of ACTH
zona fasicularis and reticularis because ACTH promotes protein synthesis and growth of each
85
Cortisol is bound to ____ which is made in the _____
CBGLiver
86
DHEA is bound to
albumin
87
This controls the amount of steroids gaininga ccess to MR receptor
11B-HSD
88
Function of NF-kB
migrates to nucleus to upregulate cytokine genes
89
How does cortisol reduce inflammation
Cortisol binds to GR and is then able to interfere with NF-kB access to the gene to prevent cytokine productionGlucocorticoids also surpress phospholipase A2 and Cox-2
90
Cortisol effect on metabolism of carbohydrates
increase GluconeogensisHyperglycemiaIncrease Glucose 6 phosphatase
91
Cortisol effect on metabolism of protein
inhibit protein synthesisincrease blood urea nitrogenincrease nitrogen excretionpromotes muscle degradation in muscle to mobilize amino acids
92
Cortisol effect on metabolism of lipids
enhance lipolysis free fatty acids typically migrate to trunk 
93
Cortisol deficiency - effect on cardiovascular system
responsiveness to vasoconstricters is diminished thus producing hypotensive state 
94
Cortisol effect on lymph response
decrease antibody productionlimite immune reactions so as to not damage the organism
95
cortisol effect on CNS 
can pass blood brain barrierchanges in mood and behavior 
96
Excess androgen production can lead to 
appreciable masculinizaiton 
97
fetal zone of adrenal cortex produces
DHEA and sulfated form
98
Hypofunction of adrenal cortex
loss of appetitefatigue; muscle weaknesshypoglycemia
99
Addisson's Disease
adrenal gland is destroyedlack of negative feedback from cortisol ; therefore, ACTH and POMC are overproducedLeads to hyperpigmentation due to MSH
100
Cushing's Disease
Hyperfunction of adrenal-- excess cortisolbilateral adrenal hyperplasia (due to excess ACTH)HyperglycemiaMuscle WeaknessThin extremitiesFat redistribution to face and trunk
101
Congenital Adrenal Hyperplasia. Most commonly caused by? 
cortisol not produced in adequate amounts to activate negative feedback loop; therefore, ACTH hypersecretion results causing adrenals to enlarge Salt wasting due to no aldosteroneMost commonly caused by deficiency in 21 hydroxylase 
102
Congenital Adrenal Hyperplasia effect on males and females
Females: masculanizaiton of external genetaliaMales: precocious puberty
103
Goiter
Enlarged thyroid
104
Follicle of cells that secrete thyroid hormone contain ______
colloid
105
This gland is well vascularized and has one of the highest rates of blood flow per gram of tissue
thyroid gland
106
Colloid is surrounded by ____ type of epithelium
cuboidal 
107
______ essential for synthesis of thyroid hormones 
dietary iodine
108
Recommended iodine intake per day. If this is below the normal value what happens? 
150 micrograms/day; if below 100 the gland will be unable to secrete normal levels of thyroid hormone leading to hypothyroidism along with goiter
109
What constitutes the iodine pump and what is it connected to
Na/I co transporter on basolateralcoupled with Na/K ATPase
110
Inhibitors of Na/I symporter
perchlorate (HClO4 -) and thiocyanate (SCN-)compete for sites on symporter
111
How does TSH affect the Na/I pump
increases synthesis of pump
112
Pendrin
apical transporter of iodine
113
Function of thyroid peroxidase
changes I to I+couples thyroglobulin to form MIT (iodinated in one location) or DIT (iodinated in two locations)
114
What is functional significance of thyroglobulin? Where is it made?
thyroglobulin is made in the thyroidIt contains tyrosine which is then incorporated with I+ Forming MIT and DIT
115
Once TGB forms T3/4 how is T3/4 released?
TGB is endocytosed and then broken down via lysozymesT3/4 are then released through basolateral membrane into blood (Iodide is recycled)
116
Function of thiouracils
inhibit peroxidase enzyme to inhibit T3 and T4 production
117
TSH secretion is inhibited by ______
somatostatin-- decreases pituitary response to TRH
118
Which steps of T3 and T4 synthesis is TSH involved with?
All of them (iodine symporter, coupling, endocytosis, proteolysis of thyroglobulin)
119
More potent thyroid hormone: T3 or T4?
T3many tissues can convert T4 to T3
120
Wolff Chaikoff effect
excess iodine inhibits synthesis of T3 and T4 via peroxidase enzyme
121
Is most of T3/4 bound or unbound? Which state(s) are the active form
BoundUnbound is active
122
Molecules which bind T3/4. which has the highest affinity
thyroxine binding globulin (TBG) -- highest affinity (binds both)transthyretin (TTR) - binds T4 but low amounts of T3Albumin- binds both but with low affinity
123
Half life for T3?
