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Neuro Flashcards

1
Q

central nervous system (CNS)

A

brain and spinal cord

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2
Q

hydrocephalus

A

abnormal accumulation of cerebrospinal fluid in the ventricles;
due to genetic defect, tumor, traumatic injury, or other factors;
infants and young children: abnormal enlargement of the head;
adults: headaches, loss of balance, impaired cognitive skills, and bladder control problems

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3
Q

spinal cord

A

carries information between the brain and peripheral nervous system;
consists of 31 segments that are divided into 5 groups;
damage depends on its location and severity - may produce a complete or incomplete injury

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4
Q

5 groups of the spinal cord

A

from top to bottom: cervical, thoracic, lumbar, sacral, coccygeal
CTLSC

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5
Q

damage to spinal cord at various locations

A

cervical: quadriplegia (AKA tetraplegia) - loss of sensory and/or motor functions in the trunk, upper limbs, and lower limbs;
thoracic, lumbar, or sacral: paraplegia - loss of sensory and/or motor functions in the lower limbs

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6
Q

complete injury

A

total loss of sensation and voluntary movement (paralysis)

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7
Q

incomplete injury

A

loss of sensation but no loss of movement or vice versa or a limited loss of sensation and/or movement

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8
Q

peripheral nervous system (PNS)

A

afferent nerves (AKA sensory or receptor nerves) that carry information from the sense organs to the CNS;
efferent nerves (AKA motor or effector nerves) that carry information from the CNS to the muscles and glands;
divided into the somatic nervous system and the autonomic nervous system

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9
Q

somatic nervous system

A

controls the actions of the skeletal muscles;
responsible for voluntary movement;
relays signals from the senses of sight, hearing, smell, taste, and touch

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10
Q

autonomic nervous system

A

contains nerve fibers that innervate (supply with nerves) the smooth muscles, cardiac muscle, and glands;
regulates primarily involuntary activity (digestive processes, respiration, heartbeat);
changes in level of autonomic arousal are associated with changes in emotionality;
divided into the sympathetic and parasympathetic nervous systems

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11
Q

sympathetic nervous system

A

mobilizes the body’s resources and prepares the organism for “fight-or-flight” by causing increased heart rate, pupil dilation, increased blood flow to the extremities, inhibition of digestive processes, and conversion of energy stores (fat and glycogen) to glucose

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12
Q

parasympathetic nervous system

A

deactivates responses that the sympathetic nervous system activates and is active during states of relaxation;
decreased heart rate, activation of digestive and elimination processes, and conversion of glucose to glycogen and fat

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13
Q

neuron

A

nerve cell;
information processing unit of the nervous system;
brain consists of about 100 billion neurons and about 10 times as many glial cells (also called glia), which provide physical support, nutrients, and a means of cleaning debris in the nervous system

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14
Q

3 main parts of neuron

A

1) cell body (soma): contains the neuron’s nucleus, mitochondria, and other specialized structures - responsible for most of the cell’s protein synthesis
2) dendrites: short fibers that project outward from the cell body - respond to stimulation from other neurons and carry this information toward the cell body. most neurons have many dendrites.
3) axon: fiber, sometimes quite long, that carries information away from the cell body. most neurons have only one axon, but it usually has several branches (collaterals) with each branch ending in a terminal button

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15
Q

conduction

A

the electrochemical process by which information is received and processed within a nerve cell

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16
Q

action potential

A

an electrical impulse that travels quickly through the cell;
operates on the all-or-none principle

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17
Q

all-or-none principle

A

whenever the stimulation received by a neuron from adjacent cells exceeds a minimum threshold, the resulting action potential is always of the same magnitude;
additional stimulation beyond the minimum threshold does not increase the magnitude of the action potential

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18
Q

Conduction Within Neurons

A

1) at resting potential: inside of cell is negatively charged while outside is positively charged
2) when cell receives sufficient stimulation from other cells, the electrical balance between the interior and exterior of the cell changes, and the interior of the cell becomes less negative (depolarized)
3) depolarization triggers an action potential
4) speed of conduction within a cell is affected by:
the larger the diameter of the axon, the greater the speed of the nerve impulse
the thicker the myelin, the greater the speed

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19
Q

multiple sclerosis (MS)

A

muscular weakness, impaired coordination and balance, sensory loss, and blurred or double vision;
loss of myelin

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20
Q

synaptic transmission

A

transmission of information from one neuron to an adjacent neuron

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21
Q

Transmission Between Neurons

A

release of a neurotransmitter from the presynaptic cell’s terminal button into the synapse (synaptic cleft), which is the small space between the presynaptic and postsynaptic (adjacent cell that receives neurotransmitter) cells;
the neurotransmitter is released into the synapse when the action potential arrives at the axon’s terminal button where the neurotransmitter is stored;
the released neurotransmitter then spreads across the synapse and binds to receptor sites on the dendrites or cell body of the postsynaptic neuron;
the binding of a neurotransmitter to receptors initiates the electrochemical process that may result in an action potential in the postsynaptic cell

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22
Q

reuptake

A

occurs when terminal buttons take up the excess neurotransmitter and store it for future use

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23
Q

enzymatic degradation

A

occurs when enzymes in and around the synapse break down the neurotransmitter into inactive metabolites that are ultimately removed as waste

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24
Q

neurotransmitters

A

released by neurons and transmit information to other neurons and organ and muscle cells;
can have an excitatory (increase likelihood) or inhibitory (decrease likelihood) effect on postsynaptic cells that an action potential will occur

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25
Q

neuromodulators

A

increase or decrease the sensitivity of neurons to the effects of other neurotransmitters

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26
Q

types of neurotransmitters

A

acetylcholine (ACh), dopamine, norepinephrine, serotonin, GABA, glutamate
ANDSGG

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27
Q

acetylcholine (ACh)

A

cholinergic neurons;
found in the CNS and PNS;
involved in the control of voluntary movement, learning and memory, sexual behavior, and sleep;
acts as an excitatory or inhibitory neurotransmitter depending on the location:
* excitatory effect: junctions between neurons and muscle fibers - causes muscles to contract - defect in ACh transmission to muscle receptors impairs voluntary movement
* inhibitory effect: heart, respiratory muscles - accumulation of ACh paralyzes respiratory muscles;
brain: ACh important in learning and memory - degeneration of ACh in hippocampus and certain areas of the cortex contribute to the memory loss associated with normal aging and Alzheimer’s disease

