organ systems III: exercise physiology

this lecture by Dr. Frangos, PT ND, focused on the effects of exercise on the body. we looked at both how the body responds acutely to exercise, as well as how the body adapts long term to regular endurance exercise. acute effects of exercise on the heart include a increase in cardiac output (CO) mainly due to increased heart rate, with only a slight increase in stroke volume (SV), which is dependent on myocardial contractility. regular endurance exercise also increases CO, which is mainly due to increased SV from increased myocardial contractility. other adaptive effects on the heart include a lower resting heart rate and increased maximal oxygen intake. exercise's acute effects on the lungs mainly revolve around an increase in ventilation rate (exercise intensity has a linear relationship with ventilation rate up until moderate intensities, beyond which the relationship becomes supralinear), but also includes an increase in alveolar ventilation for both rate and volume.

hormone release also markedly shifts with exercise, mainly to facilitate efficient utilization of glucose in skeletal muscle. sympathetic stimulation causes release of stress hormones such as epinephrine and cortisol, and insulin release is decreased so that glucose is available in the blood for metabolism. also, thyroid hormones such as T3 and T4 are increased so that metabolism can increase. repeated endurance training causes adaptive changes such as increased insulin receptors on cells, which increases the efficiency of glucose uptake in endurance athletes.

exercise affects skeletal muscle by increasing blood flow to muscle, body temperature due to contraction, and use of creatine phosphate / glycogen to form ATP. additionally, during intense exercise, lactic acid is produced in the muscles and can contribute to a metabolic acidosis, which can be compensated by excreting CO2 through ventilation. sustained endurance exercise increases the oxidative capacity of skeletal muscle through more mitochondria, as well as increasing the size of myofibrils through increased synthesis of myofilaments, and increased fast oxidative-type muscle fibers.


questions
acute effects of exercise on different systems...
1. describe the acute effects of exercise on the heart.
2. what are the increases in HR and SV attributed to?
3. describe the difference in SV and HR as exercise intensity increases to maximum.
4. describe the effect of exercise on mean arterial pressure.
5. describe the acute effects of exercise on the lungs.
6. describe the function of minute ventilation rate vs. exercise intensity.
7. describe the function of the lungs in maintaining pH during exercise.
8. describe how exercise affects hormone release.
9. how does exercise affect thyroid related hormones?
10. describe the effects of exercise on skeletal muscle.
11. describe the acute effects of exercise on metabolism.
12. describe how exercise affects GI function.

adaptive effects of exercise on different systems...
13. how does the heart adapt to endurance exercise?
14. how does endurance training affect hormone release?
15. how does endurance training affect skeletal muscle?
16. how does endurance training affect metabolism?
17. how does endurance training affect bone and connective tissue?

answers
1. drastic increase in CO due to increased HR (small increase in SV) and increased venous return from skeletal muscle pumps and respiratory pump.
2. increased HR due increased sympathetic stimulation of SA node and decreased parasympathetic. increased SV due to increased myocardial contractility.
3. HR continues to max, but SV plateaus relatively early.
4. increases slightly; CO is increased but total peripheral resistance is decreased.
5. increased ventilation rate, increased alveolar ventilation (rate and volume)
6. a linear relationship at low to moderate intensities, then a supralinear relationship.
7. high intensity exercise produces lactic acid in the muscles, which causes metabolic acidosis; the lungs compensate for this by increasing ventilation and excreting CO2 from the blood.
8. causes an increase in hormones related to stress (cortisol, EP, glucagon, GH) due to sympathetic stimulation. also causes a decrease in insulin release (so that glucose can be used as fuel).
9. increased TSH, T4, T3, which stimulates metabolism.
10. increased bloodflow from increased CO, increased body temperature from increased contraction, and increased use of creatine phosphate/glycogen to form ATP.
11. increased liver supply of glucose via glycogenolysis. increased lipolysis causes increase in glycerol and free fatty acids. increased utilization of free fatty acids.
12. decrease in blood flow to GI tract. slower gastric emptying and intestinal absorption. increased caloric expenditure and thus increased appetite.

13. increased contractility of myocardium increases CO, and increased mitochondria increases oxidative capacity. increased efficiency lowers resting heart rate. also, increased maximal oxygen uptake.
14. increased insulin receptor density on cells increases sensitivity to insulin and allows for increased efficiency of glucose transport into muscles.
15. increased mitochondria causes increased oxidative capacity. hypertrophy of muscle fibers due to increased synthesis of myofilaments. increased number of fast oxidative fibers. increased synthesis of glycolytic enzymes. increased capillaries surrounding muscles. finally, increased myoglobin synthesis.
16. improved GI function (motility and elimination in particular), increased BMR, increased endurance from usage of fatty acids, increased WBC count leads to better immune function.
17. decreased chance of injury due to increased strength and density of tissues. decreased joint pain.

organ systems III: thyroid

this lecture (sadly, dr. brons' last lecture during our time here) covered the thyroid anatomy and thyroid hormones release and physiological effects on the body. the thyroid hormone is situated between the thyroid cartilage and the 6th tracheal cartilage ring and is composed of functional units called follicles. these follicles are vesicles that are lined with cuboidal cells which take in iodine and secrete it, along with thyroglobulin, into the lumen of the follicles. in the lumen, iodine combines with thyroglobulin and tyrosine to form mono and di-iodotyrosine, which can be combined to form the main thyroid hormones T3 and T4, which are stored in the lumen of the follicles.

the release of T3 and T4 from the thyroid gland is mediated by the HPA axis; the hypothalamus releases TRH (thyrotropin releasing hormone) into the portal veins and anterior pituitary, which then releases TSH (thyroid stimulating hormone) into the circulation. the thyroid reacts to TSH by endocytosing T3/T4 from the lumen into follicle cells, where thryoglobulin is removed from T3/T4 via phagolysosomes. T3/T4 then enter general circulation in the approximate ratio of 10:1 T4:T3. high T3 levels allow for feedback inhibition of the hypothalamus, causing it to downregulate TRH receptor sites as well as disrupting synthesis of TSH, homeostatically lowering T3 levels.

in peripheral cells, T4 is converted to T3; T3 has a host of effects on virtually all organs and tissues in the body. on a cellular level, it functions as a modulator of cell metabolism (rather than an on-off switch, it simply amplifies existing metabolic processes) by acting as a transcription factor which can upregulate certain metabolic proteins; such as the ATP-ase Na+/K+ pump. the net effect of T3 on cells is to increase basal metabolic rate, oxidative metabolism (except in the brain, spleen, and testes) by increasing O2 consumption, facilitating hormonal actions on metabolic fuels (such as glucose, fatty acids, etc), and increasing cardiac output by upregulating beta-receptors. due to this close relationship to metabolism, the release of thyroid stimulating hormones is regulated by body temperature; higher body temperatures will inhibit release of TSH and lower body temperatures will stimulate TSH release.

hyperthyroidism is an excess production of T3/T4 and the accompanying metabolic frenzy, and is either caused by reduced feedback inhibition or an immune dysfunction where antibodies produced against the thyroid stimulates excess release of T3/T4; in this case, the high levels of T3/T4 would cause feedback inhibition and thus low levels of TSH. hyperthyroidism results in a goiter due to hyperplasia of thyroid cells, heat intolerance, weight loss, exophthalamos, nervousness, irritability, tachycardia, arrhythmia. hypothyroidism is the opposite condition of low T3/T4 levels which can be the result of autoimmune destruction of thryoid, iodine deficiency, or excess consumption of goitrogens. the symptoms include lethargy/sluggishness, colloid goiter, cold intolerance, delayed tendon reflexes, high cholesterol, hair loss, enlarged liver/kidney/tongue, and myxedema, among other things.

questions
thyroid anatomy and functional anatomy...
1. what is the endocrine axis that regulates release of thyroid hormone?
2. what is TRH? how is it released?
3. what is TSH? how is it released?
4. how does the thyroid respond to TSH?
5. where is the thyroid gland located?
6. what is the functional unit of the thyroid and what does it consist of?

T3, T3 synthesis, release, feedback...
7. describe the synthesis of T3 and T4.
8. how long can T3 and T4 be stored in the lumen of thyroid follicles?
9. describe the release of T3 and T4 from the thyroid into the blood.
10. what is the ratio of T4 to T3 at release from the thyroid?
11. in cells, what happens to T4?
12. describe the feedback inhibition of T3.
13. how does temperature affect T3/T4 release?

physiological and metabolic effects of T3...
14. which organs does T3 affect?
15. describe the role that T3 plays in regulating cellular functioning.
16. what is cretinism and what does it result in?
17. in peripheral cells, T3 enhances...
18. in which tissues does T3 not enhance oxidative metabolic functioning?
19. describe T3's effects on metabolism.

pathologies...
20. what is hyperthyroidism and what are its causes?
21. describe relative levels of T3/T4 and TSH in hyperthyroidism that results from autoimmune dysfunction.
22. what are some of the symptoms of hyperthyroidism?
23. what is hypothyroidism and what are its causes?
24. describe the relative levels of T3/T4 and TSH in hypothyroidism.
25. what are the symptoms of hypothyroidism?

answers
1. HPA axis.
2. thyrotropin releasing hormone is released from the PVN of the hypothalamus into the portal veins and anterior pituitary.
3. thryoid stimulating hormone is released from the anterior pituitary into general circulation.
4. by releasing T3 and T4 into the circulation.
5. between the thyroid cartilage to the 6th tracheal cartilage ring.
6. a follicle which is a vescicle surrounded by cuboidal cells that incorporate iodine and synthesize thyroglobulin, and a colloid interior where T3 and T4 are synthesized and stored, bound to thyroglobulin.