~1 day
124
Half life for T4
~6/7 days
125
How does pregnancy affect amount of T3/4 in active state
estrogen increases binding globulins (including TBG) thus causing more to be bound and inactive
126
Enzymes involved in deiodination use
selenium
127
Which deiodinase are found in glial cells? Why?
Type II To maintain high levels of T3 even if T4 concentrations drop
128
Is reverse T3 an active form? When do you see elevated levels of reverse T3
No does not bind to thyroid receptorstarvation (to decrease metabolic rate and fuel consumption)
129
How do T3 and T4 enter the cell?
Monocarboxylate transporter (MCT8)Organic Anion Transporting family (OATP)
130
what is function of T3 once it is converted from T4
alter transcription rate and production of mRNA
131
where is thyroid receptor in absence of ligand
in nucleus associated with chromatin
132
T3 effect on carbohydrate metabolism
increase uptake of glucose and glycolysisincreased carbohydrate metabolism
133
T3 effect on lipid metabolism
increase lipolysispromote mobilization of fatty acidsdecrease in plasma TAGs
134
how does hypothyroidism alter basal metabolic rate (BMR). why?
decreases it due to decrease in oxygen consumption
135
Thyroid hormone effect on heat? carbon dioxide?
increase both
136
Hypothyroidism associated with hypo or hyper thermia
hypothermia (generate less heat and lower tolerance to cold)
137
What happens if thyroid hormone is absent during development of fetus
Dimished growth of cerebral cortexdecrease in proliferation of axonsdecreased myelinationlack of maturation for bone growth centers 
138
Effect of elevated thyroid hormone in adults
emotional instabilityhyperexcitability
139
Effect of hypothyroidism in adults
slow speechdecreased memorydecreased conduction in peripheral nerves
140
Effect of thyroid hormone on catecholamines
increases number of receptors (NOT increase blood levels of catecholamines)
141
Hyperthyroidism on heart
increased contractility due to increase in alpha myosin heavy chain, calcium channels, calcium ATPase, B-adrenergic receptorsPositive inotropic and chronotropic effects 
142
Common finding to explain hyperthyroidism
1) benign thyroid adenoma 2) elevated levels of thyroid stimulating immunoglobulin which binds normal TSH receptors to over stimulate production of T4/T3
143
Grave's Disease. Clinical findings? treatment? 
TSI (produced by B-lymphocytes) binds to TSH receptor on thyroid gland causing enlarged/overactive thyroidEyes protrudeTreated with thioamides
144
Causes of hypothyroidism
Iodine deficiencyhypothalmic or pituitary dysfunction chronic thyroid inflammationremoval of thyroid
145
myxedema. treated with?
synonym for hypothyroidismmucinous edema that gives skin puffy appearancetreatment: synthetic levothyroxine
146
(A nitpicky one) Name the positions of Iodine on T3, T4, and rev T3
T3: 3,5,3T4: 3,5,3,5Rev T3: 3,3,5
147
Where does thyroid hormone not increase oxygen consumption in humans
brain, gonads, spleen
148
How does somatostatin alter TSH secretion?
Somatostatin decreases pituitary response to TRH (RELEASING HORMONE!)
149
Why is such a large population of T3/T4 bound?
To insure hormone solubilitymaintain large circulating reservoir of T3/T4 that is unaffected by shifts in secretionminimize loss of hormones via kidney/liver
150
How does T3 impose its negative feedback?
reduces number of TRH receptorsinhibits gene responsible for TSH synthesisT4/T3 suppress mRNA levels for TRH
151
What is the name of the zone of adrenal cortex present in gestation that eventually proliferates at a young age?
Definitive Zone
152
How would you treat Cushing's Disease
metyrapone - blocks 11 hydroxylase enzyme to lower cortisol levels
153
What is the most abundant hormone in the adenohypophysis?
growth hormone
154
What is the GH-like hormone secreted during pregnancy?
hCS
155
What hormone stimulates GH release?
growth hormone release hormone
156
What hormone inhibits growth hormone?
somatostatin
157
How does GHRH affect somatotrophs?
increase GH mRNA transcription, synthesis of GH protein, GH release
158
What tissue secretes somatostatin?
hypothalamus
159
How does somatostatin affect somatotrophs?
decrease GH secretion
160
What is another name for IGF1?
somatomedin
161
What tissue produces somatomedin?
liver
162
How does somatomedin affect somatotrophs?
GH transcription
163
In adults, when are the highest GH levels observed?
during sleep
164
How many GH surges are seen per day around puberty?
4-6
165
What conditions increase GH?
stressexerciselow glc
166
What is the assumed endogenous ligand for GH secretagogue receptor?
ghrelin
167
What carries GH in the blood stream?
GH binding protein
168
What downstream signaling mechanism does GH use?
JAK/STAT
169
What tissue has the most GH receptors?
liver
170
Which IGF isoform is the most important?
