S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani

S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani Thursday, January 15, 2009 Proof: Sally Hamissou Dr. Banos Brainstem II Page 1 of 8 RF= reticular formation BSRF=brainstem reticular formation ARAS = Ascending Reticular Activating System CN= cranial nerve I. Introduction [S1]: Brain Stem II II. Today. [S1] a. Brain Stem Reticular Formation b. Talk about the corticobulbar tract briefly. c. The coverage of the cranial nerves and their nuclei is not exhaustive, and he wants us to understand the big picture. He will be introducing the cranial nerves, nuclei, and their basic function, and more things will be added later. III. Major Brain Stem Activities [S3] a. Conduit ascending and descending pathways. We have talked about it already. b. Integrative functions are what we are going to hit today. i. Complex motor patterns ii. Vegetative things iii. Arousal c. Cranial Nerve functions. IV. Integrative Functions: Brain Stem Reticular Formation [S4] V. Brain Stem Reticular Formation [S5] a. Reticular means “net like” in Latin. That is appropriate because the BSRF is really a set of loosely defined nuclei and tracts. b. It extends through the brainstem. c. There are tons of ascending/descending pathways and intimate connections with cranial nerves/nuclei. d. It’s this nebulous/ wispy nucleus that connects to everything. e. Input and output is everywhere! Put that on your note card! VI. Brain Stem Reticular Formation [S6] a. This is location of the BSRF. It’s illustrating that it runs the entire length of the brainstem. It does not have straight fast boundaries so don’t memorize it like that. b. It looks like a tight normal nucleus that exploded out and became a cloud of cell bodies and nuclear functions spread out to the brainstem. VII. Brainstem Reticular Formation [S7] a. It can be roughly divided into three longitudinal zones: i. Midline - Raphe Nuclei -Longitudinally ii. Medial Zone is long ascending and descending projections Furthest projections. b. Lateral Zone - Cranial nerve reflexes and some visceral functions VIII. Brain Stem Reticular Formation [S8] a. Connectivity is extremely complex b. Many different types of neurons. They descend down multiple levels of the spinal cord. Many have numerous ascending and descending collaterals. b. Even the complex neurons in there are not going from point A to point B. You have neurons that are connecting to multiple simultaneously. Some have bifurcating collaterals. c. Many have very large dendritic fields across multiple levels of the brain stem. So you are bringing input to these neurons from multiple levels. Sending output to different points of bifurcation. IX. Brain Stem Reticular Formation [S9] a. So this is a cross-section of the brainstem on the side. Pons, midbrain, medulla at bottom. This is single neuron in the BSRF. b. Various nuclei all over this place. Think of millions of neurons like that connecting all these things together. X. Reticular Formation Functions [S10] a. RF participates in control of movement through connections with both the spinal cord and cerebellum. i. So we have talked about the corticospinal tract as the motor movement. The corticospinal cord is one player in motor movement that controls your most voluntary and conscious movements. Like reaching for the pencil to take notes- things that you are aware of, conscious motor movement. ii. Think about the motor things that you are not aware of like balance, posture, staying in your seat- you are not consciously deciding what muscle needs to exert of force. iii. There are several systems that contribute that over the course. The BSRF also plays a role in that as well. iv. You have two reticulospinal tracts (reticulo-starts in the brainstem and travels to the spinal cord) originate in the rostral pontine and medullary reticular formation v. There are major alternate route by which spinal neurons are controlled vi. Can help regulate sensitivity of spinal reflex arcs and tonic inhibition of flexor reflexes. If you take the innervation away from the spinal cord (like cut the brainstem pretty high) you can get weird postural S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani Thursday, January 15, 2009 Proof: Sally Hamissou Dr. Banos Brainstem II Page 2 of 8 extensor and strange things happen to your muscle that you don’t think about it because you never have it happen when you have voluntary controls. The reticulospinal tracts are inhibiting the reflex that would cause the limbs to draw up if the reflexes ran unchecked. vii. It also mediates some complex behavioral reflexes like yawning (sort of voluntary but mostly an involuntary reflex) - not like a spinal cord reflex, which