7. iodine is pumped into follicular cells and subsequently into the lumen of the follicles, along with thyroglobulin. in the lumen, thyroglobulin is combined with iodine and tyrosine to form mono and di-iodo tyrosine (MIT and DIT), and T3 and T4 are formed by combining MIT and DIT or two DIT's.
8. 2-3 months.
9. T3 and T4 are endocytosed back into follicle cells where the thyroglobulin is degraded into amino acids via phagolysosomes. T3 and T4 are then released into the circulation.
10. 10:1
11. it is converted to T3.
12. high T3 levels can act on the anterior pituitary to downregulate TRH receptors as well as inhibiting signal transduction in the TSH pathway, ultimately reducing the level of T3/T4 that is released from the thyroid.
13. high temperature inhibit T3/T4 release and cold temperatures stimulate T3/T4 release via hypothalamic temperature centers.

14. all organs.
15. acts as a modulator of cell function rather than an on/off switch.
16. an early thyroid deficiency; abnormal development of bones and CNS. results in stunted bones, malformation of facial bones and mental retardation.
17. basal metabolic rate, oxidative metabolism, upregulation of ATP-ase sodium/potassium pump.
18. brain, spleen, testes.
19. increases O2 consumption, facilitates hormonal actions on metabolic fuels (glucose, lipids, etc.), increases cardiac output by upregulating beta-receptors.

20. increased synthesis of T3/T4, caused by reduced feedback inhibition or autoimmune dysfunction, where antibodies to thyroid gland stimulate excess release of T3/T4.
21. high T3/T4 levels and low TSH levels due to feedback inhibition of the anterior pituitary.
22. goiter due to hyperplasia of thyroid cells, heat intolerance, weight loss, exophthalamos, nervousness, irritability, tachycardia, arrhythmia.
23. decreased synthesis of T3/T4 due to autoimmune destruction of thyroid, iodine deficiency, or goitrogens in the diet such as turnips or cabbage (but only in ridiculous, comical quantities according to dr. brons)
24. low levels of T3/T4 but high levels of TSH; results in increased colloid volume in thyroid due to synthesis and storage of T3/T4 without release.
25. colloid goiter, cold intolerance, fatigue/somnolescence, delayed tendon reflexes, bradycardia, high cholesterol, hair loss, enlarged liver/kidney/tongue, myxedema (mucopolysaccharide gel in skin osmotically holding water).

organ systems: limbic system part 1

the limbic system is a set of brain structures that are involved in a variety of neurological and physiological functions such as emotion and memory formation. the outer brain structures included in the limbic system include the parahippocampal cortices, cingulate gyrus, prefrontal cortex, entorhinal cortex, and the insula. the deeper brain structures include the amygdala, septum, the nucleus accumbens of the ventral striatum, and the hippocampus.

a sidebar on neuromodulatory pathways that are related to limbic functioning. the pathway involving norepinephrine begins in the locus ceruleus in the pons, and mediates attentional selection during stress, activating wide areas of the brain. the dopamine pathway starts at the ventral tegmentum in the midbrain and is involved in maintaining working memory and also reward seeking behavior via the mesolimbic system. the serotonin pathway begins in the raphe nucleus in the medulla, and regulates mood and the sleep/wake cycle. finally, the acetylcholine pathway begins in the diagonal band of broca, septum, and nucleus basalis, and is involved in memory formation and cognition.

the hippocampus is a structure in the limbic system that is centrally involved in formation of memories. it has an "archicortex" (a term that denotes a cortical area that has less than 6 layers) that bulges into the lateral ventricle. it receives sensory afferents from various areas of the brain; in particular, the septum and various cortical areas (sensory, premotor, association, cingulate), allowing it to form episodic memories-- the auto-noetic, contextual experiences of an event. this information is then projected to the hypothalamus for neuroendocrine function, as well as back to the cortical areas (prefrontal, cingulate, temporal) for storage of semantic memories: the abstracted, noetic, non-contextual knowledge which is parsed from episodic memories.

the next sections focused on the limbic system's role in mediating sleep / wake states. it introduced the EEG as a tool to measure synchronous brain activity, used as a tool to detect various brain states during different stages of sleep. during the night, humans alternate between stage 1-4 sleep and REM sleep, which have markedly different neurological and physiological features: stage 4 sleep has a high EEG amplitude and low frequency and thus is called slow wave sleep; it also features decreased afferent input to cortical areas, decreased metabolism, and sleepwalking / tossing. on the other hand, REM sleep is characterized by low amplitude, high frequency EEGs, paralysis of large muscles, and an extremely active mind- leading to dreaming and hallucinations.

the states of arousal and wakefulness are mediated by the thalamus, which receive afferents from the cholinergic pontine pathways which are active during waking and REM states, and then project to the cortex. when the pathways that stimulate the thalamus are activated, the thalamus is activated to send information to the cortex. the cortex receives afferents from monoaminergic pathways (norepinephrine, serotonin, dopamine), cholinergic pathways from the basal forebrain nucleus, and the orexin and hypocretin pathways (which are defective in narcolepsy). when these pathways are stimulated, the cortex is activated to process the input from the thalamus.

sleep regulation is mediated by the hypothalamus and SCN. the VLPO nucleus of the hypothalamus inhibits hypothalamic and brain stem nuclei involved in arousal via GABA and galanin, thus inducing drowsiness. the SCN, as covered in the optic system, receives light/dark information from the eyes and projects to the supraventricular zone and dorsal medial nuclei of the hypothalamus, which promotes wakefulness by inhibiting the VLPO nuclei of the hypothalamus via GABA as well as stimulating the orexin pathway via glutamate.

questions
anatomy and neuromodulators...
1. what are the cortical regions included in the limbic system?
2. what are the deeper brain regions included in the limbic system?
3. what are the brain areas involved in planning, cognition, stress, fear, and memory?
4. where does the neuromodulatory pathway for norepinephrine begin and what is it involved in?
5. where does the neuromodulatory pathway for dopamine begin and what is it involved in?
6. where does the neuromodulatory pathway for serotonin begin and what is it involved in?
7. where does the neuromodulatory pathway for acetylcholine begin and what is it involved in?

hippocampus and memory...
8. describe the structure and location of the hippocampus.
9. what are the structures that project afferents to the hippocampus?
10. describe the pathway of neural activity that leads in and out of the hippocampus.
11. where does the hippocampus project efferent neurons to?
12. what are the two types of explicit/declarative memory?
13. where are episodic memories processed and what are they?
14. where are semantic memories processed and what are they?
15. describe the encoding of episodic memories by the hippocampus.
16. describe the formation of semantic memory.

sleep: EEG's and REM...
17. what does an EEG measure?
18. what are the two stages of sleep that humans oscillate between? how often does this occur?
19. what happens to EEG waves when sleep progresses through stage 1 to stage 4?
20. describe the physiological and neurological state during stage 4 non-REM sleep.
21. describe the physiological and neurological state during REM sleep.
22. what types of sleep (REM vs. slow wave) are the first and second halves of sleep dominated by?

arousal pathways, regulation...
23. what pathways are wakefulness and arousal mediated by?
24. what do pathways that activate the thalamus facilitate?
25. what are the specific pathways that activate the thalamus during wakefulness / arousal? when during the day or night are they the most active?
26. what do pathways that activate the cortex facilitate?
27. what are the specific pathways that activate the cortex during arousal / wakefulness?
28. which of these pathways degenerates during narcolepsy?
29. sleep is regulated by which brain structure?
30. describe the specific action of this brain structure in regulating sleep.
31. describe the regulation of sleep via circadian cycles.

answers
1. parahippocampal cortex, cingular cortex, prefrontal cortex, entorhinal cortex, insula.
2. amygdala, septum, ventral striatum / nucleus accumbens, hippocampus.
3. planning: frontal and cingulate cortices. cognition: cerebral cortex. stress: HPA axis, amygdala, hippocampus. fear: amygdala. memory: hippocampus, entorhinal cortex.
4. begins in locus ceruleus in pons, involved in attentional selectivity during stress and activating large areas of brain.
5. begins in the ventral tegmentum in midbrain, involved in facilitating working memory in prefrontal cortex, and reward seeking behavior via the mesolimbic dopamine system.
6. begins in raphe nucleus in medulla, involved in mood regulation and sleep-wake cycles.
7. begins in nucleus basalis, diagonal band of broca, septum, involved in memory formation and cognition.

8. has an archicortex that bulges into the temporal lobe / lateral ventricle.
9. the septum, and cortical regions such as prefrontal, association, sensory, cingulate cortices.
10. parahippocampal cortex, entorhinal cortex, hippocampus, amygdala.
11. from the fornix of the hippocampus to the hypothalamus for neuroendocrine function, and the prefrontal, cingulate, and temporal cortices for memory consolidation.
12. episodic and semantic.
13. processed in the hippocampus and hippocampal cortices; an auto-noetic, context based memory of the experience of an event.
14. non-contextual, noetic, long term representations based on knowledge of the world. encoded in the limbic cortices: anterolateral temporal and ventrolateral prefrontal.
15. sensory cortices project particular experiences, contexts, and relationships to the hippocampus to form the basis for episodic memory formation.
16. episodic memories are projected to the temporal and prefrontal cortices, where they are encoded into semantic memories; patterns and relationships are parsed from episodic memories and stored.

17. synchronous activity of large groupings of neurons which are producing EPSP's or IPSP's in unison.
18. REM sleep and non REM sleep, every 90 minutes.
19. amplitude of EEG waves increases and frequency gets slower.
20. decreased neural afferent input to cortices. decreased metabolism: heart rate, breathing rate, blood pressure. sleepwalking and tossing/turning. inactive mind, relatively active body.
21. decreased EEG amplitude/increased EEG frequency. rapid eye movements. increased metabolism. paralysis of large muscles. hallucinations and dreaming. active mind, inactive body.
22. first half dominated by slow wave sleep and second half dominated by REM sleep.