IGF1
171
What effects does IGF have?
increase: glc uptakemitosisbone cel differentiationcollagen productiongrowth of the epiphyseal cartilage plate
172
How does GH affect adipose tissue?
decrease glc uptakeincrease lipolysis
173
How does GH affect chondrocytes?
increase aa uptake and protein synthesis
174
How does GH affect metabolism?
increase plasma glc and FFAdecrease plasma aa
175
How does GH affect skeletal growth?
stimulate epiphyseal cartilageincreased chondrocyte metabolism
176
What happens to epiphyseal plates without GH?
narrowcartilage redued
177
How is hormone sensitive lipase affected by GH?
increase
178
How do insulin and GH cross-talk?
GH inhibits insulin in muscle and adipose
179
GH deficiency causes __.
dwarfism
180
GH excess causes __.
gigantism
181
What does octreotide do?
somatostain analog
182
perfusion of brain increases proportional to increase in _____________
arterial CO2
183
Cerebral blood flow remains nearly constant between ____ and ___ mmHg. Beyond these limits blood flow becomes _____ dependent
60 and 160pressure dependent 
184
How does autoregulation in CNS blood flow work when BP is high or low?
Low BP- dilation of arterioles which decreases resistance to flow to promote flowHigh BP - constrict arterioles to increase resistance This promotes constant flow desired
185
How does chronic Hypertension alter autoregulation of CNS blood flow. What negative effects can this have?
shifts autoregulation to the right (increasing autoregulation pressure boundaries)Neg Effect- brain is now at risk for damage during periods of low pressure as CBF will decrease
186
Injuries such as ________ (multiple answers) can cause CBF to have a linear relationship with ______
head trauma, ischemia, subarachnoid hemorrhageCBF varies directly with Cerebral Perfusion Pressure
187
Brain lacks ____ and ______ ; therefore, it requires continuous supply of _____
creatine phosphate / glycogenO2
188
What is the normal extracellular [K+] and what happens when the value is below and above this normal 
4 mMol is normalBelow 4- flow decreasesAbove 4- flow increases
189
__________ causes the extracellular [K+] to be above ____ mMol which leads to this undesirable response (much higher than normal K value)
neuronal damage10arterioles contracting -- shutting down flow to sacrifice local neurons to save surrounding neurons
190
Lack of oxygen results in the release of ___________ which produce ______ and ______ blood flow
acid metabolitesvasodilationincreased
191
Anterior Cerebral Artery supplies? Penetrating branches supply?
inferior frontal lobesmedial surface of frontal lobesmedial surface parietal lobesanterior corpus callosumPenetrating: Limbic structures, head of caudate, anterior limb of internal capsule
192
middle cerebral artery supplies? penetrating branches?
frontal lobesparietal lobestemporaloccipitalinsularpenetrating: posterior internal capsule, putamen, outer globus pallidus, body of caudate
193
Posterior cerebral artery supplies? 
occipital lobeinferior temporal lobethalmusposterior limb of internal capsule
194
penetrating anterior choroidal artery supplies?
anterior hippocampusposterior internal capsule
195
What arteries supply the ventral side of the brain?
PCACerebellar arteries (superior, ant. inf. , post. inf. )Brainstem branchesAnterior Spinal Artery
196
what is the most common brainstem stroke?
posterior inferior cerebllar artery stroke
197
A stroke affecting this artery could lead to possible ________ (a disease) symptoms.
posterior inferior cerebllar arteryptosis and miosis
198
posterior inferior cerebllar artery stroke is also known as what other syndromes?
Wallenberg SyndromeLateral Medullary Syndrome
199
contralateral loss of pain and temp to the body and ipsilateral loss of pain and temp to the face is seen in a stroke of _______
posterior inferior cerebellar artery (PICA)
200
Other random symptoms of stroke to PICA
vertigodifficulty swallowingataxia
201
Symptoms associated with stroke to AICA. also known as _______
vomitingvertigoipsilateral deafnessnystagmusipsilateral facial weaknesslateral pontine syndrome
202
Interesting symptoms of stroke to superior cerebellar artery
ipsilateral ataxiaslurred speechipsilateral horner's syndromecontralateral loss of pain/temppartial deafnessRARE
203
What is contained in paramedian midline territory?
corticospinal tractmedial lemiscus
204
what is contained in the paramedian short circumferential territory?
pontocerebellar fibersmedial leminiscusALS
205
What is contained in the paramedian long circumferential territory
middle and superior cerebellar pedunclesvestibular and cochlear nerves/nucleiCN 5 (spinal and trigeminal nucleus)CN 7ALS
206
How is spinal artery supplied with blood?
anterior spinal artery - anterior 2/3 of cordposterior spinal artery- posterior 1/3 of cord
207
_____ strokes are when blood vessel in brain ruptures and blood seeps into brain. This is most commonly caused by ____ and ____
hemorrhagic strokehigh BP aneurysm (weakness of vessel wall causing it to balloon outward)
208
What are some secondary mediators released from O2 deprived tissue? What does this cause?