is more complex. viii. Stretching is kind of voluntary but you can do it involuntarily also. ix. A baby suckling is a reflex that is not voluntary. This is where RF is exerting some control over these types of things. x. It also has some interconnectivity with cerebellar motor control circuitry XI. Clinical Correlation [S11]: Pseudobulbar Affect a. A big clinical correlation is Pseudobulbar affect. A good example is Amyotrophic Lateral Sclerosis. Although you can see it in stroke and head injury. b. Do you know what Affect is? Affect is the behavioral display of your emotional state. It’s not the emotional state. Sad can be the emotional state. Affect is that I am quiet, looking at the ground etc. Laughing is affect. Usually affects can be reflective of your moods and be correlated. But they are two separate issues. c. When you have degeneration of descending motor pathways from the cortex to the brainstem- like LMN and UMN disease, behavioral reflexes are dis-inhibited. d. Pseudobulbar affect is uncontrollable laugher and crying. It’s constant. Usually it’s crying, but there are people that will cry at the drop of hat and they don’t feel sad. They are embarrassed by it. e. It maybe appropriate to the situation but it may not be. The classic is I was watching TV and sad commercial came on, and I burst into tears. And why am I crying? Good marketers don’t want you to cry because of their commercial. f. Sometimes mentioning the sadness or crying like in stroke patients. If you distract them it goes away. g. Conceptually analogous to upper motor neuron hyperreflexia except it’s a brainstem reflex that’s coming out. Any sudden emotional burst pulls an emotional response. h. [SQ]: Is this like when you laugh at funeral or something like that. i. [A]: That’s the border line. There are more sophisticated cortical things going on. It’s related to that except but we do have more control over this, then someone who has had a stroke. ii. A good example is children; a lot of reflexes aren’t well-developed obviously. A child drops the toy and the crying just starts. It’s extreme response of dropping the toy. Because there isn’t sophisticated inhibition developed for their reflexes. That’s a normal manifestation of something like that. XII. Clinical correlation [S12]: Terri Schiavo Case a. This case was big news because there was debate on whether the behaviors that she was exhibiting was conscious thought. A lot of neurologists were saying these were brain stem reflexes. If there are sounds near by, you are going orient to them. You can have emotional responses in the facial muscles that are very sophisticated and that are just reflexive. There was an argument of no real higher level activity; it was a series of dis-inhibited brainstem reflexes that looked like normal behavior. b. More about the background of the case found [21:46] XIII.Reticular Formation Functions [S13] a. Second big function of RF is modulation of transmission in the pain pathways. We talked about the spinothalamic tract, the pain comes in and zoom it goes to the brain. Pain is extremely complex phenomenon. There are lots of things that modulate pain experiences. Part of that is the involvement is by RF. b. You have Spinomesencephalic (starting spine and go midbrain) fibers bring information and go to the periaqueductal grey (found around the cerebral aqueduct if we are talking about midbrain). c. Periaqueductal grey also receives input from the hypothalamus and cortex about behavioral and conscious intention, cognitive states, and drive state from the hypothalamus. d. Efferent from the periaqueductal grey project to one of the raphe nuclei (help modulate pain) and medullary reticular formation. e. All this projects to the spinal cord and can suppress transmission of pain information in the spinothalamic tract f. He said to think concepts and not get caught up in this. XIV. Reticular Formation Functions [S14] a. Red line is the spinothalamic tract b. This is all the supporting players that are modulating that. c. This is going to be a recurring theme. The big four pathways don’t do everything by themselves. There are lots of supporting pathways that modulate how they function. d. Periaqueductal grey is getting information from the spinal cord about pain and cortex and hypothalamus to the raphe and then to spinal cord. e. This little arrow here for a psychologist is huge. That means the behavioral therapeutic techniques we use have a neural mechanism of action. People don’t believe that what you think in your thoughts and perception of pain S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani Thursday, January 15, 2009 Proof: Sally Hamissou Dr. Banos Brainstem II Page 3 of 8 can alter your