Reticular formation, limbic, hypothalamus, hippocampus, basal ganglia
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| What is the reticular formation? | Collection of nuclei running vertically throughout the brainstem in three columns
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| What is the function of the reticular formation? | Control of skeletal muscle, pain modulation, control of autonomic and endocrine system, circadian rhythms, and consciousness
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| What structure receive influence from the reticular formation for motor responses? | Red nucleus, substantia nigra, subthalamus, basal ganglia, cerebellum
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| For sensory, what tract sends in info to the reticular formation? | Spinal: spinoreticular, cranial: bulboreticular
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| What tract does the reticular formation send info to influence ANS? | Reticulobulbar or reticularspinal
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| What is the reticular activating system? | Network of neurons that project to cortex that uses external stimuli to alert people to bring them to consciousness
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| How does the reticular formation incorporate a stimulus for consciousness? | Stimulus (alarm clock, bright light, etc.) carried to RF by appropriate nerves and feed into RAS
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| What is an example of RAS? | Ammonia smelling salts stimulate CN V sensory fibers in nose and can be used to rouse an unconscious patient
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| What is the implication of RAS if it deals with consciousness? | General anesthetics work to suppress this system
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| What is the limbic system in charge of? | Emotion, mood, behavior, and memory
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| What are the main components depicted in the following figure? | Amygdaloid body, olfactory bulb, hippocampus, fornix, limbic cortex
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| What does the amygdaloid body control? | Behavior, mood, emotion
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| What does the olfactory bulb do? | Sends info to the amygdaloid body
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| What does the hippocampus do? | Involved in learning new information and in recent memory
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| What does the fornix do? | Contains output fibers of the hippocampus
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| What does the limbic cortex do? | Involved in behavioral control, learning, and brief storage of memories
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| What are mammillary bodies? | Part of hippocampus, travels through mammillothalamic tract to anterior nucleus of thalamus to function with hippocampus in memory
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| What does the amygdala send info to? | Facial nerve, hippocampus, hypothalamus, limbic cortex, thalamus, reticular formation, temporal/parietal/occipital lobe
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| What structure is involved in short term memory becoming long term? | Amygdala
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| How does a short term memory become long term? | Process of consolidation must occur through rehearsal and meaningful association which involves changes in the neurons
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| What would higher the increase in amygdalar activity? | Stronger emotional component of info. Activity correlates with retention and retrieval of the memory
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| What emotions are attributed to the amygdala? | Anger or rage
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| What structure in the brain controls anger produced in amygdala? | Prefrontal cortex, which applies judgment and awareness of underlying issues to the emotions
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| How does the stimulation of the hypothalamus and amygdala compare? | Stimulation can cause same effects in both strucgures
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| What can destruction of the amygdala result in? | Decreased aggression, impaired emotional recognition and emotional learning, increased weight gain, increased sex drive, anxiety, and depression
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| How can destruction of the amygdala result in decreased aggression? | Anger feelings produced in amygdala, so without amygdala, there would be no anger
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| Why is there impaired emotional recognition and learning when the amygdala is destroyed? | Amygdala is involved in emotional learning so lesion would prevent attachment of emotional meaning to sensory stimuli
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| What is an example of impaired emotional recognition/learning? | Theory in autism for social deficits is damaged amygdala - why they don't connect faces with comfort, food, or water → don't form social bonds necessary for normal developments
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| How does a lesion in the amygdala induce anxiety? | Part of amygdala contains GABAergic neurons with a high density of GABA receptors
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| How does a lesion in the amygdala induce depression? | Many projections from reticular system to amygdala release serotonin in amygdala - imbalance of NT release in amygdala (decreased serotonin) can lead to depression
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| What kind of functions does the hypothalamus have | Vegetative, endocrine, and behavioral functions
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| What is the relationship between functions of the hypothalamus and hypothalamic area? | Functions of the hypothalamus are dependent on which hypothalamic area is active
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| How is hunger regulated in the hypothalamus? | Medial - satiety center. Lateral - initiation of eating
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| For hunger, what would happen if there was a lesion in the ventromedial hypothalaimc nuclei? | Voracious appetite - can't stop eating
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| For hunger, what would happen if there was a lesion in the lateral hypothalaimc nuclei? | Loss of appetite → weight loss
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| What emotions are associated with the hypothalamus? | Fear and rage
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| What areas of the hypothalamus promote tranquility and rage? | Medial - tranquility, lateral - rage
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| Where is the hippocampus? | Temporal lobe
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| What is the function of the hippocampus? | Memory and learning
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| What is the main pathway associated with memory and learning | Hippocampus → fornix → mammarillary bodies → anterior nucleus of thalamus → limbic cortex → hippocampus
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| Mammillary bodies are relay centers for olfactory info, what is the implication of this? | Memories are closely associated with smell - considered a survival function → reminds us how bad food smells
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| What kind of memories are formed with the hippocampus? | Formation of new memories - not recalling distant memories
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| What would happen if hippocampus were to be removed? | Can't remember anything after removal of hippocampus. Can watch same movie over and over again and feel like new.