glutamateCaprostaglandinsfree radicalsprolong and extend neuronal damage
209
Major risk factors for stroke
High BPSmokingDiabetesCarotid artery disease ( narrow Cartoid artery can be blocked by clot) - peripheral artery disease- narrowed blood vessel Atrial FibrillationBlood disorder- sickle cell anemia or high RBC count
210
Comparison of blacks vs whites for strokes
blacks 2x more likely to have stroke for first timeblacks have higher death rate 
211
What is an effective treatment for ischemia of brain. Who should this not be given to?
tissue plasminogen activatorsshould not be given to someone with hemorrhagic stroke b/c they will bleed out
212
treatments for hemorrhagic stroke
1. drain/remove blood2. endovascular coli embolization (insert coil to repair aneurysm3. Place clip around aneurysm  
213
Vessel Occluded : anterior spinal artery (posterior to last radicular artery)
bilateral paralysis caudal to blockagebilateral loss of Pain/Temp below blockage
214
Vessel Occluded : branch from anterior spinal artery at C5
Ipsilateral UMN paralysis below C5Ipsilateral LMN paralysis at C5Contralateral loss of pain/temp below C5
215
Vessel Occluded : lateral branch of vertebral artery
contralateral loss of pain/temp from neck downipsilateral loss of pain/temp from faceipsilateral unsteadiness on feet
216
Vessel Occluded : Penetrating branch from anterior spinal artery
ipsilateral tongue deviationcontralateral loss of touch from neck downcontralateral paralysis (UMN) from neck down
217
Vessel Occluded : Medial Penetrator from basilar artery
contralateral loss of touch from neck down and some facecontralateral paralysis (UMN) from neck down and vocal and tongue
218
Vessel Occluded : Penetrator from AICA
contralateral loss P/T and ipsilateral faceipsilateral loss facial motoripsilateral eye- no lateral movement - abducens nucleus ipsilateral vestibular response loss
219
Vessel Occluded : long circumferential from basilar
CL loss P/TCL loss touch from body and faceIP LMN of jaw musclesdecrease CL auditory perception
220
Vessel Occluded : Medial penetrating from Basilar
CL UMN from headIP CN3 PalsyIP ataxia 
221
Vessel Occluded : Penetrating branch of superior cerebellar 
CL paralysis (UMN) from neck downCL loss of touch, P/T from face and bodyDecrease CL auditory perception
222
Vessel Occluded : Blockage of penetrating branch of posterior cerebral artery
CL loss of touch, position, P/T from body face
223
Anterior Limb of Internal capsule is supplied by
lenticulostriate branch of Anterior Cerebral Artery 
224
Genu/Rostral Internal Capsule blood supply
lenticulostriate from MCA and anterior choroidal 
225
Blood supply to caudal posterior limb
penetrating branches of PCA 
226
Vessel Occluded : Anterior Cerebral Artery (ACA)
CL UMN paralysis from waist downCL loss of somatic sensation from waist down
227
Vessel Occluded : Posterior Cerebral Artery (PCA)
CL homonymous hemianopsia
228
Vessel Occluded : Middle Cerebral Artery (MCA)
CL UMN paralysis from waist upCL loss of somatic sensation from waist up
229
What is the last brain structure to mature?
uncinate
230
ADHD is characterized by a __ in cortical maturation.
delay
231
What is neuroplasticity?
gene expression changes that lead to learning and behavioral adaptation
232
How do heteromodal cortices differ from primary?
They integrate signals from multiple sensory inputs
233
What does the arcuate/association fiber connect?
cortical areas of same hemisphere
234
What do corticofugal fibers connect?
subcortical structures
235
Name the 2 main arcuate fibers for learning.
uncinate fasciculusarcuate fasciculus
236
List the 4 parts of the corpus callossum.
rostrumgenutrunksplenium
237
What tissue is made up of archicortex?
hippocampus
238
What tissue makes up paleocortex?
temporal lobe
239
What is the allocortex made up of?
hippocampusamygdalaprepyriform cortex
240
How does the cortex connect to the pons?
radiationsinternal capsulecerebral peduncle
241
List some components of the limbic lobe.
cingulate gyrushippocampusparahippocampal gyrusnucleus accumbensamygdaladentate
242
The hippocampus is right on top of what cortex?
perirhinal
243
What tracts go from the hippocampus to the thalamus?
fornix to mammillary body to mammillothalamic tract
244
ADHD is characterized by a __ in cortical maturation.
delay
245
How do heteromodal cortices differ from primary?
