Exam 4 Textbook Notes

8/9/2019 Exam 4 Textbook Notes

1/22

Chapter 13: HumanCommunication

I. Speech Production and Comprehension: Brain Mechanisms

a. Aphasia: difficulty in producing or comprehending speech not caused by deafness or

a simple motor deficit; caused by brain damage.i. Patient must have difficulty comprehending, repeating, or producing

meaningful speech, and this difficulty must not be caused by simple sensory

or motor deficits or by lac of motivation.b. !esearchers have used P"# and functional M!I to gather information about language

processes form normal sub$ects

c. %aterali&ationi. 'erbal behavior is a laterali&ed function.

(. Most language disturbances occur after damage to the left side of the

brain.ii. !ight )emisphere

(. Involved in the e*pression and recognition of emotion in the tone of

voice.

+. Involved in control of prosody the normal rhythm and stress found inspeech.

d. Speech Production

i. Must have something to tal about(. Involved posterior part of the cerebral hemisphere

a. Involved in perceptions of current events and memories of

events that occurred in the past.ii. Conversion of perception, memories, and thoughts into speech maes use of

neural mechanisms located in the frontal lobes.

iii. Brocas aphasia: a form of aphasia characteri&ed by agrammatism, anomia,

and e*treme difficulty in speech articulation.(. !esult of damage to the inferior left frontal lobe -disrupts ability to

spea.

+. Slo/, laborious, and nonfluent speech.0. #rouble /ith function words preposition, article, or other /ord that

conveys little of the meaning of a sentence but is important in

specifying its grammatical structure.1. Manage to say content words a noun, verb, ad$ective, or adverb that

conveys meaning.2. Brocas area: a region of the frontal corte*, located $ust rostral to the

base of the left primary motor corte*, that is necessary for normalspeech production.

a. Motor memoriesmemories of the se3uences of muscular

movements that are needed to articulate /ords.

b. 0 ma$or speech deficits produced be lesions of the area:


2/22

i. Agrammatism: one of the usual symptoms of Broca4s

aphasia; a difficulty in comprehending or properly

employing grammatical devices, such as verb endingsand /ord order.

1. 5ppears to disrupt patients4 ability to use

grammatical information, including /ord order,to decode the meaning of a sentence.

ii. Anomia: difficulty in finding -remembering the

appropriate /ord to describe an ob$ect, action, orattribute; one of the symptoms of aphasia.

iii. 5rticulation difficulties

(. Patients mispronounce /ords, often altering the

se3uence of sounds.e. Speech Comprehension

i. 5ccomplished be neural circuits in the middle and posterior portion of the

superior temporal gyrus of the left hemisphere

(. Wernickes area: a region of the auditory association corte* on theleft temporal lobe of humans, /hich is important in the comprehension

of /ords and the production of meaningful speech.ii. Wernickes aphasia: a form of aphasia characteri&ed by poor speech

comprehension and fluent but meaningless speech.

(. 6ses fe/ content /ords, and the /ords that he or she strings together$ust do not mae sense.

+. Receptive aphasia

0. 7isrupts recognition of spoen /ords, comprehension of the meaning

of /ords, the ability to convert thoughts into /ords.iii. Pure word deafness: the ability to hear, spea, and -usually to read and /rite

/ithout being able to comprehend the meaning of speech; caused by the

damage to 8ernice4s area or disruption of auditory input to this region.(. 7amage to left temporal lobe

+. Brain in$uries can cause this

a. 7isruption of auditory input to 8ernice4s areai. Produced by bilateral damage to the primary auditory

corte*

ii. 7amage to the /hite matter in the left temporal lobes

b. 7amage to 8ernice4s area itselfiv. Mirror neurons neurons activated either /hen /e perform an action or see

another person performing particular grasping, holding, or manipulating

movements or /hen /e perform these movements ourselves.v. Transcortical sensory aphasia: a speech disorder in /hich a person has

difficulty comprehending speech and producing meaningful spontaneous

speech but can repeat speech; caused by damage to the region of the brainposterior to 8ernice4s area.

(. !esults from damage to the posterior language area alone

+. Patients can repeat /hat other people say to them


3/22


4/22

i. Speech disorder characteri&ed by fre3uent pauses, prolongations of sounds, or

repetitions of sounds, syllables, or /ords that disrupt the normal flo/ of

speech.ii. ( of population; 0< more prevalent in men then /omen.

