Chapter 6 Flashcards
diencephalon
includes the thalamus (inner room), epithalamus (upper room), hypothalamus (lower room), and subthalamus
thalamus
- 20 nuclei each projecting to a specific area of cerebral cortex
- a “hub”
epithalamus
- pineal gland
- stria-medullaris thalami
- habenula
- posterior commissure
hypothalamus
- 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
subthalamus
a component of the basal ganglia (subthalamic nucleus [STN])
pineal gland
- 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
stria-medullaris thalami
a white matter tract that connects the forebrain to the midbrain, and is part of the limbic system
habenula
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
posterior commisure
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)
subthalamus
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
three C’s of the function of the thalamus
consciousness, control, cognition
internal medullary lamina of the thalamus divided into 3 major nucleus groups
- 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
posterior group of the thalamus
contains the pulvinar, medial, and lateral geniculate body
anterior nuclear group of the thalamus
- 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
anterograde amnesia
- poor forming of new memories
- caused by Bilateral A lesions
retrograde amnesia
- poor recall of information from past years
- caused by Bilateral A lesions
medial nucleus group of the thalamus
- 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]
main three groups of the lateral nuclear group of the thalamus
ventral posterior nucleus (VP), ventral lateral nucleus (VL)-cerebellum, ventral anterior nucleus (VA)-basal ganglia
ventral posterior nucleus (VP) of the lateral nuclear group of the thalamus
- 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
ventral lateral nucleus (VL)-cerebellum of the lateral nuclear group of the thalamus
- 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
ventral anterior nucleus (VA)-basal ganglia of the lateral nuclear group of the thalamus
- 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
three main groups of the posterior nuclear group of the thalamus
pulvinar, lateral geniculate nucleus, medial geniculate nucleus
pulvinar of the posterior nuclear group of the thalamus
- 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)
lateral geniculate nucleus (LGN) of the posterior nuclear group of the thalamus
- input/output: receives input from optic tract/output to visual cortex
- function: vision
medial geniculate nucleus (MGN) of the posterior nuclear group of the thalamus
- input/output: receives input from inferior colliculus; output to auditory cortex
- function: hearing
optic radiations
from the lateral geniculate nucleus, neurons radiate out to the striate cortex in the occipital lobe
auditory pathway
ears –> cochlear nerve –> inferior colliculus –> medial geniculate body –> temporal cortex
visual pathway
eyes –> optic nerve –> optic chiasm –> optic tract –> lateral geniculate body –> optic radiation –> striate (visual) cortex in occipital lobe
superior colliculus
orienting movements of head and eyes
contralateral hemianesthesia, hemihypoacusis, and contralateral hemianopsia
- 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
hemihypoacusis
- can occur if the thalamic relay nuclei of the somatosensory auditory or visual pathways are damaged
- contralateral loss of hearing
- ventral lateral nucleus
contralateral hemianopsia
- can occur if the thalamic relay nuclei of the somatosensory auditory or visual pathways are damaged
- contralateral visual defect
- ventral lateral nucleus
clinical considerations concerning the thalamus
- 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
alcoholic-Korsakoff or Wernicke-Korsakoff Syndrome
damage occurs to MD and REN and may or may not have accompanying mamillary body damage; nearly always accompanied by thiamine deficiency
Dejerine-Roussy or Thalamic Pain Syndrome
- VPL and VPM damaged by stroke in left thalamus –> clinical signs in right face and body
- hemianesthesis
- astereognosis
- paroxysmal pain
- dyesthesia
- hyperpathia
paroxysmal pain
severe and intolerable occuring spontaneously
dysesthesia
highly unpleasant emotional reactions to tactile or temperature stimuli that may not be perceived, or only slightly perceived
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
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
summary of diencephalon functions
- 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
key functions of hypothalamus
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
clinical signs of alterations in endocrine and autonomic function and the hypothalamus
- appetite and weight and temperature
- metabolism
- sexual behavior
- sleep cycles
- body growth
- mood
hypothalamus is closely linked to the pituitary gland and controls the release of most hormones in the body through 2 functional systems
- hypothalamo-hypophysial tract or Magnocellular neuroendocrine system: hypothalamus-posterior pituitary
- tubero-hypophysial tract or Parvocellular neuroendocine system: hypothalamus-anterior pituitary
lateral hypothalamus
regulates hunger
ventromedial hypothalamus
regulates satiety
ghrelin signals
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
basic findings of the brain mechanisms of hypothalamus
- 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
what the lateral hypothalamus (LH) secretes when activated
melanin-concentrating hormone (MCH) orexin
- orexigens = appetite-inducing chemicals
pathway from the lateral hypothalamus
- 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)
brain mechanisms in the hypothalamus for hunger
- neuropeptide Y (NPY)
- dopamine
- paraventricular nucleus (PVN)
- agouti-related protein (AGRP)
- endocannibinoids
endocannabinoids
facilitate release of MCH and orexin
action of hunger signals on feeding circuits in the brain
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)
brain mechanisms in hypothalamus for satiety
- leptin
- CART (for cocaine and amphetamine-regulated transcript)
- Alpha-MSH
CART
- activated by cocaine and amphetamine
- system of neurons in the arcuate nucleus (in ventromedial hypothalamus)
- suppresses appetite
leptin
- inhibits neurons secreting NPY/AGRP
- activates neurons for CART/Alpha-MSH
Alpha-MSH
also released by CART neurons
action of satiety signals on hypothalamus
- 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
possible causes of eating disorders
- brain changes
- starvations: symptoms as cause or consequence
- excessive exercise
- genetic factors
treatment of eating disorders
- very difficult to treat successfully
- cognitive behavior therapy considered most effective approach
- pharmacology
- alterative therapies
criteria for anorexia nervosa
- 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
criteria for bulimia nervosa
- episodes of binge eating
- compensatory behaviors to prevent gaining weight that follow binge eating
- critical evaluation of body weight or shape
criteria for binge-eating disorder
- episodes of binge eating
- distress related to binge eting
- no use of compensatory behaviors