They integrate signals from multiple sensory inputs
246
How does the cortex connect to the pons?
radiationsinternal capsulecerebral peduncle
247
List some components of the limbic lobe.
cingulate gyrus hippocampus parahippocampal gyrus nucleus accumbens amygdala dentate
248
List the 4 parts of the corpus callossum.
rostrum genu trunk splenium
249
Name the 2 main arcuate fibers for learning. 
uncinate fasciculus arcuate fasciculus
250
The hippocampus is right on top of what cortex? 
perirhinal
251
What do corticofugal fibers connect?
subcortical structures
252
What does the arcuate/association fiber connect?
cortical areas of same hemisphere
253
What is neuroplasticity? 
gene expression changes that lead to learning and behavioral adaptation
254
What is the allocortex made up of? 
hippocampus amygdala prepyriform cortex
255
What is the last brain structure to mature? 
uncinate
256
What tissue is made up of archicortex? 
hippocampus
257
What tissue makes up paleocortex?
temporal lobe
258
What tracts go from the hippocampus to the thalamus? 
fornix to mammillary body to mammillothalamic tract
259
MDD patients have a __ activation of the limbic system.
high
260
What frequency are EEG gamma waves?
25+ Hz
261
What frequency are EEG beta waves?
13-25 Hz
262
What frequency are EEG alpha waves?
13-Aug
263
What frequency are EEG theta waves?
4-7 Hz
264
What frequency are EEG delta waves?
<4 Hz
265
What EEG wave occurs during deep sleep?
delta
266
What EEG wave occurs during early sleep?
theta
267
What EEG wave occurs during binding of information?
gamma
268
What EEG wave occurs during the alert stage?
beta
269
What frequency EEG wave is the awake but relaxed state?
8-13 Hz
270
How does encephalitis affect EEG?
general slowing
271
How do siezures present on an EEG?
hyperactivity of neurons
272
What makes up the classic reticular activating system?
rostral ponsthalamic relay nucleiintralaminar thalamic nucleicortex
273
What NTS are used by the reticular activating system?
AChNE
274
What nuclei start the reticular activating system?
parabrachial nucleilocus ceruleuspedunculopontine nucleusdorsal and median raphe nuclei
275
What fiber drives the secondary arousal pathway?
medial forebrain bundle
276
What NTS are used in the secondary arousal pathway?
orexinAChhistamine
277
How do thalamic neurons fire during a synchronized EEG?
oscillatoryhyperpolarization by inhibitory input from thalamic reticular cells, which leads to Ca influx
278
How do thalamic neurons fire during a desynchronized EEG?
tonic modecholinergic brainstem afferents from the reticular activating system
279
What would happen if you were napping and then your EEG became desynchronized?
You would be awake
280
What neural structure secretes histamines?
tuberomammillary nucleus
281
Non-REM is regulated by activation of GABA neurons in the __. 
ventrolateral preoptic area (VLPO)
282
How long is REM sleep in each sleep cycle?
5-15 min
283
How long is a sleep cycle?
90-120 min
284
How is muscle tone affected in REM sleep?
relaxed
285
GABA inhibition of what neuron initiates sleep?
NE 5HT ACh neurons in the midbrain
286
During REM sleep, what part of the sleep neurons turns back on?
AChNE/5HT axis stays off
287
What does the NE/5HT axis of sleep control?
motor output
288
What nucleus is the circadian pacemaker?
suprachiasmatic nucleus
289
What happens in narcolepsy?
onset of sleep starts with REM sleep
290
What happens in cataplexy?
loss of muscle tone by active inhibition of skeletal muscleduring consciousness
291
What sort of stimuli does sleep help encode?
positive stimuli
292
What is encoding?
newly learned info is attended to and processed
293
What is consolidation?
hippocampus-dependent short memories being encoded into cortex-dependent long memories
294
Hippocampal damage results in __.
anterograde amnesia
295
What type of memory is the hippocampus important for?
spatialshort term
296
What updates faster, visual or auditory memory?
visual
297
Does short term memory require the hippocampus?
no
298
What is the molecular basis of memory?
long term potentiation/depression
299
What are examples of nonassociative learning?
habituationsensitization
300
What is habituation?
repeated exposure to same stimulus decreases response
301
What is sensitization?
repeated exposure to same stimulus increases response
302
What neural structures are important in associative memory?
amygadala and hippocampus
303
What brain region does the central amygdala go to?
brainstemhypothalamus
304
What brain region does the basolateral amygdala go to?
orbital cortexanterior cingulatemedial thalamus
305
What part of the amygdala controls emotional cognition?
basolateral
306
What part of the amygdala controls autonomic response?
central
307
Simple associative learning of emotional response involves __.
amygdala
308
Simple associative learning of the skeletal muscle involves the __.
cerebellum
309
What is the common example of procedural memory?
riding a bike
310
What sort of memory underlies our ability to create stereotypes?
perceptual
311
What is episodic memory?
remembering experiences
312
What is semantic memory?
remembering specific facts
313
What lobe do Alzheimer plaques concentrate on?
parietal
314
How does frontal lobe damage affect memory?
more work to get info in and out of storage
315
How does hippocampal damage affect memory?
impossible to get info into storagecan still get memory from cortex
316
What does the basal ganglia motor loop do?
the putamen sequences somatic movements by the motor and premotor cortex
317
What does the basal ganglia oculomotor loop do?
regulates saccades using the caudate and frontal eye fields
318
What does the basal ganglia prefrontal loop do?
dorsolateral prefrontal cortex innervates the caudate to use memory
319
What does the basal ganglia limbic loop do?
anterior cingulate and orbital frontal cortex innervate the ventral striatum to regulate emotional behaviors
320
What causes syndrome of Cretinism
decreased thyroid hormone during fetal development which leads to poor mental development
321
How is GH affected by presence of Thyroid Hormone?