II. 7isorders of !eading and 8ritinga. Pure Alexia: loss of the ability to read /ithout loss of the ability to /rite; produced

by brain damage.

i. Perceptual disorderb. 6nderstanding of !eading

i. #/o processes of reading:

(. 7irect recognition of the /ord as a /hole

+. Sounding it out letter by letterii. Wholeword reading: reading by recogni&ing a /ord as a /hole; =sight

reading>.

iii. Phonetic reading: reading by decoding the phonetic significance of letter

strings; = sound reading>.iv. 7ysle*ia4s

(. !urface dyslexia: a reading disorder in /hich a person can read /ordsphonetically but has difficulty reading irregularly spelled /ords by the

/hole?/ord method.

a. Must listen to their o/n pronunciation to understand /hat theyare reading

+. Phonological dyslexia: a reading disorder in /hich a person can read

familiar /ords but has difficulty reading unfamiliar /ords or

pronounceable non?/ords.a. Cannot sound out /ordsdifficulty figuring out ho/ to read

unfamiliar /ords.0. "irect "yslexia: a language disorder caused by brain damage in /hich

the person can read /ords aloud /ithout understanding them.v. #isual wordform area $#W%A&: a region of the fusiform gyrus on the base

of the temporal lobe that plays a critical role in /hole?/ord recognition.

(. 5lso involved in perception of faces and other shapes+. Studies have found damage to the '8@5 produces surface dysle*ia

vi. #he fusiform face area of the right hemisphere has the ability to 3uicly

recogni&e uni3ue configurations of peoples eyes, noses, lips, and otherfeatures of their faces even /hen the differences bet/een t/o peoples4 faces

are very similar.

vii. #he brain regions responsible for phonetic reading and /hole?/ord reading

are each independently connected /ith brain regions responsible for speech.c. 6nderstanding of 8riting

i. Argani&ation of the motor aspects of /riting involves the dorsal parietal lobe

and the premotor corte*.ii. Phonological dysgraphia: a /riting disorder in /hich the person cannot

sound out /ords and /rite them phonetically.


5/22

(. 5ppears to be caused by damage to regions of the brain involved in

phonological processing and articulation.

a. 7amage to Broca4s area, the ventral precentral gyrus, and theinsula cause this disorder, and phonological spelling tass

activate these regions.

iii. 'rthographic dysgraphia: a /riting disorder in /hich the person can spellregularly spelled /ords but not irregularly spelled ones.

a. Caused by damage to the '@85 on the base of the temporal

lobe.d. "e(elopmental "yslexia: a reading difficulty in a person of normal intelligence and

perceptual ability; of genetic origin or caused by parental or perinatal factors.

i. %inages suggests chromosomes (, +, 0, , (2, ( may contain genes

responsible for different components of this disorderii. Common deficit is deficient phonological a/arenessdevelopmental

dysle*ia people have difficulty blending or rearranging the sounds of /ords

that they hear.


6/22

Chapter 14: Neurological DisordersI. Tumor: a mass of cells /hose gro/th is uncontrolled and that serves no useful function

a. )alignant: a cancerous tumor; lacs a distinct border and may metastasi&e.

i. )etastasis: the process by /hich cells brea off of a tumor, travel throughthe vascular system, and gro/ else/here in the body.

b. Benign: a non?cancerous tumor; has a distinct border and cannot metastasi&e.

i. Encapsulated: /hether there is a distinct border bet/een the mass of

tumor cells and the surrounding tissue.c. #umors damage brain tissue:

i. Compressionii. Infiltration

d. 5rise from other cells found in the brain or from metastases originating else/here

in the body.

e. Most serious tumorsi. Metastases

ii. *liomas: a cancerous brain tumor composed of one of several types of

glial cells.(. 'ery malignant and fast gro/ing

f. )eningioma: a benign brain tumor composed of the cells that constitute the

meninges.

i. "ncapsulatedii. Ariginate in the part of the dura mater that is found bet/een the t/o

cerebral hemispheres or along the tentorium, the sheet of dura mater that

lies bet/een the occipital lobes and the cerebellum.II. !ei+ure "isorders: the preferred term for epilepsy.

a. 5ppro*. +.2 million people in the 6S have.

b. Seizure: a period of sudden, e*cessive activity of cerebral neuronsc. Con(ulsion: a violent se3uence of uncontrollable muscular movements caused by

a sei&ure.

i. !esults /hen neurons that mae up the motor system are involved

d. Partial vs. Denerali&ed sei&ures

i. Partial !ei+ures: a sei&ure that begins at a focus and remains locali&ed,not generali&ing to the rest of the brain.

(. !imple partial sei+ures: a partial sei&ure, starting from a focusand remaining locali&ed, that does not produce loss of

consciousness.

+. Complex partial sei+ures: a partial sei&ure, starting from a focusand remaining locali&ed, that produces loss of consciousness.


7/22

ii. *enerali+ed sei+ures: a sei&ure that involves most of the brain, as

contrasted /ith a partial sei&ure, /hich remains locali&ed.

e. Tonicclonic sei+ure: a generali&ed, tonic?clonic sei&ure, /hich results inconvulsions.

i. Includes motor systems of the brain

ii. Aura: a sensation that precedes a sei&ure; its e*act nature depends on thelocation of the sei&ure focus.

iii. Tonic phase: the first phase of a tonic?clonic sei&ure, in /hich all of the

patient4s seletal muscles are contracted.iv. Clonic Phase: the phase of a tonic?clonic sei&ure in /hich the patient

sho/s rhythmic $ering movements.

f. A,sence: a type of sei&ure disorder often seen in children; characteri&ed by

periods of inattention, /hich are not subse3uently remembered; also called petitmal sei&ure.

i. Accur /ith children

ii. Denerali&ed sei&ure disorder

g. 2E of patients /ith sei&ure disorders sho/ evidence of damage to thehippocampus.

i. !tatus epilepticus: a condition in /hich a patient undergoes a series ofsei&ure /ithout regaining consciousness.