23. reticular pathways to the thalamus and cortex.
24. transmission of information from the thalamus to the cortex.
25. cholinergic pontine pathways: pedunculopontine and lateral dorsal tegmental nuclei- most active during waking and REM sleep.
26. processing of information from the thalamus.
27. monoaminergic pathways (norepinephrine, dopamine, serotonin pathway), cholinergic pathway from basal forebrain nucleus, orexin/hypocretin pathway from lateral hypothalamus. (base forbes, t rex hypocrit)
28. the orexin/hypocretin pathway.
29. VLPO nucleus of the hypothalamus.
30. inhibits hypothalamic and brain stem nuclei involved in arousal via GABA and galanin; thus inducing drowsiness.
31. the suprachiasmatic nucleus regulates sleep according to light-dark cycles- projecting neurons to supraventricular zone and dorsal medial nuclei of hypothalamus, which promotes wakefulness by inhibiting VLPO nuclei of hypothalamus via GABA, stimulates orexin via glutamate.

organ systems: motor system part 2

this was the second unit in the motor system (apologies for not getting to motor systems part 1 in time for the last test) and dealt with the motor pathways that start in the CNS, the different motor cortices and their roles, and some aspects of higher motor processing.

upper motor neurons originate in various places within the brain and project downwards through various descending tracts: the lateral corticospinal tract (recall that this was the major descending motor pathway from the spinal cord unit) represents 90% of the corticospinal tract which decussates in the medulla, follows the lateral funiculus, and is involved in fine movements. the remaining 10% does not cross over, follows down the anterior funiculus, and is involved in trunk muscles and posture. the vestibulospinal is a descending tract which receives information from the vestibular portion of the vestibulocochlear nerve and projects down to the spinal cord, ultimately to the flexors of the lower limb and extensors of upper limb. the reticulospinal is another descending tract which projects down to trunk muscles, extensors of lower limb, and flexors of the upper limb.

lower motor neuron disease happens when alpha motor neurons are damaged and thus dysfunctional motor innervation leads to muscle atrophy and flaccid paralysis. on the other hand, upper motor neuron disease occurs because a stroke in the higher motor centers disrupts the descending tracts' communication with cranial nerves and spinal motor neurons.

there are different motor cortices which all play different roles in processing and executing motor tasks. for example, the association cortex is involved in setting up tasks or sequences of motor programs, which it then sends to the primary motor cortex which executes the programs by contraction of fine muscles. the supplementary cortex is involved in mental rehearsal of the motor task, regardless of the external environment (also regardless of whether the action is actually performed). the premotor cortex is involved in "conditional motor tasks"-- deciding the appropriateness of movements and encoding intention behind them. broca's area is a part of the prefrontal cortex which controls the motor aspects of speech production.

different areas of the motor cortex are also involved in higher processing of motor information with incoming sensory input to both predict the future states of motion or position of a body part, as well as generally create the sensations of self-agency, ownership, and thus contributes to self-awareness. the motor cortex receives sensorimotor input from the posterior parietal cortex and visual cortex, which it then integrates with the motor program and feeds an "efference copy" into the somatosensory cortex for prediction of future limb states. when the efference copy matches the intention of a person, a feeling of self-agency is created; the sense that one is in control of one's actions- that the predicted body position or movement has occured. when incoming sensory data matches the intention, this creates the feeling of self-ownership.

another higher order function of the motor cortex occurs with mirror neurons, which are in the "core mirror area": inferior premotor cortex and inferior parietal cortex. these neurons were originally discovered in monkeys and are shown to fire when both performing certain movements as well as simply observing them. it is proposed that in humans they are fundamental in acquiring social behavior and thus the development of mirror neurons might have been an evolutionary landmark that allowed us to adapt and acquire behaviors that facilitated survival simply by observing and imitating.

questions
overview...
1. what do upper motor neurons control?
2. which areas of the brain have upper motor neurons that mediate balance, posture, and fine extremity movement?
3. what are the descending tracts in the spinal cord related to motor control?
4. what are the ascending tracts in the spinal cord related to motor control?
5. what does the vestibulospinal nuclei in the medulla receive and project?
6. what does the vestibulospinal tract activate in the upper and lower limbs?
7. what does the reticulospinal tract project down to?

descending tracts...
8. corticospinal tracts includes tracts to...
9. what are the three tracts that the motor cortex forms?
10. where does the somatosensory cortex send tracts down to?
11. how does the corticoreticular tract smooth general movements?
12. describe the lateral corticospinal tract.
13. describe the anterior corticospinal tract.
14. what other CNS structures do the corticospinal tracts pass through?

motor neuron disease...
15. what is lower motor neuron disease?
16. what is upper motor neuron disease?
17. why does upper motor neuron disease lead to a decrease in fine control of movement?
18. why does upper motor neuron disease lead to spasticity?
19. what does spasticity involve?
20. what is the babinski sign?
21. what is the babinski sign due to and who is it generally found in?

primary, association, supplementary, premotor cortices...
22. what role does the association motor cortex play in producing movements?
23. what role does the primary motor cortex play in producing movements?
24. where is the primary motor cortex located?
25. what is the role of the supplementary motor cortex in producing movements?
26. what is the role of the premotor cortex in producing movements?
27. what is broca's area?

higher functioning...
28. what does selecting appropriate movements require of the motor cortex?
29. where does the motor cortex receive information from during sensorimotor integration?
30. why are copies of the motor program fed back into the somatosensory cortex?
31. what does self-awareness or self-recognition depend upon?
32. what is the forward model?
33. what is self-agency and how is it manifested in the brain?
34. what is self-ownership and how is it generated in the brain?
35. what are mirror neurons?
36. what is the "core mirror area" in humans?
37. mirror neuron activity often represents what aspects of observed behavior?

answers
1. posture, balance, movements.
2. brainstem has pathways for balance and posture. motor cortex has fine extremity movement pathways.
3. lateral and anterior corticospinal tract, vestibulospinal, reticulospinal tracts.
4. spinocerebellar, gracile/cuneate fasciculi.
5. receives input from vestibular system (semicircular duct, utricle, saccule) about head position and movement, relays to spinal cord.
6. extensors in upper limb, flexors in lower limb.
7. trunk muscles, flexors of upper limb and extensors of lower limb.

8. brainstem and spinal cord.
9. corticospinal to the ventral spinal cord, corticonuclear to the cranial nerve nuclei, and corticoreticular to the medullary and pontine reticular formation.
10. to the brainstem to regulate sensitivity of sensory pathways.
11. by limiting inhibition in the extensors of the lower limb.
12. represents the 90% of corticospinal tract that crosses over in the medulla and goes down the lateral funiculus. fine control of movement.
13. represents the 10% of corticospinal tract that does not cross over; goes into the anterior funiculus and projects bilaterally. posture of neck and trunk.
14. the internal capsule, cerebral peduncles, and pyramids in medulla.

15. lesions in the alpha motor neurons blocking motor input to muscles, resulting in atrophy and flaccid paralysis.
16. a stroke in the motor cortex disrupting descending pathways to the cranial nerves and spinal motor neurons.
17. because of the disruption of the corticospinal tracts.
18. because of the disruption of the cortical projections to the reticular formation.
19. hypertonicity, clasp knife reflex, hyperreflexia, antigravity posture. (gravity causes the knife reflex in tonic water)
20. the fanning of toes due to upward stroking of the sole of the foot.
21. present in newborns, due to unmyelination of corticospinal tracts

22. develops strategies and programs/sequences of movements, which are then sent to the primary motor cortex.
23. activates small groups of muscles for fine movements.
24. in the precentral gyrus.
25. ensures correct motor sequences independent of external conditions; activated during mental rehearsal of movements.
26. involved in encoding intention of a movement and selection of movements based on environment or memory.
27. a part of the premotor cortex that controls motor aspects of speech production.

28. integration of the spatial aspects of environment with proprioceptive and somatosensory data.
29. the posterior parietal and visual cortex.
30. for integration with incoming sensory input to predict future sensation and limb position / movement.
31. sense of agency and ownership, possible through the integration of intention and sensory feedback in the "forward model".
32. the combination of the efference motor program copy, incoming sensory information, and internal model of the dynamics of the limb to predict the current state of the limb.
33. knowing that one's intentions lead to external actions; occurs when efference copy matches subject's intentions.
34. the sense that you are the one who is undergoing the experiences, generated when sensory feedback matches intentions.
35. the neurons that fire during an action as well as the observation of that action in others.
36. the inferior premotor cortex, and inferior parietal cortex.
37. the intention or goal of the action.

organ systems III: cranial nerves

this lecture covered the pathways, functional components, target structures, CNS connections of each of the cranial nerves.
















questions
embryology...
1. all but one of the cranial nerves exit from...
2. after neurulation, the neural tube differentiates into...
3. what separates the alar and basal plates?
4. the 4th ventricle pushes both plates...

cranial nerve classification...
5. GSA
6. GVA
7. SSA
8. SVA
9. GSE
10. GVE
11. SVE

12. describe the arrangement of nuclei for cranial nerves.
13. what are two examples of how a given nucleus can project to or receive from several cranial nerves?
14. describe the orientation of the nuclei with respect to the 4th ventricle.

cranial nerves I, II, III, IV, VI...
15. what is the functional component of the olfactory nerve?
16. where is the primary olfactory cortex?
17. which brain areas are responsible for conscious perception of smell?
18. which brain areas are responsible for association between smell and emotions?
19. describe the course of the optic nerve.
20. what is the functional component of the optic nerve?
21. describe the course of the oculomotor nerve.
22. what are the functional components to the oculomotor nerve?
23. what is the course of the trochlear nerve?
24. what is the functional component of the trochlear nerve?
25. what is the course of the abducens nerve?
26. what is the functional component of the abducens nerve?
27. what are two tests that measure the function of the oculomotor nerve?

trigeminal nerve...
28. what are the courses for the three components of the trigeminal nerve?
29. what are the target structures for the three branches of the trigeminal nerve?
30. where do sensory and motor nulcei from the trigeminal nerve project to?
31. what are the functional components to the trigeminal nerve?
32. what are some tests that measure the function of the trigeminal nerve?

facial nerve...
33. what is the course of the facial nerve?
34. the chorda tympani passes along...
35. what are the visceral nerves of the chorda tympani?
36. what are the functional components to the facial nerve?
37. describe the taste pathway of the facial nerve.
38. what are some tests to gauge proper functioning of the facial nerve?

vestibulocochlear...
39. describe the course of the vestibulocochlear nerve.
40. what are the functional components of the vestibulocochlear nerve?
41. describe the pathway from the auditory system to the CNS via the vestibulocochlear nerve.
42. describe the pathway from the vestibular system to the CNS via the vestibulocochlear nerve.
43. what are the vestibulocochlear nerve tests?

glossopharyngeal, vagus...
44. what is the course of the glossopharyngeal nerve?
45. what is the test for the function of the glossopharyngeal nerve?
46. what are the functional components to the glossopharyngeal nerve?
47. what is the course of the vagus nerve?
48. what are the functional components of the vagus nerve?
49. what are the CNS components/connections from the vagus nerve?
50. what are the tests for vagal functioning?

accessory, hypoglossal...
51. what is the course of the accessory nerve?
52. what is the functional component of the accessory nerve?
53. what is the test for accessory nerve functioning?
54. what is the course of the hypoglossal nerve?
55. what is the functional component of the hypoglossal nerve?
56. what is a test that indicates proper hypoglossal nerve functioning?

answers
1. the ventral side of the brainstem.
2. the dorsal alar and the ventral basal plate.
3. the sulcus limitans.
4. ventrally.