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28
Q

dopamine

A

found in several areas of the brain: basal ganglia, limbic system, frontal lobes of the cortex;
involved in movement, learning, mood, and the reinforcing effects of stimulants, opiates, and nicotine;
abnormal levels linked to: depression, Schizophrenia, Tourette’s Disorder, ADHD, Huntington’s disease, and Parkinson’s disease

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29
Q

norepinephrine

A

plays a role in mood, dreaming, learning, and autonomic responses;
abnormal levels: depression, mania, panic disorder

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30
Q

Serotonin (5-HT)

A

regulation of anxiety, mood, memory, aggression, pain, sleep, appetite, and sexuality;
low levels: depression, aggression, PTSD, OCD, bulimia;
higher-than-normal levels: Schizophrenia, ASD, decreased appetite associated with anorexia

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31
Q

Gamma-Amino Butyric Acid (GABA)

A

main inhibitory neurotransmitter in the CNS;
contributes to motor control and regulates anxiety;
abnormal levels: sleep, eating, anxiety, seizure disorders, Parkinson’s disease, and Huntington’s disease;
anti-anxiety drugs work by increasing GABA activity

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32
Q

glutamate

A

major excitatory neurotransmitter in the CNS;
involved in long-term potentiation (LTP), which is essential for the formation of memories;
abnormal levels: anxiety disorders, mood disorders, Schizophrenia;
overactivity at glutamate synapses (“excitotoxicity”): seizures, stroke, TBI, Alzheimer’s disease, Huntington’s disease, and Parkinson’s disease

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33
Q

endorphins (“endogenous morphine”)

A

act as neuromodulators;
involved in reducing feelings of pain and producing feelings of pleasure;
believed to contribute to “runner’s high” and the pain-relieving effects of acupuncture and placebos

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34
Q

hormones

A

endocrine system is comprised of endocrine (ductless) glands that secrete hormones which travel through the bloodstream and influence the functioning of organs

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35
Q

thyroxin

A

released by thyroid gland;
controls metabolism;
undersecretion: hypothyroidism (slows metabolism, causes reduced appetite), weight gain, lowered heart rate, cold intolerance, decreased sex drive, fatigue, depression, and impaired memory;
oversecretion: hyperthyroidism (AKA Grave’s Disease) - speeds up metabolism and causes increased appetite, weight loss, accelerated heart rate, nervousness and agitation, heat intolerance, insomnia, and decreased attention span

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36
Q

insulin

A

released by pancreas;
stimulates the uptake of glucose and amino acids into cells
undersecretion: diabetes, if untreated with injections of insulin, leads to high blood glucose levels (hyperglycemia) and causes increased appetite with weight loss, frequent urination, increased thirst, frequent infections, fatigue, apathy, sexual dysfunction, and, eventually, kidney failure, strokes, and heart attacks;
oversecretion: hypoglycemia - intense hunger, weakness, headaches, visual disturbances, palpitations, anxiety, depression, confusion

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37
Q

cortisol

A

secreted by the adrenal cortex (the outer layer of the adrenal gland);
helps regulate blood glucose levels;
undersecretion: Addison’s disease - muscle weakness, fatigue, low blood pressure, decreased appetite and weight loss, irritability, depression, and darkening of skin pigmentation;
oversecretion: Cushing’s disease - obesity, hypertension, impaired concentration and memory, depression, anxiety, and decreased libido
b/c cortisol is elevated by psychological stress, a cortisol blood, urine, or saliva test is sometimes used to monitor stress level

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38
Q

3 areas of the brain

A

hindbrain, midbrain, and forebrain

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39
Q

hindbrain

A

referred to as the brainstem;
contains the medulla oblongata, pons, and cerebellum

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40
Q

midbrain

A

referred to as the brainstem;
contains the reticular activating system and the substantia nigra

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41
Q

medulla oblongata

A

contains vital centers that control breathing, heart rate, blood pressure, and digestion;
stimulate coughing, swallowing, salivating, and other reflexive actions;
damage to the medulla is often fatal

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42
Q

pons

A

connects the two halves of the cerebellum;
involved in relaying sensory and motor information;
plays an important role in arousal, sleep, and respiration

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43
Q

cerebellum

A

maintains balance, coordinates movements, and controls posture;
damage can produce ataxia (slurred speech, severe tremors, loss of balance)

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44
Q

reticular activating system (RAS)

A

part of the reticular formation, which is a complex network of interconnected neurons that extends from the spinal cord to the midbrain to relay vital info;
regulates the sleep-wake transition and screens incoming sensory information, especially during sleep;
arouses higher centers in the brain when important information should be paid attention to

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45
Q

substantia nigra

A

helps control movement;
degeneration of dopamine-producing neurons in this structure contributes to Parkinson’s disease;
plays a role in reward-seeking and addictive behaviors

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46
Q

Forebrain – Subcortical Structures

A

hypothalamus, thalamus, basal ganglia, and limbic system

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47
Q

hypothalamus

A

exerts control over the autonomic nervous system and endocrine system via its influence on the pituitary gland;
.(a) maintains the body’s homeostasis by monitoring the body’s internal states and controlling temperature, metabolism, and other functions;
(b) plays a role in the control of many motivated behaviors such as drinking, feeding, sex, aggression, and maternal behavior;
(c) involved in the physical expression of strong emotions, especially rage, fear, and excitement;
contains the suprachiasmatic nucleus and the mammillary bodies

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48
Q

suprachiasmatic nucleus (SCN)

A

regulates the body’s circadian rhythms primarily through its sensitivity to light and dark;
at night, signals the pineal gland to release melatonin which induces sleepiness; then, at the first sign of daylight, it signals the pineal gland to stop secreting melatonin which alerts the body to wake up

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49
Q

mammillary bodies

A

play a role in memory;
damage to them and certain areas of the thalamus (often as the result of a thiamine deficiency caused by chronic alcoholism) causes Korsakoff’s syndrome

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50
Q

thalamus

A

acts as a “central relay station” by relaying incoming sensory information to the cortex for all of the senses except olfaction;
processes information sent between different cortical regions and between the cortex and subcortical regions;
involved in language, memory, and motor activity

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51
Q

basal ganglia

A

includes the caudate nucleus, globus pallidus, and putamen;
help make up the extrapyramidal motor system - control of posture and gross muscle movements and the coordination of movement on the right and left sides of the body;
process and relay information necessary for the control of voluntary movement, the motor (outward) expression of emotion, and sensorimotor learning;
abnormalities linked to Tourette’s Disorder, Huntington’s disease, Parkinson’s disease, Schizophrenia, mood disorders, OCD, ADHD.