(. Can cause damage to hippocampal region

+. Caused by e*cessive release of glutamate during the sei&ure.h. Causes of sei&ures:

i. Most common is scarring, /hich may be produced by an in$ury, a stroe, a

developmental abnormality in the brain, or the irritating effect of a

gro/ing tumor.ii. 7rugs and infections that cause a high fever

iii. Denetic factors

i. #reatments:i. 5nticonvulsant drugsincrease the effectiveness of inhibitory synapses

ii. Brain surgery to remove the part of the brain surrounding the focus

iii. Ketogenic dietmost of the calories come from fats, /ith a moderate

amount of proteins and a very lo/ amount of carbohydrates.

(. Carbohydrates increase the ris of having a sei&ure

+. +?7D reduced sei&uresIII. Cerebrovascular 5ccidents

a. Stroesappro*. EE,EEE per year.

i. -emorrhagic strokes: a cerebrovascular accident caused by the rupture

of a cerebral blood vessel.(. Bleeding /ithin the brain, usually from a malformed blood vessel

or from one /eaened by high blood pressure.

ii. ',structi(e strokes: a cerebrovascular accident caused by occlusion of ablood vessel.

(. Plug up a blood vessel and prevent the flo/ of blood

+. schemia: the interruption of the blood supply to a region of thebody.


8/22

0. Throm,us: a blood clot that forms in blood vessels, especially in

places /here their /alls are already damaged.

iii. /m,olus: a piece of material that forms in one part of the vascular system,breas off, and is carried through the bloodstream until it reaches an artery

to small to pass through.

iv. Produce permanent damage to the brainv. #he immediate cause of neuron death is the presence of e*cessive amounts

of glutamate.

vi. Clot dissolving drugtP5

vii. 7esmodus rotundus plasminogen activator -7SP5 FdesmoteplaseGviii. !is factors that can be reduced:

(. )igh blood pressure, cigarette smoing, diabetes, high blood levels

of cholesteroli*. "ndarterectomy has been sho/n to reduce the ris of stroe by 2E in

people under H2 years of age.

*. Stent in narro/ed carotid artery

I'. 7isorders of 7evelopmenta. #o*ic Chemicals

i. Babies born to alcoholic /omen are typically smaller than average and

develop more slo/ly.(. %etal alcohol syndrome: a birth defect caused by ingestion of

alcohol by a pregnant /oman; includes characteristic facial

anomalies and faulty brain development.b. Inherited metabolic disorders

i. "rrors of metabolismgenetic abnormalities in /hich the recipe for a

particular en&yme is in error, so the en&yme cannot be synthesi&ed.

ii. Phenylketonuria $P0&: a hereditary disorder caused by the absence of

an en&yme that converts the amino acid phenylalanine to tyrosine; theaccumulation of phenylalanine causes brain damage unless a special diet is

implemented soon after birth.

(. #reated by lo/?phenylalanine dietiii. Tay!achs disease: a heritable, fatal, metabolic storage disorder; lac o

en&ymes in lysosomes causes accumulation of /aste produces and

s/elling of cells of the brain.

(. Mainly children of "astern "uropean e/ish descentc. "own !yndrome: a disorder caused by the presence of an e*tra t/enty?first

chromosome, characteri&ed by moderate to severe mental retardation and often by

physical abnormalities.i. %ined to mothers age, + +(stchromosomes

'. 7egenerative 7isorders

a. Transmissa,le spongiform encephalopathy $T!/&: a contagious brain disease/hose degenerative process gives the brain a sponge?lie appearance; caused by

accumulation of misfolded prion protein.

i. Prion: a protein that can e*ist in t/o forms that differ only in their three?dimensional shape4 accumulation of misfolded prion protein is responsible

for #S".


9/22

(. @ound primarily in the membrane of neurons

+. 7ifference bet/een PrPc and PrPScthe /ay the protein is

folded.ii. !poradic: a disease that occurs rarely and is not obviously caused by

hereditary or an infectious agent.

iii. Caspases: a =iller en&yme> that plays a role in apoptosis, or programmedcell death.b. Parinson4s 7isease

i. Caused by degeneration of the nigrostriatal system the dopamine?

secreting neurons of the substantia nigra that sends a*ons to the basalganglia.

ii. Symptoms: muscular rigidity, slo/ness of movement, a resting tremor,

postural instabilityiii. 2ewy ,odies: abnormal circular structures /ith a dense core consisting of

alpha?synuclein protein; found in the cytoplasm of nigrostriatal neurons in

people /ith Parinson4s disease.