Thyroid Hormone is required by pituitary somatotroph for GH synthesis and secretion. Also, maintains sensitivity to GH and IGF
322
What is the purpose of carotid endarterectomy
Restore blood flow to the brain by removing atherosclerotic plaque
323
Where does atherosclerotic plaque build up (what layer of vessel)
intimia (endothelial layer)
324
What are some consequences of stable and unstable plaque
occlusionthrombosishemorrhageembolism
325
layers of vessel. features? 
intima- endothelial ; basement membranemedia- smooth muscle ; Extracellular matrixadventitia- loose connective tissue ; vaso vasorum 
326
Infection, Inflammation, trauma, or toxic exposure can cause this type of interaction between the layers of the vessel 
smooth muscle cells invade intima (intimal thickening)
327
Which specific vessels does atherosclerosis predominantly affect?
Coronary and Carotid vessels
328
What is a stroke?
embolus from broken plaque reaches cerebral vessels thus causing ischemic hypoxia in the brain
329
Describe events in pre-clinical phase of atheroma 
normal artery -- 1) fatty streak 2) fibrofatty plaque (can also skip fatty streak stage) 3)advanced vulnerable plaque ---> clinical phase
330
Describe clinical phase of atheroma
Continuation of advanced plaque from pre-clinical : 1) mural thrombosis/ embolization/ leading to wall weakening-->aneurysm and rupture2) plaque ruptures or erodes/embolizaiton --> occlusion by thrombus 3)progressive plaque growth --> critical stenosis
331
Partial or complete blockage of internal carotid or vertebral arteries leads to what change in blood flow?
None. Patients come in with 80% blockage in both carotids without symptoms 
332
What percent of patients have an incomplete circle of willis
20-50%
333
How are carotid occlusions detected?
cerebrovascular event may be first sign: 1) stroke ; 2) transient ischemic attack
334
Whaaaaaat is a bruit? 
rush sound heard with a stethoscope (blood moving past occlusion)
335
What is used to assess degree of infarct in patients who have just had a stroke?
CT/MRI
336
Carotid Endarterectomy is recommended for patients with what symptoms?
70%+ stenosisstroketransient ischemic attackSignificant carotid artery disease
337
What are possible fatal events associated with carotid endarterectomy
cardiac eventspost op stroke : plaque emboli ; platelet clotting ; improper flushinghyperperfusion syndrome
338
Describe vascular anatomy of Pre Carotid Endarterectomy patients
vertebral artery flow compenstates for lack of carotid flowcommunicating branches become strongerautoregulation functions to decrease resistance to maintain CBF
339
Describe vasculature of post Carotid Endarterectomy patient
Higher BP and oxygen is sensed; therefore arterioles try to constrict to prevent excess CBF
340
3 clinical features of hyperperfusion syndrome
ipsilateral headache - migrainefocal motor seizuresintracerebral edema and hemorrhage
341
What is main impaired ability with respect to autoregulation after Carotid Endarterectomy
vessels are unable to constrict in presence of high blood pressure
342
Characteristics, prior to operation, of patients who have hyperperfusion syndrome
had high grade carotid stenosis (>80%)recent infarctbilateral carotid occlusionpoorly regulated post operative systemic blood pressure
343
How does cardiovascular reactivity % correlate to hyperperfusion syndrome
low % are likely to suffer from hyperperfusion syndrome
344
How are free radicals produced in hyperperfusion?
when clamping is removed, influx of blood and oxygen results in free radical formation and thus produces evidence of lipid peroxidaiton (within minutes of declamping)
345
How is baroreceptor affected during Carotid Endarterectomy
1) nerves to carotid body may be severed or damaged by cytokines (from inflammatory response)--> hypertension and tachycardia2) stimulation of carotid sinus during procedure --> leads to hypotension which cannot be handled by autoregulation as vessels cannot constrict
346
Where does the hippocampus project to 
limbic cortexmammallary body septum(Kalivas diagram)
347
What is the input to the nucleus accumbens
anterior cingulate (+)oribital cortex (-)
348
What does the inucium griseum connect
hippocampus to anterior cingulate/orbital cortex
349
What is the corticostriatal thalmic loop? Purpose?
limbic cortex (ant cingulate/orbital cortex) to accumbens to medial anterior thalmus back to limbic cortex modifies behavior
350
Phases of addiction.
social useregulated relapsecompulsive relapse
351
Neurocircuitry associated with social use
mesocorticolimbicdopamine
352
Neurocircuitry associated with regulated relapse
prefrontal cortexglutamate
353
Neurocircuitry associated with compulsive relapse
striatal habit circuitry
354
How does dopamine contribute to addiction?