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52
Q

limbic system

A

“emotional brain”;
mediates the emotional component of behavior;
contains the amygdala, septum, cingulate cortex, and hippocampus

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53
Q

amygdala

A

integrates and directs emotional reactions, attaches emotion to information it receives from the senses, and mediates defensive/aggressive behavior;
in humans, damage may cause a lack of emotional response (especially fear) to environmental stimuli and an inability to recognize facial and vocal expressions of emotion;
in monkeys, bilateral lesions in the amygdala and anterior temporal lobe produce hypersexuality and Kluver-Bucy Syndrome (reduced fear and aggression, increased docility, altered dietary habits, “psychic blindness”- inability to recognize the significance of objects or situations)

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54
Q

septum

A

inhibits emotionality;
septal lesions in rats produce septal rage syndrome (hyper-emotionality and vicious behaviors)

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55
Q

cingulate cortex

A

plays a role in the regulation of emotional responses and pain perception;
believed to play an excitatory role in emotions and in motivating behaviors;
acts as a “satisfaction center” and mediates the feelings of satisfaction that follow eating and sex

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56
Q

hippocampus

A

memory and learning;
responsible for memory consolidation (the transfer of information from short- to long-term memory);
bilateral destruction of hippocampus, amygdala, and medial temporal lobes produces severe permanent anterograde amnesia;
normal age-related declines in memory and memory loss associated with Alzheimer’s disease have been linked to a degeneration of neurons in the hippocampus

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57
Q

cerebral cortex

A

involved in a variety of higher-order cognitive, emotional, sensory, and motor functions;
more developed in humans than other animals;
divided into the right and left hemispheres, which look very similar but serve different functions

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58
Q

contralateral representation

A

the right hemisphere controls the functions of the left side of the body and the left hemisphere controls the functions of the right side of the body;
2 exceptions: olfaction and vision: olfactory information from the right nostril goes directly to the right hemisphere and vice-versa, for each eye, information from the right visual field is transmitted to the left hemisphere, while information from the left visual field is transmitted to the right hemisphere

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59
Q

lateralization of function

A

for over 90% of right-handers and over 60% of left-handers, the left hemisphere is responsible for written and spoken language, logical and analytical thinking, and the expression of positive emotions (e.g., cheerfulness, euphoria);
the right hemisphere is responsible for understanding spatial relationships, creative and holistic thinking, and the expression of negative emotions (fearfulness, sadness);
(The hemisphere that is responsible for language is referred to as the “dominant hemisphere,” while the other hemisphere is referred to as the “nondominant hemisphere.”)

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60
Q

corpus callosum

A

fibers that transfer information between the right and left hemispheres, which allows information that is available to the left hemisphere to also be available to the right hemisphere and vice-versa;
if cut, the two hemispheres seem to operate as independent brains

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61
Q

split-brain patients

A

corpus callosum had been cut to relieve severe epileptic seizures;
surgery didn’t cause noticeable changes in personality or intelligence, but did produce some unusual behaviors:
when a pic of an object was presented to a patient’s left visual field only (so that information was transmitted to the right hemisphere), the patient could not verbally identify the object or pick out the object from several objects with his/her right hand, but the patient could pick out the object with his/her left hand;
in contrast, when a picture of an object was projected to a patient’s right visual field only (so that information was transmitted to the left hemisphere), the patient could verbally identify the object and pick out the object with his/her right hand but was unable to do so with his/her left hand

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62
Q

Forebrain – Lobes of the Cerebral Cortex

A

4 lobes – frontal, temporal, parietal, occipital

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63
Q

frontal lobe

A

motor behavior, expressive language, and higher-level cognitive functions;
includes: primary motor cortex, premotor cortex, Broca’s area, prefrontal cortex

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64
Q

primary motor cortex

A

part of the pyramidal motor system;
involved in the control of voluntary movement;
lesions may produce contralateral motor weakness, paralysis, and/or apraxia

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65
Q

pyramidal motor system

A

pathway of neurons descending from the motor cortex to the brain stem and spinal cord;
mediates fine, intricate movements and the speed and strength of movement

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66
Q

premotor cortex

A

anterior to the primary motor cortex;
active during the performance of motor actions as well as during observations of others performing familiar motor actions

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67
Q

Broca’s area

A

one of the primary language areas of the brain;
in most people, is located in the left frontal lobe;
damage produces Broca’s (expressive) aphasia: deficits in the production of written and spoken language - speak slowly and with great difficulty, can use only a few words (mostly nouns and verbs), have poorly articulated speech, have difficulty repeating phrases, may have anomia (an inability to name familiar objects), and are aware of their deficits

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68
Q

anomia

A

inability to name familiar objects

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69
Q

prefrontal cortex

A

essential for higher-order cognitive functions (planning, judgment, problem-solving), certain aspects of memory (working memory and prospective memory), the regulation of emotion, and motor responses;
damage depends on location:
* dorsolateral prefrontal area: “dysexecutive syndrome” - impaired problem-solving, planning, and abstract thinking, distractibility, motor perseveration, and apathy
* medial frontal area: “pseudodepression” - apathy, lack of motivation and spontaneous movement, reduced verbal output
* orbitofrontal area: “pseudopsychopathy” - sexual disinhibition, coarse language, peculiar and facetious sense of humor, inappropriate social behavior, and a lack of concern for others;
abnormal functioning: Schizophrenia, Bipolar Disorder, and ADHD

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70
Q

temporal lobe

A

auditory processing (including receptive language) and long-term memory;
contains the auditory cortex and Wernicke’s area

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71
Q

auditory cortex

A

involved in the mediation of auditory input;
damage: auditory agnosia (an inability to distinguish sounds), auditory hallucinations, and other auditory abnormalities

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72
Q

Wernicke’s area

A

located in the left temporal lobe;
involved in the comprehension of language;
damage: Wernicke’s (receptive) aphasia - trouble understanding language, produce fluent speech that is normal sounding in terms of rate, rhythm, and articulation but makes little or no sense, display anomia and difficulties with repetition, and they are usually unaware of their deficits

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73
Q

H.M.