(. Mutation of chromosome 1 /ill produce this disordera. Produces gene alphasynuclein a protein normally found

in the presynaptic membrane, /here it is apparently

involved in synaptic plasticity. 5bnormal accumulations areapparently the cause of neural degeneration in Parinson4s

disease.

b. Toxic gain of function: said of a genetic disorder causedby a dominant mutation that involves a faulty gene that

produces a protein /ith to*ic effects.

iv. Parkin: a protein that plays a role in ferrying defective or misfoldedproteins to the proteasomes; mutated parin is a cause of familial

Parinson4s disease.(. Chromosome

+. Causes a loss of function said of a genetic disorder caused by arecessive gene that fails to reproduce a protein that is necessary for

good health.

0. Proteasome: organelles responsible for destroying defective ordegraded proteins /ithin the cell.

1. Parin assists in tagging of abnormal or misfolded proteins /ith

numerous molecules of u,i3uitin? a protein that attaches itself tofaulty or misfolded proteins and thus targets them for destruction

by proteasomes.

v. Causes: may be by to*ins in the environment, faulty metabolism, or

unrecogni&ed infectious disorders.vi. #reatment:

(. %?7AP5 -precursor of dopamine

a. Increased levels in the brain cause a patient4s remainingdopaminergic neurons to produce and secrete more

dopamine and alleviate the symptoms.

+. 7eprenyl


10/22


11/22

(. Dene encodes the production of the Bamyloid precursor protein$APP&: a protein produced and secreted by cells that serves as the

precursor for B?amyloid protein.a. Chain of HEE amino acids.

+. 5PP is cut in t/o places by en&ymes no/n as secretasesto

produce 5B.a. 5 class of en&ymes that cut the B?amyloid precursor

protein into smaller fragments, including B?amyloid.

b. Cuts head and tale off0. !esults in 1E or 1 amino acids.

vi. Presenilin: a protein produced by a faulty gene that causes B?amyloid

precursor protein to be converted to the abnormal short form; may be a

cause of 5l&heimer4 disease.(. Chromosomes ( and (1

+. PS( and PS+ appear to be subunits of gamma?secretase

vii. Apolipoprotein / $Apo/&: a glycoprotein that transports cholesterol in

the blood and plays a role in cellular repair; presence of the "1 allele ofthe apo" gene increases the ris of late?onset 5l&heimer4s disease.

(. Mutation of this might cause 5l&heimer4s disease+. "1 increases the ris of late?onset 5l&heimer4s disease, by

interfering /ith the removal of the long form of 5B from the

e*tracellular space in the brain.viii. Pharmalogical treatments acetylcholinesterase inhibitors and an JM75

receptor antagonist.

e. Amyotrophic 2ateral !clerosis$A2!&: a degenerative disorder that attacs the

spinal cord and cranial nerve motor neurons.i. 7eath occurs 2 (E years after the onset of the disease as a result of

failure of respiratory muscles.

ii. (E cases hereditary; KE sporadic(. )ereditarysupero*ide dismutase ( -SA7(

iii. Pharmacological!ilu&olereduces glutamate induced e*cito*icity

-decreases release of glutamate.

f. Multiple Sclerosis -MS

i. 5n autoimmune demyelinating disease

ii. Myelin sheaths are attaced by the person4s immune system, leavingbehind hard patches of debris called sclerotic pla3ues

iii. More common in /omen; usually late +Es to 0Es

iv. Promising treatments:(. Interferon Bprotein that modulates the responsiveness of the

immune system

+. Dlatiramer acetatemi*ture of synthetic peptides composed from

random se3uences of the amino acids tyrosine, glutamate, alanine,

and lysine.'I. 7isorders Caused by Infectious 7iseases

a. /ncephalitis: an inflammation of the brain; caused by bacteria, viruses, or to*ic

chemicals.


12/22

i. -erpes simplex (irus: a virus that normally causes cold sores near the

lips but that can also cause brain damage.

(. 'iruses live 3uietly in the trigeminal nerve ganglia nodules on thefifth cranial nerve that contain the cell bodies of somatosensory

neurons that serve the face.

+. )erpes encephalitis

attacs the frontal and temporal lobesii. Acute anterior poliomyelitis $polio&: a viral disease that destroys motorneurons of the brain and spinal cord.

(. 7amages motor neurons of the brain and spinal cord, neurons in

the primary motor corte*, and motor nuclei of the thalamus,hypothalamus, and brain stem; cerebellum; and in the ventral horns

of the gray matter of the spinal cord.

iii. 6a,ies: a fatal viral disease that causes brain damage; usually transmittedthrough the bite of an infected animal.

b. )eningitis: an inflammation of the meninges; can be caused by viruses or

bacteria.

i. Stiff nec 9 most important symptom


13/22

Chapter 15: Schizophrenia,

Afectie Disorders, and An!iet"Disorders

I. !chi+ophrenia: a serious mental disorder characteri&ed by disordered thoughts,

delusions, hallucinations, and often bi&arre behaviors.a. #hree categories of symptoms

i. Positi(e symptom: a symptom of schi&ophrenia evident by its presence:

delusions, hallucinations, or thought disorders.(. Though disorder: disorgani&ed, irrational thining.