physical experience of pain but it’s true. It doesn’t make the pain go away, but it can alter the experience of pain. XV. Clinical Correlation [S15]: Pain Management a. Pain Management is clinical correlation. i. Periaqueductal grey has high concentration of opiate receptors 1. Endogenous opiates that help control of modulation of pain. 2. Exogenous opiates, our hardcore medicines, act of opiate receptors and use that pathway to influence pain. XVI. Pause for Contemplation [S16], [S17] a. Really drill this in (TEST): The major recurring theme of LOOPS. There is very little in neural function that is actually linear. As we add on more pathways, we need to realize that everything is continuously running in loops. i. Brain function seems to be up regulating or down regulating a loop system. So you tend to have an external influence that will help adjust it. ii. We have already talked about muscle tone modulated by the UMN. iii. We have talked about reflex loops and the LMN reflexes and brainstem reflexes. iv. Pain modulations is a linear pathway if you are looking at the spinothalamic tract. But it is kind of a loop system that has some feedback that can modulate the experience. b. A lot of pathology and treatment of pathology deals with getting these loops back in balance or loops falling out of balance. c. A lot of medical and neurological things that go on are usually hyper-this or hypo-that, and that illustrates the concepts: you have too much or too little of some aspect of the balance. Keep that in mind. d. [S17] This is the linear pathway, but here is the feedback loop that completes the modulatory circulatory. XVII. Autonomic Reflex Circulatory [S18] a. The third function of the RF is autonomic reflex circuitry. b. Reticular formation gets input from environmental changes from various conduits including the cortex and the hypothalamus. c. RF sends output to: cranial nerve nuclei and Intermediolateral cell column of the spinal cord that’s involved in autonomic processes. i. Involved in breathing, heart rate, and blood pressure, the very basic vegetative types of things. d. You have heard that the brainstem is where breathing and heart rate is involved. XVIII. Clinical Correlation [S19]: Damage to the Medulla and Horner’s Syndrome a. The clinical correlation is damage to the medulla often kills you. So it’s not the entire brainstem, you can have midbrain damage, pons damage- and those are not always fatal if not extremely extensive. The medulla is hard to sustain a lot of damage to and survive because that’s where lot aspects of RF that control the vegetative functions are located. b. Another clinical correlation is Horner’s Syndrome. So you have pathways that go to intermediolateral cell column (in spinal cord) that control a lot of autonomic functions. c. Horners Syndrome (syndrome is grouping of common symptoms, it’s not a disease process necessarily) which include: i. Ipsilateral Miosis (small pupil) ii. Ipsilateral Ptosis (drooping eyelid) iii. Ipsilateral Flushing/lack of sweating d. You can have various lesions and disease processes that can interrupt this system. So Horner’s Syndrome is a grouping of symptoms. e. Leave it to you if you want to study that vigorously. Clinically it’s not a bad thing to now. It might suggest to you that there’s a lot more going than what the patient is presenting. XIX. Reticular Formation Functions [20] a. BSRF is involved in control of arousal and consciousness. b. Theme is input from multiple modalities/sources. Pain is big one that gives input in this system. c. Ascending pathways from RF project to thalamus, cortex, and other structures. d. Thalamus is important in maintaining arousal and “cortical tone.” Again this idea of tonic stimulation, which is a loop system. These projections go to the thalamus which keeps the cortex stimulated enough so that can respond to environmental stimuli quickly. e. This system which is loosely defined (not a single pathway or structure) is called the Ascending Reticular Activating System (ARAS). f. The important point is that it’s a functional system not a distinct structure, and the RF is a big part of it. XX. Clinical correlation [S21]: Sleep/wakefulness S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani Thursday, January 15, 2009 Proof: Sally Hamissou Dr. Banos Brainstem II Page 4 of 8 a. It’s going to be involved in normal functions like sleep/wakefulness. If you were talking about regulation of arousal, it would make sense the sleep and wakefulness would be involved. b. Loss of Consciousness for various reasons. i. Traumatic brain injury- if you take a good hit to the head, you get knocked unconscious. Part of the reason is the way the brain is positioned in the