A

had a bilateral medial temporal lobectomy;
STM and memory for information acquired long before the operation were intact but unable to acquire new information or recall information that was acquired shortly before the surgery

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74
Q

parietal lobe

A

contains the somatosensory cortex - processes somatosensory input (touch-pressure, kinesthesia, pain, and temperature) and integrates somatosensory information with other sensory information

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75
Q

somatosensory agnosia

A

tactile agnosia (an inability to identify objects by touch), asomatognosia (an inability to recognize one’s own body parts), and/or anosognosia (an inability to recognize one’s own symptoms)

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76
Q

apraxia

A

inability to execute purposeful movements despite normal motor and sensory functions

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77
Q

ideomotor apraxia

A

can’t carry out a request to pantomime or actually perform a particular action (e.g., blow out a candle) but may be able to perform that action spontaneously

78
Q

constructional apraxia

A

can’t draw or copy simple figures or arrange blocks in a pattern

79
Q

contralateral neglect

A

loss of knowledge about or interest in one side of the body and things in the environment on the same side;
most often involves the right (nondominant) parietal lobe

80
Q

Gerstmann’s syndrome

A

caused by lesions in the left (dominant) hemisphere;
involves a combination of agraphia (difficulties with writing), acalculia (difficulties with math), finger agnosia (inability to recognize and distinguish the fingers), and left-right disorientation

81
Q

occipital lobe

A

contains the visual cortex;
involved in the processing of visual information;
total destruction = cortical blindness, less extensive damage = blind spots, persistent after-images, loss of depth perception, alexia (inability to recognize printed words), or visual agnosia (inability to recognize familiar objects by sight);
damage that affects the junction of the occipital, temporal, and parietal lobes may produce prosopagnosia (inability to recognize familiar faces)

82
Q

arcuate fasciculus

A

fibers connecting Wernicke’s to Broca’s area;
damage: conduction aphasia - comprehends language and speaks fluently but has anomia and difficulty repeating what they heard

83
Q

3 components of emotion

A

autonomic arousal, feelings, and behavior

84
Q

universal emotions

A

happiness, sadness, fear, anger, disgust, and surprise

85
Q

Papez’s circuit

A

neural circuit mediates both the experience and expression of emotion;
includes: hippocampus, mammillary bodies, anterior thalamic nuclei of the thalamus, and cingulate gyrus

86
Q

hypothalamus, amygdala, and cerebral cortex role in emotions

A

1) hypothalamus: physical expression of emotion through its effects on the autonomic nervous system and pituitary gland;
2) amygdala: attaching emotional content to memory (especially fear and anxiety), mediating defensive/aggressive behaviors, and recognizing fear in human facial expressions;
3) cerebral cortex: two hemispheres play different roles:
* left (dominant): positive emotions, while lesions can produce a “catastrophic reaction” - severe depression, anxiety, and fearfulness
* right (nondominant): negative emotions, while lesions can result in an “indifference reaction” - apathy and indifference or, in some cases, inappropriate euphoria

87
Q

James-Lange theory

A

emotions occur when people experience autonomic arousal in response to environmental stimuli and then interpret that arousal as an emotional state;
we’re afraid because we tremble and we’re sad because we cry

88
Q

Cannon-Bard theory

A

physical arousal and the experience of emotion occur together when, in response to an environmental stimulus, the thalamus simultaneously stimulates the sympathetic nervous system and cerebral cortex;
views all emotions as essentially identical in terms of physical arousal

89
Q

Schachter and Singer’s cognitive-arousal theory

A

views emotion as due to a combination of physical arousal and cognitive attributions for that arousal;
physical sensations are similar for most emotional states, and the specific emotion experienced depends the attribution for the cause of those sensations;
“epinephrine study”: environmental cues often determine our attributions for arousal

90
Q

how sex hormones are released

A

stimulation from the hypothalamus –> pituitary gland produces the gonadotropic hormones –> gonads secrete the sex hormones – estrogen and progesterone from the ovaries and testosterone and other androgens from the testes

91
Q

Sexual Development at Puberty

A

production of sex hormones is fairly low during childhood but increases during puberty, resulting in the development of the secondary sex characteristics and maturation of the reproductive organs;
onset of puberty is initiated by increased activity in the hypothalamus-pituitary-gonadal (HPG) axis;
this activity appears to be genetically programmed but is also affected by diet, physical health, climate, and other factors

92
Q

sexual dimorphism

A

differences in physical appearance between individuals of different sex in the same species

93
Q

Sexual Differences and the Brain

A

sex-related differences have been found in the size, shape, or volume of the corpus callosum, hippocampus, amygdala, and cerebellum;
may be due to differences in exposure to testosterone and other androgens during prenatal and early postnatal development

94
Q

Sex Hormones and Adult Females

A

animals: sex hormones have a strong impact on adult sexual behavior - higher an animal is on the phylogenetic scale, the lower the impact of the sex hormones and the greater the impact of other factors;
humans: link is weaker due to attitudes and beliefs, physical attraction to their partner, and other factors;
sex drive not strongly affected by menopause or the removal of the sex organs; and, when women do experience a reduction in sexual interest in these situations, testosterone is usually more effective than estrogen for restoring the sex drive

95
Q

effects of menopause

A

reduction in estrogen, progesterone, and testosterone levels;
symptoms: hot flashes, insomnia, mood swings, urinary incontinence, and vaginal changes (dryness and loss of elasticity) as well as an increased risk for osteoporosis and heart disease;
estrogen replacement therapy (ERT) and hormone replacement therapy (HRT), which combines estrogen and progesterone, alleviate many of the symptoms of menopause and reduce the risk for osteoporosis and heart disease but may increase the risk for breast cancer and produce side effects of nausea, headaches, weight gain or loss, depression, changes in libido

96
Q

Sex Hormones and Adult Males

A

effects of androgens on libido vary somewhat from person to person;
minimum level of testosterone seems to be necessary to maintain the sex drive, with levels above the minimum having little or no additional effect:
men who develop hypogonadism in adulthood have abnormally low levels of testosterone and also report a reduced sex drive (which can be restored with androgen replacement therapy);
unusually high levels of testosterone aren’t associated with a high sex drive

97
Q

5 sleep stages

A

1) transitional stage between wakefulness and sleep in which fast alpha waves (which are characteristic of an awake, relaxed state) are replaced by slower theta waves - drowsy state, muscles relax, heart rate becomes slower;
2) begins after a few minutes and is characterized by theta waves with intermittent sleep spindles and K-complexes (bursts of faster activity and higher amplitude activity, respectively) - moderately light sleep and can be easily awakened;
3) transitional stage between 2 and 4 and is marked by the appearance of large (high amplitude), slow delta waves;
4) large, slow delta waves - breathing deeply, slowed heart rate, lowered blood pressure; deep state of sleep and difficult to awaken;
5) REM sleep - rapid eye movements and EEG pattern similar to the patterns of 1 and 2. Although the sleeper’s heart and breathing rates are similar to those of an awake person, he/she is in a deep state of sleep and difficult to arouse. Consequently, REM sleep is also known as “paradoxical sleep.” Dreaming occurs during both REM and non-REM sleep but, during REM sleep, dreams are more vivid, bizarre, and emotionally laden and are more likely to be remembered when the sleeper awakens