+. "elusion: a belief that is clearly contradiction to reality.a. Persecution false beliefs that others are plotting andconspiring against oneself.

b. Drandeur false beliefs in one4s po/er and importance

c. Control belief that one is being controlled by othersthrough such means as radar or tiny radio receivers in the

brain.

0. -allucinations: perception of a non?e*istent ob$ect or event.

a. 6sually auditory.ii. 5egati(e symptom: a symptom of schi&ophrenia characteri&ed by the

absence of behaviors that are normally present: social /ithdra/al, lac of

affect, and reduced motivation.iii. Cogniti(e symptom: a symptom of characteri&ed by cognitive difficulties,

such as deficits in learning and memory, poor abstract thining, and poor

problem solving.b. )eritability

i. Is a heritable trait

ii. Studies suggest a large number of rare mutations play a role in the

development of schi&ophrenia.c. Pharmacology

i. "vidence suggest the positive symptoms are caused by a biochemical

disorderii. Dopamine hypothesissuggests that the positive symptoms are caused

by over activity of synapses bet/een dopaminergic neurons of the ventral

tegmental area and neurons in the nucleus accumbens and amygdala.

iii. 7rugs have one thing in commonbloc dopamine receptors.

iv. 7rug Category: production of the positive symptoms(. 5ct as dopamine agonists

+. Include amphetamine, cocaine, methylphenidate, and %?7AP5


14/22

v. Mesolimbic path/ay is believed to be involved in the symptoms

activity of dopaminergic synapses in the nucleus accumbens appears to be

a vital lin in the process of reinforcement.vi. @ibiger suggest that paranoid delusions maybe caused by increased

activity of the dopaminergic input to the amygdala.

vii. 5typical antipsychotic medications

reduce both the positive symptomsand negative symptoms of schi&ophrenia

(. Clo&apined. Jegative and cognitive symptoms are similar to those produced by brain damage

caused by several different means.

e. Brain 5bnormalities

i. Studies have found loss of brain tissue in C# and M!I scansii. @ound that the rate of tissue loss is greater in schi&ophrenic patients.

f. Possible Causes of Brain 5bnormalities

i. /pidemiology: the study of the distribution and causes of diseases inpopulations.

(. People born during the late /inter and early spring have greaterchancea. !easonality effect: the increased incidence of

schi&ophrenia in people born during late /inter and early

spring.b. Pregnant /omen might contract a viral illness during a

critical phase of their infants development

+. 'itamin 7 deficiency

g. "videncei. Behavioral evidence:

(. Children /ho later become schi&ophrenic had poorer social

ad$ustment and did more poorly in school.ii. Physical

(. )igh?steepled palate, partial /ebbing of t/o middle toes, or

especially /ide?set or narro/?set eyes.iii. Mono&ygotic #/ins

(. #/o types of mono&ygotic t/ins

a. Monochorionic

b. dichorionich. !elationship bet/een positive and negative symptoms

i. Positive symptoms may be caused by hyperactivity of dopaminergic

synapses, and the negative and cognitive symptoms may be caused bydevelopmental or degenerative changes in the brain.

ii. Jegative symptoms are caused primarily by -ypofrontality(. 7ecreased activity of the prefrontal corte*; believed to be

responsible for the negative symptoms of schi&ophrenia.

iii. PCP is an indirect antagonist of J7M5?receptor

iv. 7ecreased activation of the prefrontal corte* causes an increase in therelease of dopamine in the nucleus accumbens


15/22

v. )as a gradual onset: negative symptomsfollo/ed shortly by cognitive

symptomsseveral years later positive symptoms.

vi. =Classic> anti?schi&ophrenic drugs fail to reduce negative and cognitive

symptoms

(. Ane of the causes of these symptoms is decreased activity of

dopamine receptors in the prefrontal corte*, and drugs that bocdopamine receptors /ould mae these symptoms /orse.

vii. 5typical anti?schi&ophrenic drugsincrease dopaminergic activity in the

prefrontal corte* and reduce it in the nucleus accumbens.(. 5ripipra&oleacts as a partial agonist at dopamine receptors

a. Partial agonist: a drug that has a very high affinity for aparticular receptor but activates that receptor less than the

normal ligand does.

b. Serves as an antagonist in regions such as the nucleusaccumbens, but serves as an agonist in regions such as the

prefrontal corte*

II. )a7or affecti(e disorders: a serious mood disorder; includes unipolar depression andbipolar disorder.

a. Bipolar "isorder: a serious mood disorder characteri&ed by cynical periods of

mania and depression.i. "pisodes of mania are characteri&ed by a sense of euphora that does not

seem to be $ustified by circumstances.

b. )a7or "epressi(e "isorder $)""&: a serious mood disorder that consists of

unremitting depression or periods of depression that do not alternate /ith periodsof mania.

i. 8ithout mania

c. )eritability

i. Denes on several chromosomes may be implicated in the development ofthe affective disorders.