skull, the spinal cord and brainstem don’t have much room to move, but the cortex can pivot around the brainstem (the fulcrum) including the medulla. You are twisting the area where the ARAS is, and that’s how you turn the lights off by disrupt the ARAS. ii. If you have severe traumatic brain injury, you loose consciousness for other reasons but especially for boxers this is usually why they can get knocked in the head and they can come around afterwards. iii. Things that wake you up when you loose consciousness, like smelling salts (not used extensively anymore). Smelling salts will wake you up, it usually ammonia, adverse smells that are really pain sensations. They activate the pain pathway and that activates ARAS and jolts it back in. It gives a good stimulation to the cortex to bring the arousal back around. iv. Sternal rubs- If you have seen someone unconsciousness EMTs will do this. Take a knuckle and rub vigorously on the sternum because that hurts. It causes a pretty stout pain, so it will jolt the ARAS pretty quickly. It will help you figure out if someone fainted or if there is something else going on. Don’t recommend a sternal rub because you don’t know the medical history (cardiac etc). You can pinch someone’s fingernail. Just enough pain to perk them-arouse them. c. You can be in a coma for a couple of reasons. You can be in a coma because your entire cortex is damaged. You can also have a coma because of focal damage to ARAS. A stroke to the medulla is hard to survive. You can have brainstem strokes that hits the ARAS at the right spot and it permanently turns the lights out and the patient ends up in a coma. d. There is a lot of medical controversory. Part if is from Terri Schiavo case about coma vs. minimally conscious state. They argued is she completely vegetative or is there something cognitive going on? e. Recent literature shows a lot of distinction between coma and minimally conscious state. It depends on whether you have intact sleep and wake cycles and brain activity. Part of it is reduced down to ARAS: whether you have the system doing its function and trying to stimulate the cortex or that it can’t get stimulated enough versus is the system completely non-operational and the person can’t wake up at all. f. The boundaries between actual meaningful cognition and what is vegetative is extremely blurry. XXI. The Corticobulbar Tract [S22] a. Not in much detail. It will be built on to in later lectures. Bulb is the brainstem, referring to brainstem to overall. Its a more anatomical term. Clinically, it shouldn’t be used. Be specific. Cortex to the brainstem. b. The reason they don’t say corticopanotine tract etc, because it’s actually a tract that goes to several different levels of the brainstem, essentially the cranial nerve nuclei. XXII. The Corticobulbar Tract [S23] a. Corticospinal tract have descending motor pathways. i. We have HAL-head arm and legs on the homunculus b. And they decussates at a single point in the pyramids of the medulla (pyramidal decussation) XXIII. The Corticobulbar Tract [S24] a. Corticobulbar tract i. Descending motor pathways to cranial nerve nuclei ii. Basically they include HAL’s head because they time you are in the spinal cord, you should have no motor pathways that are related to the head because it’s late to dive off the spinal cord to go and make it back to the head. iii. Fibers for each CN nucleus decussate at the level of that nucleus. So there are multiple points of decussation in that pathway. Really remember that especially for CN symptoms and cases. Remember that corticospinal desiccates once, corticobulbar desiccates many times and the level of the individual nuclei. XXIV. Cranial Nerves and Their Nuclei [S25] a. I want to cover the basics of the CN. There are a couple of pathways thrown in the lecture. The more clinically relevant CN will be built on later in the course and today is just an overview. XXV. A word about organization [S26-29] a. Various CN and nuclei b. Sensory and motor spinal nerves can be divided into sensory and motor. c. Sensory tends to be dorsal. Motor tends to be ventral. d. Within sensory, you have somatic and visceral. i. Somatic sensory - pain, temperature, mechanical stimuli. This is dorsal column in the spinal cord and the spinothalmic tract. ii. We haven’t talked about visceral pathways. Receptive endings of the viscera. iii. Be aware that you have a somatic and visceral in the spinal cord. S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani Thursday, January 15, 2009 Proof: Sally Hamissou Dr. Banos Brainstem II Page 5 of 8 e. Motor (ventral) i. Motor Somatic - Innervate skeletal muscle. And that’s the corticospinal tract. ii. Motor Visceral – You are not