5. general somatic afferent: muscle, connective tissue, skin receptors.
6. general visceral afferent: organs and blood vessel receptors.
7. special somatic afferents: for audition and vision.
8. special visceral afferents: for olfaction and taste.
9. general somatic efferents: control of skeletal muscle.
10. general visceral efferents: smooth and cardiac muscle.
11. special visceral efferents: muscles of face, mastication, larynx, pharynx.

12. nuclei for cranial nerves are arranged in longitudinal columns that are functionally distinct (fit one of the classifications above) and can be connected with multiple cranial nerves.
13. SVA (solitary nucleus) receives from VII, IX, X. SVE (nucleus ambiguus) projects out on IX and X.
14. most of the nuclei line up on the floor of the 4th ventricle except for the SVE and the GSA which migrate ventrally.

15. olfactory bulb for smell.
16. medial temporal lobe.
17. thalamus and cortex.
18. amygdala and entorhinal cortex.
19. optic nerve projects information from retina to thalamus, which projects to visual and association cortices.
20. the lateral geniculate nucleus (SSA)
21. from the midbrain to the cavernous sinus, through the superior orbital fissure to the extraocular muscles.
22. oculomotor nucleus (GSE) involved in external eye movements. edinger westfal nucleus (GVE) involved in parasympathetic constriction of pupil in response to incoming light.
23. posterior midbrain, cavernous sinus, superior orbital fissure.
24. trochlear nucleus (GSE)-- innervates superior oblique.
25. pons, cavernous sinus, superior orbital fissure.
26. abducens nucleus (GSE)-- innervates lateral rectus.
27. equal ocular motion test measures the somatic aspect and the pupils equal round reactive to light test measures the parasympathetic function of the oculomotor nerve.

28. V1: pons, cavernous sinus, SOF. V2: pons, cavernous sinus, foramen rotundum. V3: pons, foramen ovale.
29. V1: orbital cavity, upper face, eyes sensory innervation. V2: palate, nasal cavity, middle face innervation. V3: oral cavity sensory innervation and mastication muscles motor innervation.
30. thalamus (and from there to face area in primary somatosensory cortex) for sensory, and muscles for motor.
31. the primary sensory nuclei (GSA) which receives discriminative touch, the mesencephalic (GSA) which receives proprioceptive input, the spinal trigeminal tract (GSA), which receives pain and temperature input, and the motor nucleus (SVE) which innervates
32. somatosensory tests (sharp or dull sensations), clenching jaw (to test masticating muscle function), and the corneal blink test (irritation causes eye closure via V and VII reflex loop).

33. pons, internal acoustic meatus, stylomastoid foramen.
34. the interior of the tympanic membrane.
35. parasympathetic branches which innervate the submandibular and sublingual glands. special visceral afferent branches receive visceral input from the anterio 2/3 of the tongue via the lingual nerve.
36. the motor nucleus (SVE) which innervates the muscles of facial expression and the stapedius, the salivatory nucleus (GVE) which innervates nasal, lacrimal, and palatine glands via the pterygopalatine ganglion and the submandibular and sublingual glands via the submandibular ganglion. also, the solitary nucleus (SVA) receives taste input from the anterior 2/3 of the tongue via the lingual nerve, and the spinal trigeminal nucleus (GSA) which receives somatosensory input from the ear.
37. solitary nucleus (SVA) receives visceral sensory information from tongue from VII, IX, X, which then projects to the VPM nucleus of the thalamus, and then to the cortex in the insula.
38. facial muscle tests: various facial expressions.

39. vestibular apparatus / cochlea through the internal auditory meatus to the nuclei in the medulla.
40. cochlear and vestibular nuclei (SSA) for hearing and balance.
41. cochlear nuclei in medulla to superior olive to inferior colliculus to primary auditory cortex and association cortices.
42. vestibular nuclei, cerebellum, III, IV, VI, spinal cord.
43. conductive vs. sensorineural defect tests; humming/tuning forks

44. medulla, jugular foramen, descends neck.
45. the gag reflex.
46. the nucleus ambiguus (SVE), inferior salivatory nucleus (GVE), solitary nucleus (SVA and GVA), spinal trigeminal nucleus (GSA).
47. medulla, jugular foramen, down into pharynx/larynx/lungs/GI/kidney, etc.
48. nucleus ambiguus (SVE) for motor innervation of pharynx/larynx, dorsal vagal nucleus (GVE) for parasympathetic innervation of lung, GI, kidney, solitary nucleus (SVA) for taste from epiglottis/palate and (GVA) afferents from viscera and blood vessels, and spinal trigeminal nucleus (GSA) for sensory from ear.
49. GVA from solitary nucleus relayed to hypothalamus, reticular formation, limbic system for homeostatic organ regulation, memory, emotion. SVA from solitary nucleus projected to thalamus and gustatory cortex. GSA from spinal trigeminal nucleus projects somatosensory input from ear to thalamus and somatosensory cortex.
50. raising the tongue to the roof of the mouth, deviated palate, and gag reflex.

51. medulla, jugular foramen, into neck.
52. accessory nucleus (SVE) for motor innervation of SCM and trapezius.
53. shrugging the shoulders, resisting pressure on forehead, chin
54. medulla, hypoglossal canal, oral cavity.
55. hypoglossal nucleus (GSE) for motor innervation of tongue.
56. deviation of tongue.

organ systems III: vestibular system

the vestibular system is located in the inner ear and is involved in detecting head movement, maintaining balance and posture, and formation of the perception of one's physical boundaries. it is located within the petrous portion of the temporal bone and has several components: the bony labyrinth is the outer covering which contains the 3 mutually perpendicular semicircular canals and the vestibule. inside the semicircular canals are the semicircular ducts which contain endolymph and the crista receptors in the ampulla of each duct. inside the vestibule are the utricle and saccule, which contain the macula receptor.

the crista receptors inside the semicircular ducts are designed to sense angular acceleration- rotation of the head causes the fluid inside the semicircular ducts to shift due to the inertia of the fluid itself. the fluid pressing against the crista receptors causes a distortion of the cilia embedded within the crista, which causes a receptor potential. each semicircular canal is in a different orientation such that any given rotation will produce a different set of shifts in each duct, the combination of which is then integrated and processed downstream.

the macula receptors inside saccule and utricle are designed to sense linear acceleration. these are made of receptor cells with cilia embedded within a gelatinous otolith layer, on top of which there are calcium carbonate stones. when the head is tilted, the stones distort the otolith layer and therefore the cilia from the receptor cells, producing a receptor potential. occasionally the otoliths can detach and enter the semicircular ducts, causing benign paroxysmal positional vertigo.

the vestibular pathway starts at the vestibular nerve, which carries information to the vestibular nuclei in the pons. from there the vestibular nuclei projects to cranial nerves III, IV, VI in order to coordinate eye movement along with head movement (to enable tracking of an object in space- the vestibulo-ocular reflex), and also to the vestibulospinal tract, for control of muscles involved in posture and balance. damage to the vestibular pathway might result in vertigo, a loss of equilibrium and balance and a sense of falling.

information from the vestibular system is also projected to the vestibular cortex, which is located at the temporal-parietal junction, insula, somatosensory cortex, and the superior parietal cortex. in the parietal association cortex, vestibular information is integrated with other modalities such as somatosensory, visual, audition, etc. in order to form an integrated sense of one's environment and body. the vestibular cortex is also known to be involved in the sense of localization; ie, where one perceive's one's center of awareness to be. dysfunctions within the temporal-parietal junction in particular have been demonstrated to cause such hallucinations (of increasing intensity and of vestibular dysfunction) as autoscopy, where one sees one's own body in another space, heatoscopy, where one sees one's own body in another space and feels one's awareness might be located there as well, and out of body experiences, in which the person's center of awareness is completely removed from their body.

questions
anatomy and receptor physiology...
1. where is the vestibular system located?
2. the bony labyrinth is divided into...
3. what is the membranous labyrinth and what is it divided into?
4. what is endolymph secreted by? where does it drain?
5. what is perilymph secreted by? where does it drain?
6. what is meniere's disease?
7. what are the three semicircular ducts/canals? describe their orientation.
8. rotation of ducts with head causes...
9. what are crista and cupula?
10. how does the crista sense rotation?
11. describe the sensory receptor system within the saccule and utricle.
12. the macula is sensitive to what type of acceleration as opposed to the crista?
13. what happens in benign paroxysmal positional vertigo?

innervation...
14. vestibular nerve conducts to...
15. from where do the vestibular nuclei in the pons receive input?
16. where do the vestibular nuclei project to?
17. what is the vestibulo ocular reflex?
18. what is nystagmus?
19. what do the vestibulospinal tracts project to?
20. what is vertigo and what can it be caused by?

perception and sensation...
21. what does the parietal association cortex do?
22. how was the vestibular cortex mapped out?
23. where is the vestibular cortex?
24. which part of the vestibular cortex is mainly responsible for creating the sense of being in one's body?
25. what is autoscopy?
26. describe an out of body experience.
27. describe an autoscopic hallucination.
28. describe "heatoscopy".
29. which of these illusions has the most vestibular dysfunction? which has the least?

