Neurology Quick Facts Week 2 Flashcards
1
Q
Location of CN III
A
in midbrain, just ventral to the superior and inferior colliculi respectively
2
Q
CN III: How many nuclei, and why so many?
A
5 nuclei because controls 5 eye muscles
3
Q
Names of the nuclei of CN III
A
Dorsal inferior nuclei, central caudal nucleus, medial nuclei, ventral nucleus and intermediate nucleus
4
Q
CN III provides ipsilateral innervation to?
A
The inferior oblique, the medial rectus, and the inferior rectus.
5
Q
CN III contains a nucleus that sends axons contra-laterally. Which is it?
A
The medial nuclei innervate contra-laterally.
6
Q
CN III passes between the superior cerebellar artery and posterior cerebral artery, then alongside the posterior communicating artery and underneath the internal carotid artery. What does this mean for possibility of injury to this cranial nerve? What is the risk association between the cavernous sinus and CN III?
A
CN III is at risk of a lesion due to aneurysm from one of the many blood vessels by which it passes.
CN III travel with the cavernous sinus, which drains blood from the eyes and cortical veins to empty eventually into the jugular vein.
7
Q
Function of the ciliary muscle of the eye
A
It produces a change in the lens shape as the eyes converge on a target moving toward the eyes. The resulting pupillary constriction produces the accommodation reflex.
8
Q
Medial recti do what to the eye? How are they innervated?
A
Medial recti move the eye globe toward the nose (adduction)
The medial rectus is innervated by CN III
9
Q
What do the superior and inferior recti do to the eye? How are they innervated?
A
Vertical movement up and down; innervated by CN III
10
Q
What does the superior oblique muscle do, and how is it innervated?
A
The superior oblique muscle causes intorsion of the eye (think of a cross-eyed person). It is innervated by the trochlear nerve, or CN IV
11
Q
What does the inferior oblique muscle do, and how is it innervated?
A
The inferior oblique muscle causes extortion of the eye and is innervated by CN III
12
Q
What do the lateral recti do, and how are they innervated?
A
Lateral recti away from the nose respectively.
The lateral rectus is innervated by CN VI.
Remember! LR 6, SO4, 3
13
Q
The dorsal nucleus innervates which muscle?
A
Inferior rectus muscle
14
Q
The intermediate nucleus innervates which muscle?
A
Inferior oblique muscle
15
Q
The medial nucleus innervates which muscle?
A
The superior rectus muscle
16
Q
The ventral nucleus innervates which muscle?
A
The medial rectus
17
Q
The central caudal nucleus innervates which muscle?
A
The levator palpebrae superioris muscle, which VOLUNTARILY elevates the upper eyelids. Again, it is innervated by CN III
18
Q
How do you test the superior rectus muscle of the eye in a physical exam?
A
Ask the patient to look laterally and upward (therefore test one eye at a time). This test works because when either eye is in the abducted position, looking laterally, elevation of the eye is controlled primarily by the superior rectus muscle. If the patient has trouble with this, it means his superior rectus muscle is weak or that the nerve innervating it is injured.
19
Q
How do you test the lateral rectus of the eye?
A
Ask the patient to fully abduct the eye (look laterally). If the eye does not fully abduct, then the lateral rectus is weak or CN VI is not functioning normally.
20
Q
How do you test the inferior rectus muscle of the eye in a physical exam?
A
Ask the patient to fully abduct the eye (look laterally) and then look down. In the abducted position, depression of the eye is controlled primarily by the inferior rectus muscle and its CN III.
21
Q
How do you test the inferior oblique muscle in a physical exam?
A
Ask the patient to adduct the eye (look toward his nose), then look up.
22
Q
How do you test the medial rectus muscle of the eye?
A
Ask the patient to adduct his eye (look toward his nose)
23
Q
While testing a patient, Dr. Bad Mother Shut Yo Mouth asks the patient to look to the patient’s right, then up, then down. What muscles are being tested by Dr. Bad Mother Shut Yo Mouth?
A
Of the right eye, the lateral rectus, then superior rectus, and inferior rectus.
Simultaneously of the left eye, the medial rectus, the inferior oblique muscle, and the superior oblique muscle
24
Q
What does the tarsal muscle do and how is it innervated?
A
The tarsal muscle has sympathetic innervation that allows for INVOLUNTARY elevation the eye
25
What is the consequence of a completely damaged CN III?
Complete paralysis of the superior rectus (of both eyes), inferior rectus, medial rectus, and inferior oblique, as well as the levator palpebrae superioris that results in eye closure.
26
What is the consequence of a partially damaged CN III?
Incomplete lesions produce paresis of the superior rectus, inferior rectus, medial rectus, and inferior oblique, as well as the levator palpebrae superioris with partial lid closure.
27
Describe the sympathetic pathway to the pupillary dilator muscle
The pathway originates in the hypothalamus, travels through the lateral brainstem, and eventually synapses with a secondary neuron located in the intermediolateral gray area of the spinal cord at the C8-T2 level. The secondary neuron sends its axon to the paravertebral sympathetic ganglia chain and and travel upward to synapse in the superior cervical ganglion. The tertiary neuron sends its fibers, along with the internal carotid artery, through the carotid sheath and into the calvarium. Sympathetic fibers then join the nasociliary nerve to innervate the superior tarsal muscle. They also join the long and short ciliary nerves to innervate the dilator muscle of the pupil.
28
Which nerve do sympathetic fibers join in order to innervate the superior tarsal muscle?
The nasociliary nerve
29
Which nerve do sympathetic fibers join in order to innervate the dilator muscle of the pupil?
The long and short ciliary nerves
30
Where does the sympathetic pathway for eye innervation originate?