98
Q

Age and Sleep

A

first 6 months of life: EEG shows only 2 distinct patterns — REM and non-REM sleep;
during first 2-3 months, sleep period begins with REM sleep;
sequence of REM and non-REM sleep then reverses, and total sleep time, stages 3 and 4 sleep, and REM sleep all decrease in duration from childhood to adulthood, with stages 3 and 4 and REM sleep continuing to decrease throughout adulthood;
newborns sleep 16 hours a day, preadolescents 10, and adults 8 or less hours;
during infancy, REM is 50% of total sleep period while, in adulthood, 20%;
while older adults do not require less total sleep than younger adults do, they often have more trouble falling asleep, awaken during the night more frequently, and experience an advanced sleep phase, which is a shift in the timing of sleep that involves going to sleep earlier at night and waking up earlier in the morning

99
Q

sleep deprivation

A

doesn’t produce serious maladjustment, but alters sleep patterns and can increase anxiety and irritability and impair cognitive functioning;
effects disappear when the REM-deprived person is allowed to sleep;
when REM sleep is no longer interrupted following deprivation, the person exhibits an REM rebound - spends more time than normal in REM sleep on subsequent nights

100
Q

brain structures linked to memory

A

1) hippocampus: memory consolidation (converting short-term memories into long-term memories)
2) amygdala: formation of emotional memories (linking emotions to specific stimuli and events)
3) prefrontal cortex: working memory and prospective memory (the ability to remember to do something in the future)
4) temporal lobes: storage of long-term declarative memories

101
Q

long-term potentiation (LTP)

A

observed in glutamate receptors in the hippocampus and other areas of the brain;
persistent strengthening of synapses based on recent patterns of activity - believed to underlie memory formation

102
Q

protein and memory

A

needed for the production of neurotransmitters and the growth of dendrites and axons;
STM involves a modification of pre-existing proteins and LTM involves the synthesis of new proteins;
studies have found that administering a drug that blocks the synthesis of protein or RNA (which is needed for protein synthesis) during or shortly after the time of training prevents the formation of long-term (but not short-term) memories

103
Q

sensation

A

receipt of information by the sensory receptors and translation of that information into nerve impulses that are sent to the brain

104
Q

perception

A

process of becoming aware of and interpreting what has been sensed

105
Q

physical stimuli for vision

A

light waves (electromagnetic energy) that are absorbed by photoreceptor cells in the retina of the eye

106
Q

visual pathway

A

light waves entering the eye pass through, in order, the cornea, pupil, and lens before they are received by the retina

107
Q

cornea

A

the transparent covering in front of the eye

108
Q

pupil

A

the opening within the iris (the colored part of the eye);
opens and closes to regulate the amount of entering light

109
Q

lens

A

focuses light waves on the retina, which is at the back of the eye;
contains 2 types of photoreceptors: rods & cones

110
Q

rods

A

sensitive to degree of brightness, are adapted to sensing stimuli in low levels of light, and are responsible for seeing black, white, and shades of grey;
located primarily at the periphery of the retina

111
Q

cones

A

specialized for detecting color, provide greater visual acuity than the rods, and function best in bright light;
cluster around the center of the retina, in a region called the fovea

112
Q

Young-Helmholtz trichromatic theory

A

proposes that there are 3 types of color receptors (cones) that respond to a different primary color – red, blue, or green;
applies to the first level of processing in the retina

113
Q

Hering’s opponent-process theory

A

proposes that there are 3 types of opponent-process cells – red-green, yellow-blue, and white-black;
predicts that some of these cells are stimulated by red and inhibited by green, etc., with the overall pattern of stimulation producing the various colors;
explains why we see afterimages;
applies to the second level of processing that occurs as visual signals pass from the retina to the visual cortex

114
Q

color blindness

A

often caused by a genetic defect (anomaly on X chromosome) but may also be due to an injury or disease;
affects the retina, optic nerve, or other part of the visual system

115
Q

physical stimuli for audition

A

sound waves, which are a type of mechanical energy

116
Q

Auditory Pathways

A

sound waves enter the outer ear and pass through the auditory canal to the eardrum (membrane that vibrates in response to sound waves);
vibrations are picked up and amplified by 3 small connected bones (the ossicles) and transmitted to the oval window;
movement of the oval window exerts pressure on the liquid in the cochlea (a snail-shaped tube in the inner ear);
this produces movement in the hair cells, which are the auditory receptors;
hair cells transform mechanical vibrations to neural activity, which travels via the auditory nerve to the thalamus and auditory cortex in the temporal lobe

117
Q

loudness (intensity)

A

determined by the amplitude of sound waves and is measured in decibels (db);
normal conversation = 60 db; truck traffic, lawn mowers = 90 db; pain threshold = 120 db

118
Q

pitch

A

determined primarily by the frequency of sound waves;
measured in terms of cycles per second, with 1 hertz (Hz) = 1 cycle per second;
in humans: range of audible frequencies is about 20 to 20,000 Hz

119
Q

timbre

A

tonal quality of sound and is related to a sound wave’s complexity;
makes it possible to distinguish between two different sounds that have the same loudness and pitch

120
Q

somesthetic senses

A

1) cutaneous senses: receptors that are sensitive to pain, temperature, and pressure
2) kinesthetic senses: receptors in the muscles and joints that detect body position and movement
3) vestibular senses: receptors in the inner ear that are sensitive to gravity, balance, and acceleration

121
Q

Gate-Control Theory

A

activation of large nerve fibers that carry information about touch, pressure, and vibration inhibits transmission of pain by small nerve fibers;
activation of the large fibers “closes the gate”;
activities that close the gate: massaging or applying heat or cold to the injured area, information traveling from the brain (why engaging in distracting mental activities can reduce the sensation of pain)

122
Q

neuropathic pain

A

caused by nervous system trauma, surgery, disease, and certain drugs;
phantom limb pain cause is unknown, but believed to be the result of damage to neurons in the central or peripheral nervous system - psychological factors play a role in its course and severity

123
Q

pharmacological treatments for neuropathic pain

A

antidepressants (esp the TCAs amitriptyline, doxepin, and imipramine and the SNRI venlafaxine), opioids, anticonvulsant drugs, and topical analgesics;
some evidence that transcutaneous nerve stimulation (TENS) helps reduce phantom pain for some patients

