Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSYC 424: Neuropsychology > Chapter 6 > Flashcards

Chapter 6 Flashcards

1
Q

diencephalon

A

includes the thalamus (inner room), epithalamus (upper room), hypothalamus (lower room), and subthalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

thalamus

A
  • 20 nuclei each projecting to a specific area of cerebral cortex
  • a “hub”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

epithalamus

A
  • pineal gland
  • stria-medullaris thalami
  • habenula
  • posterior commissure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hypothalamus

A
  • 22 small nuclei involved in feeding, sexual behavior, sleeping, temperature regulation, emotional behavior, and movement
  • connects to pituitary gland
  • ventral component of diencephalon surrounding third ventricle
  • small size but wide range of functions
  • rarely affected by stroke (rich blood supply)
  • can be affected by: tumors, developmental disorders, infections, alcoholism, head trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

subthalamus

A

a component of the basal ganglia (subthalamic nucleus [STN])

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pineal gland

A
  • function not well understood in humans
  • important for gonadal functions and circadian rhythms (a lot of melatonin secretion)
  • prone to calcification
  • early tumors in this gland (which overstimulate the gland) depress gonadal functions and delay puberty
  • early lesions lead to precocious (earlier) onset of puberty (suggestion: this gland plays an inhibitory role in gonadal functions)
  • secretes melatonin
  • secretes DMT
  • makes neurosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

stria-medullaris thalami

A

a white matter tract that connects the forebrain to the midbrain, and is part of the limbic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

habenula

A

receives the stria medullaris thalami
- in turn it projects to areas in the midbrain involved in motivational and emotional behaviors (areas that have dopamine, noreadrenaline, serotonin, and acetylcholine cell bodies)
- a part of a neural network tha tincludes limbic and olfactory systems that are concerned with mechanisms of emotion and behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

posterior commisure

A

connect one pre-tectal region to the other
- important for vertical gaze and pupillary light reflex
- tumors in the region during adulthood usually interfere with vertical gaze
- the tumor also pressures the posterior commissure (PC), leading to loss of indirect or consensual light reflex (this condition known as Parinaud’s syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

subthalamus

A

from a functional point of view, it is part of the basal ganglia system
- some of the treatments of Parkinson’s involve deep brain stimulation of the subthalamic nucleus
- under the thalamus and above the substantia nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

three C’s of the function of the thalamus

A

consciousness, control, cognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

internal medullary lamina of the thalamus divided into 3 major nucleus groups

A
  • medial group –> on the medial side ofo the internal medullary lamina
  • lateral group –> on the lateral side of the internal medullary lamina
  • anterior group –> bordered by the 2 arms of the “Y” of the internal medullary lamina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

posterior group of the thalamus

A

contains the pulvinar, medial, and lateral geniculate body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

anterior nuclear group of the thalamus

A
  • input/output: have heavily reciprocal connections with hypothalamus, specifically mammillary bodies; receives input from hippocampus via fornix; connects to cingulate gyrus
  • function: limbic/emotional and memory
  • clinical significance: bilateral A lesions –> memory impairments –> anterograde amnesia; retrograde amnesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

anterograde amnesia

A
  • poor forming of new memories
  • caused by Bilateral A lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

retrograde amnesia

A
  • poor recall of information from past years
  • caused by Bilateral A lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

medial nucleus group of the thalamus

A
  • main nucleus in the mediodorsal nucleus (MD)
  • input/output: receives input from subcortical structures that are involved in the processing of signals related to emotional/affective behaviors (e.g., amygdala), reciprocally connected with the prefrontal cortex, and the expression of motor behaviors via output to the substantia nigra
  • function: control of emotion and complex behaviors (e.g., decision-making and judgment)
  • clinical significance: bilateral MD lesions –> syndrome characterized by indifference and poor motivation; lack of insight (unaware that they have a problem); apathy (indifference and incapacity to keep an ongoing activity) [symptoms similar to frontal lobe syndrome]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

main three groups of the lateral nuclear group of the thalamus

A

ventral posterior nucleus (VP), ventral lateral nucleus (VL)-cerebellum, ventral anterior nucleus (VA)-basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ventral posterior nucleus (VP) of the lateral nuclear group of the thalamus

A
  • VPL: for spinothalamic and medial lemniscal systems
  • VPM: for trigeminal sensory; therefore, unilateral lesions lead to contralateral loss of sensation on both the body and the face
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ventral lateral nucleus (VL)-cerebellum of the lateral nuclear group of the thalamus

A
  • receives input from cerebellum
  • connects to motor cortex
  • therefore, function is motor and clinical signs after a stroke resemble those of cerebellar lesions, e.g., dysarthria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ventral anterior nucleus (VA)-basal ganglia of the lateral nuclear group of the thalamus