really moving the viscera that much, maybe in some aspects of the digestive system. But you do have some efferent pathways down to the autonomic ganglia that control the viscera. f. When we talk about CN nuclei, we will get more specific in these distinctions and we will add more to it. g. There are also special sensory and special motor in the CN. These are things that your head and face do that rest of your body doesn’t do. i. Special sensory fibers: 1. Hearing 2. Equilibrium applies to the rest of the body but it’s really the mechanism of the inner ear that really takes care of it. 3. Taste h. Have to take these special sensory fibers into account with CN nuclei because they don’t occur in other places of the body. i. Special motor fibers or Branchial motor (term from embryological tissue that they develop from) i. Muscles of the head and face that are otherwise structurally and functionally the same as other muscles i.e. movement of jaw. ii. But since they originate differently, we call them special motor fibers. j. There are also distinct autonomic fibers (he said we won’t go into much detail on). k. Think of basic motor/sensory and basic visceral/somatic divisions and then add on special sensory and motor. l. [S28] This shifting of the neural tube around the pons (not really a specific level), the pons illustrates the best where you have sulcus limitans. The motor and sensory are organized, so since you add a special sensory and motor, so you end up with 3 nuclei on either side. This is very abstract generic picture. In every level you are not going to have 6 nuclei lining up neatly like that. m. Look longitudinally [S29], this is where things will be organized. It’s the same thing from [S28], sensory is more peripheral, motor on the medially. (I believe that’s what he was trying to show). He continued to point our things. Whole purpose: the six nuclei are not going to be neatly everywhere. But, when you spread them out longitudinally, they are represented everywhere. This picture is in the book. It has the nuclei named and is helpful.

XXVI. CN I [S30,31] a. [S30] Look at their location and function. The CN are numbered top to bottom, anterior to posterior, rostral to caudal. They follow a linear logical ordering except for the last couple CN. If you don’t know where to look for a nerve, start at the top and count down. It is extremely important you know what they do and learn where they are located! It’s really important for OPT and DENT to know the location of these nerves. You can get various symptoms around the head; you need to know physically where they run together, what symptoms tend to cluster together, because nerves are together. You rarely will get a clinical case with a patient that has a single CN defect, more likely multiple nerve things that you have to sort out and find out to what extent it is related to your specialty and to what extent it is related to other specialties. b. Starting at top CN I olfactory. c. Fiber types are special sensory—Smell. No other part of your body has sensory fibers for smell. d. In the picture [S31] you are looking at the olfactory bulb, it’s not technically CN I. CN I is actually the fibers that originate in the olfactory mucosa of the nasal cavity, pass through the cribiform plate, and synapse onto the olfactory bulb. e. So when you take the brain out of the skull, the fibers get ripped of. Know that the olfactory bulb is technically not the nerve! f. It’s’ the only one that there is no brain stem nucleus for CNI. Why? It’s one of the oldest sensory systems that we have. It’s wired in a primitive way, and the other nuclei that have been added over the course of evolution to the CN tend to be more sophisticated to their wiring. Smell is old and a crude sense that is hard-wired simply. XXVII. Diagram [S32] a. The cribiform plate looking in the anterior cranial fossa is a sieve (holes). Here is the cross-section. Here are the nerve fibers which is CN I. They cross through the cribiform plate and synapse to the olfactory bulb XXVIII. Clinical Correlation [S33]: Olfactory Nerve Dysfunction a. Olfactory nerve dysfunction is alteration of taste or smell. Taste and smell as we perceive them are hard to differentiate. If you lose your sense of smell, you also lose what our brain assembles as taste. Not what we literally think as the taste from the taste buds. Taste and smell merge in our perception. b. Know that someone with CN I dysfunction will often tell you that I can’t smell or food doesn’t taste right. c. Upper respiratory tract infection will affect CN I temporarily d. Traumatic Brain Injury (TBI). S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani Thursday, January 15, 2009 Proof: Sally Hamissou