124
Q

synesthesia

A

“joining senses”;
most common form is grapheme synesthesia: numbers or letters are associated with specific colors;
limbic system, neural connections, genetic contributions

125
Q

psychophysics

A

Fechner
study of the relationship between the magnitude of physical stimuli and psychological (internal) sensations

126
Q

absolute threshold

A

weakest stimulus that a person can detect;
presenting stimuli of various intensities to many subjects for many trials, and he defined the absolute threshold as the intensity at which a physical stimulus is detected 50% of the time

127
Q

just noticeable difference (JND)
AKA difference threshold

A

smallest physical difference between two stimuli that is recognized as a difference;
vary, depending on type of stimulus and its initial intensity

128
Q

Weber’s Law

A

predicts that the JND for any stimulus increases in size in direct proportion to the magnitude of the stimulus;
example: JND for weight is 2% - this means that, if the first object weighs 50 oz, you would not notice a difference in weight unless the second object weighs at least 51 oz. however, if the first object weighs 100 oz, you would not notice a difference unless the second object weighs at least 102 oz

129
Q

Fechner’s law

A

predicts that there is a logarithmic relationship between psychological sensation and the magnitude of a physical stimulus;
the intensity of an internal sensation increases arithmetically as the intensity of the physical stimulus increases geometrically;
doesn’t work for all types of stimuli

130
Q

Stevens’s power law

A

there is an exponential relationship between psychological sensation and the magnitude of a physical stimulus, with the exponent varying for different kinds of stimuli;
magnitude estimation - asked subjects to assign numbers to stimuli based on their relative sensations;
example: subject arbitrarily assigned a value of 2 to one tone and believed a second tone was twice as loud, he/she would assign the second tone a value of 4. using this method, Stevens found that the relationship between physical stimuli and psychological sensation differs for different stimuli - doubling the intensity of a light may double the sensation of brightness, but doubling the temperature of a hot object more than doubles the sensation of heat

131
Q

structural brain imaging techniques

A

identify structural changes due to tumors, strokes, degenerative diseases, inflammation, infection, and other abnormalities;
include CT or CAT scan and MRI - both techniques provide images of cross-sections of the brain and are sensitive to tissue density

132
Q

advantages of a CT scan

A

costs less than an MRI, provides images more quickly, and, unlike an MRI, doesn’t require the patient to remain motionless for an extended period of time

133
Q

advantages of MRI

A

produces three-dimensional images, provides images with more precise detail, and doesn’t require the use of x-rays

134
Q

functional brain imaging techniques

A

provide information about brain structure and activity;
include PET, SPECT, fMRI
PET: injected radioactive material to assess neural activity by measuring regional cerebral blood flow, glucose metabolism, or oxygen consumption; mapp the distribution of neurotransmitters and identify brain dysfunction;
SPECT: similar to PET but provides images with lower resolution;
fMRI: similar to MRI but also provides information on brain activity by detecting changes in blood oxygenation

135
Q

stroke

A

cerebrovascular accident (CVA);
onset of neurological symptoms caused by an interruption or severe reduction of blood flow to the brain

136
Q

ischemic strokes

A

most common;
occur when an artery that supplies blood to the brain becomes blocked

137
Q

hemorrhagic strokes

A

occur when a weakened blood vessel in the brain ruptures or leaks

138
Q

risk factors for stroke

A

leading risk factor: hypertension;
atherosclerosis (thickening of the lining of the arterial walls), atrial fibrillation and other types of heart disease, diabetes, cigarette smoking, age over 55, male, African American race, and family history of stroke

139
Q

middle cerebral artery

A

supplies blood to parts of the frontal, temporal, and parietal lobes and the basal ganglia;
artery most often involved in a stroke;
common consequences: contralateral hemiplegia (paralysis) and hemiparesis (muscle weakness) (usually in the face and arm) and contralateral visual field loss in both eyes, aphasia if the dominant hemisphere is affected or contralateral neglect and denial of deficit if the nondominant hemisphere is affected

140
Q

anterior cerebral artery

A

supplies areas of the frontal and parietal lobes, the corpus callosum, and the caudate nucleus;
consequences: contralateral hemiplegia, usually in the leg, impaired judgment and insight, personality change, and incontinence

141
Q

posterior cerebral artery

A

supplies blood to the thalamus, temporal lobe, and occipital lobe;
consequences: cortical blindness, visual agnosia and other visual deficits, language impairment, and memory loss

142
Q

open head injury

A

when the skull is penetrated by, for example, a gunshot or knife;
symptoms are usually focal (related to the area of brain damage) and may resolve relatively rapidly;
many people with an open head injury do not lose consciousness

143
Q

closed head injury

A

occurs when a blow to the head doesn’t penetrate the skull;
usually causes more widespread damage than an open head injury and is often followed by a loss of consciousness
upon consciousness, he/she is likely to experience a combination of emotional, behavioral, physical, and cognitive symptoms

144
Q

severity measures for TBI

A

classified as mild, moderate, or severe, with score on the Glasgow Coma Scale (GCS), duration of post-traumatic amnesia (PTA), and/or duration of loss of consciousness (LOC)

145
Q

severity scores for TBI

A

1) mild: GCS: 13 to 15; PTA: <1 hour; LOC: 30 minutes or less or none
2) moderate: GCS: 9 to 12; PTA: 1 to 24 hours; LOC: 30 minutes to 24 hours
3) severe: GCS: 8 or less; PTA: more than 24 hours; LOC: more than 24 hours

146
Q

TBI prognosis

A

related to the severity and location of the injury, the person’s age and pre-injury health, and other factors;
in general, the greatest amount of recovery occurs during the first 3 months with substantial additional improvement continuing during the first year;
many individuals, esp those with a moderate or severe injury, continue to experience some physical, emotional, and/or cognitive symptoms indefinitely;
duration of post-traumatic (anterograde) amnesia is considered to be a good predictor of outcome

147
Q

postconcussional syndrome (PCS)

A

ppl with TBI (especially mild TBI) develop a PCS that lasts several months and involves multiple symptoms: dizziness, headaches, memory impairment, fatigue, and emotional instability;
would receive the DSM-5 diagnosis of Major or Mild Neurocognitive Disorder due to TBI when meets the following diagnostic criteria:
(a) symptoms meet the criteria for Major or Mild Neurocognitive Disorder
(b) evidence of a TBI with one or more of the following symptoms – loss of consciousness, posttraumatic amnesia, disorientation and confusion, neurological signs (e.g., a new onset of seizures, visual field cuts, hemiparesis)
(c) neurocognitive disorder presents immediately after the TBI or recovery of consciousness and persists past the acute post-injury period