(. #he strongest candidate is the gene for the serotonin transporter,/hich plays a role in brain development.

d. Biological #reatments

i. Several treatments:

(. Monoamine o*idase -M5A inhibitors+. 7rugs that inhibit the reuptae of norepinephrine or serotonin

0. "lectroconvulsive therapy -"C#

1. #ranscranial magnetic stimulation2. 7eep brain stimulation

. 'agus nerve stimulation

H. Bright light therapy. Sleep deprivation

ii. Tricyclic antidepressants: a class of drugs used to treat depression;

inhibits the reuptae of norepinephrine and serotonin but also affects otherneurotransmitters; named for the molecular structure.

(. Inhibit reuptae of 2?)#

+. Monoaminergic agonist


16/22

iii. !pecific serotonin reuptake inhi,itors $!!6&: an antidepressant drug

that specifically inhibits the reuptae of serotonin /ithout affecting the

reuptae of other neurotransmittersiv. !erotonin and norepinephrine reuptake inhi,itor $!56&: an

antidepressant drug that specifically inhibits the reuptae of

norepinephrine and serotonin /ithout affecting the reuptae of otherneurotransmitters.

v. /lectrocon(ulsi(e therapy $/CT&: a brief electrical shoc, applied to the

head, that results in an electrical sei&ure; used the therapeutically toalleviate server depression.

(. 7ecrease brain activity and raises the sei&ure threshold of the

brain, maing it less liely for another sei&ure to occur

a. Increased sei&ure threshold appears to be caused by anincreased release of D5B5 and neuropeptide L.

vi. !u,genual anterior cingulate cortex $!u,genual ACC&: a region of the

medial prefrontal corte* located belo/ the =nee> at the front of the

corpus callosum; plays a role in the symptoms of depression.vii. 'agus nerve stimulation provides an indirect form of brain stimulation

viii. 2ithium: a chemical element; lithium carbonate is used to treat bipolardisorder.

(. "ffective in treating the manic phase

e. )onoamine -ypothesis: a hypothesis that states that depression is caused by alo/ level of activity of one or more monoaminergic synapses.

i. 5 monoamine antagonist produces the symptoms of depression, and

monoamine agonists alleviate them.

ii. Tryptophan depletion procedure: a procedure involving a lo/tryptophan diet and a tryptophan?free amino acid =coctail> that lo/ers

brain tryptophan and conse3uently decreases the synthesis of 2?)#.

f. "vidence for Brain 5bnormalitiesi. %ong and Short alleles of the 2?)## promoter

(. Study found that people /ith one or more short alleles had a +2

reduction in the gray matter of the region around the genu of thecorpus callosum

+. #he possession of one or t/o short alleles of the 2?)## promoter

increases e*tracellular levels of 2?)#, affects prenatal

development, and causes a reduction in the si&e of the subgenual5CC.

g. !ole of Jeurogenesis

i. #here is no /ay to measure the rate of neurogenesis in the human brain.h. Circadian !hythms

i. Most effective antidepressant treatments is sleep deprivation

(. 5n important effect of successful antidepressant treatment may beto suppress !"M sleep

ii. #otal sleep deprivation produces immediate effects

iii. )ypothesis sleep produces a substance /ith a depressogenic effect


17/22

i. !easonal affecti(e disorder $!A"&: a mood disorder characteri&ed by depression,

lethargy, sleep disturbances, and craving for carbohydrates during the /inter

season /hen days are short.i. #reatment

(. Phototherapy: treatment of S57 by daily e*posure to bright light.

a. Serves as a &eitgeber

synchroni&es the activity of thebiological cloc to the day?night cycle.III. Anxiety "isorders: a psychological disorder characteri&ed by tension, over?activity of

the autonomic nervous system, e*pectation of an impending disaster, and continuous

vigilance for danger.a. Panic "isorder: a disorder characteri&ed by episodic periods of symptoms such

as shortness of breath, irregularities in heartbeat, and other autonomic symptoms,

accompanied by intense fear.i. Anticipatory anxiety: a fear of having a panic attac; may lead to the

development of agoraphobia.

(. Agorapho,ia: a fear of being a/ay from home or other protected

places.b. *enerali+ed anxiety disorder: e*cessive an*iety and /orry serious enough to

cause disruption in people4s lives.

c. !ocial Anxiety "isorder: a disorder characteri&ed by e*cessive fear of beinge*posed to the scrutiny of other people that leads to avoidance of social situations

in /hich the person is called on to perform.

d. Causes:i. )ereditary component

ii. %actic acid and carbon dio*ide both increase heart rate and rate of

respiration, $ust as e*ercise does.iii. #he presence of one or t/o short alleles of the promoter region of the

serotonin transporter -2?)## gene is associated /ith increasedemotionality and susceptibility to depression, apparently because of

differences in the structure and activity of the amygdala and subgenual5CC.

iv. Studies suggest that the amygdala and the cingulate, prefrontal, and insular

cortices are involved in an*iety disorders.e. #reatment

i. Ben&odia&epines

(. #arget D5B5 receptors.f. ',sessi(eCompulsi(e "isorder $'C"&: mental disorder characteri&ed by

obsessions and compulsions.

i. ',session: un/anted thought or idea /ith /hich a person is preoccupied.

ii. Compulsions: feeling that one is obliged to perform a behavior, even ifone prefers not to do so.