Dr. Banos Brainstem II Page 6 of 8 i. The frontal lobes sit on top. It can slosh forward, and move the olfactory bulb; you shear of these fibers. Disconnect the sense of smell. TBI patients with good/moderate TBI will tell you that they can’t smell anything and food doesn’t taste the same and can be a big problem down the road. ii. [SQ]: How do you fix that? [A]: We can’t do anything but over the course of time, it can regain most function back. If you have mild loss, you can get functional recovery but not because of us. e. Subfrontal meningioma is tumor of the mengines. It can damage CN I. f. Dementia- Recent research has shown that there is degeneration of the olfactory bulb. i. Now there is a lot of testing companies that are developing “smell markers.” Smell the different markers and tell you what they smell like. It can lead to screening tools for dementia. g. Some basic definitions [S34] i. Anosmia - Total loss of smell ii. Hyposmia - Partial loss of smell iii. Hyperosmia - Exaggerated sense of smell, less common iv. Dysomia - Distorted sense of smell; People report that they can smell things but they don’t smell right (ie foods smell like other foods) v. Olfactory hallucinations- usually not a CN I defect. But it is associated with the olfactory system. People can hallucinate auditory and visual things for many different reasons. But if they have olfactory hallucinations, that can indicate seizures and they would need to see a neurologist. XXIX. CN II OPTIC TRACT [S35, 36] a. Special Sensory –Vision b. Retinal ganglion cells to fibers going to all three of these pathways: i. Thalamus to the lateral geniculate nucleus 1. Primary visual pathway ii. Superior colliculus 1. Reflexes involving vision and light. Something comes at you fast, you turn your head that way or turn away, because of the superior colliculus. iii. Hypothalamus 1. Light-dependent behavioral cycles that are regulated. 2. Does not have a specific nucleus in the brain stem c. Blind sight (clinical case) is damage to visual cortex and patient is completely blind but they can respond to visual stimuli. They can’t see anything but if you shine light, they can tell you accurately where it is but can’t consciously perceive light. The hypothesis is that the information is going to the superior colliculus is getting processed, even though no conscious sensory experiences of vision. d. Optic tract doesn’t have a specific brainstem nucleus unless you counting the thalamus as the brainstem. It goes to LGN to thalamus and then off to the specific cortex. XXX. CN III Oculomotor [S37,38] a. CN III- oculomotor is coming out the inner peduncular system. The cerebral peduncles on their side, and the two nerves coming out. b. CN III- Somatic Motor involved Eye movement. The somatic motor goes to the superior, inferior, medial recti , Inferior oblique and levator palpebrae superioris (lifting the eyelid) c. Autonomic component is responsible for pupillary constriction d. Edinger-Westphal nucleus responsible to constriction. Sends efferent to pupillary sphincter i. So you want to associate Edinger-Westphal nucleus with CN III and with pupillary constriction response. e. [SQ]: It is autonomic because we don’t realize that we’re constricting our pupil? i. A: Autonomic response is fight or flight response. If you are frightened or excited, your pupils get really big. No conscious control. XXXI. Diagram [S39] a. Typical midbrain slice. Nucleus of III is there, and Edinger-Westphal nucleus is right there with it. XXXII. CN III Oculomotor [S40-42] a. The muscles of eye movement: i. Superior rectus (straight muscle)- on top of the eye elevation of eye when you are looking straight ii. Inferior rectus (straight muscle) - depression iii. Medial rectus – adduction, pulling inwards b. Obliques work differently depending on if you are looking straight ahead or looking at one extreme or another c. Levator muscle that elevates the lid. d. To help remember the muscles: i. CN Ill Oculomotor is “Pillars” that hold the eye open if you look at a roman numeral. ii. CN VII (Arabic number 7) Facial is “Hook” that pulls the eye closed. Remember which one closes the eye, and which opens the eye. S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani Thursday, January 15, 2009 Proof: Sally Hamissou Dr. Banos Brainstem II Page 7 of 8 e. [S42] Edinger-Westphal nucleus i. This is the efferent component of the pupillary light reflex ii. The pupillary light reflex is when the light is shine in the pupil, and the pupil should constrict depending on ambient conditions. XXXIII. Clinical Correlation [S43-47]: Damage to CN III a. Damage to CN Ill or nucleus of Ill i. The classic is “Down and out” eyeball –depressed and out, medial rectus is not working and the eye drifts outwards ii. Diplopia –double vision iii. Ptosis –eyelid dropping iv. Dilated and fixed pupil – because the pupillary accommodation response is not working v. Paralysis of pupillary accommodation vi. Overall: down and out eyeball, pupil is blown, and no response when you shine a light in the eye. b. Can be caused by i. Uncal/transtentorial herniation 1. uncus of the temporal lobe herinates over the tentorium cerbelli and impinges onto the CN III. So all TV shows talk about “blown pupil”, it’s basically a symptom of stroke, bleed, large mass lesion that’s causing hearniation. 