In the hypothalamus
31
Explain what happens upon stimulus (with a flash of bright light) applied to the front of the left eye
The bright flash of light causes afferent signals of the optic nerve to be sent through the optic chasm and optic tract to synapse in the left and right pretectal nuclei. The pretectal nuclei send their BILATERAL axons to the Edinger-Westphal nucleus. The EW nucleus sends axons to both the right and left pupillary constrictor muscles.
32
Does the Edinger-Westphal nucleus become stimulated regardless of which eye receives a flash of light?
Yes, because it is a single, midline nucleus with neurons that send signals to BOTH the left and right pupillary constrictor muscles. This is the basis for direct and consensual light reflex tests. You want to make sure both eyes are responding to the nudge from the EW nucleus.
33
What neural pathways are you testing with the light reflex test?
You're testing the integrity of the afferent pathway - the fibers from the retina and optic nerve traveling to the EW nucleus.
You're testing the efferent pathway - the Edinger-Westphal projections to both eyes via the ciliary ganglia that produce pupillary constriction.
34
Does the Edinger-Westphal nucleus contain parasympathetic fibers?
Yes.
They travel along the dorsal medial surface of CN III on their way to the Edinger-Westphal nucleus.
35
What type of aneurysm most commonly compresses CN III?
Posterior communicating artery aneurysms
36
Which arm of the autonomic nervous system is first compromised when an aneurysm begins to compress CN III? How would a patient initially present?
The parasympathetic nerves that cause pupillary constriction are first compromised.
Patient would present with unilateral pupillary dilatation. If the aneurysm enlarged more to completely compress CN III, unilateral paresis would then occur. An aneurysm that compresses CN III is an emergency since rupture can cause either death or permanent disability.
37
A diabetes patient presents with oculomotor paresis withOUT enlargement of the pupil. What pathophysiology is on your differential? Why is the pupil not enlarged?
The patient has developed a vascular disease from the diabetes that is occluding small arteries that supply the center of CN III. The pupil is not enlarged because the parasympathetic pupillary constrictors and their superficial blood vessels are not affected by vasculopathies occurring in the center of the nerve - they are too superficial.
38
By which areas of the brain is the accommodation reflex initiated?
Prefrontal eye field and occipital-parietal fields cause a pretectal activation that triggers parasympathetic output through the Edinger-Westphal nucleus to produce pupil constriction and lens thickening. CN III is also bilaterally activated to produce eye convergence.
39
Which axons running through the Edinger-Westphal nucleus allow for the accommodation reflex, and what actions of the result?
Parasympathetic output is triggered and causes pupil constriction and lens thickening.
40
CNIII provides contralateral innervation to? Via what nucleus?
The superior rectus muscle.
The medial nucleus
41
The trochlear nerve, CN IV, provides (ipsilateral / contralateral) innervation to?
CN IV provides contralateral innervation to the superior oblique muscle.
42
CN VI provides (ipsilateral / contralateral) innervation to?
CN VI provides ipsilateral innervation to the lateral rectus muscle.
43
What structure connects CN VI to CN III to achieve horizontal movement of the eyes?
The medial longitudinal fasciculus (MLF), which leaves the abducens nucleus, decussates, and travels rostrally to synapse on the ventral nucleus of CN III.
44
What structure controls the MLF connection between CN III and CN VI?
Phasic firing of MLF is regulated by the paramedian pontine reticular formation (AKA: horizontal gaze center and parabducens nucleus)
45
Saccadic eye movement - definition and other facts. Give an example of a situation in which saccadic eye movement is voluntarily activated and one in which it is reflexively activated.
This is fast conjugate movement of the eye. Saccadic eye movement is under the control of the frontal eye field and is either voluntarily or reflexively triggered.
E.g. 1: Holding the head still whilst looking from one side of the room to the other
E.g. 2: A bug crawling on the wall in your peripheral vision causes you to automatically look at it.
46
Describe the saccadic pathway.
The saccadic pathway from one frontal eye field travels with ipsilateral corticobulbar fibers through the internal capsule to the ipsilateral superior colliculus and on to the contralateral PPRF. Thus, the RIGHT frontal eye activates the LEFT PPRF, which in turn activates the left abducens nucleus and right ventral nucleus of CN III, causing the eyes to conjugately look to the left.
47
Notes on lesions: CN VI palsy is a problem with the lateral rectus. If the patient is asked to look to the right, one eye fine and the other not. Right abducens nucleus palsy - the abducens nerve is affected so that the right eye cannot move laterally, but it can no longer send the axons across the MLF to the conjugal medial rectus. Therefore, neither eye makes it over if you infarct the abducens nucleus on the right side. If you infarct the parabducens nucleus, you can look to the left just fine but on the right side, it's the same as if you had a right abducens nucleus infarct. They are actually clinically indistinguishable. MLF lesions: if you have a left MLF lesion, you look to your left and all is well, but when you look to the right, the axon sent by the abducens across the midline and up the MLF to the contralateral medial rectus is not working, so you look to the right, the left medial muscle just sits there and the left eye cannot move over. How do we know this is the MLF and not CN III and its nucleus? Bring your finger to the tip of their nose to converge the eyes, and see that they can, in fact, converge. This occurs in MS because these are highly myelinated nerves. You'll likely see left MLF on USMLE. The last lesion: Left MLF and left abducens nucleus are affected. The left abducens nucleus pulls the eyes toward it, so there's failure of that to happen. You cannot move the eyes conjugately across the midline. Because the left MLF is also affected, when you want to move the eyes to the right side, that right abducens sends its axon to the MLF, but MLF is out, so that does not work. Medial rectus does not move when you try to look. The right eye moves only when it is abducting. CN VI function preserved on the right. On the left side, cannot look right or left - stuck in the middle.
Write this information down.
48
Pursuit movement: description and other facts. Give an example in which pursuit movement is used.
Slow pursuit movements are under the control of the parietal-occipital-temporal (POT) area. The POT area directs eye movement in the ipsilateral direction (unlike the frontal eye field).
E.g.: Hold your index finger in front of you and move it from right to left, keeping your eyes on the finger. Your LEFT POT area controls your eyes as you track the finger to the left.
49
Explain how saccadic and slow pursuit eye movements work together during the OKN test (striped cloth that patient is asked to follow with eyes). Explain what you'll see if things are awry.
As the striped bars are moving from right to left, the RIGHT POT tracks with slow pursuit (ipsilateral). Then, the LEFT frontal eye field (contralateral) causes the eyes to saccade back toward the right for the next stripe.
If the patient had problems, you'd see an OKN nystagmus - that is to say, the saccadic movement beating to the right, instead of moving smoothly to the right.
50
Describe the difference between a left frontal cortex lesion and a left pontine lesion in regards eye movement.
Lesion of the left frontal lobe produces a right hemiparesis and loss of input to the right PPRF. This leaves only the left PPRF to work on the eyes (recall PPRF operates ipsilaterally); thus, the right frontal eye field and the left PPRF drive the eyes to the left, away from the paresis; that is to say, the muscle weakness.
A lesion to the left pons produces a right hemiparesis and loss of input to the left PPRF. This leaves only the right PPRF, which will drive the eyes to the right (because of its ipsilaterally operation), toward the paresis.
51
Describe the function of the cerebellum
Compares intention with performance to compensate for error in movement.
Coordinates somatic motor activity to influence and maintain equilibrium
Cognition, emotion, and affective processing
Sequencing of incoming sensory patterns and detecting temporal changes in the sequence of sensory events.
52
List the cranial nerves that are sensory only
I, II, and VIII
53
Describe the location of the motor nucleus of the trigeminal nerve, as well as how CN V exits the skull
The motor nuclei is located at the mid pons level. Motor fibers are located ONLY in V3, the mandibular branch of CN V. V3 exits the calvarium via the foramen ovale
54
What does the V3 division of CN V innervate?
The muscles of mastication, including the masseter, temporalis, and medial and lateral pterygoid. It also innervates the tensor tympani, the tensor veli palatini, the anterior belly of the digastric, and the mylohyoid muscle
55
Describe the jaw jerk reflex and why a physician uses it to test a patient.
Tapping the lower jaw triggers muscle spindles in the masseter muscle to send an impulse through the sensory fibers of sensory cranial nerve V. The fibers synapse in the mesencephalic nucleus of V. An interneuron connects the mesencephalic nucleus to a motor nucleus of V. The motor nucleus of V sends an impulse to the masseter muscle to contract.
A physician can perform the muscle stretch reflex to ensure that the efferent fibers from the motor nucleus of CN V are functioning properly.
56
What are the functions of the tensor tympani and the tensor veil palatini?
Tensor tympani dampens sound, and tensor veil palatini opens the eustachian tube.
57
What is the function of the mylohyoid muscle and the anterior belly of the digastric?
They elevate the hyoid bone.
58
What is the result of a lesion to CN V?
Lesions of CN V or its nuclei will cause unilateral weakness of jaw closure, reduced jaw jerk, and atrophy of the temporals and masseter muscles.
59
Which and what part of the cranial nerve are you testing when you ask a patient to bite on a tongue depressor as aggressively as possible?
You're testing the motor fibers of V3, as well as the motor nuclei, of CN V.
60
How many sensory nuclei are associated with the trigeminal nerve? What are their names?
There are 3 nuclei. They are the chief sensory nucleus, the spinal nucleus, and the mesencephalic nucleus.
61
Describe the function of the chief sensory nucleus and how it gets its information.
The chief sensory nucleus receives epicritic inputs from afferents for fine touch and vibration sense from the face. Epicritic afferent cell bodies are located in the trigeminal/gasserian ganglion outside of the brainstem. They send their processes into the brainstem to the chief sensory nucleus.
Important: other cranial nerves also help with touch and vibration sensations of the face. Though they initially synapse in peripheral nuclei other than the trigeminal, they also synapse in the chief sensory nucleus of V; therefore, the chief sensory nucleus of V is the first integration center for all fine touch and vibration inputs for the face region.
62
Describe the function of the mesencephalic nucleus of V and how it gets its information.
The mesencephalic nucleus of V is a peripheral ganglion that contains cell bodies of proprioceptive afferents like spindle organs and Golgi tendon organs from the muscles of mastication. it is located in the tegmentum of the mesencephalonm despite it's being considered peripheral. The peripheral processes of these cells form the mesencephalic tract of V.
Cells projecting from the mesencephalic nucleus project bilaterally to the trigeminal motor nucleus to mediate the monosynaptic stretch reflexes.
63
Describe the function of the spinal nucleus and how it gets its information.
The spinal nucleus receives inputs from pain and temperature afferents for the face that run in cranial nerve V, as well as in CNs VII, IX, and X. Cell bodies for the afferents of V are located in the trigeminal ganglion. The processes from the various ganglions project and synapse in the spinal nucleus of V. These axons and the second-order axons run in the spinal tract of V
64
Which nucleus of CN V receives pain and temperature afferents?
The spinal nucleus
65
Which nucleus of CN V receives proprioceptive (Golgi tendon organ, spindle organ) afferents from the muscles of mastication?
The mesencephalic nucleus
66
Which nucleus of CN V receives afferents for fine touch and vibration sense?
The chief sensory nucleus.
67
Which nucleus integrates afferents from the peripheral ganglion of many cranial nerves, but is mainly associated with CN V?
The chief sensory nucleus is the main dude own for this, but the spinal nucleus also does some incorporating
68
Describe the path of the trigeminal lemniscus
The trigeminal lemniscus runs from the chief sensory nucleus of V to the ventroposteromedial nucleus (VPM) of the thalamus.
69
Describe the path of the trigeminothalamic tract
The trigeminothalamic tract runs from the spinal nucleus of V to the VPM (ventroposteromedial nucleus) of the thalamus.
70
List the tracts associated with the chief sensory nucleus of V
Cell bodies for afferents are located in the trigeminal ganglion (cell bodies for VII, IX, and X are also there). Central processes of these cells project to the chief sensory nucleus of V.
2nd order neurons travel in the contralateral trigeminal lemniscus and terminate in the VPM of the thalamus.
2nd order neurons from afferents from inside of the mouth travel in the ipsilateral posterior trigeminothalamic tract
71
List the tracts associated with the spinal nucleus of V
Several cranial nerve afferents for pain and temperature contribute to the spinal nucleus - CNs V, VII, IX, and X. Their central processes project into the spinal tract of V and synapse in the spinal nucleus of V.
2nd order neurons from afferents travel in the contralateral trigeminothalamic tract
72
List the tracts associated with the mesencephalic nucleus of V
Central processes travel to reticular formation, cerebellum, and motor nucleus of V
73
List the tracts associated with the motor nucleus of V
Afferents travel in the corticospinal tract to motor neurons.
74
Afferents from which spinal nerves hold the most dorsal position in the spinal tract?
Afferents from CNs VII, IX, and X.
75
Afferents from which branch of CN V hold the most dorsal position in the spinal tract relative to the other CN V branches?
The mandibular, or V3 afferents
76
Where does CN VII exit the brainstem?
CN VII exits with the nervus intermedius at the cerebellopontine angle.
77
The facial nucleus axons create a bulge on the floor of the fourth ventricle called the?
Facial colliculus
78
Describe the path of CN VII as it exits the calvarium and beyond
CN VII and nervus intermedius exit the brainstem at the cerebellopontine angle. They enter the auditory canal. Within the auditory canal, CN VII bends ventrally to enter the facial canal and exits the skull via the stylomastoid foramen.
79
What muscles does CN VII innervate?
CN VII innervates the muscles of facial expression and the stapedius muscle, which dampens sound.
80
How do you test for CN VII motor lesions?
Ask the patient to furrow his forehead, close his eyes tightly, and show you his teeth. Make sure these movements are symmetrical.
81
Which parts of the face have bilateral CN VII innervation, and which parts have unilateral? What does this mean clinically?
The forehead muscles have bilateral innervation, but the rest of the face muscles have unilateral innervation.
Clinically: unilateral lesions to the motor cortex or corticobulbar fibers causes unilateral weakness of contralateral lower facial muscles, but spares the forehead muscles (because these are bilaterally innervated).
Unilateral lower motor neuron lesions cause ipsilateral weakness of the lower face and forehead muscle. Ipsilateral hyperacusis and dry eye may also occur.
82
With which reflex is CN VII associated?
Motor CN VII mediate the efferent arm of the corneal reflex.
83
Where are the cell bodies of the somesthetic afferent fibers of CN VII located?
The geniculate ganglion
84
Where do fibers from the geniculate ganglion project to?
Central processes from the geniculate ganglion project to the chief sensory nucleus of V (epicritic) or the spinal nucleus of V (pain and temperature)
85
From which CNs doe the gustatory nucleus receive inputs?
CNs VII, XI, and X
86
What is the the nucleus solitarius?
It runs as a column through the pons and medulla; it's rostral portions are also called the gustatory nucleus and are concerned with taste sensation
87
The rostral part of the nucleus solitarius, or gustatory nucleus, receives input from a few different cranial nerves. Each cranial nerve is communicating taste from a specific area of the oral cavity. Pair each cranial nerve with the area from which it brings taste.
Cranial nerve VII: Taste input from the anterior 2/3 of the tongue
Cranial nerve IX: Taste input from the posterior 1/3 of the tongue
Cranial nerve X: Taste input from the pharynx and epiglottis
88
The caudal part of the nucleus solitarius is called the?
Cardiorespiratory nucleus
89
The cardiorespiratory nucleus is located? From which nerves, and which type, of input does it receive?
It receives visceral sensory (glands, baroreceptors, chemoreceptors) from CNs VII, IX, and X.
90
What two main pathways are associated with CN VIII?
The auditory pathway (hearing) and the vestibular pathway (balance and acceleration)
91
Name the nuclei in which auditory afferents from CN VIII synapse
Auditory afferents begin at hair cell receptors and leave the ear to synapse in the spiral ganglion, the dorsal cochlear nucleus, the inferior colliculus, the medial geniculate body, and finally, Herschel's gyrus
92
What do auditory receptors in the ear do?
They are tuned to different frequencies of sound and are sensitized to airborne pressure waves
93
Where are vestibular hair cells located?
They are located in the saccule, utricle, and the three semicircular canals.
94
What do the vestibular receptors in the ear do?
They are important for the adjustment of posture, regulating muscle tone, and coordination of eye movements.
95
What nuclei are associated with the vestibular pathway?
The medial, lateral, superior, and inferior nuclei.
96
What tracts are associated with each nuclei of the vestibular pathway?
The lateral nucleus gives rise to the lateral vestibulospinal tract. The medial and inferior vestibular nuclei give rise to the medial vestibulospinal tract.
The medial and superior nuclei give rise to the medial longitudinal fasciculus (MLF).
97
What does the lateral vestibulospinal tract control?
Balance and extensor tone
98
What does the medial vestibulospinal tract control?
It extends to the cervical levels of the cord and controls head and neck position.
99
What does the medial longitudinal fasciculus control?
It coordinates eye movements.
100
What nucleus is associated with the motor component of CN IX?
The nucleus ambiguus
101
What the motor component of CN IX innervate?
The stylopharyngeus muscle, which raises the pharynx during talking and swallowing
102
Clinical testing of CN IX is best done how?
Via sensory function, as the only motor innervation is of the stylopharyngeus muscle.
103
Upper motor and lower motor lesions may produce?
Dysphagia
104
What is the motor nucleus for CN IX?
The nucleus ambiguus
105
List the sensory roles of CN IX
Taste from the posterior 1/3 of the tongue
Chemo- and baroreceptor afferents from the carotid sinus and carotid body respectively.
Pain and temperature afferents from the posterior 1/3 of the tongue, pharynx, tonsils, tympanum, and a small area around the external ear.
Afferents for epicritic touch from the posterior 1/3 of the tongue, pharynx, tonsils, tympanum, and a small area around the external ear.
106
What nucleus is associated with the taste afferents from CN IX?
Afferents from the posterior 1/3 of the tongue terminate in the rostral solitary tract (AKA: the gustatory nucleus)
107
What CN IX nucleus is associated with the carotid sinus baroreceptors and the carotid body chemoreceptors?
The caudal part of the solitary nucleus and tract
108
What CN IX nucleus is associated with pain and temperature afferents from the posterior 1/3 of the tongue, pharynx, tonsils, tympanum, and a small area around the external ear?
The spinal nucleus and tract of CN V
109
What CN IX nucleus is associated with the afferents for epicritic touch from the posterior 1/3 of the tongue, pharynx, tonsils, tympanum, and small area around the external ear?
The chief sensory nucleus of V
110
Motor components of CN X are served by which nucleus?
The nucleus ambiguus, located near the lateral medulla.
111
What do the motor fibers of CN X innervate?
CN X innervates the soft palate. It also innervates the pharynx and larynx, for the purposes of talking and swallowing.
112
Which nucleus sends preganglionic, parasympathetic fibers to the heart, lungs, and digestive tract?
The dorsal motor nucleus
113
Where does CN X exit the brainstem and skull?
CN X exits the brainstem between the inferior olive and the inferior cerebellar peduncle. It exits the skull at the jugular foramen.
114
What reflex does CN X participate in?
The gag reflex. Remember that CN IX is also involved in the gag reflex. The gag reflex can be tested to investigate the integrity of the cranial nerves.
115
What is the consequence of a lower motor neuron lesion of CN X?
Hoarseness of the voice, dysphagia, and reduced gag reflex on the stimulated side.
116
Is there strong or weak bilateral upper motor neuron input of CN X nuclei?
Very strong, so an upper motor neuron lesion is not as severe as a lower motor neuron lesion.
117
What are the sensory roles of CN X?
Taste from the pharynx, larynx, and the epiglottis.
Visceral info from the aortic arch baro- and chemoreceptors.
Somatic info from the pharynx and larynx.
Touch and pain/temp info from a small portion of the external ear.
118
Is CN XI mixed, motor, or sensory?
It is a pure motor nerve.
119
What two nuclei are associated with CN XI?
Nucleus ambiguus and the spinal accessory nucleus
120
Explain the path of CN XI fibers from the nucleus ambiguus.
Fibers from nucleus ambiguus travel with proximal fibers of CN XI, then joint CN X to innervate the pharynx and larynx
121
Explain the path of CN XI fibers from the spinal accessory nucleus
The spinal accessory nucleus has neurons that lie in the intermediolateral gray area of spinal cord segments C1 - C4/5. The fibers exit the cord, ascend alongside it, enter the skull through the foramen magnum, then exit it through the jugular foramen. They then innervate the sternocleidomastoid and trapezius muscles.
122
Is CN XII motor, mixed, or sensory?
CN XII is purely motor.
123
What nucleus serves the hypoglossal nerve?
The hypoglossal nucleus, which is in the posterior medulla at the junction of the spinal cord and medulla.
124
Describe the path of the hypoglossal nerve
Axons exit the brainstem ventrally between the inferior olives. It exits the skull through the hypoglossal foramen, which is at the posterior aspect of the petrous temporal bone. It travels to innervate the tongue muscles.
125
What are the clinical applications of a lesion to the UMN and LMN of the hypoglossal nerve
Recall that right tongue muscle pushes tongue to left and left tongue muscle pushes tongue to the right. If both are working, contraction of the muscles pushes the tongue out straight
Unilateral LMN lesion of CN XII or nucleus causes tongue to protrude TOWARD the side of the lesion; there is unilateral tongue atrophy and fasciculations of the tongue muscle.
Unilateral UMN lesion of the motor cortex or corticobulbar fibers cause tongue to protrude AWAY from the lesion since corticobulbar fibers decussate to innervate the hypoglossal nuclei.
126
To which nucleus do CN X and IX project taste?
The nucleus solitarius, also known as the gustatory nucleus
127
To which nucleus do CN X and IX project information from the chemo- and baroreceptors?
The caudal parts of the nucleus solitarius
128
To what nucleus do CN IX and X afferents for general visceral sense of the pharynx and larynx project fibers?
The nucleus solitarius
129
Fine touch, pain, and temperature from around the external ear are projected via CN IX and X to which nucleus?
The nucleus of the spinal tract of CN V
130
The afferent limb of the gag reflex is carried by which CN, and to where?
How is the afferent limb connected to the efferent?
Who carries the efferents to the target?
Afferents are carried by afferents of CN IX and projected to the caudal solitary nucleus. An interneuron connects afferents to efferents in the nucleus ambiguus.
The efferent response is mediated by motoneurons in the nucleus ambiguus, whose axons travel with CN X back to effect the reflex.
131
What do the vermis and paravermian structures of the cerebellum do?
They control axial musculature (neck and trunk muscles)
132
What do the lateral hemispheres of the cerebellum do?
They control limbs - legs and arms
133
What does the flocculonodular lobe of the cerebellum do?
It maintains balance and coordinates head and eye movements with the vestibular system.
134
What is the function of the deep nuclei of the cerebellum?
They serve as primary relay points for efferent fibers traveling from the Purkinje cells of the cerebellar cortex to other brain regions.
135
To which nucleus do fibers in the lateral hemispheres of the cerebellum project?
Lateral hemispheres project to the dentate nuclei.
136
To which nuclei do fibers in the paravermis of the cerebellum project?
To the globose and emboliform nuclei, which together are known as the iterpositus nuclei.
137
To which nucleus do fibers in the vermis of the cerebellum project?
The fibers of the vermis project to the fastigial nuclei.
138
What is the consequence of damage to deep cerebellar nuclei?
Severe ataxia.
139
What is the major outflow pathway to forebrain from the cerebellum?
The superior cerebellar peduncle is the major outflow pathway to the forebrain; it uses the dentatorubrothalamic tract and the dentathalamic tract.
140
What do dentatothalamic tract fibers carry?
They carry information from the lateral portions of the anterior and posterior cerebellar cortices to the contralateral ventrolateral nucleus of the thalamus and then onto the motor cortex
141
What do fibers of the dentatothalamic tract fibers do?
They smooth out the movement in the limbs ipsilateral to the cerebellar hemisphere of origin. They are efferent fibers that connect the superior cerebellar peduncle to the thalamus and motor cortex.
142
Describe the path of cortical motor intent
Cortical motor intent is sent to nuclei in the pons, then forwarded to the contralateral cerebellar hemisphere for processing.
143
What nuclei send processed information about cortical motor intent back to the cortex after it has run through the cerebellum?
Dentate nuclei
144
What are the afferents of the superior cerebellar peduncle of the cerebellum?
The anterior spinocerebellar tract and acoustic/optic information
145
What are the afferents of the middle cerebellar peduncle?
The pontocerebellar tract
146
What are the afferents of the inferior cerebellar peduncle?
Vestibulocerebellar tract, olivocerebellar tract, and posterior spinocerebellar tract
147
What are the efferents of the superior cerebellar peduncle?
The dentatorubrothalamic tract and the dentatothalamic tract
148
What are the efferents of the inferior cerebellar peduncle?
The cerebellovestibular tract and the cerebelloolivary tract
149
What information does the cerebelloolivary tract carry?
It carries info from the vermis and flocculonodular lobes through the emboliform, globose, and fastigial nuclei (EGF) to the vestibular nuclei, the olivary nuclei, and the brainstem reticular formation, which all help maintain balance.
150
What are the three layers of the cerebellar cortex?
There are three layers of gray matter: the outer molecular layer, the Purkinje Cell layer, and the granule cell layer.
151
What types of cells does the outer molecular layer of the cerebellar cortex contain?
Basket and Stellate cells
152
What type of cells does the Purkinje Cell layer of the cerebellar cortex contain?
Purkinje cells
153
What type of cells does the granule cell layer contain?
Golgi and granule cells
154
Which type of cell in the cerebellar cortex is the output neuron?
The Purkinje Cell, which synapses on one of the deep nuclei. The deep nuclei then send fibers outside of the cerebellum.
155
What afferent fibers that begin outside of the cerebellum input DIRECTLY to the Purkinje Cells of the cerebellar cortex ?
Climbing fibers that originate in the olivary nuclei of the medulla.
156
What occurs in the cerebellar glomeruli in regards to input from mossy fibers?
Mossy fibers from outside of the cerebellum enter said cerebellum and synapse in the cerebellar glomeruli with granule cells and with Golgi cell dendrites and axons.
157
What do granule cells of the cerebellum do?
They pass information brought to them by mossy fibers and Golgi cells to the Purkinje cells
158
What effect to basket and stellate cells have on the Purkinje cells?
An inhibitory effect.
159
What are the three functional divisions of the cerebellum?
The Vestibulocerebellum, the spinocerebellum, and the cerebrocerebellum.
160
What is contained in the vestibulocerebellum?
The flocculonodular lobe, the inferior paravermis, and the fastigial nucleus.
161
What is the function of the vestiblocerebellum?
It has both feed-forward and feedback loops though the cerebellum from both the motor and vestibular systems that provide continuous correct to and anticipation of changes in the body's axial stability and balance.
162
What is the consequence of injury to the vestibulocerebellar system?
Severe truncal and gait ataxia.
163
What is contained in the spinocerebellum?
The anterior lobe, vermis, and superior paravermis
164
What is the consequence of a lesion to the anterior cerebellum/spinocerebellum by stroke?
Truncal instability and peripheral limb dis-coordination
165
In which lobe of the cerebellum is limb movement coordinated?
The anterior lobe. Output is via emboliform and globose nuclei to the ventral lateral nucleus of the thalamus, which projects to the motor cortex. From there, adjustments can be made in movement instructions via the corticospinal tract.
166
What does the cerebrocerebellum contain?
The lateral aspects of the posterior lobes.
167
From where does the cerebrocerebellum receive information?
The pontine nuclei, which have received cortical input from many areas of the cortex.
168
What does the cerebrocerebellum do?
It is important for eye-hand coordination needed to reach or manipulate an object.
It also compares past sensory experiences to learn and predict sensory consequences of current movements.
It is also important for movements that become automatic with practice, like playing the piano and handwriting.
It is responsible for grammar, fluidity of language, and prediction of sentence structure and flow.
169
A patient presents to you with oculomotor paralysis with a wide, fixed pupil, contralateral hemiplegia (paralysis of one side of the body), contralateral facial weakness with the lower face weaker than the upper face, and contralateral weakness of the tongue causing it to protrude toward the weaker side. Where is the lesion?
What is the blood supply to the area of the lesion?
The cerebral peduncle and the oculomotor nerve fascicles passing just medial of the peduncle.
This is called Weber Syndrome.
The ipsilateral oculomotor paralysis is caused by a lesion to the oculomotor nerve fascicle.
The contralateral hemiplegia is caused by the lesion to the cerebral peduncle.
The tip of the basilar artery and the PCA
170
A patient presents with ipsilateral oculomotor nerve palsy and contralateral cerebellar ataxia. Where is the lesion?
Most likely the fascicle of the oculomotor nerve and the fibers from the superior cerebellar peduncle passing below and medial to the red nucleus.
This is called Claude's Syndrome.
171
What does a lesion to the medial lemniscus cause?
Loss of discriminative touch on the contralateral side of the body
172
What does a lesion to the red nucleus cause?
Contralateral tremor and ataxia
173
What does the red nucleus do?
It has control over involuntary movement.
It is one of four main parts of the midbrain. The midbrain's four parts are the tectum, red nucleus, substantia nigra, and the crus cerebri.
174
What does a lesion to the oculomotor nuclear complex and the Edinger-Westphal nucleus do?
It causes ipsilateral CN III palsy and loss of pupillary constriction.
175
What structures can be affected in Benedikt's Syndrome?
Fascicles of the oculomotor nerve, the medial lemniscus, the red nucleus, the superior cerebellar peduncle, and the substantia nigra.
176
What syndrome does Benedikt's Syndrome closely resemble?
Weber Syndrome, except that Benedikt's features hemi-ataxia, and Weber's features hemiplegia.
177
What is the blood supply to the midbrain, specifically the base and the tegmentum?
The tip of the basilar artery and/or branches of the PCA.
178
What structures can be affected in Weber's Syndrome?
CN III fascicles and the cerebral peduncle.
179
What is the cerebral peduncle?
It is everything in the mesencephalon except the tectum. Cerebral peduncles are on the most anterior part of the midbrain and act as connectors between the rest of the midbrain and the thalamic nuclei...and thus the cerebrum.
180
What structures are affected in Claude's Syndrome?
CN III fascicles, red nucleus, and the superior cerebellar peduncle.
181
What artery supplies the medial pons?
The paramedian branches of the basilar artery
182
What symptoms are seen with a lesion to the corticospinal and corticobulbar tracts, as well as to CN VII fascicles?
Contralateral hemiparesis
Ipsilateral LMN facial paresis
183
What symptoms are seen with a lesion to corticospinal and corticobulbar tracts, as well as CN VII fascicles and the PPRF and/or CN VI?
Contralateral hemiparesis, ipsilateral LMN facial paresis, and ipsilateral gaze paresis.
184
What part of the brainstem does Wallenberg's Syndrome affect?
The lateral medulla
185
What is the blood supply to the lateral medulla?
The vertebral artery or the posterior inferior cerebellar artery
186
What structures are affected when the lateral medulla experiences a stroke or other lesion?
Vestibular nuclei, inferior cerebellar peduncle, CN V and tract, spinothalamic tract, sympathetic fibers, nucleus ambiguus, and nucleus solitarius
187
A lesion to nucleus ambiguus causes?
Dysarthria and dysphagia
188
A lesion to the spinothalamic tract causes?
Loss of pain and temperature on the contralateral side of the body
189
A lesion to the spinocerebellar tract causes?
Gait ataxia on the ipsilateral side of the body
190
A lesion to the spinal trigmeminal nucleus and tract causes?
Loss of pain and temperature from the ipsilateral side of the face.
191
Where does CN III exit the brainstem?
It exits ventrally at the level of the midbrain
192
Which CN is the only one to exit the brainstem dorsally?
CN IV. It exits dorsally, just caudal to the inferior colliculus
193
Does CN IV innervate ipsilateral or contralateral structures?
It innervates the contralateral superior oblique muscle.
194
Which two cranial nerve nuclei controlling eye movement serve the contralateral eye muscles?
The trochlear nucleus and the medial nucleus of CN III.
195
What eye movement ability is classically lacking in a patient who has had a dorsal midbrain stroke?
Upgaze in both eyes. This is because though the medial nucleus exhibits contralateral control, the fiber that innervates the opposite eye crosses over immediately to join the rest of the "same-side" dudes. Therefore, a lesion that knocks out one oculomotor nucleus means that the medial nucleus of the broken dude can't send his fiber to the opposite side, AND the fiber that crossed over super early to join the now-injured guys...is also now injured.
196
What five CNs nerves travel within the cavernous sinus?
What arteries?
How about sympathetics?
Oculomotor nerve, trochlear nerve, ophthalmic nerve, abducent nerve, and maxillary nerve (III, IV, V1, V2, and VI)
The internal carotid artery.
Sympathetic fibers traveling with the internal carotid artery on their way to dilator muscles of the pupil
A lesion in the cavernous sinus may affect some or all of these structures.