A
  • receives input from basal ganglia
  • connects to premotor cortex
  • therefore, function is motor and clinical signs after a stroke resemble those of basal ganglia movement disorders, e.g., dystonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

three main groups of the posterior nuclear group of the thalamus

A

pulvinar, lateral geniculate nucleus, medial geniculate nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

pulvinar of the posterior nuclear group of the thalamus

A
  • input/output: receives input from superior colliculus and pretectum; connected (output) to lateral geniculate body; connects reciprocally to extensive areas of parietal, occipital, and temporal cortices
  • function: visual (especially those related to eye movements in visual attention, i.e., damage leads to visual neglect); language (speech mechanisms and language)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

lateral geniculate nucleus (LGN) of the posterior nuclear group of the thalamus

A
  • input/output: receives input from optic tract/output to visual cortex
  • function: vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

medial geniculate nucleus (MGN) of the posterior nuclear group of the thalamus

A
  • input/output: receives input from inferior colliculus; output to auditory cortex
  • function: hearing
26
Q

optic radiations

A

from the lateral geniculate nucleus, neurons radiate out to the striate cortex in the occipital lobe

27
Q

auditory pathway

A

ears –> cochlear nerve –> inferior colliculus –> medial geniculate body –> temporal cortex

28
Q

visual pathway

A

eyes –> optic nerve –> optic chiasm –> optic tract –> lateral geniculate body –> optic radiation –> striate (visual) cortex in occipital lobe

29
Q

superior colliculus

A

orienting movements of head and eyes

30
Q

contralateral hemianesthesia, hemihypoacusis, and contralateral hemianopsia

A
  • can occur if the thalamic relay nuclei of the somatosensory auditory or visual pathways are damaged
  • loss of sensation in half of the body
  • ventral lateral nucleus
31
Q

hemihypoacusis

A
  • can occur if the thalamic relay nuclei of the somatosensory auditory or visual pathways are damaged
  • contralateral loss of hearing
  • ventral lateral nucleus
32
Q

contralateral hemianopsia

A
  • can occur if the thalamic relay nuclei of the somatosensory auditory or visual pathways are damaged
  • contralateral visual defect
  • ventral lateral nucleus
33
Q

clinical considerations concerning the thalamus

A
  • contralateral hemiasnesthia, hemihypoacusis, hemianopsia
  • both abnormal voluntary and involuntary movements can occur with thalamic pathology
  • memory impairments can occur with thalamic pathology, most notable being the alcoholic-Korsakoff or Wernicke-Korsakoff Syndrome
  • somatosensory changes following pathology in the posterior and ventral thalamus; Dejerine-Roussy or thalamic pain syndrome
34
Q

alcoholic-Korsakoff or Wernicke-Korsakoff Syndrome

A

damage occurs to MD and REN and may or may not have accompanying mamillary body damage; nearly always accompanied by thiamine deficiency

35
Q

Dejerine-Roussy or Thalamic Pain Syndrome

A
  • VPL and VPM damaged by stroke in left thalamus –> clinical signs in right face and body
  • hemianesthesis
  • astereognosis
  • paroxysmal pain
  • dyesthesia
  • hyperpathia
36
Q

paroxysmal pain

A

severe and intolerable occuring spontaneously

37
Q

dysesthesia

A

highly unpleasant emotional reactions to tactile or temperature stimuli that may not be perceived, or only slightly perceived

38
Q

in Dejerine-Roussy or Thalamic Pain Syndrome, clinical signs 3-5 in terms of mechanisms seem paradoxical, or not understood and may take time (2-3 weeks) to develop

A

possible explanations:
- a few surviving and/or damaged neurons in the injured left thalamus are sending abnormal messages to the cortex
- there may be pathways not known about carrying information that bypasses the somatosensory thalamus (VPL + VPM)
- peripheral stimuli to tissue receptors may trigger dual (1) somatosensory messages such as pain, temperature, and touch and (2) emotional messages
- somatosensory message is altered by thalamic damage, but the emotional message is perceived in other brain areas not damaged

39
Q

summary of diencephalon functions

A
  • regulating states of sleep and wakefulness via the epithalamus and pineal gland (melatonin)
  • sensation and pain via the ventrolateral nuclei
  • vision via the lateral geniculate body
  • hearing via the medial geniculate body
  • support of motor systems: the thalamus receives input from cerebellum (VL nuclei) and basal ganglia (VA nuclei) and connect them to motor cortex
  • learning and memory: anterior thalamic nuclei are connected via the fornix to the hippocampus
  • language and speech: the link of the thalamus to motor systems gives it a key role in speech (damage to motor thalamic nuclei could cause slurred or impaired speech); the link of the pulvinar of the thalamus to cortical language areas gives it a role in language –> damage to those areas could give rise to some forms of aphasias, but they tend to recover quickly
  • thalamic nuclei have strong reciprocal connections with the cerebral cortex, forming thalamo-cortico-thalamic circuits that are believed to be involved with consciousness
  • the thalamus plays a major role in regulating arousal, the level of awareness, and activity
  • extensive bilateral damage to the thalamus can lead to permanent coma
40
Q

key functions of hypothalamus

A

homeostasis (regulating and maintaining normal body function)
- this includes: body weight and temperature; food, salt, and water intake; sexual cycles, orientation, and onset of puberty; circadian rhythms; body growth; stress response