answers
1. within the petrous portion of the temporal bone.
2. the vestibule and the semi-circular canal.
3. membranous tube containing receptors for head movement; divided into semicircular ducts (in the semicircular canals) and saccule and utricle (within the vestibule).
4. secreted by cochlear duct and drains into dural sinuses via endolymphatic duct.
5. secreted by periosteum and drains into CSF via perilymphatic duct.
6. excess endolymph secretion or fluid pressure causing nausea/vomiting, vertigo/dizziness, abnormal saccadic eye movements.
7. anterior, horizontal, posterior. mutually perpendicular.
8. flow of endolymph within ducts.
9. the receptor organ in the ampula of each canal; the cupula is the gelatinous mass which the cilia of receptor cells are embedded in.
10. rotation of the head in the same alignment as the semicircular canals produces pressure against the crista because of the inertia of the endolymph.
11. maculae is the sensory device which is composed of ciliated macular receptor cells which have cilia embedded in the gelatinous otolithic membrane, which is then covered by calcium carbonate stones which produce shifts in the otolithic membrane when the head is tilted.
12. linear acceleration as opposed to angular acceleration.
13. when otoliths from utricle fall into the semicircular canals and produce "apparent motion" in the crista, resulting in dizziness, vertigo, imbalance, nausea

14. the vestibular nuclei in brain stem, cerebellum.
15. directly from the vestibular nerve or indirectly from the cerebellum.
16. CN III, IV, VI for control of eye movement.
17. a reflex that requires the cerebellum which causes movement of eyes opposite to rotation of head.
18. involuntary saccadic movements when the eyeball is at rest.
19. to the muscles that control posture and balance.
20. disorientation and a sense of spinning-- can be caused by a tumor in vestibular system or meniere's disease.

21. integrates somatosensory, proprioceptive, visual, auditory, vestibular input to form body schema- body, personal space, extra personal space.
22. by looking at brain responses to vestibular illusions in epilepsy, or to galvanic/caloric vestibular stimulation.
23. the temporal-parietal junction, insula, somatosensory cortex, superior parietal cortex.
24. the temporal-parietal junction.
25. the experience of perceiving one's own body in another place because of the lack of congruence among the sensory inputs integrated in the association cortices.
26. seeing one's own body from an elevated position, feeling that the center of awareness is located outside of the body (disembodiment).
27. seeing a double of oneself in extrapersonal space, with the center of awareness remaining inside the body.
28. seeing a double of oneself in extrapersonal space with the center of awareness being split between the body and the extrapersonal space.
29. out of body has the most TPJ dysfunction, then heatoscopy, then autoscopy.

organ systems III: auditory system

this lecture covered the anatomy of the ear, the sound transduction mechanism of the cochlea, and the auditory pathways of the CNS. the ear can be roughly divided into three sections. external ear is the auricle (the skin covered elastic tissue which includes the helix/antihelix, tragus/antitragus, concha and lobule), up to the tympanic membrane. the middle ear contains the ossicles, which transmit sound from the tympanic membrane to the inner ear. the pathway for vibration goes from the tympanic membrane to the malleus, then the incus, then the stapes. the stapes transfers its vibrations through the oval window into the cochlea. a few other middle ear notes: the tegmen tympani is the bony membrane that separates the CNS from the middle ear (middle ear infections can thus lead to meningitis by spreading through the tegmen typmani). the tensor tympani attaches to the malleus, is innervated by V3, and absorbs low frequency vibrations from the malleus. the stapedius is a muscle that is innervated by the facial nerve which absorbs extreme vibrations from the stapes.

the stapes transfers its vibrations into one of the two channels within the helical bony structure of the cochlea, the scala vestibuli (the other being the scala tympani). separating these two channels is the cochlear membrane which contains the organ of corti, which contains the sensory receptors in the form of ciliated receptor cells. the organ of corti is covered by the basilar membrane, which contacts the scala vestibuli, and the tectorial membrane, which contacts the cilia of the receptor cells. vibrations pass through the oval window into the perilymph fluid in the scala vestibuli, which causes a distortion of the basilar membrane- this causes a shift in the ciliated cells via the tectorial membrane, which produces a receptor potential. along the length of the cochlea, the basilar membrane gets wider and the cilia cells get longer, such that higher frequency vibrations are absorbed closer to the oval window. each sound thus produces a characteristic deflection pattern along the length of the basilar membrane.

the cochlea is innervated by the cochlear portion of CNVIII, the vestibulocochlear nerve, via the spiral ganglion. from there, the auditory pathway goes to the cochlear nuclei in the medulla, to the superior olive nuclei in the medulla (which receives input from both ears), to the inferior colliculus in the midbrain, to the middle geniculate nucleus of the thalamus via the lateral lemniscus, to the primary auditory cortex in the temporal lobe. from there, the information can be sent to the auditory association areas, such as wernicke's area for language comprehension or the parietal areas for reading/writing. music comprehension is divided between the hemispheres; the left hemisphere processes rhythm and the right processes melody.

questions
ear anatomy, innervation...
1. describe the transduction of sound from pressure waves in the air to the inner ear.
2. what is the auricle and what are its components?
3. what type of glands are around the external auditory meatus?
4. what is the umbo of the tympanic membrane?
5. what are the landmarks of the ear visible with an auriscope?
6. what are the sensory nerves to the ear?
7. which nerves innervate the tympanic membrane?
8. where is the chorda tympani and what does it convey?

middle ear...
9. tympanic cavity contains...
10. the auditory tube connects tympanic cavity to...
11. what is the tegmen tympani?
12. what is an otitis media? what might it lead to?
13. what do the ossicles do?
14. what is the tensor tympani and what does it do? what is it innervated by?
15. what is the oval window?
16. what does the stapedius do? what is it innervated by?

inner ear...
17. describe the shape of the cochlea.
18. what are the two channels in the cochlea? what are they separated by? where do they meet?
19. what is endolymph? perilymph?
20. describe the different roles of the oval and round windows.
21. describe the role of the basilar and tectorial membrane in the inner ear.
22. describe how the basilar membrane encodes a specific pitch.
23. closer to the apex, the basilar membrane becomes...
24. closer to the apex, the hair cells become...

innervation and auditory pathways...
25. describe the sensory innervation of the cochlea.
26. describe the auditory pathway from the cochlea to the primary auditory cortex.
27. disparity in time and intensity between right and left sounds...
28. how are low frequency sounds localized as opposed to high frequency sounds?
29. what are the three types of deafness and what are they caused by?
30. what are the auditory association cortices?
31. describe where rhythm and melody are processed in the brain.

answers
1. pressure waves enter the external ear and vibrate the tympanic membrane, which transmits vibration to the middle ear: malleus, incus, stapes, which translates the vibration into the fluid filled cochlea.
2. the elastic cartilage around the external ear which is covered by skin. has the helix/antihelix, tragus/antitragus, concha and lobule.
3. ceruminous.
4. the central depression formed by tension from the malleus.
5. umbo, malleus, incus, stapes, cone of light, flacid/tense portions of tympanic membrane.
6. greater auricular / lesser occipital, auriculotemporal (V3), facial (VII), glossopharyngeal (IX), vagus (X)
7. V3 and vagus innervate lateral side, glossopharyngeal innervates medial side.
8. deep to the tympanic membrane, conveys taste from anterior 2/3 tongue, parasympathetic to submandibular and sublingual glands via submandibular ganglion.

9. ossicles and their muscles.
10. nasopharynx.
11. the thin bone between the tympanic cavity and the brain.
12. a middle ear infection that can spread through the tegmen tympani to cause meningitis or brain abscesses.
13. transmit the vibrations from the wide tympanic membrane through the narrow base of the stapes.
14. the muscle that attaches to the malleus and dampens extremely low frequency vibrations. innervated by V3.
15. the area which the stapes transmits vibrations into the cochlea.
16. dampens extreme vibrations of the stapes. innervated by facial nerve.

17. a helical bony canal.
18. scala vestibuli and scala tympani: separated by cochlear duct, meet at the helicotrema at the apex.
19. endolymph is the fluid in the cochlear duct which has high K+. perilymph is the fluid in the scala vestibuli and tympani which has high Na+.
20. oval window is the area through which the stapes triggers fluid vibrations in the perilymph, and the round window is the area which absorbs the outward displacements of fluid vibrations.
21. vibrations of perilymph in the scala vestibuli are translated to the basilar membrane, which causes a distortion of the organ of corti. tectorial membrane is the membrane that contacts the cilia of the auditory receptor cells and causes the actual auditory signal.
22. the pitch of an incoming sound is encoded by the stretch and width of the basilar membrane from the oval window to the helicotrema. each sound or pitch has a maximum amplitude at a characteristic point along the basilar membrane.
23. wider
24. taller

25. provided by cochlear branch of vestibulo-cochlear nerve (CNVIII). synapses at spiral ganglion.
26. cochlea, cochlear nerve, cochlear nuclei in medulla, superior olive nuclei (each nuclei receives from both ears), inferior colliculus, medial geniculate nucleus of thalamus via lateral lemniscus, primary auditory cortex.
27. localizes object in space.
28. low frequency sounds are localized via time differences and high frequency sounds are localized via intensity differences.
29. conductive deafness due to damage of tympanic membrane or ossicles. sensorineural deafness due to damage of cochlea or cochlear nerve. central deafness due to damage of central auditory pathways.
30. wernicke's area on the left side of the temporal lobe (language comprehension), parietal areas for reading and writing.
31. rhythm is processed on the left side, melody on the right.

organ systems III: visual system part 4- central visual pathways

this is the last lecture in the series on the visual system and deals with the processing of visual information through the visual cortices and other pathways. visual information is received through 3 types of ganglionic cells- Y type cells receive input from rods and thus detect peripheral movement or light intensity changes. X type cells receive input from cones and as such detect fine detail and color, and W type cells receive peripheral rod input. the center-surround receptive field information then projects to the lateral geniculate nucleus, which then projects information to the primary visual cortex.