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| What is another disorder related to the pathway associated with memory and learning? | Korsakoff's syndrome
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| What is Korsakoff's syndrome? | Memory disorder caused by deficiency of vitamin B1, commonly from alcoholism
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| What is the implication of deficiency of B1? | Affects cells with highest metabolic need → shrinkage of anterior thalamic nucleus and mammillary bodies
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| What are the symptoms of Korsakoff's syndrome? | Anterograde amnesia, confabulation
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| What is anterograde amnesia? | Difficulty in processing memory of events occuring after a traumatic incidence
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| What is retrograde amnesia? | Difficulty remembering events that occured before a brain disruption
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| What is confabulation? | Plausible but imagined memory that fills in gaps in what is remembered
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| The hippocampus is also active in spatial memory and navigation, what is the implication of this? | London taxi drivers who must remember a large number of place,s routes, etc → larger hippocampus than general public
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| Where is the basal ganglia located? | They are masses of grey matter lateral and caudal to the thalamus
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| What are the structures that make up the basal ganglia? | Caudate nucleus, putamen, globus claustrium
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| What is the neostriatum? | Caudate nucleus + putament
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| What is the lentiform nucleus? | Putamen + globus palidus
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| What is the corpus striatum? | Caudate nucleus + putament + globus pallidus
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| What are the parts of the globus pallidus? | Globus pallidus internal (medial), globus pallidus external (lateral)
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| What structures work closely with the corpus striatum and are considered to be part of the basal ganglia? | Subthalamus and substantia nigra
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| What is the function of the claustrium? | No known function
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| What makes up the caudate nucleus? | C shaped → anterior head, body that makes spine of C, posterior tail
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| Where is the caudate nucleus? | Above thalamus
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| What structures does the internal capsule separate? | Caudate and lentiform nuclei
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| What is at the tip of the tail of the caudate nucleus? | Amygdaloid nucleus
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| What two parts make up the substantia nigra? | Pars compacta - contain dopamine and more neurons, Pars reticulara - contain GABA, less neurons and project to superior colliculi and parts of the thalamus
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| What is the importance of the internal capsule? | Anything that has to go to and from the cortex passes through there
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| What happens if there's a tumor in that area? | Squeezes fibers passing through which starts to affect face but then paralysis of limbs from all fibers being pressed.