2. In the ER, you want know if someone has a herniation extremely quick, that’s they check the eye first and check pupils, this is the first things that are checked when people are not responsive. ii. Also cause by aneurysm c. [S44] Pupillary light reflex is basically a direct and consensual response. So direct response is if I shine in your left eye, your left pupil should constrict and the right pupil should also constrict with it (consensual response). They don’t function independently in the reflex. i. CN II is the input of the reflex to the Edinger-Westphal nucleus and sends separate efferent out to CN III, which controls the pupil. d. [S45] If you have lesion (lightning bolt), if you shine the light in the left eye, you don’t get a direct response. And you don’t get a consensual response of pupillary constriction to the right eye either because there is not input to the reflex system. i. If I shine the light in your right eye, I get a response from both eyes– direct and consensual. e. [S46] If I have a lesion there, if I shine light in the left eye, I lose direct, but keep the consensual. i. If shine in the right eye, lose the consensual and keep the direct. ii. Testing the reflex is good way to localize where on the pathway the lesion could be. It’s part of the basic neurological exam. iii. There is another reflex system that functions similarly that we will later discuss. Need to understand direct and consensual response f. [S47] If you hit right there, right in the middle brain at Edinger-Westphal nucleus. You have nothing for either.

XXXIV. CN IV Trochlear [S48-50] a. CN IV - Trochlear is also involved in eye movement. It controls the Superior Oblique which intorts, depresses, adducts the eye. The obliques are more complicated because it depends on where your gaze is. Not doing all these movements at the same time. b. [S50] Mapping onto the brainstem. Look at the midbrain, where the eyes are so it makes sense. CN IV lower than CN III. Conceptually where they are, not exactly near the surface. c. Trochlear is ONLY CN to exit out of the dorsal aspect of the brainstem. d. In the picture, it is actually coming out from the behind, it’s not origin point. But, peel down the cerebellum and peak down on the brainstem around the corpus quadrigemena, and right there (dots) you’ll see little thin nerves coming of there. They are usually torn before they make it to the front of brain. CN IV is hard to find.

XXXV. CNVI Abducens [S51-53] a. CNVI somatic motor that controls Lateral rectus. CNIII was medial rectus. It’s responsible from the abduction of the eye or pulling outward. b. Look at the longitudinally arrangement, CN 3, 4, 6, in cross-section are located about there. [S53] c. Introduction to pathway that is crucial for oculomotor things and neurological syndromes. XXXVI. Finally Lets Add a Pathway [S55,56] a. Think about what muscles are being used when we look to the left or right? i. You may think the eyes are doing the same thing when eyes look to left, but really one is abducting and the other is adducting. b. What cranial nerves are going to be responsible for horizontal movement that is coordinated? S1: Neurosciences 9:00-10:00 Scribe: Sunita Jagani Thursday, January 15, 2009 Proof: Sally Hamissou Dr. Banos Brainstem II Page 8 of 8 i. Adduction (CN III) on one side ii. Abduction (CN VI) on the other side iii. Wired so they do the opposite when you are doing that. c. [S56] Accomplished by cross-wiring the medial longitudinal fasciculus (MLF). It looks like kind of like that. i. The signal comes from the brain. It comes to CN VI and causes the eye to abduct. There is a cross pathway that goes to the contra-lateral CN III so it can do the adduct, they will do the opposite thing because of the cross-wiring. ii. Then, when you have various lesions, you get different neurological syndromes if you understand the pathways. Be aware there is inter-wiring these because eye movements need to be coordinated. XXXVII.Learn more [S57] a. Good website. Knock out individual muscles or CN and then see what happens with oculomotor function [End 49:40]