within the primary visual cortex there are "ocular dominance columns" that the LGN projects to that are cortical columns that receive input from one eye or another. within these ocular dominance columns there are distinct layers of cells: "simple cells" in the middle layers receive input from ganglionic cells that receive input from receptive fields that are aligned within the same line-- and are thus stimulated by bars of light in the particular orientation of the ganglionic cells. complex cells receive input from several simple cells and therefore detect movement of bars of light. simple cells in layer 4 also receive "monocular input" and complex cells in the upper and lower layers process "binocular" visual information, processing the disparity between retinal information of each eye.

the primary visual cortex then sends information to the neighboring visual cortices, V2 through V5, each cortex processing the visual information in a progressively complex fashion. for example, whereas V1 receives simple light/dark/color input, V2 processes the object/background differences as well as formation of illusory/incomplete boundaries. V2 then projects into two streams: the dorsal stream then goes to V3, then to the middle temporal cortex, and is the "motion processing" or "how and where" of visual processing. the ventral stream goes to V4, then to the inferotemporal cortex, and is the detail oriented "what" pathway of visual processing. (the right side of the inferotemporal cortex is involved in processing complex shapes such as faces, and the left side is involved in language processing).

a few other brain areas involved in visual processing: the superior colliculus is part of the midbrain that receives Y-type visual information, audition, and somatosensory information and is involved in orienting the head and eyes towards visual stimuli via the "extrageniculate" pathway- via the posterior thalamic nuclei and the amygdala. the superior colliculus is also involved in producing the saccadic eye movements (and thus modulates the cranial nerves that innervate the extrinsic eye muscles, CN III, IV, VI), rapid fixations that break up scanning movements and allow the brain to put together bits of visual information in a process analogous to a film movie. the superior colliculus is also involved in the phenomenon of "blindsight", where a lesion in V1 blocks the primary (primitive) visual processing pathway, and visual information flows through the intact "extrastriate" (mammalian) pathway through the superior colliculus.

the suprachiasmic nucleus is a thalamic nuclei that receives receptive field information from ganglionic cells and is involved in mediating the circadian clock. the circadian clock receives information about light/dark cycles and via transcription factor cycles mediates different autonomic regulatory pathways in the body. the factors in the positive transcriptional loop are BMAL1 and PER2; the ones in the negative loop are CRY1,2 and PER1,3. the "central heterodimers" are BMAL1 and CLOCK. the output of these transcriptional loops produces transcription of CLOCK controlled genes which produce proteins that ultimately alter cellular function. the SCN also projects to the liver, adrenals, and pineal, where is mediates melatonin release.

questions
pathways...
1. each side of the visual field projects to the ... side of the brain.
2. what can total blindness in one eye be caused by?
3. what is heteronymous hemianopsia and what can it be caused by?
4. what is homonymous hemianopsia and what is it caused by?

lateral geniculate nucleus...
5. what are the three types of ganglion cells that the lateral geniculate nucleus receives signals from?
6. describe the role of Y type ganglion cells.
7. describe the role of X type ganglion cells.
8. describe the role of W type ganglion cells.
9. lateral geniculate nucleus projects center-surround receptive fields to...

primary visual cortex...
10. what is the primary visual cortex surrounded by?
11. what is the role of simple, complex, and hypercomplex cells in the primary visual cortex?
12. describe how a simple cell in the visual cortex can sense a "bar of light".
13. what do complex cells do?
14. thalamic neurons project contralateral visual field input to...
15. why are ocular dominance columns so named?
16. which layer is monocular input found in the visual cortex?
17. which layer is binocular input found?
18. retinal disparity provides information regarding...

V2-V5...
19. what does the visual association cortex do?
20. describe the dorsal stream from the visual association cortex.
21. describe the ventral stream from the visual association cortex.
22. both streams converge into...
23. what is a difference between the cells of V2 and V1?
24. what is V4 tuned for?
25. what is the inferotemporal cortex tuned for?

wernicke's area, fusiform gyrus, superior colliculus...
26. what is Wernicke's area associated with?
27. how is Wernicke's area connected with Broca's area?
28. inappropriate activity in the fusiform gyrus can lead to...
29. what is synesthesia and how is it related to the fusiform gyrus?
30. describe the superior colliculus: what it is, what it receives, projects to, what function it is involved in.
31. what are saccadic eye movements and how is the superior colliculus involved in producing them?
32. which cranial nerves does the SC modulate?

blindsight, SCN, circadian clock...
33. lesion of primary visual cortex leads to...
34. what is the pathway for visual information in blindsight?
35. what is the suprachiasmatic nucleus and what is it involved in?
36. circadian rhythms depend on...
37. positive transcriptional loops are mediated by...
38. negative transcriptional loops are mediated by...
39. what are the central heterodimers that are activated or inactivated by these transcriptional loops?
40. output from the circadian clock manifests in...
41. where does the SCN project to? which neurotransmitters does it use to do so?
42. what do the hypothalamic nuclei that the SCN projects to involved in?
43. SCN contains neurons that specifically target...
44. what does effect does the SCN have on the pineal gland?

answers
1. contralateral
2. damage to the optic nerve of one eye distal to the optic chiasm.
3. loss of opposite visual fields due to lesions of the optic chiasm.
4. loss of same side visual fields due to a lesions between the optic chiasm and the visual cortex on one side.

5. Y type, X type, W type.
6. receive input from rods in the periphery of the retina and thus are more sensitive to rapid movement or light intensity changes.
7. receive input from cones in the fovea and thus are more sensitive to fine details of objects, and color.
8. also receive input from rods, detecting movement in periphery of visual field.
9. primary visual cortex, V1.

10. secondary, association, and tertiary visual cortices.
11. developing perception of form, color, direction of movement, and binocular vision through hierarchical organization of these cells.
12. it can receive the receptive fields for ganglion cells that are all oriented along the same line and thus the simple cell can be maximally stimulated only when a bar of light hits the retina at the same location and orientation.
13. detect information about movement of bars of light by combining input from several simple cells.
14. ocular dominance columns in the primary visual cortex.
15. because they only receive input from one eye or the other.
16. simple cells in layer 4.
17. the complex cells in the upper and lower layers.
18. the depth of vision.

19. projects visual information into two streams, dorsal and ventral.
20. the dorsal stream is loosely involved with the "how" and "where" of visual processing. the dorsal stream goes from V2 to V3 to the middle temporal cortex to the posterior parietal cortex.
21. the ventral stream is loosely involved with the "what" of visual processing- identifying complex shapes, forms, colors. the stream goes from V2 to V4 and into the inferotemporal cortex, then to the posterior parietal cortex.
22. prefrontal cortex to form working memory.
23. V2 cells are tuned to more complex stimuli, such as the formation of illusory boundaries and distinguishing between object and background.
24. color, simple geometric shapes.
25. recognition of faces and other complex shapes on the right side, perception of language on the left side.

26. understanding symbolic systems.
27. via the arcuate fasciculus.
28. visual hallucinations.
29. the phenonemon in which a subject experiences different sensory modalities simultaneously such as sound and color, possibly related to cross-activation of color and number neurons in fusiform gyrus.
30. a midbrain structure that has an "extrageniculate" visual pathway involved in orienting the head and eyes towards visual stimulus. receives Y type ganglionic signals, audition, somatosensory input, projects to posterior thalamus (pulvinar nuclei) and amygdala.
31. saccadic eye movements are coordinated movements of the eyes which breaks scanning motion into quick
fixations on different points; the superior colliculus mediates these movements along with the frontal eye field in the motor cortex.
32. III, IV, VI.

33. lack of consciousness of visual information.
34. because the primary pathway to the visual cortex is blocked, the extrastriate pathway takes over and compensates.
35. the nucleus that receives light information from the melanopsin ganglion cells and mediates the circadian rhythm.
36. positive and negative transcriptional loops.
37. BMAL1 and PER2
38. CRY1/2 and PER1/3
39. CLOCK and BMAL1.
40. CLOCK-controlled gene expression, which leads to altering of cellular function.
41. to the dorsomedial and paraventricular hypothalamic nuclei, using vasopressin, GABA, and glutamate.
42. autonomic activity, and HPA axis hormone release.
43. liver, pineal, adrenal.
44. mediates release of melatonin which regulates sleep wake cycles, temperature, cortisol release.

organ systems III: visual system part 3- the retina

this lecture covered basic ideas about the structure and function of the retina. the retina is the layer in the back of the eye that contains the photoreceptor cells that transduce light energy into neural signals. the fovea is the area in the back of the eye which focuses light most readily and the macula lutea is the yellow region surrounding the fovea. the retina is made up of several layers: at the base is the retinal epithelial layer, then the photoreceptor cells, then the integrative cells (horizontal, amacrine, bipolar), then the ganglionic cells. this configuration is called "inverted" because the light has to travel through the ganglionic and integrative cells before hitting the photoreceptors. the photoreceptors need to be close to a blood supply, the choroid vessels (see previous lecture), and thus the inverted configuration serves to keep the thick blood supply from blocking the light from hitting the photoreceptors.

rods and cones are the two types of photoreceptors in the retina, and have complementary properties to each other. cones are better suited for bright light sources while rods are better suited for dim light sources. cones have a lower concentration of pigments and thus a lower sensitivity, while rods have a higher concentration and thus a higher sensitivity (making them better suited for detecting dim light sources). cones have a high concentration in the fovea, the area where light focuses best, and thus provide high visual acuity and spatial resolution while rods are diffusely spread peripherally to the fovea and are more involved in movement and have lower spatial resolution. finally, cones have three colored pigments (isomers of iodospin?) while rods have one color pigment (rhodopsin).

the retinal epithelial layer is the layer that supports the photoreceptor in several ways. first, the pigments within the layer absorb light, preventing the bounceback of light from obscuring the image. during the absorption of light by the photoreceptors, pigments create trans-retinol, which is converted back to cis retinol and transported back into the photoreceptors. this process also creates debris, which is phagocytosed by the retinal epithelial layer. finally, the pigments in this layer absorb blue light preferentially, which helps prevent the production of free radicals.

photoreceptor cells create a graded receptor potential via their pigments, which change conformation after light absorption, opening sodium channels and changing membrane potential. the photoreceptor cells then send signals to the layer of integrative cells which includes the horizontal, amacrine, and bipolar cells. bipolar cells receive signals from several photoreceptor cells, whereas amacrine and horizontal cells integrate signals from several photoreceptors. ganglionic cells receive the processed signal, which it sends to the optic nerve. the receptive field of the ganglionic cell, which spans the photoreceptors that it receives signals from, undergoes lateral inhibition via the integrative cell layer, which creates "center-surround" receptive fields. these are either stimulatory in the center and inhibitory in the periphery, or vice versa. the receptive fields are most stimulated when the edge between the center and periphery "subtends" the light and dark edge; these receptive fields, and thus the signals that the ganglionic cells send to the optic nerve, are most receptive to the contrast between dark and light, making it well suited for distinguishes edges and borders. center surround receptive fields are also involved in color perception; ganglionic cells can receive impulses from colored pigments from cones, creating a receptive field which sends a signals based on the wavelengths of incoming light; thus providing the neural information necessary to construct a colored image.

questions
1. what is the retina?
2. where do the receptor cells lie in relation to the retinal cells?
3. what is the fovea?
4. what is the macula lutea?
5. what is the blind spot?
6. where does the retina blood supply come from?
7. what are the retinal layers starting from the retinal epithelium?
8. what do bipolar, horizontal, amacrine and ganglion cells do?
9. what is the physical makeup of the fovea?
10. what are the pigments in rods and cones that respond to the visible light spectrum?
11. how do photoreceptors produce a receptor potential?
12. what do the retinal integrative cells do?

difference between rods and cones...
13. bright light sources vs. dim light sources...
14. sensitivity / concentration of pigment...
15. acuity / concentration in the fovea...
16. direct vs. scattered light...
17. color...

18. why do photoreceptors need to be close to the choroid blood layer?
19. what does it mean that the retina is inverted and what is the purpose of this orientation?
20. why do the ganglionic and bipolar cells not distort the incoming light?
21. what is the retinal pigment epithelium (RPE)?
22. what is the purpose of the RPE?
23. what is retinal detachment?
24. what causes retinal detachment?

25. bipolar cells receive input from...
26. what do horizontal and amacrine cells do?
27. lateral inhibition of horizontal and amacrine cells creates...
28. what do ganglionic cells do?
29. what are the glial cells that support the optic nerve?
30. what is papilledema?
31. what are on-center and off-center ganglionic cells?
32. both off-center and on-center ganglionic cells produce the most stimulation when...
33. what is the implication of the receptive field of ganglionic cells responding most to the light/dark edge?
34. how do ganglionic cells code color?
35. what is the blind spot?

answers
1. the back inner lining of the eyeball.
2. deep to the retinal cells.
3. the central area in the back of the eye where the light most clearly focuses.
4. the yellow area surrounding the fovea.
5. the area in the back of the retina where the optic nerve exits; contains ganglion cells but no receptor cells.
6. internal carotid provides the central artery which supplies the retina.
7. retinal epithelium, photoreceptors, bipolar/horizontal/amacrine cells, ganglion cells.
8. bipolar, horizontal, amacrine cells integrate visual information and ganglion cells send information to brain stem.
9. fovea has the highest concentration of cone receptor cells which receive more incoming light by the outward spreading of the other retinal layers.
10. rhodopsin in rods and iodopsin in cones.
11. the pigments contained within photoreceptors absorb light and change conformation, causing the opening of sodium channels and the production of a receptor potential.
12. generate EPSP's and IPSP's and summate the potentials from neighboring retinal cells to send an integrated signal to the ganglion cell.

13. rods for bright light, cones for dim light.
14. rods have high concentration of pigment and thus sensitivity, cones have low concentrations of pigment and thus low sensitivity.
15. high concentration of rods in the fovea and thus high sensitivity. low concentration of cones in the fovea and thus low sensitivity.
16. rod receptors are best with direct axial light and cones receptors are best with scattered light.
17. rod receptors have 3 pigments which absorb different colors; cones only have one color pigment.

18. because photoreceptor turnover requires a large oxygen supply.
19. the inverted retina refers to the fact that the photoreceptor cells are the last layer that the light hits. this orientation prevents the blood supply to the photoreceptor cells from blocking the light from hitting the photoreceptors.
20. because the bipolar and ganglionic cells have the same refractive index as the vitreous humor.
21. the pigmented layer deep to the photoreceptors.
22. absorbing light that passes through the photoreceptor to prevent the bounceback of light which could potentially cause blurring. absorbing blue light in particular, which is particularly involved in the production of free radicals. regeneration of trans-retinal back into cis-retinal in the retinal cycle. delivery of nutrients such as glucose and retinol to photoreceptor cells. phagocytosis of debris which might accumulate from the photoreceptor's light absorption. (bouncing blue ball regenerates nutrient debris)
23. when the retinal layer mechanically detaches from the RPE.
24. buildup of pressure in the macula region, or buildup of cellular waste material.

25. several receptor cells.
26. integrate signals from several receptor cells.
27. center-surround receptive fields.
28. transmit signals to the optic nerve which then transmits to the lateral geniculate nucleus of the thalamus.
29. oligodendrocytes myelinate the axons and astrocytes surround the cell bodies and dendrites.
30. limited venous return from the retina caused by increased CSF pressure.
31. on-center ganglionic cells produce receptive fields that produce stimulatory signals from light shining in the middle and the opposite effect from light shining in the periphery. off-center ganglionic cells produce the opposite type of receptive field.
32. their receptive fields subtend the light-dark edge.
33. the purpose of this mechanism is for the photoreceptors to be sensitive to contrasts between light and dark; to distinguish fine features.
34. the summation of the excitatory / inhibitory activity of receptive fields of ganglionic cells which receive signals from different colored pigments within cone cells.
35. the spot on the retina where there are no receptor cells, where the optic nerve exits.

organ systems III: visual system part 2b

this lecture covered a few last concepts about the iris, the lens, and the sympathetic / parasympathetic innervation of the muscles that mediate the aperture of the pupil. the iris is the colored part of the eye, the specific color of which results from the particular distribution of melanin pigments scattered throughout the iris-- if the melanin is deep in the iris, this results in a blue color, and a more general distribution results in a brown or green color.

the iris can be dilated or constricted, allowing varying levels of light into the pupil, depending on the contraction of the dilator pupillae vs. the sphincter pupillae. the more the pupil is constricted by the sphincter pupillae, the less light is let into the eyeball, and the greater the "range of focus" is. this constriction is mediated by a parasympathetic pathway. it can be initiated by light hitting melanopsin ganglion cells in the back of the eye, which innervate the pretectal nuclei, which innervates the edinger westfall nuclei of both eyes, which projects to the ciliary ganglion behind the eyeball, which then projects post ganglionics to the dilator pupillae, constricting the pupil. it also projects to the ciliary muscles, increasing the convexity of the lens as well.

the dilation of the pupil is mediated by a sympathetic pathway which can be initiated by local reflexes or descending influences from the limbic system or hypothalamus. the sympathetic preganglionics originate from the T1-T2 level and synapse at the superior cervical ganglion, which then project post ganglionics via the arterial system to the dilator pupillae, as well as to the tarsal muscle- which connects to the tarsal plate and raises the eyelid when constricted.

questions
1. the iris contains...
2. where does eye color come from?
3. where is the melanin mainly distributed in blue eyes?
4. where is the melanin mainly distributed in brown or green eyes?
5. what does the iris control?
6. what is the relationship between pupil aperture size and the range of focus?
7. describe the action and innervation of the sphincter pupillae.
8. describe the action and innervation of the dilator pupillae.

9. describe the parasympathetic pathway of autonomic innervation of the lens muscles.
10. describe the sympathetic pathway of autonomic innervation of the lens muscles.
11. what is the edinger-westfall nucleus?
12. describe the net effect of parasympathetic innervation on the eye muscles.
13. describe the pathway by which incoming light can cause an autonomic constriction of the pupil.
14. sympathetic innervation of the iris and upper eyelid muscles is initated by...
15. describe the pathway by which sympathetics can cause dilation of the pupil.
16. what is the tarsal muscle? what does it do? where does it insert?
17. what is "ptosis"? what syndrome is this phenomenon seen in?

answers
1. pigmented striations of connective tissue, blood vessels, smooth muscle.
2. the refraction of light from the different distributions of melanin pigment in the iris.
3. on the deep surface of the iris.
4. evenly distributed throughout the iris.
5. the aperture of the pupil.
6. smaller aperture increases range of focus.
7. constricts the pupil aperture, increasing focal length. innervated by parasympathetics.
8. opens the pupil aperture, decreases focal length. innervated by sympathetics.