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| Why can nothing be done if theres a tumor in that area? | Too deep
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| What is predominantly involved in regulation of motor control? | Corpus striatum
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| What are the two main functions of the basal ganglia? | Helps cortex execute learned patterns of movement and plans sequential movements
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| What kind of movements would be considered a learned pattern? | Writing, throwing a ball
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| What would be an example of planning of sequential movements? | See lion - turn around - run - climb tree
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| What kind of movement would you see if there is a problem with the basal ganglia? | Resting tremor, jerking movements
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| Why would there be unconscious proprioception? | Problem with cerebellum - conscious would be if it reached cortex
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| Why would there be a problem with conscious proprioception? | Inferior cerebellar peduncle damage
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| What are the two prominent pathways from input to output nuclei through basal ganglia? | Direct and indirect
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| How does information flow for the direct pathway? | Travels from neostriatum directly to internal segment of the globus pallidus or substantia nigra pars reticulata
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| How does information flow for the indirect pathway? | Takes detour from striatum, first to external segment of globus pallidus and then to subthalamic nucleus before reaching internal segment of globus palliidus or substantia pars reticulata
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| What is the output of the basal ganglia? | Towards frontal lobe, particularly pre-motor and supplementary motor cortex
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| What is the function of the direct and indirect pathway? | Direct - facilitates cortical output, indirect - inhibits thalamus, aggravating cortical output
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| What NT are used for excitatory and inhibitory actions of the pathway? | Excitatory - glutamate, inhibitory - GABA
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| If lower motor neurons receive input from upper motor neuron, how is it connected to basal ganglia? | Message from basal ganglia will go out of GPi then goes to thalamus then goes to cortex (upper motor neurons) which send to lower motor neurons
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| What are the three main conditions with dysfunction of the basal ganglia? | Parkinson's, huntington's, hemiballismus
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| What is the pathology behind Parkinson's? | Degeneration of dopaminergic neurons within substantia nigra pras compacta
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| What are the symptoms of Parkinson's? | Rigidity, resting tremor, akinesia, bradykinesia, hypokinesia, unblinking stare, losing autonomic movements of face and eyes, mask-like expression, dementia, loss of postural reflexes, affected gait
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| What is akinesia? | Difficulty initiating movements which can progress into speech difficulties
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| What is bradykinesia? | Gradual loss of spontaneous movement and slow voluntary
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| What is intentional tremor a sign of? | Cerebellar damage
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| What does it mean loss of postural reflexes? | Forward bending of the head and trunk - flexion of elbows, hips, and knees
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| How does Parkinson's affect gait? | Akinesia makes it difficult for patient to begin walking and once they start, stopping is difficult
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| What does a combo of bradykinesia and hypokinesia gait look like? | walking steps short and shuffling, with hands in front of the body
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| What is the hypothesis behind Parkinson's | Inhibition of GPe within indirect pathway → disinhibition of STN →increased basal ganglia output nuclei (GPi/SNr) →excessive thalamic inhibition . Reinforced by reduced inhibitory input to Gpi/SNr through direct pathway
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| What is the result of the hypothetical mechanism that causes Parkinson's? | Increased inhibition of thalamus and decreased excitatory inputs to cortex
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| What is chorea? | Involuntary, dance-like movements of the limbs
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| What is the pathology behind Huntington's? | Hereditory disorder in which cell bodies of GABA-secreting neurons projecting to the Gpe in the caudate nucleus and putamen are lost - cells of caudate nucleus and putamen degenerate and these nuclei atrophy
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| What are the symptoms of Huntington's? | Involuntary, hyperkinetic movements; dementia develops
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| What is the hypothesis behind Huntington's | Reduced GABA from neostriatum to Gpe leads to increased inhibitory outflow from Gpe to STN and less excitatory to Gpi/Snr and less inhibitory to thalamus and more excitatory to cortex. Increased Glu to cortical areas → hyperkinetic movements
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| What is hemiballismus? | Hyperkinetic disorder common caused by a stroke of the subthalamic nucleus
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| What are symptoms of hemiballismus? | Involuntary ballistic movements of the arm and leg on opposite side of the body from lesion
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| What is the hypothesis behind hemiballismus? | Reduced Glu from STN to GPi leads to reduced inhibitory outflow from Gpi/Snr to thalamus and increased excitation ofmotor cortex. Increased Glu to cortical areas → hyperkinetic movements
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