148
Q

motor disorders

A

caused by damage to the spinal cord, the structures of the extrapyramidal motor system, or motor areas of the cortex;
Hutington’s and Parkinson’s affected by extrapyramidal motor system

149
Q

Huntington’s disease

A

degenerative disease that involves a combination of affective and personality changes, cognitive deterioration, and abnormalities in movement;
causes: autosomal dominant gene, and offspring of a person carrying the gene have a 50% chance of inheriting the disorder;
linked to abnormalities in the basal ganglia and cortex - MRI shows reduced volume in basal ganglia structures, PET shows reduced metabolic brain activity;
glutamate, ACh, GABA, and dopamine abnormalities

150
Q

onset of symptoms Huntington’s

A

first apparent between 30 - 50;
initial signs are affective (e.g., depression, anxiety, mania, emotional lability) and may be erroneously diagnosed;
followed by forgetfulness, personality changes, and motor symptoms (clumsiness, fidgeting, and incoordination);
later, athetosis (slow writing movements) and chorea (involuntary rapid, jerky movements) become increasingly prominent;
may develop dysarthria (difficulty with articulating words), dysphagia (difficulty swallowing), immobility, and Major or Mild Neurocognitive Disorder;
suicide risk is high, esp among younger individuals

151
Q

Parkinson’s disease

A

degenerative brain disorder characterized by abnormalities in movement;
caused by loss of dopamine-producing cells in the substantia nigra which affects the functioning of the basal ganglia, thalamus, and cortex;
no known cure but symptoms are temporarily alleviated by L-dopa and other drugs that increase dopamine levels in the brain

152
Q

4 primary symptoms of Parkinson’s disease

A

1) tremor: hands, arms, and legs and is often an initial symptom, “pill-rolling”: movements of the thumb and forefinger, common resting tremor
2) rigidity: muscles of the neck, arms, and legs, “cogwheel rigidity”: combo of rigidity and tremor characterized by short, jerky (ratchet-like) movements
3) postural instability: (impaired balance and equilibrium) causes unsteadiness, a stooped posture, and gait disturbances
4) bradykinesia: (slowness of voluntary movement) causes difficulty initiating and completing movements and affects both fine and gross motor functions, produces a blank (mask-like) facial expression

153
Q

mental health and Parkinson’s

A

40% have comorbid depression; and, in 20% of these cases, depressive symptoms precede the onset of motor impairments by an average of 5 years;
some develop Major or Mild Neurocognitive Disorder that involves cognitive slowing, impaired memory retrieval, and executive dysfunction

154
Q

epileptic seizure

A

caused by abnormal electrical activity in the brain that causes transient symptoms which may include a loss of consciousness, sensory changes, and/or motor disturbances;
categorized as partial or generalized

155
Q

partial (focal) seizures

A

originate in a localized area in one side of the brain and affect one side of the body (although they may spread and become generalized);
two types:
1) simple partial seizures: don’t cause a loss of consciousness and involve uncontrollable movements, sensory symptoms (e.g., paresthesias, visual or auditory hallucinations), and/or autonomic symptoms (e.g., nausea, sweating) - arise in various regions of the brain but are most often due to abnormal electrical activity in one of the lobes of the cerebral cortex, especially the temporal lobe
2) complex partial seizures: may begin with an aura, include some alteration in consciousness, and often include automatism (involuntary complex movements that may include lip smacking, involuntary chewing, or walking in circles)
temporal lobe seizures are characterized by automatisms, auditory hallucinations or other sensory phenomena, a sense of déjà vu or depersonalization, and autonomic symptoms

156
Q

generalized seizures

A

bilaterally symmetric, don’t have a focal onset;
tonic-clonic seizures: AKA grand mal seizures, involve an alteration in consciousness and include a tonic stage (stiffening of muscles in the face and limbs) followed by a clonic stage (jerky rhythmic movements in the arms and legs) - when consciousness returns, the person may be depressed, irritable, or confused and have amnesia for events that occurred during the seizure;
absence seizures: AKA petit mal seizures, brief loss of consciousness with a “vacant stare” but few or no other symptoms

157
Q

migraine headaches

A

intense, throbbing pain that is usually on one side of the head and may be accompanied by nausea or vomiting, dizziness, and sensitivity to sound, light, and odors;
triggered by a variety of factors including emotional stress or relaxation after stress; abrupt weather changes; alcohol (especially beer and red wine); and certain foods and food additives (e.g., aged meat and cheese, chocolate, MSG);
intensity may be increased by routine physical activity such as walking or climbing stairs;
theory: related to a low level of serotonin that produces a constriction of blood vessels in the brain;
treatments: nonsteroidal anti-inflammatory drugs (NSAIDs); ergotamine, sumatriptan, SSRIs, and other drugs that act at serotonin receptors; beta-blockers; and a combination of thermal biofeedback and autogenic training

158
Q

classic migraine

A

starts with an aura (specific visual, motor, or sensory symptoms)

159
Q

common migraine

A

does not begin with an aura

160
Q

tension headaches

A

dull and diffuse mild to moderate pain that is experienced as a tight band (pressure) around the head;
may be due to sustained contractions of muscles in the forehead, scalp, and neck but, for others, the cause is unknown;
abnormalities in serotonin or other neurotransmitters may be involved;
treatments: OTC and prescription pain relievers, EMG biofeedback, and, for chronic tension headaches, antidepressants

161
Q

cluster headaches

A

severe (often burning or piercing) non-throbbing pain that lasts for 15 to 90 minutes and occurs more than once each day over several weeks or months;
pain is unilateral and usually located behind one eye but may spread to the face, cheek, and/or temple;
treatments: oxygen therapy (breathing 100% oxygen through a mask), sumatriptan or other triptan, and lidocaine or other local anesthetic

162
Q

sinus headaches

A

caused by sinusitis, which is an inflammation of the membranes that line the sinuses (the cavities around the nose, eyes, and cheeks);
produce a dull throbbing pain and pressure around the eyes and in the cheeks and forehead, with the pain being worsened by a sudden movement of the head, leaning forward, and cold, damp weather;
common accompanying symptoms: runny or stuffy nose, coughing, sneezing, a mild to moderate fever, sore throat, and fatigue;
treated with antihistamines, decongestants, antibiotics, and corticosteroids

163
Q

quantitative genetic methods

A

calculate the net impact of genetic and environmental variables on specific traits