the dopamine release caused by a drug is directly related to how addictive it is
355
characteristics of drugs which cause addiction
1) more dopamine release2) rapid drug onset3) greater drug availability 
356
Primary pathology in addiction?
inability for prefrontal cortex to regulate behavior via nucleus acumbens due to imbalance of glutamate projection to accumbens 
357
What types of drugs may be useful in treating addiction
drugs that restore normal glutamate transmission
358
Cocaine addiction reduced ______ activity
prefrontal metabolic (anterior cingluate and orbital cortex)
359
When cocaine addicts watched a cocaine video where was the greatest stimulation seen?
amygdala and anterior cingulate
360
Cocaine use leads to a loss of ______
plasticity -- decreased LTP and LTD
361
Replacement therapies are effective for what stage of addiction
regulated relapse as it provides similar effect
362
This drug helps to restore LTP and LTD 
N-acetylcysteine
363
NAC reduced activity in ______ for cocaine users shown a cocaine video
anterior cingulate
364
Why is addiction so common in adolescents?
Adolescents have 30% more dopamine enabling them to become more easily addicted 
365
Most drug addicts begin between what ages?
14 and 23
366
How did NAC affect days to relapse in cocaine addicts
increased the number of days to relapse
367
In experiment to determine NAC effect on marijuana users what was found?
NAC increased number of people who produced NEGATIVE urine samples for THC vs placebo
368
Purpse of ventral stream of visual processing
visual cortex to anterior temporal lobe facial recognition
369
Purpse of dorsal stream of visual processing
visual cortex to medial temporal and parietal cortexspatial orientation and spatial cognition 
370
If a patient could not recognize faces where would you look for a lesion
ventral temporal/occipital junctionmust be in right hemisphere but can also be bilateral
371
prosopagnosia
inability to recognize faces
372
what are some associated problems that arise in conjunction with prosopagnosia 
achromatopsia- inability to recognize colormetamorphopsia- object has distorted shape
373
Balint's syndrome
bilateral lesions of parietal cortexsimultangagnosia- loss of awareness for overall object (big picture loss) optic ataxia- inability to reach out and grasp object (hand eye coordination) 
374
What is the function of the parietal cortex in dorsal stream visual processing
analysis of motion and spatial relations
375
What is the function of the temporal cortex in dorsal stream visual processing
analysis of form and color
376
A unilateral parietal lesion will cause what problems with respect to hand eye coordination
Normal function in the ipsilateral fieldContralateral hand makes errors when in contralateral visual field 
377
Explain relationship between R/L visual field stimulus and increased activity in R/L parietal cortex
stimulus presented in the L visual field will cause firing in right parietal cortexstimulus presented in R visual field will cause firing in both right and left parietal cortex
378
Lesion in which parietal cortex (R or L) is more devastating? What is this known as?
Right because both L and R visual field excites right parietal cortexLEFT NEGLECT
379
The Go circuit is ______ as it is involved in ____ and _____
anterior cingulatemotivationattention
380
The Stop circuit is the ______ as it is involved in providing _____
Orbital Cortexinhibitory control over behavior
381
Drug addicts show blunted activity in the ______ indicating compulsive behavior
orbital cortex(also Kalivas states diminished anterior cingulate in a different lecture) 
382
This portion of the cortex is activated during emotional pocesssing
Insula (and Amygdala)
383
Lateral frontal cortex of temporal lobe provides memory about _____
objects
384
Anterior Cingulate cortex provides memory about _____
people corresponding to emotional/motivational content
385
In experiment where subject is given a series of nouns and required to provide a verb to fit. Where was brain activity most prominent for the naive subject
prefrontal cortex and temporal lobe
386
In experiment where subject is given a series of nouns and required to provide a verb to fit. Where was brain activity most prominent for the novel subject (experienced but given new words)
prefrontal cortex and temporal lobe
387
Broca's area? Function?
posterior frontal lobe-- production of language
388
Lesion of Broca's area
expressive aphasia- can understand but difficulty expressing
389
Wernicke's area? Function?
posterior temporal lobeunderstanding language
390
Lesion to Wernicke's area
receptive aphasia-- can't make sense but speaking is ok
391
Arcuate fasiculus purpose?
connects Wernicke's and Broca's area
392
Lesion to arcuate fasiculus
conduction aphasia -- paraphrasic speech and inability to produce appropriate response
393
Stroke to ____ of temporal lobe may cause loss of ability to read and spell
posterior 
394
How do brains of deaf people adapt?
more easily activated parietal and frontal area associated with visual attention
395
Language functions are lateralized with ______ on the left and _____ on the right
speech on leftemotional context on right
396
What is Aprosodia? It comes about with a lesion in ______.
loss of emotion in speechLesion to right Broca's area
397
Dyscalculia? Lesion/Damage to what?