41
Q

clinical signs of alterations in endocrine and autonomic function and the hypothalamus

A
  • appetite and weight and temperature
  • metabolism
  • sexual behavior
  • sleep cycles
  • body growth
  • mood
42
Q

hypothalamus is closely linked to the pituitary gland and controls the release of most hormones in the body through 2 functional systems

A
  • hypothalamo-hypophysial tract or Magnocellular neuroendocrine system: hypothalamus-posterior pituitary
  • tubero-hypophysial tract or Parvocellular neuroendocine system: hypothalamus-anterior pituitary
43
Q

lateral hypothalamus

A

regulates hunger

44
Q

ventromedial hypothalamus

A

regulates satiety

45
Q

ghrelin signals

A

when the stomach is empty, the ghrelin (hormone produced in the stomach) relays singlas from the stomach to the hypothalamus (lateral hypothalamus) to start a meal

46
Q

basic findings of the brain mechanisms of hypothalamus

A
  • after lateral hypothalamus (LH) was destroyed, animals stopped eating or drinking
  • electrical stimulation of same region would produce eating, drinking, or both behaviors
  • lesions of ventromedial hypothalamus produced overeating that led to gross obesity, whereas electrical stimulation suppressed eating
47
Q

what the lateral hypothalamus (LH) secretes when activated

A

melanin-concentrating hormone (MCH) orexin
- orexigens = appetite-inducing chemicals

48
Q

pathway from the lateral hypothalamus

A
  • MCH goes to thalamus, cerebral cortex, and periaqueductal gray matter
  • Orexin goes to reticular formation, locus coeruleus, and neurons in spinal cord that control the ANS (has effects on metabolism)
49
Q

brain mechanisms in the hypothalamus for hunger

A
  • neuropeptide Y (NPY)
  • dopamine
  • paraventricular nucleus (PVN)
  • agouti-related protein (AGRP)
  • endocannibinoids
50
Q

endocannabinoids

A

facilitate release of MCH and orexin

51
Q

action of hunger signals on feeding circuits in the brain

A

ghrelin secretion increases when stomach empties, meanwhile neuropeptide Y (NPR) in the ventrolateral medulla –> arcuate nucleus with neuropeptide Y (NPY) and agouti-related protein (AGRP) –> lateral hypothalamus with endocannabinoids that facilitate release of MCH and orexin (has an excitatory effect on eating, reduction of metabolic rates) OR paraventricular nucleus –> brain stem nuclei that control ANS (decreased insulin secretion, decreased breakdown of fatty acids, decreased body temperature)

52
Q

brain mechanisms in hypothalamus for satiety

A
  • leptin
  • CART (for cocaine and amphetamine-regulated transcript)
  • Alpha-MSH
53
Q

CART

A
  • activated by cocaine and amphetamine
  • system of neurons in the arcuate nucleus (in ventromedial hypothalamus)
  • suppresses appetite
54
Q

leptin

A
  • inhibits neurons secreting NPY/AGRP
  • activates neurons for CART/Alpha-MSH
55
Q

Alpha-MSH

A

also released by CART neurons

56
Q

action of satiety signals on hypothalamus

A
  • gastrointestinal system –> inhibitory effects of PYY secretion after meal –> arcuate nucleus with NPY/AGRP and CART/Alpha-MSH –> lateral hypothalamus with endocannabinoids that facilitate release of MCH and orexin (has an excitatory effect on eating, reduction of metabolic rates) OR paraventricular nucleus –> brain stem nuclei that control ANS (decreased insulin secretion, decreased breakdown of fatty acids, decreased body temperature)
  • adipose tissue –> leptin secretin by well-nourished fat cells to paraventricular nucleus then to brain stem nuclei that control ANS AND excitatory effect of leptin to arcuate nucleus then to lateral hypothalamus
57
Q

possible causes of eating disorders

A
  • brain changes
  • starvations: symptoms as cause or consequence
  • excessive exercise
  • genetic factors
58
Q

treatment of eating disorders

A
  • very difficult to treat successfully
  • cognitive behavior therapy considered most effective approach
  • pharmacology
  • alterative therapies
59
Q

criteria for anorexia nervosa

A
  • restricting eating that leads to low body weight
  • fear of gaining weight
  • persistent behavior to prevent weight gain
  • disturbance in self-perception or failure to perceive seriousness of low body weight
60
Q

criteria for bulimia nervosa

A
  • episodes of binge eating
  • compensatory behaviors to prevent gaining weight that follow binge eating
  • critical evaluation of body weight or shape
61
Q

criteria for binge-eating disorder

A
  • episodes of binge eating
  • distress related to binge eting
  • no use of compensatory behaviors

PSYC 424: Neuropsychology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions