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Neuro Test 03


2012-04-07 19:38:45

Description: Neuro Test 03

Flashcards app available on theAndroid Marketplace as well as on the Apple App Store foriOS. Give the name and basic function of all the cranial nerves? Olfactory smell pure sensory, no motor component Optic nerve sight pure sensory Oculomotor nerve control movements of the eye balls specifiably 4 extrinsic muscles of the eye (there are 6 extrinsic muscles of the eyeball), muscles that go around the eye, also controls the diameter of the pupil and changing the shape of the lens for focusing on things there are parasympathetic fibers go along with this cranial nerve to the eyeball to cause constriction of the pupils. Also controls the papillary muscle that lifts the eye lid. Trochlear nerve controls the superior oblique muscle which points the eyeball down. Trigeminal nerve controls chewing muscles and moving the jaw up and down, but mostly up also handles face sensation all the touch pressure, pain , temperature. abducens goes to the lateral recutus muscle which adbucts the eye , points it outward or laterally. Fascial nerve all the muscle of the face except the four used in chewing are this nerve , also handles the anterior 2/3 of the tongue so taste. Also controls tears and some of the saliva glands

vestibularcochlear nerve handles balance , head movement and sound. Glossopharyngeal (literally means tongue and throat) taste in the back of the tongue and the throat muscles Vagal is a very important autonomic nerve , it innervates all the organs of the thorax and upper abdomen. Accessory nerve innervates traps and SCM Hypoglossal (tongue movement) muscles of the tongue are supplied by this nerve. 1. Name the three sensory divisions of the trigeminal nerve (CN#5)? o Opthalmic division also called V1 o maxillary division also called V2 o mandibular division also called V3

2. Name the nerve(s) that carry sensations from the tongue? o anterior taster buds = facial o Posterior taste buds = glosopharngeal nerves o pressure on the tongue = trigeminal nerve, also handles pressure for the cornea over the eye and the sinuses.

3. What does the trigeminal nerve do? Trigeminal nerve - Three of its branches give the face sensation from the three regions of the face the ophthalmic,maxillary and the mandibular division so sensation of all the face pain and temp touch and pressure sensations - this includes pressure on the tongue and the cornea over the eye and the sinuses. innervates the Chewing muscles (4 strong muscles) the temporalis, masseeter, lateral pterygoid and medial pterygoid. All but the lateral pterygoid close the mouth and elevate the jaw were as the later pterygoid opens the jaw or mouth.

4. Explain the pathway for pain and temperature with the trigeminal nerve? Pain and temperature for the face is carried up the unipolar neuron (first order neuron) past the semilunar ganglion and down into the pons/medulla at which point It synapses with the second order neuron which crosses the midline and ascends in the trigeminal lemniscus and ends in the thalamus at the VPM (Ventral posterior medial nucleus) and then the third order neurons goes out to the somatosensory cortex.

5. Explain the pathway for touch and pressure within the trigeminal nerve? Touch and pressure on the face and tongue is carried by a unipolar neuron (first order neuron) past the semillunar ganglion to the main sensory nucleus on the side of the body it originates from. Then the pathways splits and the second order neurons ascend bilaterally into the thalamus to the VPM in both sides of the body and from there the third order neurons takes it to the somatosensory cortex in both hemispheres.

6. What would a lesion of the left middle cerebral artery cause in the face? a left middle cerebral artery lesion would cause a loss in sensation of pain and temp from the right hand side of the face

7. Cranial nerves are divided into 3 functional groupsname those groups and the nerves within each? 3 pure sensory optic, olfactory, vestibulocochlear 4 pure motor trochlear, abducences, accessory, hypoglossal 5 mixed nerves oculomotor, trigeminal, facial , glossopharyngeal and vagus all have PS fiber except for the trigeminal. Example: this is why olculomotor is some times called mixed because it has skeletal fibers and PS fiber which in this case are also motor fibers

8. What is the smallest cranial nerves name and number? 4 trochlear nerve

9. What does the trochlear nerve do and were does the trochlear nerve (CN#4) start? it innervate one muscle of the eye the superior oblique which moves the eye down as in looking down. It originates from a Nucleus in the mid brain and the motor nerve comes out the back of the brain stem beneath the the corpora quadrigemina which is made of the inferior and superior colliculi and the pineal gland sits right above this

10. What is the most common lesion to the trochlear nerve? the most common lesion to the trochlear nerve is caused by Parinaud's syndrome which is when a tumor of the pineal gland swells and pushs on the superior and then inferior colliculi and then on the trochlear nerve which causes vertical gaze palsy. Parinaud's syndrom can also cause a problem with the pupil's reaction to light, so the pupil of the effected side doesn't get smaller in reaction to light because it is the superior colliculi that mediates the change in size of the pupil. Parinaud's syndrome can also cause a problem with our reactions to sound do to the damage to the inferior colliculi.

11. Name all six muscles of the eye? and what nerve innervates them? inferior oblique superior rectus medial rectus lateral rectus superior oblique inferior rectus All are innervated by the occulomotor nerve except for the superior oblique (trochlear) and the lateral rectus (abducens).

12. What does the Abducens nerve do? and what is it number?

o o

innervates the lateral rectus (abductor of the eye) muscle of the eye CN #6

13. Were is the abducens nucleus located? and what is it called? It is found in the pons and it is called nucleus IV

14. What is the most commonly damage CN going to the eye? what does damage to it cause? The abducens is the most commonly damaged nerve going to the eye because it has a long course to the eye. If damaged you would lose the ability to turn the eye ball outward due to the loss of control of the lateral rectus muscle and hence you would develop medial strigmus or medial squint due to the unopposed action of the medial rectus muscle.

15. Were does the spinal acessory nerve come from and what does it do? The accessory nerve comes form two place part of it is a displaced loop of the cervical plexus and so cervicle rootlets emerge in the neck and go up to merge with the other portion of this nerve that comes out of the brain stem and descends to meet the cervical portion. Then this combined nerve comes back down the neck and innervates the SCM and trapezius. The cranial portion is also one of several cranial nerves that mediates swallowing

16. What would damage to the acessory nerve (CN 11) cause? Swallowing - Damage to the accessory nerve can cause problems with swallowing torticolis - (which is a spasm in the SCM which cause the childs head to flex ipsilaterally and to turn to the contralteral side. Loss of trapezius muscle - You may also have issues with the

trapezius muscle which would impair your ability to shrug your shoulder, or lift your scapula. If this becomes chronic you may also see a flatting of the effected shoulder. Or the neck on the effected side may take on an L shape due to the atrophy Breathing issues - There may be issues with breathing due to failure of the CSM which has the reverse action of lifting the rib cage.

17. If you have a child who is stuck looking left because of torticolis, what nerve is effected and how would you fix this? it is the R SCM that is effected so it is the the R accessory nerve and to fix it you would stretch them by flexing them away from the effected side (L side) and turning there head toward the effect side (R side).

18. Which cranial nerve is located lowest in the brain stem? Hypoglossal nerve CN: XII

19. Were does the Hypoglossal CN: XII start and what does it do? The hypogloseal nerve starts on a nucleus located in the medulla and it goes to the muscle of the tongue. You have two hypoglossal nerves one for each side of the tongue (left/right).

20. What would a lesion of the hypoglossal nerve CN: #12 cause? If one of these two hypogloseal nerve is damaged the tongue will deviate to the side of the lesion when extended , this is due to the unopposed action of the muscle of the uneffected side. This can cause Dysarthria due to the tongue being half paralyzed, which can cause things like slurred speech and issues with chewing and swallowing, because they can't move the food around there mouths as easily. Long term loss of this nerve can result in the atrophy of the effected tongue muscles, which will look like ridges or furrows in the tongue.

21. How are the nucleus from which the cranial nerves start arranged in the CNS? Top four nerves are in the mid brain then 4 in pons and then 4 in the medulla in order from 1-12 Mid brain Olfactory I Optic II Oculomotor III Trochlear IV Pons Trigeminal V Abducens VI Facial VII Auditory (vestibulocochlear) VIII Medulla Glossopharyngeal IX Vagus X Spinal Accessory XI Hypoglossal XII

22. Explain the basics of the pathways of the autonomic nervous system? In the ANS there is always a chain of two neurons to the effectors (always two in PNS and ANS). This is chain is made of the pre and post ganglionic neurons and were the Preganglionic neurons starts is a nucleus with specific name. The preganlionic neuron then synapses at the post ganglion neuron (which also tend to have specific name for each pathway) and then this post ganlionic fiber goes to the effector.

23. Why is the oculomotor nerve (CN: #3) sometimes considered a mixed nerve? The oculomotor nerve is considered a mixed nerve because it contains two types of motor fibers, one set for the PNS and the other for the normal skeletal muscle nerve supply.

24. What does the skeletal muscle fibers within the oculomotor nerve (CN: #3) innervate? Four of the intrinsic muscles of the eye and one muscle of the eye lids Inferior oblique medial rectus inferior rectus superior rectus Levator palpebrae the muscle that lift the superior eye lid

25. Explain the pathways for the PSN fibers and the skeletal fibers of the oculomotor nerve (CN:3)? and what does the PSN part of this nerve do? The skeletal muscle fibers start at the oculomotor nucleus and go to four intrinsic eye muscles, inferior oblique, medial rectus, inferior rectus ,superior rectus. The PSN part of the oculomotor nerve starts at the Edinger-Westphal nucleus and then travels along with the other oculomotor nerve fibers to synapse with the ciliary ganglion (which is the end of the preganglionic fibers). The post ganglionic fibers then go to the pupil sphincter muscle, which when stimulated constrict the pupil. It also innervates the cilliary muscles which is a sphincter muscle or circular muscle which control the shape of the lens. So when stimulated it contract around the eye causing it to bunch up and thicken, which is called accommodation and is done to see things close up.

26. What is the cause of oculomotor palsy? Oculomotor paralysis is a result of the paralysis of the medial rectus, often do to damage to the oculomotor nerve.

27. Why do people need reading glasses when you get older? As you age the lens looses it elasticity. This elasticity normally lets the lens bunch up which is called accommodation. Without accommodation you need glass to read or see things close up because though the muscle contract the lens cant bend enough to let you focus on things near the eye.

28. Name a drug that is a PSN agonist , that is used in the eye? o Atrophine is a drug that is a PSN agonist so it will dilate the o pupil.

29. Name to syndromes that can cause oculomotor paralysis? and explain give the key signs of both disorders? Damage to the oculomotor nerve can be caused by Webbers or Benedict's syndrome both of which can cause oculomotor paralysis. Webbers causes oculomotor palsy and hemiplegia and Benedicts causes oculomotor palsy and contralateral loss of sensation to the Face.

30. Explain oculomotor palsy? Oculomotor nerve palsy is an eye condition (usually unilateral) resulting from damage to the third cranial nerve or a branch thereof. As the name suggests, the oculomotor nerve supplies the majority of the muscles controlling eye movements. Thus, damage to this nerve will result in the affected individual being unable to move their eye normally. In addition, the nerve also supplies the upper eyelid muscle (Levator palpebrae superioris) and so can cause ptosis or drooping of the eyelid and the muscles responsible for pupil constriction (sphincter pupillae), which causes the eye to be dilated and unreactive to light. The limitations of eye movements resulting from the condition are generally so severe that the affected individual is unable to maintain normal alignment of their eyes when looking straight ahead, leading to strabismus and, as a consequence, double vision (diplopia). Commonly can cause lateral strabismus due to the failure of the medial rectus muscle, causing the unopposed lateral rectus (which is innervated by the abducens nerve CN:#6) to abduct the eye. THis can also cause problems with seeing close up do to damage to the PSN fibers within this nerve.

31. Define ptosis? Dropping eye lid

32. Define Mydriasis? Mydriasis dilated pupil.

33. Define aniscoria? Anisocoria is when the two pupils are unequal in size. So one may be dilated or constricted but either way they not the same side.

34. What muscle dilates the eye? sympathetic nervous system control the radial muscle which dilates the pupils.

35. List some of the signs of trigeminal nerve (CN: #5) damage? Trigeminal nerve damage can cause problems with chewing and speaking (dysathria), deviations of the jaw, Tic douloureux and loss of the corneal reflex. To test this have the pt open there jaw. If the jaw deviates to the side of the lesion do to the unopposed action of the lateral pterygoid muscle of the oposite side.

36. What is Tic douloureux? and explain how it can be treated? Tic douloureux Trigeminal neuralgia (most common issue with this nerve) a idiopathic pathology were there is a shooting electrical shock pain that goes down the course of one of the branches of the nerve, usually the maxillary or opothalmic nerve tracts that can last a few seconds or up to 15 minutes. Can be caused by trauma or other pathologies. In severe cases it is treated by giving the pt anti convalescents and analgesics to decrease the pain.

37. What is the corneal reflex? and why do we have it? what pathway does it follow? Corneal reflex is when something touches the cornea of the eye causing the eye to blink or close to protect itself. Without this reflex you don't blink when things get in the eye and this can lead

to issues with infection and lack off lubrication of the eye. The sensation of something touching the cornea is carried by the trigeminal nerve into the head were it synapses at an interneuron (also called an internuncial neuron) which connects to the facial nerve, which then sends a signal to the orbicularis oculi muscle which shuts/blinks the eye. Loss of this reflex is common in people above 40 years old though we don't know why this happens we do know it can be brought on by odd things like eating very hot or cold food or from dental work. This is treated with modalities for the pain and usually goes away within a year.

38. What is the Glabellar reflex , what do we use it for? what pt might lack this reflex? Glabellar reflex the glabellar is the bit of the forehead between your eye brows. When you tap yourself you don't blink but when something else touches this spot on your forehead you will blink. But if they do it three or four times you stop blinking because you have adjusted to it. This is used to test of the functioning of the trigeminal nerve which opposes this People with parkinsons disease (early sign), dementia (advanced) or frontal lobe damage will not be able to suppress this reflex. Myerson's sign is when they don't stop blinking it is an early sign of parkinsons disease. Travels same path as the corneal reflex.

39. What is the Supraorbital foreamen and why do we care about it? Supraorbital foreamen little groove in top of eye socketthrough which a branch of the trigeminal nerve runs and it is this branch which causes the Glabellar reflex and corneal reflex.

40. What does the Ciliospinal reflex test? what is this reflex? Explain the pathway it uses? Ciliospinal reflex tests the function of the trigeminal nerve and the oculomotor nerve

when you pinch some ones neck and create a sharp pain, watch the pupil on the side of there face you pinched. The pain should causes the ipsilateral pupil to dilate. This works because the trigeminal nerve carries this pain signal to the brainstem were it synapses with an interneuron that connects to the occulomotor nerve and facilitates the Sympathetic pathway to the pupil. Pain creates a instinctive response to escape so this reflex is a fight or flight response.. You can also test this reflex electronicly.

41. Explain a mono-synaptic neuron reflex? o receptor sensory neurons synapse motor neuron o you dont need a conscious brain for this.

42. What are the major componets of the facial nerve (CN: #7) do? It has three major components Special sensory fibers - taste on anterior two thirds of the tongue (back of the tongue is glosopharnygeal). These PS fibers also go to the submandibular and sublingual glands which produce salivia and to the nose for nasal mucous and the lacrimal glands for tears. Skeletal muscle (largest component) all the muscle of the face except for those of the trigeminal are controlled by this nerve. So all the muscle of facial expression.

43. Explain the pathway for taste from the anterior tongue through the facial nerve? Taste from the anterior 2/3 of the tongue is carried on a first order neuron past the Geniculate ganglion to the nucleus solitarius were two things happen a second order neuron picks up the signal and cross the mid line of the body ascend through the brainstem to the end on the VPM (ventral posterior medial

nucleus) in the thalamus. From there a third order neuron takes it into the cortex to the gustatory center deep within the lateral sulcus. An interneuron takes the signal to the superior salivatory nucleus (located beside the nucleus solitarius) which is the start of the PS fibers to the saliva glands. So the preganglionic fibers start at the superior saliuvatory nucleus and end at either the submandibular or submaxillary ganglion from which a post ganglionic fiber carries the stimulus to the submandibular and sublingual glands which are then stimulated to produce saliva.

44. Name all the branches of the facial nerve that innervate muscles? there are five major branches of motor fibers from the facial nerve based on there location Twelve zulu's became my clients Temperal Zygomatic Buccal Mandibular Cervical There are a couple little branches that go to other things like the two little muscles that go to the hyoid bone Stylohyoid goes from the styloid process down to the hyoid and help elevate the hyoid bone. P diagastric goes from the mandibale to the hyoid and help elevate and control it.

45. What does the stapedius muscle do? Stapedius muscle another small branch of the facial nerve goes to this muscle which attaches to the stapes in the ear and is responsible for dampening the motion of the stapes so it doesnt vibrate like crazy so damage to it or the facial nerve can cause hyperacusis

46. What is hyperacusis? Hyperacusis when things that shouldn't be loud sound very loud do to loss of the stapedius muscles dampening effect.

47. What is the most common disorder caused by damage to the facial nerve (CN: #7)? Most common damage to facial nerve is Bell palsy

48. What is bells palsy? What are some the signs of this diseases? This is an ideopathic disease with an unknown ideology which usually occurs unilaterally (if bilateral may be from Myasthenia gravis), in people 20-40 years old. In this disorder the facial nerve is inflamed were it goes through the temporal bone which leads to the paralysis of all the muscles around the eye. Signs: lose of the orbicularis oculi muscle and hence wont be able to close there eye even when asleep. lose of the ability to create tears which can lead to infection. Weird facial expression and a grotesque smile due to drooping on one side of the face do to lost tone on the effect side of the face. Lose of the ability to lose or frown Lose of the orbicularis oris muscle and hence the ability to close lips on one side of the mouth, may lead to drooling Lose of saliva from the submadibular glands which will decrease the amount of saliva in the mouth but other gland will still provide some Treatment though there is no known cure for bells palsy, the condition usually only last a few months to a year. This being said it can be a side effect of lime disease in which case curing the lime disease will cure the bells palsy but this is less likely. In some cases surgeons may widen the facial nerves passage through the temporal nerve with a drill.

This disease can be mistaken for RA.

49. What does the Corticobulbo tract do? Corticobulbo tract - is the upper motor neurons or tract that goes to the start of the motor cranial nerves

50. Explain how the facial nerve innervates the muscles of the face? The lower face is innervated from the contralteral hemisphere, but the upper face is innervated bilaterally so the motor cortexs from both hemisphere innervate the muscles.

51. What motor effects would a lesion of the facial nerve cause? what motor effect would a supra nuclei lesion, UML, corticobulbo tract lesion or motor cortex lesion have? A lesion to the facial nerve will cause unlateral palsy to whole face A lession above the facial nerve will cause lose of the contralateral lower face but not the upper face due to the bilateral supply of those muscles. This is why stroke pts upper face will be fine, even if there lower is paralyized.

52. What artery supplies the facial part of the motor cortex? Middle cerebral artery supplied facial part of motor cortex.

53. What is Crocodile tears syndrome? Crocodile tears syndrome When you taste something good you cry. This is due to a short circuit between the sensory nerves for taste and the autonomic fibers going to the lacrimal glands. The taste fibers coming up meet with the fibers to the lacrimal gland right near the Geniculate ganglion so this has to happen proximal to the Geniculate ganglion because this is the only place these two nerves are close together.

54. What the easist way to dignoise a facial nerve issue? To Dx problem with facial nerve just have the pt make a facial expression and if it only happens on one side of their face then it is a facial nerve issue such as bells palsy. You can also can test taste sensations, mucous and tear production.

55. What does the Glossopharyngeal nerve (CN: #12) do? taste neurons from posterior part of the tongue (facial is anterior part) PS fibers going to a saliva gland the parotid gland (parotid gland big gland makes saliva, its ganglion is the otic ganglion). nucleus were the neurons start is the inferior salivatory nucleus. (superior salivatory nucleus is the start of the facialnerves saliva glands) Sensory neurons from the throat the soft palate , the ustation tube (the tube that you blow to equalize pressure in the middle ear) and the sensory nerves form the carotid sinus. Skeletal muscle one muscle the stylopharyngeus which is involved in swallowing

56. Explain how the saliva reflex is triggered in the Glossopharyngeal nerve (CN: #12)? Saliva we have a reflex to make saliva so you put something on the back of the tongue and the 1st order neurons send a signal past the petrosal ganglion and then this tract goes to the nucleus solitarius and then there is a internueron which goes to the inferior salivatory nucleus which sends the signal down PS fibers to the parotid gland and this causes us to salivate. (parotid gland is big gland makes saliva, its ganglion is the otic ganglion

57. Explain the pathway for tast from the Glossopharyngeal nerve (CN:#12)? Same pathways for taste from facial or Glossopharyngeal nerve for conscious perception of taste.

Taste from the posterior 1/3 of the tongue is carried on a first order neuron past the Geniculate ganglion to the nucleus solitarius were two things happen a second order neuron picks up the signal and crosses the mid line of the body ascend through the brainstem to the end on the VPM (ventral posterior medial nucleus) in the thalamus. From there a third order neuron takes it into the cortex to the gustatory center deep within the lateral sulcus.

58. Explain the role the Glossopharyngeal nerve (CN:#12) plays in controling O2, CO2, heart rate and blood pressure. Sensory fibers from the Glossopharngeal nerve are found within the carotid sinus. Hence there are Baroreceptor within the sinus which can sense changes in the blood pressure. You also find carotid body in the carotid sinus which senses (specialized cells) partial pressure of O2 and to a lesser extent the partial pressure of CO2. So if there is a changes in blood pressure and/or O2 level it get sensed by these receptors and it sends this information up the brainstem through the Glossopharyngeal nerve which ends in the brainstem at the nucleus solitarius. Which synapses through a direct connection (interneuron) with the vagus nerve and alters heart rate and vasoconstriciton of the arterial walls and hence blood pressure and O2 levels.

59. Explain how the glossopharyngeal nerve (CN:#12) triggers gagging or swallowing? Why is this reflex important? Sensory receptors at the back of the throat from the Glossopharyngeal nerve react to touch or the feel of food going down and cause you to gag or swallow through a connection to other nerves such as the vagus nerve (CN:#10). These receptors also close of the epiglottis when you feel something going down/up your throat. This is why when go under a general anesthetic you dont eat for 10-12 hours before because it deadens the reflex to close the epiglottis, so if you puke you could vomit into your lungs and choke to death.

60. What does the vagus nerve do? Vagus nerve is an important nerve in the ANS, specificly it is one of the

primary sources of PS innervation to the organs of the thorax. Also most of the organs it runs to have sensory fibers either in them or in the membranes around them which send there sensations but up the vagus nerve. It also has a skeletal motor supply within it which controls many of the oddly named muscles of the the throat and voice box area. It is also the motor nerve involved in the gag reflex and in swallowing. It is also the PS nerve involved in the carotid body and baroreceptor reflexes, causes a change in breathing and heart rate. PS stimulus through this nerve also decreases the activity of most organs with the exception of parastolis and the digestive process which are increased. IT also increases the produciton of mucous in the bronchial tree and decreases bronchial diameter, which means it shuts down the lungs but increases mucous production.

61. What is Vasovagal Syncope? Vasovagal Syncope also called vasovagal reflex, vasovagal attach , vasovagal response, emotional fainting or neurally mediated hypotension - (This can run in families) which means to faint this is when the pt get a blood see's blood and faints or there in high stress situation and they faint , can be caused in several ways

62. Explain the vasovagal reflex? The limbic system or emotional centers of the cerebral cortex stimulate the anterior hypothalamus to increase PS activity due to panic or other strong emotions and this causes the vasomotor center in the medulla to become stimulated which sends a signal down the vagal nerve which causes vasodiliation and a decrease in heart rate and blood pressure. This mechanism occurs because you body is trying to make sure the brain has enough blood and oxygen so if it is deprived of blood due to something like standing on your feet all day or a panic attack then the body will cause this fainting spell to get your head at the level of your heart or below there by preventing ischemia. Due to this baroreceptors and carotid bodies can also feed into this mechanism sense they can also act to decrease heart rate and blood pressure.

63. Explain what happens to light as it enters the eye? light comes into the pupil pass through the lens and hits the retina which houses our receptors.. The lens will invert the image left and right and up and down

Example:so what we see in the world is on the opposite side of the retina - so if your looking straight ahead at some one there feet are on the top of the retina and there head on the bottom, and there left and right would be reversed as well

64. What is the blind spot? It is the place in the eye with no receptors because it si were the optic nerve enters the eye

65. Name the receptors of the eye, their type of neuron and one neurological difference between them? There are two types of receptors in the eye rods and cones , both of which are bipolar neurons. One of the difference between the two is that cones have there own specific neuron attached were as with rods multiple rods can link to the same neuron.

66. Explain the basic neural pathway for the optic nerve? 1st order Light hits the bipolar neurons which act as receptors and this goes to the retinal ganglions 2nd order which come together to make up what we consider the optic nerve which runs out the back of the eye to the optic chaism (were some of the fibers cross) after which the nerve is renamed the optic tract this nerve goes to the thalamus and the lateral geniculate nucleus 3rd order from the later geniculate nucles optic radiations (also called geniculocalcarine fibers) leave the thalamus and spread out and go along the back of the brain to the occipital pile (visual cortex). They do this in two paths optic radiations caring the lower visual field go straight back to end on cuneate gryus above the carlcarine fissue. Optic radiations caring the upper visual field make a sweep through the temporal lobe and then go back. This sweep around the lateral ventricle is called Meyer's loop and it ends on the lingual gryus.

67. Explain the visual and retinal fields? and explain how visual defiecits are named? Retina is broken into two Visual field, Nasal retinal field - the of the field by the nose is the nasal retina field (C and B on diagram). (near nose) sees the temporal visual field Temporal retinal field the Half nearest to the temporal bone is temporal field. (near outside of eye) see the nasal visual field Retinal fields see the opposite visual field. So the left retinal field see the right nasal field.

When talking about visual deficits you always refer to the visual field not the retinal field, so when using diagrams of visual deficits they will show you the visual field the pt can't see, so never think of the retinal field damage only think of the visual field problem.

68. Some fibers cross at the optic chiasm were are these fibers from and which visual field do they carry? At the optic chaism the temporal retinal field (nasal visual field) stays ipsilateral and the nasal retinal field (temporal visual field) cross over to the other side. So this how we get the left side of the world to the right hemisphere

69. What does the R nasal retinal field see? R temproal visual field Nasal retinal fields see temporal visual fields, just as temporal retinal field sees a nasal visual field.

70. Explain the geography of the visual cortex? is right along the calcarine fissure which is a horizontal line/fissure which has a crack down the middle that separates the hemisphere (longitudinal fissure).

The calcarine fissure separates the gryus into the cuneate (means wedge) gryus on top and lingual gryus on bottom.

71. What would you have lost if you lose the left side of the combined visual field of the right eye. IF you lost the left side of the combined visual field of the right eye then you have lost the temporal field of the right eye.

72. Define anopsia? Anopsia: loss of one eyes parts of the visual fields.

73. Name two things that can cause lesion to the optic nerves path? o aneurysm in the internal carotids o Tumor of the pituitary gland (paurnads syndrome)

74. Explain the inderect and direct reflexes of the eye? 1% of our neurons coming along the optic tract do not go to the lateral geniculate body instead they peel off and go to the pretectile nucleus which is within the superior coliculi in the brainstem. Then this signal goes to two placesit travels through the white commissure to the opposite hemisphere pretectile nuclei and then from the pretectile nucleus of both sides the signalpasses through an inter-neuron to the eddinger walthall nucleus, which is the start of the PS fibers of the oculomotor neuron. From there it travels through the PS fibers to the sphincter muscle of the pupil. This connection to the oculomotor nerve causes the direct reflex which cause the pupil of the eye to constrict when a light is shined into it . The bilateral connection is why the consensual light reflex happens which is when you shine light in R eye and left eye shutdowns a little bit. Th bilateral connection through the white commissure is what creates the indirect reflex were the opposite pupil starts to constrict a little bit from light being shined in the opposite eye. SN: these relfexes aren't controlled by the cortex so they will work in a pt who is blind or unconcious and so are a good way to make sure there is no bleeding into the brianstem whcih can also shutdown these reflexes.

A similiar pathway through the tectospinal path is also responsible for the jumping we may do when startled or suprised by a bright light.

75. What is Blind sight? Blind sight if a pt is blind but they can still see in a reflexive way , so if you ask them to grab some thing they can grab it even though they can't see. This is because the brainstem can see some what so they can see reflexively.

76. What is the Cilliospinal reflex? what does it test? Cilliospinal also test the oculomotor nerve. - this is when you pinch someones neck hard the pupil dialtes.

77. Lot of things effect the pupil name a few and why we want to know this? o Pupil will dilate from stress and other such factors. o You can measure the amount of cognition a person is using based on dialtion of the pupil. o An anesthisoligist can tell by the pts pupil how under a pt is. So show level of consciousness.

78. Why do doctors look in the back of the eye with an othalmoscope? They are look for cerebral herniation. Which can cause a papilloedema or choked or swollen disk.Which is when the meninges come around the optic nerve and this can push the optic disk into the back of of the retina. This bulge is vsiable in the back of the eyeball using a special scope.

79. Why don't you use morphine when you suspect a head injury? Because Morphine causes more bleeding because it causes dilation of blood vessels which is why you never give a pt with a cerebral hernia because you will make it worst. Plus it pin points the pupils so you can't check the state of the brainstem once there on this drug.

80. Explain the near point reaction reflex? anything that comes close to you will cause the lens to gets thicker (accommodation) from the cilliary muscle , which you cant see this. To let you focus on the approaching finger so you accommodate the approaching finger. Eye balls went inward so went cross eyed (medial rectus controlled by the oculomotor nerve) to track the finger, so this test the medial rectus. pupil constricted which increases the depth of focus. A smaller hole increases the depth of focus. This test the PS part of the oculomotor nerve.

81. What is the Argyll Robertson pupil? Some disease will cause a pupil not to react to light but it will react to the near point reflex. Seen in diabetes and in neurosyphilis. So in general means something is messed up with the nervous system.

82. Name the receptors of the vestibule? semicircular canals detect angular movement or angular acceleration of the head Don't dissect these for it a pain - they about 15 mm long with superior being bigger then the lateral one if cut in half (cross section) they less the mm in width. The size of them in animals is related to how fast and agile the animal is, so a cheetah has big ones but a sloth would have smaller semicircular canals. otolith organs utricle and saccule linear acceleration or movement of the head forward backward left right but no angular or in between movement

83. Name the 2 major functions of vestibular aparatus?

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posture and balance detects the changes in head position which cause changes in balance to keep us upright. eye movement - help keep the eye fixed on something. So when the head moves the eye can keep locked onto somehting to prevent visual slip or blurred vision which we don't want.

84. Explain the Semicircular canals ? Semicircular canals there are 3 of them one in each plane though none are in the exact cardinal plane , but they called the anterior (or superior) , posterior and lateral (or horizontal) it is a boney tube , inside of that is perilympth and inside of that is a membranous pipe and within that is endolympth (liquid in the dead center of the pipe) at the end of each canal there is an ampullae or a swelling. These canal don't lie exactly in saggital and other planes they are tilted and the horizontal plane is not horizontal it 25-30 degrees tilted up in the front. This tilt is important in treatment.

85. Explain the orientation of the semicircular canals? The Right anterior canal is parallel to the left posterior canal and vica versa the right posterior lines up with the left anterior canal. so anterior and posterior on opposite sides run in the same direction, because of how they are orientated. The posterior canal aim from the ear at the eye on the opposite side.

86. Explain the structure of the ampulla? Ampullae - within these swellings there is a projection of a lump of jelly called the cupula The cupula floats in edolympth and usual isn't effect by gravity. There are hairs from the dendrites sticking out of the cupula. These hairs are made up of one kinocillium and a series of sterocillia in a step like path leading up to it.

87. Explain what role the cupula plays in sensing motion and in dizziness? When you move your head the cupula is dragged through the endolympth and by the inertia of the endolymph. SO if flick head to the right the endolympth stays still but the cupula is dragged through that liquid. Which causes the hair cells to get knocked over or deflected and this signals to the receptor that the

head is moving. But if you keep spinning to the right for 30 sec or more the endolymopth catches up to the hair cells and the hairs cells get righted again because everything is moving in unison and sense they are vertical again they tell the body your not moving until you stop moving. When you suddenly stop moving the endolyth keep moving round and round and this hits the hair cells again and bends them over and you feel dizzy, because you think your moving again.

88. Explain how the semicircular canals know your moving and how they know which way your moving? At rest the receptor hair cells of the cupula are pointed upward but they still fire at a background rate. But if you move the stereo cilli (little hairs) and they are knocked towards the big one this excites the receptors. But if the Big kinocillia is knocked towards the stereocillia you get inhibition of the receptors, and the inhibition firing is less then the resting firing. So you know which way your head is going based on whether you your getting inhibition or increase of the resting signal. So to indicate a lack of motion you need resting firing patterns from the semicircular canals on both sides.

89. What is Vestibulo Unilateral Hypofunction and why does it happen? Vestibulo Unilateral Hypofunction lose of more hair cells from one side then the other. Which causes an unequal firing of signals between the two semicircular canals which sense it is the coupled action of these two sets of receptors and their two cranial nerves interpreted by the cerebellum and cortex that create balance loss of these hair cells can trick the brain into thinking your moving this can cause a pt to falls over get vertigo and nasua and other issues with balance.

90. Name the 4 Cardinal sign in later Parkinson's disease? o Vestibulo Unilateral Hypofunction o tremor o rigidity o bradykinesia.

91. Name and Explain the structure of the otilith organs? Otilith organs utricel and saccule contain flat saucer like apparatus of jelly called the macula and this corresponds to the cupula in the semilcircular canals it also has same specific gravity as endolymoht and hair cells stick out of them. In this jelly are little otoconia or little Ca+ carbonate crystal or rocks. Which lie within the surface of the macula and that makes the macula sensitive to gravity because it gives it weight, so lets these organs detect gravity. Sacule is upright and utricle is flattish. These respond to linear motion. Such as side to side motion, or up and down.

92. What does the saccule do? So the saccule is the one important in detecting gravity because the rocks bend the macula downward and so bend the hair cells and detects gravity, at least this is the traditional thought but the latest research says we are bad at detecting gravity and indicates that we relies more on the somnatosensory symptoms

93. Why is it bad that the Semicircular canal are continuous with the utricel and sacrule? Semicircular canal are continuous with utricel and sacrule so the endolympth in all of them is the same and interconnected. Which is bad because in certain disease (BPBD) these calcium crystal can break of the macula and float through the endolythm and land on the cupula and stick or they can hang out in the endolymopth and when you move they smack into your cupula causing it to move way to much when you move. Which can cause vertibo and other issues when the pt moves there head. However this is easily treated with pt. This disease is called BPV

94. Explain the neural pathways of the vestibocochlear nerve (CN:#8)? 1st order -the bilpolar neurons (have scarpas or vestibular ganglion) running away from the receptor enters the brainstem and most of them ends on the vestibular nuclei which is mostly in the bottom of the pons and slightly in the top of the medulla. vestibulo cerebellar pathways some fibers bypass the vestibular nuclei and go directly to the flocula cerebellum (or vestibulo cerebellum) and to the flocculus lobe. Then to the fastigial nucleus, then back

to the vestibular nuclei. Were it will go to the second major pathway leaving there the vestibulospinal tract, and go down to correct (posture) movement by triggering extensors. 2 order starts at the 4 vestibular nuclei (4 on each side) named for there relationship to each other, so superior , lateral, medial and inferior (lower one or inferior one is also called spinal or descending nuclei). Vestibular nuclei send this information to 4 major places Conscious perception goes to sensory cortex so we can perceive it out of the vestibular nuclei we get bilateral paths which go to the thalamus and specifiably the ventral posterior nucleus and the third order neuron projects out to the cortex, (just behind the somatosensory cortex) vestibulospinal tracts start at the vestibulo nuclei and go down the cord to correct the posture. There are two of these tracts (part of extra pyramidal pathways) there is a lateral and a medial one. Lateral vestibulospinal tract starts at the lateral vestibulo nuclei and goes all the way down ipsilaterally to the lumber and sacral regions and controls the legs were it's job is to increase the extensor tone of the legs and through reciprocal inhibition decreases flexor tone. Medial vestibulospinal tract comes out of the other 3 nuclei (so the medial, superior, inferior) in both hemispheres and is a bilateral tract and has crossed and uncrossed tracts. It ends in the cervical spine and increases extension of the arm and decreases flexion. Collateral fibers coming of the medial vestibulospinal tract come off and go rosterally (upward) and form the Medial longitudinal fasciculus (MLF) which ends on the three cranial nerves that go to the eye ball (oculomotor , abducens , trochlear) and control the eyeball , because they are responsible for the (VOR) vestibular ocular reflex.

95. What is the (VOR) vestibular ocular reflex? VOR is responsible for moving you eyes in the opposite direction as you head to keep your eyes fixed on something, and then when the head moves to far your eyes move quickly in the direction of the head to catch up and and prevent

visual slip. This jumping of the eyes is called physiological nystagmus. This reflex can be overcome, by the cerebellum which can cancel out the VOR

96. How do name nystagmus? you name nystagmus in terms of the direction of the fast component, so if moving you head to the right you will get right physiological nystagmus.

97. What happens if you cut an animal brainstem above the vestibulo nuclei and below the red nucleus? How can you prove that this? Sense there is no cerebellar influence the animal has rigidity in both its arms and legs, because without input other then from the inverations from the vestibulospinal tract they simply want to extend the legs, leaving the animal is bolt upright. You can Prove this by taking the animal and drilling a hole into the animals ear and poring alcohol in it which wipes out the vestibular apparatus which causes the the legs to go floppy, which proves this signal is coming from the vestibulo apparatus.

98. What is the VSR and what does it do? The lateral and medial vestibulospinal tracts are responsible for the VSR (vestibular spinal reflex). VSR controls the posture of the overall body.

99. What is pathological nystagmus and why is it bad? If a pt has nystagmus (twitching of the eye) without motion it is pathological nystagmus and this is bad, and you can get this if you have unilateral hyper function so unbalanced input. This is sometime called a saccade which is when you eyes jump to something.

100. List and explain way to test the vestibular apparatus? thermal test or caloric test tests both the lateral canals because it the most

superficial have the pt tilt head 60 degrees upward put the horizontal plane vertically then you irrigate one ear with warm water (44 degrees centigrade, 111.2 degrees F, hot tub water) and this start making a current of endolympth go upward around the canal which knocks the hair sell upward which is equivalent to the left in the anatomical position, so this knocks it to the left which in normal movement would be caused by right head movement and so you will see R nostagimus in a normal person. They may vomit because very nauseating. Put cold water (7 degrees centigrade - 67 degrees F) in their ear below body temperature cause the opposite flow of endolympth so creates downward flow of endolympth and right motion in the anatomical positions and so you will see L nystagmus. Nausea is caused form a conflict between visual and vestibular information hence sea sickness.

101. How do you test for Physiological nystagmus? use a spinningchair

102. What is Optockinetic nystagmus? Optockinetic nystagmus not due to a part of the vestibular system it caused by looking at a moving object like a train or something moving across in front of you slowly because you tract something on the train because your system hates visual blur so you track something then reset, hence creating nystagmus.

103. How do you test the VSR? Fukuda's stepping test - ask the pt to close their eyes , put their arms out and step in place for 50 steps you should not see the person moving (normal is less then 30 degrees) so no rotation. So in a fail you will see the pt begin rotating or pedestal turning and they dont know they doing it and you can measure this distance they are off. Berg balance scale classic test for balance (14 fill in the blank questions) guess questionnaire were they do a lot of things and you check them off. Good for testing VSR and balance. foam and dome test stand there eyes open test all system working together then blind fold them to remove visual system to test

vestibular and somatosensory system if dont sway they fine if they do you know vision is compensating then put a dome over there head with a fixed x on it they supposed to look at , to make visual system invalid because when moving all they can see is the unmoving down with a x on it. Then do these three conditions again but make them stand on a chunk of foam rubber to make the somatosensory system invalid because the foam moves under there feet. (Ben doesnt think the foam doesnt makes somatosensory system invalid think it makes motor system hard to adjust the feet to input. But it a very well established test)

104. Name common Vestibular symptoms? spontaneous nystgmus pathological issue were there may be vestibular damage. It is named based on the direction which the fast movement is towards. Can also have rotational nystgmus which is when there eyes roll in little circles. Barrel rotation this is rolling in a sort of length way positions Ataxia skew deviations when the eyes squint or twist to one side Oscillopsia this is when the whole visual world jerks or twitches without you moving your eye. Example: if you poke your self in the eye lid the world jerks which is what happens with this without having to move the yes or poke your self. Vertigo dizziness falls

105. Explain how you treat VSR/balance issues? do a lot of balance and gait training and look at how to improve balance and

gait training to reduce symptoms. Hopefully the cerebellum will start working with the vestibular system to improve balance but in some cases you wont be able to get into to improve so they have to relie on the other systems.

106. Explain the two treatment apraoches for the VOR? Adaptation you fix the system , by providing the brain with error information to help it try and reset the gain of the system. Times 01 treatment approach- so what you do is have the pt track an object in front of them like a pen that you move slowly infront of them, so you induce visual slip to try and get the nerves to fix this. As they get better you progress to Times 02 treatment approach now you move the object the opposite way as the head so the eyes have to go twice the speed. So you want the eyes to be able to keep up with the visual system habituation you get the pt used to the symptoms so it gradual decreases there system so do what ever makes the person feel bad and nausea over and over again until the pt adjusts to it and this decreases the severity of the symptoms. So gentle at first evoke the symptoms until the symptoms gradually decrease.


Name three typical pathologies of the vestibular apparatus? Unilateral vestibular hypofunction often caused by age, diabetes, MS , parkinsons. Caused by hair cells in one side dieing off unequal input form two sides indicates the head is moving. So vestibular system says your moving but the rest of systems say you not hence, gait ataxia, poor balance, nasuea vertigo, nystagimus , opsilopsi, scew deviations and other vestibular symptoms. Eventually/hopefully, the cerebellum will reset the balance between these system based on the other systems input but it takes time. Meneire's syndrome (Prosper Meniere discovered this in 1861) untreatable for the most part idiopathic disease which can sometimes follow head trauma or middle ear infections. Common sign is tinitus or constant ringing in the ears during an attack which is usually unilateral. Often accompanied by hearing loss particularly of lower frequency in the

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effected ear. Also see dizziness and nausea. Pt may also feel that the ear feels full. They also have Endolymph hydrodrops for some reason the pt produces to much endolymph in the effect ear and we don't know why. They try antihistomaines and salt free diets and some cases it works and some times they don't. In sever cases they destroy the vestibular apparatus on the effected side, and though this will cause other vestibular symptoms will stop the ringing and you may adapt to the other symptoms.
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Beingn paroxysmall positional vertigo (BPPV) sudd not lethal sudden attacks of vertigo So they dizzy when they make positional sudden movements. In severe cases can make you home bound because you can tolerate the ups and downs of driving. What causes this is when the oticoni or calcium crystal come off of the utrical and sacula and they float away into the semiscircular canals. And land on the cupula and then cause it to move with gravity so when you move your head these crystal that are stuck on the cupula or drifting in the semi circular canal and cause it to move to much hence messing with balance. 90% are found in the posterior canals.

108. How do you asses Beingn paroxysmall positional vertigo (BPPV)? To asses this use the Hall-pike Dix maneuver you have the pt lie on a table and quickly move them over the edge of the table head in extension and side rotated then and hold them there and watch and the eyes should start twitching in 5-10 sec and the pt should feel nausea ( similar to vertebral artery which also can cause nystagmus so to differentiate move the body to close off the vertebral artery without moving the head).

109. How do you treat Beingn paroxysmall positional vertigo (BPPV)? Brandt's exercises - have the pt goes to the one side quickly and then to the other side to try and shake the rocks of the cupula. Semont maneuver you go over to one side and hold the head there for 3 minutes and shake it a bit, then go to the

other side and hold it there for a few minutes and the stay in mid-line for 24 hours, what this does it maneuver the rock out of the posterior semicircular canal Epley maneuver or Canalith repositioning so for a R posterior canal issue lay them supine and shake the head or gently bang the head and maybe put a vibrator on it and then roll the head over the back of the plynth and you sit them up. Them have them sleep sitting upward for 24 hours , This will make them sick as a dog for hours and may take one or two or three more times, though this may reoccur.

110. Explain the neural pathways of the auditory potion of the vestiblocochlear nerve? 1st order neuron neurons coming away from the hair cells which have there cell bodies in the cochlear and are called the cochlear or spiral ganglion. They go to the pons were they synapse with the dorsal and ventral conchlear nuclei. 2nd order neuron goes up bilaterally (crossed and uncrossed pathways) through the lateral lemniscus to the thalamus and the medial geniculate body (lateral geniculate body has visual going to it) 3rd order neuron auditory radiation project into the cortex to area 42 the superior temporal gryus which is the primary auditory perception area. Collateral also go to the inferior coliculi (part of the corpa quadrigemina) and down the tectospinal tract to trigger auditory reflexes.

111. What goes through the VPM, VPL , and the medial and lateral geniculate body? Things that go to the VPM trigeminal nerve - Pain and temp , touch and pressure Facial nerve taste anterior 2/3 of the tongues VPL lateral spinothalmic tract ventral or anterior spinothalmic tract

medial lemniscus form FC, FG medial geniculate body Lateral meniscus from the auditory part of the vestibulocochlear nerve lateral geniculate body optic nerve

112. Explain the two types of deafness? and how you tell teh difference between them? Conduction deafness is due to a mechanical problem to the transmission of sound Example torn ear drum or the most common cause of this is otosclerosis which is when one of the oscicles becomes fuses it is usually the stirrup so the oscicles don't vibrate, which stop the stirup form vibrating into the oval window and hence stop the transmission of sound into the colchear.. Sensorineural the mechanical parts are fine but the brain , cochlear or the nerves are damaged so you receive the sound but your not getting it to the brain, or not ably to process it once there. Can test which form of deafness the pt has with a tuning fork. If you place it on the skull by the ear which transmits signals to the ear through the bone so will bypass the ossicles and will let you hear it even if you have conduction deafness. So if they don't here it is sensorineural deafness. If they do it is conduction deafness.

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Name some of the many causes of sensory deafness? rubella in pregnant women can cause the child to be born death large doses of antibiotics. Aging can also cause deafness. Acoustic neuromas which is a tumor on the nerve itself (usually form the glial cells) which can cut off the nerve.

114. Explain the general antomy and pathway of the olfacotry CN:#1? There are 10-15 Olfactory neurons which enter the nose through holes in the cribform plate which is part of the ethmoid bone. These neurons terminate in

little dendrites which act as rapidly adapting chemical/smell receptors for chemical dissolved in the mucous secreted by the bowmen's gland which breaks down chemicals. The olfactory neurons connect with the olfactory bulp or mitrol cells which form the ends of the olfacotry tract. Which is simple a protrusion of the brain and not a nerve. This smell information is carried all over the brain, one place it goes to is the hippocampus and the amygdalo (part of basal ganglion in some books) which are part of the limbic system which deals with memories and emotions, so this why smell is an emotional provoking sense. We also know that to get conscious perception of smell this signal goes to the medial dorsal nucleus and eventually to the thalamus and then to the orbitofrontal cortex were our conscious perception of smell is located. Which is right above the eyes. This is a mysterious part of the brain , not sure what it does though suspected to be home of many of are decision making skills.

Olfactory neurons are always dieing so the basal cells are constantly making new ones, about ever 60 days the basal cell bud of a new neuron which grows through the hole in the cribiform plate and connects to the mitrols cells.

115. Define hyposmia? less then normal ability to smell, also happens with aging

116. Define Anosmia? complete loss of smell side note - can be a sign of damage to the cribiform plate or of damge to thr frointal lobe form things like tumors whcih can daamge the olfacotry nerve as well so may wish to look for personality changes with this.

117. Define cacosmia and give two causes? Cacosmia a problem with smell were you get overwhelmed with smells that aren't there. So olfactory hallucinations. Can be caused damage to medial temporal lobe damage (because this is were

the amgiduall is) or frontal lobe damage. So if the pt has epileptic seizures in the medial temporal lobe they can develop cacosmia.

118. What is George Gershwin Syndrome? medial temporal lobe lesion which can cause issues cascosmia and issues with upper visual field problems because meyers loop passes through the medial temporal lobe. So if it was a right medial temporal lobe lesion it would create R superior homonyus quadrant apnopsia.

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Name the exta pryamidal pathways? Extra pyramidal pathway starts lower down at the basal ganglion and other nuclei tectospinal vestibulospinal rubriospinal Reticulospinal tract

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Name some UMN and LMN lesion symptoms? UPM signs = barbinski, collonus, spasticy , hyper reflexia LMN signs areflexia, fasiculations, flacid paralysis, muscle atrophy

121. Explain the basic path of extra pryamidal pathways? Motor cortex is arranged in six layers form superifical to deep (the whole cortex has six layers) with various cells starting in the cerebral layers. Most of the pryamidal tract neurons start in layer 5. So the Cell body of the multipolar neurons going into the pyramidal tracts are in layer 5 and look like a big pryamids hence the name of this tract. These neurons project out of the motor cortex and go down to the the bottle neck at the internal capsule. Most cross over at the decusiation at the pyramids of the medulla and form the lateral corticosponal tract the rest that don't cross over to form the anterior corticospinal tract and cross over at the segmental level with a few staying ipsilateral.

122. Were is the internal capsule? Internal capsule is between the basal ganglion and the thalamus.

123. How si the internal capsule orginized? The internal capsule when looked at as a transverse cut looks like a bent leg with posterior and anterior section and our extra prymidal tracts go through the posterior limb of the internal capsule and they go through organized as FAL Face goes through internal capsule close to the knee Arms behind it comes the arms Legs behind that is the legs

124. Why are there two enlargements in the spine? Because so many nerves goes to are arm and legs there is a swelling or cervical and lumbar enlargement in the spinal cord due to the 100 of alpha/gamma motor neurons that have to go out form those areas, which take up more space within the cord.

125. What would a lesion of the R internal capsule cause? lesion in the R internal capsule would effect both the anterior and lateral corticospinal tracts so everything to the L of the body would be gone.

126. What would a lesion of the lateral corticospinal tract cause? But if you lesion the lateral corticospinal tract in the cord (85% of the fibers that come out of the internal capsule cross to make the lateral corticospinal tract, 15 % stay ipsilateral to make the anterior corticospinal tract) you still have the anterior corticospinal tract going down the opposite so still have some function just not very good. (5 % of the 15% in the anterior corticospinal tract stay ipsilateral)

127. Why is the internal capsule prone to strokes? What are f Striate arteries? internal capsule is prone to strokes because there is lots of little arteries there that come of bigger arteries and so it easy for bit of fat to clog the internal

capsules arteries.

Many type of Striate arteries supply various parts of the internal capsules and other things as well also called the arteries of stroke because they are very prone to stroke, because they are the first small arteries that lead of the major arteries in the brain.

128. Explain Polio? Poliomyelitis ( used to be called infant paralysis) polio = Greek for gray, myelitis = marrow or middle of something is a LMN disease caused by a virus contracted through insect bites or ingestion which generally effects kids. Once in the body it spreads into the CNS and atatcks the ventral gray horn often at the lumbar and cervical enlargements. Sign/symptoms loss of reflexes weak muscles sever headaches fever and pain can be confused with menigitis and dypitheria Can cause death if it gets into the brainstem. Progression: symptoms get worse for weeks then it plateaus and then they get gradually better/stronger for a year or more but then they left with sever extremity problems Vaccine Johna Salk came up with the Salk vaccine which prevented infection from blood but not ingestion Sabin came up with a better vaccine which you take as a sugar drop.

129. Explain Post polio syndrome? post polio syndrome - more common in American this disorder is when you see a pt who thinks they have polio again this is called Post polio which is when the symptom reoccur, they have weakness and bad pain particular at trigger

points, but not fever. It occurs because polio eats some of the alpha motor neurons in the ventral grey horns and the surviving alpha motor neurons sprout and go over and innervate the muscle that's become deinnervated, so this is why you recover from polio but after 30 or so years these alpha motor neurons who have taken on double duty can't take it any more and then they die back to there original innervation, leading to pain and weakness again. So pt who had polio before like in the 50's can get this, sometimes they even it get it regularly like once a year..

130. Explain Cerebral palsy? Cerebral Palsy is a catch all term for brain damage to young kids so it usually is lesion of the spinal tract often due to loss of blood supply during child birth often idiopathic can be from set things like the pt's mother having had rubella or measles while pregnant. Or form shaking baby syndrome in which it can be an acquired brain injury from things like shaken baby syndrome. Many places in the CNS can be damage so many symptoms you can see, deafness, blindness, spasticity , gait posture problems and many others. It can be sever or mild. If only legs are effect it is called spastic dyplesia child. Can be hemipelsia so it can be one sided. Can also be broken down by symptoms athetoid CP (athetosis is bizarre writhing of the hands and arms) or ataxic CP so they can't walk smoothly. Hypotonic CP so very floppy muscles. Also can be mixed CP were they have mutliple symptoms. Some kids are high functions some are low functioning.

131. Explain ALS? Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrigs disease who died in 1941at age of 38 stand for (means without muscle nutrition lateral scarring) so it attacks primarily the lateral corticospinal tract this has no know cure or cause and it gradually gets worse as it attacks neurons, it can also attack the LMN at the ventral grey horns. So can be mixture of UMN and LMN symptoms , though it tends to be more UMN symptoms, first sign is usually hyperspasticity of the forearm wrist extensors worsens and if it migrates into the brain stem it can leads to eating and breathing issues and death. Usually very fatal within a few years of developing this disorder they usually have maybe 5 years more common in 40-50 year old pt more men then women. 10% of the pt who get this survivor more then 10 years Steven Hawkins has lived with this for years these pt have normal cognitive functions but can't move there body. If you get it earlier in life the progression is slower if you get

it later in life 50-60 years old, it progressive is faster and you die quickly only 1 in 50,000 get this. 3 people in one foot ball team got it at once so suggested an environmental cause of this. In Guam 1 in 100 people on this island got ALS, what they found that there is a lot of volcanic minerals in there brain and tissues now with improved diet and water system it dropped to one in 100,00 so they think it has something to do with the environment riluzole is a drug that tries to slow the progression has some effect it is a glutamate (prevenelent NT in the nervous system) antagonist. These pt will need lot of adaptive equipment.

132. Explain what/how the corticobulbo tratc innervates? Corticobulbo tract UMN going to the brain stem from the cortex only goes to the motor cranial nerves. So doesn't go to optic, olfactory and vestibular cochlear, because they are pure sensory. All cranial nerves have nuclei from which they start (like the ventral grey horn), most of this tract is bilateral, so the R/L hemisphere innervates both the left and right cranial nuclei except in two nerves the hypoglossal (tongue muscles) which only receives this contralaterally like in the body facial nerve the lower face have a contralateral supply and the upper muscles have a bilateral supply Due to this bilateral path a unilateral stroke wont effect the cranial nerves as much as the lower extremities. The exception being parts of the face and tongue.

133. What are Two of the most common problems in thefacial muscles? is bell palsy and Myasthenia gravis

134. Explain Myasthenia gravis? Myasthenia gravis (my = muscle asthenia = weakness gravis = grave) (sever muscle weakness) can attack any muscle in the body but it initially likes to attack the muscles supplied by the cranial nerves first. So attacks eye muscle before your legs. More common in women then men. 20-50 year old is common age of pts. It is easy to spot because the pt face will drop later in the

day this is usually bilateral (unilateral tends to be bells palsy), so you see ptosis were the eye lids get heavy and drops at the end of the day also may have issue with chewing and swallowing and may have issues with strabismus (due to loss of eye muscles) , or double vision these pt can get better from remission but it a progressive relapsing diseased were they get worse and worse until it attacks the heart and lung and then they can die. Ideopathic , no changes in the nerves and brain under disection, though you can see an abnormal thymus gland so it is occasionally removed to attempt to help them. You due see changes in the muscles, specificly you see antibodies at the neruo muscular junction , two types of these AntiBodies are found there, one blocks the release of ach from the motor end plate, the second anti body you find on the receptor sites for ach within the muscle itself, which blocks these receptors so these muscles can't contract and they weak, so the effect are similar to snake venom and currarie. So it block the receptor forever. A lot of research was done with snake venom (bungarotoxin = cobra venom because it bind forever with ach receptors) so it used to determine the severity of this disease, by Quantifying how many receptor are already bound by the disease. What they do is take a chunk of tissue out of a pt and look at under microscopes then they add the venom to the normal muscle and they watch what comes out of the bottom of the tube , it it hundred percent then nothing come out of the bottom because they all bind. With this disease a lot of it comes out the bottom because there is no were for it to come out because all these sites or a lot of them are bound. So a muscle with this disease usually only bind 1/3 of normal for the toxin so you can use this to quantify the severity by using the cobra venom. Treatment modalities and a lot of adaptive equipment and neostigmine which is a cholinesterase inhibitor which allows the ach to hang out in the synaptic cleft longer. Often this will be carried in a pen they use in case of respiratory distress. Eventually pt will be on a soft diet. Also may try palsmaphersis were they remove the plasma and try and filter the antibodies out of it, this and it can help sometimes.

135. Who has the best chance of getting PD? A over 60 year old Amish person with red hair living in nebraska? Parkinson's disease very common in the Amish community 1% of the pop over 60 have it. No one knows why but it May be due to pesticides. Also very common in Nebraska may be tied to agriculture. Those of use with dark hair have less chance of getting it then blonds (60% more chance then dark hair),

red head have 3x more likely then a person with dark brown hair. This is because it the Substantia nigria which dies when you get this disease and the production of dopimine is similar to the production of melanin so there a link in the way you produce melanin and the way you produce dopamine and hence why hair color may be related to the risk of developing it. Idiopathic disease. 5% rate of concordance.

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Name the signs of PD? Bradykinesia negative sign Akinesia - negative sign Mask-like face - negative sign Resting tremor (pill-rolling tremor) - happens every 3-5 seconds Hypertonia Cog-wheel rigidity -late in the disease rigidity is common Stooped Posture Micrographia Gait dyskinesia shuffling: stride length and cadence reduced, freezing festination were they hury up retropulsion go back ward can also be caused by reaching up Pedestal turning can result in retropulsion Affective and cognitive disorders emotional and cognitive deficits often ignored because the other symptoms are more obvious

137. What is the most common drug treatment for PD? Levodopa or Ldopa is given to these pt often given combined with carbidopa which is called sinemet (is a brand name). Carbidopa binds with L dopa and prevents the other parts of thebody form using it anywhere but in the brain because it can't enter the brain so it releases the l dopa and lets it cross the blood brain barrier to enter the brain and become dopamine.

138. Explain basic treatment for PD? Dopamine replacement and many other drugs may be used PT: Work against the rigidity and the brady kninesia also they develop a kyphotic posture so work on making the chest expand and trunk rotation. So

things like caiacing Cueing Instructional - walk big talk big to fight defiects cognitively Auditory - create rythme or tone for actions to speed actions Cutaneous Visual ) use visual things like lines to help them with freezing so things like line on the floor. Ben did first experiment with long term use of cueing.