(. Counting8 checking8 cleaning8 a(oidance.

iii. Causes(. Denetic origin

+. Chromosome K contains a region


18/22

0. "vidence suggests that infections illness can sometimes affect the

basal ganglia and produce the symptoms of AC7

1. Studies have found increased activity in the frontal lobes andcaudate nucleus.

iv. #reatment

(. Cingulotomy: the surgical destruction of the cingulum bundle,/hich connects the prefrontal corte* /ith the limbic system; helps

to reduce intense an*iety and the symptoms of obsessive?

compulsive disorder.


19/22

Chapter 1#: Autistic, Attention$De%cit&H"peractiit", Stress, andSu'stance A'use Disorders

I. Autistic "isorder: a chronic disorder /hose symptoms include failure to develop normal

social relations /ith other people, impaired development of communicative ability, lacof imaginative ability, and repetitive, stereotyped movements.

a. Aspergers disorder

generally less severe, and its symptoms do not include adelay in language development or the presence of important cognitive deficits.

b. Retts disordergenetic neurological syndrome seen in girls that accompanies

an arrest of normal brain development that occurs during infancy.i. Mutation of a gene on the < chromosome.

c. Childhood disintegrative disordernormal intellectual and social development

and then, some time bet/een the ages of + and (E years, sho/ a sever regression

into autism.d. 7iagnosis re3uires the presence of 0 categories of symptoms:

i. Impaired social interactions

ii. 5bsent or deficient communicative abilities

iii. Presence of stereotyped behaviorse. Possible Causes:

i. )eritability

(. #/in Studies+. Denetic studies indicate that autistic disorders can be caused by a

/ide variety of mutations, especially those that interfere /ith

neural development and communication.ii. Brain Pathology

(. !esult of structural or biochemical abnormalities in the brain

+. Increased number of gyri in the frontal lobes and abnormalities in

the number of neurons and in the spacing bet/een them.

0. 5bnormalities in /hite matter

matter containing short?rangea*ons /as increased

1. 5utism group has lo/er activation of the superior temporal sulcus

-S#S and the medial prefrontal corte*II. Attention"eficit9-yperacti(ity "isorder $A"-"&: a disorder characteri&ed by

uninhibited responses, lac of sustained attention, and hyperactivity; first sho/s itself in

childhood.


20/22

a. 7iagnosis re3uires or more of the nine symptoms of inattention and si* or more

of nine symptoms of hyperactivity and impulsivity that have persisted for at least

months.b. Methylphenidate -!italininhibits the reuptae of dopamine.

c. Possible causes:

i. )eritability of 57)7 ranges from H2 to K(ii. 6nderactivity of dopaminergic transmissiond. Symptoms: distractibility, forgetfulness, impulsivity, poor planning, and

hyperactivity

e. Short term memory 9 /oring memoryi. Prefrontal corte* uses this to guide thoughts and behavior, regulate

attention, monitor the effects of our actions, and organi&e plans for future

actions.III. Stress 7isorders

a. !tress: a general, imprecise term that can refer either to a stress response or to a

stressor -stressful situation.

b. %ightorflight response: a species typical response preparatory to fighting orfleeing; thought to be responsible for some of the deleterious effects of stressful

situations on health.

c. Physiology of the Stress !esponsei. Because threatening situations generally call for vigorous activity, the

autonomic and endocrine responses that accompany them are catabolic

-help mobili&e the body4s energy resources.ii. "pinephrine affects glucose metabolismnutrients stored in muscles

become available to provide energy for strenuous e*ercise.iii. *lucocorticoid: one of a group of hormones of the adrenal corte* that are

important in protein and carbohydrate metabolism, secreted especially in

times of stress.(. Cortisol

iv. Corticotrophinreleasing hormone $C6-&: a hypothalamic hormone

that stimulates the anterior pituitary gland to secrete 5C#)-adrenocorticotropic hormone.