9. follows the oculomotor nerve CN (III) and synapses at the ciliary ganglion which is posterior to the eyeball.
10. originates from the thoracic spine, synapses on the superior cervical ganglion, and follows the arterial system to the eye.
11. the nucleus of the oculomotor nerve from which the lens muscle preganglionics originate.
12. the sphincter pupillae contracts and the ciliary bodies contract lens.
13. incoming light into at least one eye hits the melanopsin ganglion cells, which innervate the pretectal nuclei, which innervates the EW nuclei of both eyes, which projects to the ciliary ganglion, which projects to the eye muscles and contracts the sphincter pupillae and ciliary bodies.
14. local reflexes, descending influences from limbic system and hypothalamus during emotional state.
15. sympathetic influences described in question 14 can cause the innervation of preganglionics from the T1-T2 level which synapse on the superior cervical ganglion, which then sends axons out to the dilator pupillae (but not the ciliary muscle) and the tarsal muscle, causing dilation of the pupil and lifting of the eyelid.
16. the muscle that lies deep to the levator palpabrae and attaches to the tarsal plate.
17. a drooping eyelid caused by damage to the sympathetic pathway which innervates the tarsal muscle.

organ systems III: visual system part 2a

this lecture covered the anatomical features of the eye which relate to its refraction and focusing of incoming light; namely, the lens and the muscles that control the convexity of the lens. a bit more of the embryology of the eyes: the eyeballs are derived from the same rostral portion of the neural tube as the cerebrum, and as such have outer layers that are analogous to those in the CNS. the eyes are surrounded by an outer fibrous layer, homologous to the dura mater, followed by a vascular layer composed of anastamosing "choroid" blood vessels which is homologous to the arachnoid and pia mater, followed by a nervous layer which is homologous to the neurons in the CNS.

in order to form focused images the eye must focus beams of light that are diverging from single point sources: in other words, any light source will emit light that diverges and needs to be converged back into a single point in the back of the retina. the lens is a transparent component of the eye (derived from ectoderm) which accomplishes this refraction through its convexity. the convexity of the lens is maintained internally by elastic fibers and externally through the suspensory ligaments, which are attached to the ciliary bodies that surround the lens radially. when these ciliary muscles contract, this relaxes the suspensory ligaments, allowing the internal elastic fibers to create a more convex shape in the lens; and the opposite effect for the relaxation of the ciliary muscles.

the general rule with convexity of lens vs. distance of light source: the further away the light source, the less the beams of light are diverging, and thus less refraction is necessary, and thus less convexity is necessary. the closer the light source, the more divergence is happening, and more refraction is necessary to refocus the light beam at the back of the retina. hyperopia is far sightedness, resulting from an eyeball that is too short- in this case, the light is being focused on a point beyond the retina. myopia is the opposite, resulting from an eyeball that is too long and light being focused in front of the retina. hyperopia is the age related loss of convexity of the lens caused by the loss of elasticity.

a few more anatomical notes: the sclera is the tough white connective tissue that covers the eyeball, from which the extrinsic muscles of the eye insert. the cornea is the translucent, avascular continuation of the sclera that covers the lens and lets light into the eyeball. the vitreous body is the gel like fluid in the eyeball itself which is made largely of water, hyaluronic acid, and type II collagen. the anterior and posterior chambers are deep to the cornea, separated by the iris, and are the site of secretion of the aqueous humor by ciliary processes, which then drains into Schlemm's canal into the vascular system.

questions
embryology...
1. what is the eyeball derived from?
2. what are the neural and pigmented retinal layers derived from?
3. what are the sclera and choroid derived from?
4. what is the lens derived from?
5. optic nerve is surrounded by...

eyeball anatomy...
6. what is the vitreous body and what is it made of?
7. what are "floaters"?
8. what is the hyaloid canal and how is it related to floaters?
9. what are the three outer layers of the eyeball and what CNS structures are they homologous to?
10. what is the sclera?
11. describe the cornea.
12. what does the vascular coat consist of?

refraction and the lens...
13. why are the cornea and lens curved?
14. describe the lens.
15. describe how the lens adjusts the refraction of light according to the distance from the light source.
16. what is hyperopia?
17. what is myopia?
18. what is the resting convexity of the lens maintained by?
19. internal elastic fibers in the lens produce...
20. what is the capsule of the lens made of?
21. describe the production of new lens cells.
22. what is presbyopia and what is it caused by?
23. what is cataracts?
24. describe the suspensory ligaments that attach to the lens.
25. what do suspensory ligaments do?
26. convexity of the lens is altered by...
27. what happens when the ciliary muscles contract?
28. where are the anterior and posterior chambers? what are they partitioned by?
29. where does aqueous humor form and travel to?
30. what does Schlemm's canal do?
31. what is glaucoma caused by?

answers
1. same part of the neural tube that produces the cerebral hemispheres.
2. optic vesicle.
3. embryonic meningeal tissues.
4. ectoderm.
5. dura, arachnoid, pia, subarachnoid space.

6. the gel-like fluid inside the eyeball made of water, hyaluronic acid, type II collagen fibers.
7. tiny clumps of gel in the vitreous body that are too large to be phagocytosed during development.
8. the hyaloid canal is the vestigial remains of the hyaloid artery, remnants of which can turn into floaters.
9. outer fibrous coat homologous to dura mater, vascular coat homologous to arachnoid/pia mater, and nervous coat homologous to CNS layer.
10. dense, white CT, which is the point of insertion for the extrinsic muscles of the eye.
11. the cornea is a transparent, avascular continuation of the sclera in the center of the eyeball which allows light into the eye.
12. a layer of anastamosing blood vessels (choroid) and the ciliary body, which regulates the refraction of light.

13. to refract light from a point source in order to converge back into one point.
14. clear, avascular, and depends on diffusion of nutrients from vitreous humor, like the cornea.
15. for close light sources, the lens becomes more convex and for far away light sources the lens becomes less convex.
16. far-sightedness: eyeball is too short and light converges behind the retina.
17. near-sightedness: eyeball is too long and light converges in front of the retina.
18. internal elastic fibers and suspensory ciliary ligaments.
19. an inherent tendency to bulge.
20. collagen IV and glycoprotein.
21. lens cells are produced from the germinal center on the side of the lens, which then migrate from the germinal zone, lose their nucleus, and become transparent.
22. age-related loss of lens resting convexity caused by loss of elasticity.
23. reduction of vision due to opacity of lens.
24. zonule fibers that extend from ciliary body to the equatorial perimeter of the lens.
25. maintain resting tension and decrease convexity of the lens via outward tension.
26. ciliary muscle.
27. the tension in the suspensory ligaments decreases, which allows the lens to increase its elasticity and convexity.
28. deep to the cornea, partitioned by the iris.
29. formed by the ciliary processes, secreted into the anterior and posterior chambers.
30. absorbs the aqueous humor into veins.
31. a buildup of fluid pressure due to inadequate drainage into Schlemm's canal.

organ systems III: visual system part 1

this lecture looked at the basic features of the eye; bones, muscles, and nerves. the orbital cavity is a spherical space that houses the eyeball which is composed of many different bones: frontal, maxilla, zygoma, ethmoid, palatine, sphenoid, lacrimal. the orbital cavity is expressly designed such that the eyes are facing forward and parallel to each other, making the line of sight parallel with the ground. the eye itself only takes up 1/3 of the orbital cavity; the rest of the cavity is filled with muscle, periorbital fat, nerves, and fascia. the fascia that surrounds the eye and suspends it above the floor of the orbital cavity is called the fascia bulbi.

a few more anatomical notes: the corners of the eyes are called the inner and outer canthus. the tarsal plates are dense connective tissue that line the eyelids, and contain tarsal glands which secrete mucus to moisten the eyeballs. the superior and inferior fornices are the space on the insides of the eyelids, which are lined with the conjunctiva, a thin covering which also lines the sclera. the lacrimal apparatus produces tears in the upper lateral edge of the orbital cavity, which migrate across the eye, then drain into through the puncta (skin pores) into the lacrimal canaliculi, which collects into the lacrimal sac, which drains into the nasolacrimal duct, which opens up into the inferior meatus (which is why crying instantaneously produces a runny nose).

eye movements are mediated by 6 muscles. the superior rectus produces a elevation / adduction motion, the inferior rectus produces depression and adduction. the medial rectus adducts and the lateral rectus abducts. the superior oblique, which hooks around the trochlea and approaches the eyeball obliquely, depresses and abducts the eye, while the inferior oblique, which originates from the medial orbital cavity floor, elevates and abducts the eye. the superior, medial, inferior rectus, the levator palpabrae, and inferior oblique are all innervated by the oculomotor nerve (CN III). the superior oblique is innervated by the trochlear nerve (CN IV), and the lateral rectus is innervated by the abducens nerve (CN VI).

questions
anatomical features...
1. what are the bones of the orbital cavity?
2. what are the bones of the orbital cavity designed for?
3. how much of the orbital cavity does the eyeball occupy?
4. what is in the remaining space of the orbital cavity?
5. what is the fascia bulbi?
6. what muscle closes and constricts the eyelids?
7. what is the name for the corners of the eyes?
8. what are the tarsal plates?
9. what are tarsal glands and what do they do?
10. what is the conjunctivum?
11. describe the lacrimal apparatus.
12. where do the tears secreted by the lacrimal glands drain into?

eye movements...
13. what are the muscles that control eye movement?
14. superior oblique hooks around...
15. inferior oblique originates from...

motion of...
16. superior rectus...
17. inferior rectus...
18. medial rectus...
19. lateral rectus...
20. superior oblique...
21. inferior oblique...

nerves...
22. where do the nerves to the eye enter the orbital cavity?
23. what are the motor nerves that innervate the eye muscles?
24. what is the sensory nerve that innervates the eyeball and orbital cavity?

answers
1. frontal, maxilla, zygoma, ethmoid, palatine, sphenoid, lacrimal.
2. to orient the eyes in a forward position (so that vision is parallel to the ground)
3. 1/3
4. muscles, fascia, nerves, periorbital fat.
5. the CT sheath that surrounds the eyeball and suspends it off of the orbital floor.
6. orbicularis oculi.
7. the inner and outer canthus.
8. dense CT that support the eyelids.
9. glands within the tarsal plates that secrete mucus to moisten the eyes.
10. the lining of the superior and inferior fornices and covering of the sclera.
11. lacrimal glands in the upper lateral recesses of the eye secretes tears into the superior fornix.
12. puncta (skin pores), canaliculi and lacrimal sac, nasolacrimal duct, inferior meatus.

13. the four rectuses (superior, inferior, lateral, medial), superior and inferior oblique, and levator palpabrae superioris.
14. trochlea
15. medial orbital floor.

16. elevation and adduction
17. depression and adduction
18. adduction
19. abduction
20. depression and abduction
21. elevation and abduction

22. the superior orbital fissure.
23. oculomotor (CN III) innervates the superior, inferior, medial rectus, inferior oblique, levator palpebrae superioris. trochlear (CN IV) innervates the superior oblique. abducens (CN VI) innervates the lateral rectus.
24. trigeminal (V1)