164
Q

molecular genetic methods

A

used to identify which genes are responsible for specific traits

165
Q

agonists

A

produce effects similar to those produced by a neurotransmitter

166
Q

inverse agonists

A

produce effects opposite to those produced by a neurotransmitter or agonist

167
Q

antagonists

A

produce no activity on their own but reduce or block the effects of a neurotransmitter or agonist

168
Q

factors influence a person’s response to drugs

A

older age is related to a decrease in metabolism, which can extend the half-life of some drugs and create an increased risk for toxicity;
Asians and African Americans have been found to metabolize certain isoenzymes more slowly than Caucasians, resulting in greater sensitivity to both the therapeutic and side effects of medications like benzodiazepines, lithium, neuroleptics, and some antidepressants;
good strategy when prescribing drugs for older adults and members of certain racial/ethnic groups is to start with a low dose and gradually titrate to higher doses as needed

169
Q

antidepressants

A

tricyclics (TCAs);
selective serotonin reuptake inhibitors (SSRIs);
monoamine oxidase inhibitors (MAOIs);
newer antidepressants (e.g., serotonin-norepinephrine reuptake inhibitors and norepinephrine-dopamine reuptake inhibitors)

170
Q

Tricyclic Antidepressants (TCAs)

A

work by blocking the reuptake of norepinephrine and serotonin at synapses;
imipramine (Tofranil)
clomipramine (Anafranil)
amitriptyline (Elavil)

171
Q

uses for TCAs

A

most effective for MDD that involves feelings of hopelessness and an inability to experience pleasure - particularly useful for relieving vegetative (physical) symptoms such as changes in appetite, sleep disturbances, and decreased energy;
also used to treat Dysthymic Disorder, panic attacks, Agoraphobia, OCD (esp clomipramine), enuresis (esp imipramine), and chronic pain (esp neuropathic pain and headaches);
effects of the TCAs on norepinephrine and depression support the catecholamine hypothesis which predicts that depression is due to lower-than-normal levels of this neurotransmitter

172
Q

side effects of TCAs

A

anticholinergic effects (e.g., dry mouth, constipation, urinary retention, blurred vision), gastrointestinal symptoms, impaired sexual functioning, drowsiness, weight gain, and confusion and memory impairment (especially in older adults) - many subside within a few weeks and, if not, they may be eliminated by lowering the dosage;
less common but more serious: cardiovascular effects such as tachycardia, orthostatic hypotension, and arrhythmia;
b/c of their toxicity in overdose, the TCAs must be prescribed with caution for individuals who have heart disease or who are suicidal

173
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A

increase the availability of serotonin at synapses;
fluoxetine (Prozac);
sertraline (Zoloft);
paroxetine (Paxil)

174
Q

uses for SSRIs

A

MDD, Dysthymic Disorder, OCD, Panic Disorder, Social Phobia, binge eating, and premature ejaculation

175
Q

side effects for SSRIs

A

nausea, loss of appetite, impaired sexual functioning, dizziness, agitation, headaches, and insomnia;
combining an SSRI with a TCA, MAOI, or other drug that increases the level of serotonin can cause serotonin syndrome - altered consciousness, agitation, and other changes in mental status; autonomic changes (e.g., sweating, dilated pupils); and tremor, muscle rigidity, akathisia (motor restlessness), and other neuromuscular abnormalities;
have a quicker onset of effectiveness, cause fewer and less severe side effects, and are safer in overdose: produce few or no anticholinergic effects, are less likely to cause sedation and cognitive impairment, and have fewer cardiovascular effects than TCAs

176
Q

Monoamine Oxidase Inhibitors (MAOIs)

A

block the action of an enzyme that breaks down norepinephrine and serotonin, making these neurotransmitters more available at synapses;
phenelzine (Nardil);
tranylcypromine (Parnate)

177
Q

uses for MAOIs

A

atypical depression (increased appetite, hypersomnia, rejection-sensitivity, mood reactivity, and symptoms of anxiety and/or hypochondriasis) as well as depression that has not responded to other antidepressants

178
Q

side effects for MAOIs

A

dry mouth and other anticholinergic effects, nausea, weight gain, dizziness, sedation or insomnia, tremor, tachycardia, and impaired sexual functioning;
MAOI overdose can cause seizures, coma, and cardiac arrest;
combining an MAOI with certain other drugs or with foods containing the amino acid tyramine can cause a potentially fatal hypertensive crisis: elevated blood pressure, severe headache, stiff neck, nausea and vomiting, and tachycardia or bradycardia. foods to avoid: beer, wine, aged cheese, smoked meat, soy sauce, avocados, bananas, eggplant, tomatoes, and yogurt

179
Q

serotonin-norepinephrine reuptake inhibitors (SNRIs)

A

venlafaxine (Effexor);
duloxetine (Cymbalta);
desvenlafaxine (Pristiq);
MDD, Generalized and Social Anxiety Disorders, and Panic Disorder;
side effects: sleep disturbances, nausea and other gastrointestinal problems, sexual dysfunction, headache, and increased blood pressure

180
Q

norepinephrine-dopamine reuptake inhibitors (NDRIs)

A

bupropion (Wellbutrin, Zyban);
depression and smoking cessation;
side effects: dry mouth, agitation, insomnia, itching, skin rash, and decreased appetite;
bupropion can aggravate pre-existing seizures or psychosis and cause anaphylaxis (a severe allergic reaction)

181
Q

hyperphagia

A

excessive eating, and extreme obesity leading;
lesions in the ventromedial and lateral hypothalamus;
VMH satiety center

182
Q

aphagia

A

complete cessation of eating

183
Q

adipisia

A

complete cessation of drinking

184
Q

stereognosis

A

process of identifying objects by touch

185
Q

paraprosopia

A

visual hallucinations of terrifying faces

186
Q

prosopagnosia

A

inability to recognize familiar faces

187
Q

Geschwind-Galaburda hypothesis

A

explain sex differences in cognitive abilities by relating them to lateralization of brain function;
differences in the rates of maturation between the two cerebral hemispheres is mediated by circulating testosterone levels in a fetus’ developing brain and impact hemispheric dominance, with high concentrations or excessive testosterone delaying development in the left hemisphere relative to the right hemisphere and male brains maturing later than females;
results in left-handedness, immune dysfunction, and developmental disorders of language and speech

188
Q

alexia

A

loss of ability to read

189
Q

agraphia

A

loss of ability to write

190
Q

neuropsychiatric manifestations of stroke

A

depression, pseudobulbar affect (frequent and easily provoked spells of emotion (typically manifested by laughing and crying)), and a catastrophic reaction (intense desperation and frustration that is uncharacteristic of the individual’s prestroke personality)

EPPP (11 decks)

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