(. Peptide secreted by the neurons of the P'J

a. Adrenocorticotropic hormone: a hormone released by the

anterior pituitary gland in response to C!); stimulates theadrenal corte* to produce glucocorticoids.

d. %ong?#erm Stress

i. Most harmful effects of stress /ere produced by the prolonged secretionof glucocorticoids

(. Increased blood pressure, damage to muscle tissue, steroid

diabetes, infertility, inhibition of gro/th, inhibition of theinflammatory responses, and suppression of the immune system.

e. "ffects on the brain

i. !esearch has sho/n that long?term e*posure to glucocorticoids destroysneurons located in field C5( of the hippocampal formation


21/22

ii. Studies have confirmed that the stress of chronic pain has adverse effects

on the brain and on cognitive behavior.

f. Posttraumatic stress disorder $PT!"&: a psychological disorder caused bye*posure to a situation of e*treme danger and stress; symptoms include recurrent

dreams or recollections; can interfere /ith social activities and cause a feeling of

hopelessness.i. #he presence of the short allele of the promoter for the 2?)# transporter

-2?)## gene produces an increased sensitivity to stress and an increased

incidence of depression and an*iety disorder.ii. Symptoms of P#S7 /ere positively correlated /ith the activation of the

amygdala and negatively correlated /ith the activation of the medial

prefrontal corte*.

g. Stress and Infectious 7iseasesi. Antigen: a protein present on a microorganism that permits the immune

system to recogni&e the microorganism as an invader.

ii. Anti,ody: a protein produced by a cell of the immune system that

recogni&es antigens present on invading microorganisms.I'. Substance 5buse 7isorders

a. 5ddictive drugs, including amphetamine, cocaine, opiates, nicotine, alcohol, PCP,and cannabis, trigger the release of dopamine in the nucleus accumbens

b. Process of addiction begins in the mesolimbic dopaminergic system and then

produces long?term changes in other brain regions that receive input from theseneurons.

c. 5egati(e 6einforcement: the removal or reduction of an aversive stimulus that is

contingent on a particular response, /ith an attendant increase in the fre3uency of

that response.d. Tolerance: the fact that increasingly large doses of drugs must be taen to achieve

a particular effect; caused by compensatory mechanisms that oppose the effect of

the drug.i. Withdrawal symptoms: the appearance of symptoms opposite to those

produced by a drug /hen the drug is suddenly no longer taen; caused by

the presence of compensatory mechanisms.e. 8ith drug abuse, the cortical regions most often activated include the 5CC and

orbitofrontal corte* -A@C and, less often, the insula and dorsolateral prefrontal

corte*.

f. !elapsei. #he mechanism that triggers relapse appears to involve the stress?induced

release of corticotropin releasing hormone -C!) in the brain.

g. Apiatesi. )eroin

ii. !eceptors in the peria3ueductal gray matter are primarily responsible for

the analgesia, those in the preoptic area are responsible for thehypothermia, those in the mesencephalic reticular formation are

responsible for the sedation, and those in the ventral tegmental area and

the nucleus accumbens are responsible for the reinforcing effects of

opiates.


22/22

h. Stimulant 7rugs: Cocaine and 5mphetamine

i. Cocaine binds /ith and deactivates the dopamine transporter proteins, thus

blocing the reuptae of dopamine after it is released by the terminalbuttons.

i. Jicotine

i. "vidence suggests that the behavior of people /ho regularly use tobaccois that of compulsive drug users.

ii. Jicotine receptors are located on the terminals of D5B5ergic neurons in

the lateral hypothalamus that form synapses /ith MC) neurons.$. 5lcohol

i. 5t lo/ doses, alcohol produces mild euphoria and has an an*iolytic effect

reduces the discomfort of an*iety

(. 5n*iolytic effects manifest themselves as a release from the

punishing effects of aversive stimuli.

ii. Both positive and negative reinforcementiii. Increases the activity of the dopaminergic neurons of the mesolimbic

system and increases the release of dopamine in the nucleus accumbensiv. Sites of action in the nervous system:(. Indirect antagonist at JM75 receptors

+. Indirect agonist at D5B5 receptors

v. !ol(2?12(0reverses alcohol into*ication by blocing the alcohol

binding site on this receptor.

. Cannabisi. Site of action of the endogenous canaboids in the brain is the CB( receptor

ii. Stimulating effect on dopaminergic neurons.

(. %o/ doses of #)C increased the release of dopamine in thenucleus accumbens

iii. )ippocampus contains a large concentration of #)C receptors.(. 5ffects peoples memory

l. )ereditary and 7rug 6sei. "nvironment plays a strong role in influencing a person to try a drug and

perhaps continue to use it recreationally, but genetics plays a stronger role

in determining /hether the person becomes addicted.ii. 7ehydrogenaseen&yme involved in metabolism of alcohol

iii. 'ariations in the genes involved in the u opiate receptor, the D5B5

receptor, and the M+ muscarinic acetylcholine receptor have been reported

to be associated /ith the lielihood of alcohol dependence.m. #herapy for 7rug 5buse

i. Methadone

ii. Buprenorphine(. Partial agonist for the u opiate receptor

+. Blocs the effects of opiates and itself produces only a /ea opiate

effectiii. 5camprosateJM75 receptor antagonist

Date post:	01-Jun-2018
Category:	Documents
Upload:	john-frandolig
View:	217 times
Download:	0 times

Exam 4 Textbook Notes

Documents