poor numeric abilitylesion to parieto-temporal 
398
Damage to ______ causes prosopagnosia
Right ventral temporal lobe
399
Capgras syndrome. Caused by Lesion to ? 
delusion that familiar person is an impostorassociated with damage between amygdyla and right temporal lobe 
400
What causes persistent developmental stuttering
lack of asymmetry in planum temporale (should be L dominant (temporal lobe) )
401
Naming color of ink in a word shows partnership between ______ and ____ (ex. green [ans: black]). What is this this is an example of
Frontal ParietalExample of Spatial cognition and attention
402
Deficits in working memory are often seen in patients suffering from _____ or ______
schizoparkinsons
403
Working memory (as exemplified with monkey trying to remember which container food is in) is established by _____ providing input to ______  (both are parts of the brain)
parietalprefrontal cortex
404
What is a severe and striking deficit in one cognitive function; memory?
amnesia
405
What is an absence of recognition and use of verbal language?
aphasia
406
What is impaired object recognition?
agnosia
407
What is chronic and substantial decline in two or more areas of cognitive function?
dementia
408
What are the two categories of memory?
declarative (what)non-declarative (implicit or procedural)
409
What is the leading cause of dementia?
aphasia
410
Which hemisphere is predominantly used in language?
left
411
What is an aphasia where you speak short phrases that make sense but takes a lot of effort?
broca's (non-fluent)
412
What is an aphasia where you speak long meaningless sentences?
wernicke's
413
What is agnosia?
characterized by an inability to recognize and identify objects or persons
414
Around what age does Alzheimer's onset?
60
415
Describe pathological qualities of Alzheimer's.
beta-amyloid plaquestau tanglesloss of gray matter
416
What causes Wernicke-Korsakoff syndrome?
thiamine deficiency
417
What population has high risk for Wernicke-Karsakoff?
alcholics
418
What characterizes Wernicke-Karsakoff?
nystagmusconfusionpupil responsecoma
419
List some common causes of memory disorders.
strokeseizureconcussion
420
How is mental retardation defined?
significant limitations in intellectual and adaptive function
421
When does mental retardation occur?
before age 18
422
What is the incidence of mental retardation?
1-3%
423
How to diagnose mental retardation by IQ?
<70
424
What sort of disease can resemble mental retardation?
metabolic disease
425
What is the histologic commonality in mental retardation?
dendrite and synapse abnormality
426
What causes down syndrome?
trisomy 21
427
What is the most common inherited form of mental retardation?
X-linked mental retardation disorder (XLMR)
428
What is the incidence of fragile X?
1:4000 in males1:6000 in females
429
What is the molecular cause of fragile X?
CGG repeat in the 5' UTR
430
Rett syndrome is __ to males. 
lethal
431
What gene is mutated for Rett syndrome?
MeCP2
432
When does autism typically present?
first 3 yrs of life
433
What is the triad of autism impairements?
socializationcommunicationimagination
434
What is the prevalence of autism?
2-6 cases per 1000
435
In addition to autism, what are the four other pervasive developmental disorders?
asperger'schildhood disintegrative disorderrett'sPDD not otherwise specified
436
How does autism affect language development?
delayed
437
How does autism affect social development?
physical and emotional distance from others
438
How does autism affect intellectual development?
poor verbal ability
439
What are the 5 signs that a child might be autistic?
does not babble at 12 monthsdoes not gesture at 12 monthsdoes not say single words by 16 monthsdoes not say two word phrases on his or her own by 24 monthsloss of language or social skills
440
What is the critical gene to activate male genital development?
srytestis-determining factor
441
What is the difference between organizational and activational effects of steroid hormones?
organize - in uteroactivation - puberty
442
What is wrong with female congenital adrenal hyperplasia patients?
masculanized females
443
What causes androgen insensitivity syndrome?
hormone receptors are insensitive
444
What are brain regions that are especially sex dimorphic?
hypothalamusamygdala
445
How do spinal motor neurons differ in males and females?
perineal motor neuron numbers are different
446
where does the tectospinal tract end? 
cervical segment of spinal cord since it primarily innervates shoulders and neck to move to follow eye movements
447
Hypothalamus function: what nuclei and hormone are responsible for water and electrolyte balance
Supraoptic (ADH)
448
What hypothalamus nuclei regulates circadian rhythm
Suprachiasmatic
449
What hypothalamus regulates of gonadal / sexual function
Anterior / preoptic, arcuate
450
What hypothalamus nuclei regulates hunger/satiety - lateral / ventromedial hypothalamus
Lateral nuclei - stimulate = start eating | Ventromedial nuclei - stimulate = stop eating (satiety)
451
What hypothalamus nuclei regulates thirst
Lateral hypothalamus
452
What hypothalamus areas activate sympathetic and adrenal medulla
Anterior and posterior areas.
453
What hypothalamus nuclei regulate temperature
Anterior and posterior nuclei