197
What does sympathetic innervation of the tarsal muscle do?
It provides autonomic elevation of the eyelid that is not subject to voluntary control
198
What muscle allows for voluntary elevation of the upper eyelid, and how is it innervated?
The levator palpebra superioris, innervated by CN III
199
What does the Edinger-Westphal nucleus do?
It sends bilateral visceral motor neurons via CN III to ciliary muscle and constrictor pupillae
200
Can the accommodation reflex still occur in the face of a lesion to the medial longitudinal fasciculus pathway?
Yes. The reflex is independent of the MLF pathway that connects the contralateral abducens nucleus to CN III nuclei.
201
Horizontal movement of the eyes requires two different nuclei: that of CN III and that of CN VI. The actions of these nuclei need to be linked so that a person can look with coordinated fashion in horizontal direction. How is this achieved?
Neurons in the abducens (CN VI) nucleus activate the contralateral ventral nucleus (controls the medial rectus) of CN III nuclei.
So when a person looks to the left, CN VI sends a neuron to the left lateral rectus, but at the same time, it also sends an axon, which synapses with the MLF (medial longitudinal fasciculus) and then immediately crosses the midline, to the right medial rectus so that the right eye can participate in looking horizontally to the left.
202
What does activation of the left PPRF (paramedian pontine reticular formation) trigger?
The left abducens nucleus and the right oculomotor nucleus
203
What is the result of dysconjugate gaze?
Misalignment of the eyes leading to diplopia, or double vision.
204
What is stimulated when the head is rotated to the right in the horizontal plane?
Rotation of the head to the right in the horizontal plane stimulates the right horizontal semicircular canal.
205
What occurs when the right horizontal semicircular canal is stimulated?
The vestibular apparatus uses the vestibular nerve to signal the right medial vestibular nucleus. The nucleus activates the contralateral PPRF, which means that the left abducens nucleus will activate the left lateral rectus and the MLF pathway will cause CN III to activate the medial rectus muscle so that the eyes look left.
206
When the head rotates right in the horizontal plane, which PPRF does the right medial vestibular nucleus activate?
The contralateral PPRF
207
Which way do the eyes look when the right horizontal semicircular canal is activated? How is this possible?
To the left
Because the right medial vestibular nucleus activates the contralateral PPRF, which means that the left abducens nerve is activated to do its thang on the left eye, as well as its thang on right eye, with the help of the MLF.
208
What is the vestibulo-ocular reflex, or VOR?
The compensatory reflex movement of the eyes to the direction opposite that of the head rotation. So, if you look right very quickly, the eyes will look left.
209
What does absence of eye movement with the oculocephalic maneuver, or Doll's eyes, indicate?
Nuclei and tracts mediating the VOR, or vestibulo-ocular reflex, are not working.
210
Does the saccadic pathway from the right frontal eye field activate the contralateral or ipsilateral PPRF?
It activates the contralateral PPRF
211
What controls saccadic eye movement - the visual cortex, the frontal eye fields, or the parietal-occipito area?
The frontal eye fields.
212
What controls slow pursuit eye movement - the visual cortex, the frontal eye fields, or the parietal-occipito area?
the ipsilateral parieto-occipital area
213
What control centers are involved in the slow pursuit eye movements?
The contralateral cerebellum and vestibular nuclei
214
As you move your finger from right to left, is the right or left parieto-occipital area tracking?
The left POT tracks the finger as it moves to the left
215
Which basal ganglia are in charge of movement control?
The somatic basal ganglia, also known as the dorsal basal ganglia.
216
What parts are included in the somatic, or dorsal basal ganglia?
The caudate and putamen, as well as in the internal and external globus pallidus.
217
What separate the caudate from the putamen?
the internal capsule
218
Are the putamen and caudate nucleus actually a part of the same structure?
Yes, they just come to be separated from each other by the internal capsule
219
What structure is at the tip of the tail of the caudate nucleus?
the amygdaloid nucleus
220
The thalamus is ________ to the putamen
medial
221
What is the collective term for the caudate and putamen?
The striatum
222
Which structure in the brain contains dopamine neurons?
The substantia nigra
223
Where is the substantia nigra located?
At the base of the midbrain
224
Where are dopaminergic terminals located?
The head and tail of the caudate and the putamen all receive axons from the substantia nigra, which contains dopamine neurons.
225
Which part of the substantia nigra contains dopamine neurons? What is the other part called?
The pars compacta
The pars reticula, which has a meshwork of fibers
226
What two types of neurons does the striatum contain?
Neurons with spiny dendrites called SN-neurons; 95% of neurons have spines on their dendrites. Usually smaller than aspiny dendrites. These guys integrate info from diverse sources. They are also called projection neurons because they are the neurons that transmit information to other areas of the brain.
Neurons with aspiny dendrites called A-neurons; 5% of neurons do not have spines on their dendrites. They are also called local circuit neurons, or interneurons.
227
Describe the axon of a spiny neuron of the striatum
The axon is long and leaves the striatum.
Axons of aspiny neurons are short and do not leave the striatum, which is why they're also called local circuit neurons, or interneurons.
228
What is the neurotransmitter used by all spiny neurons of the striatum?
GABA
229
Name two major subtypes of spiny neurons of the striatum
ENK neurons
Substance P (SP) neurons
230
What is special about ENK neurons of the striatum?
They are a type of spiny neuron that uses GABA as a neurotransmitter, but it also makes the opioid neuropeptide, enkephalin (ENK). Enkephalinergic neurons in the caudate and putamen project to the globus pallidus external
231
What is special about a SP neuron of the striatum?
It is a spiny neuron that uses GABA as its neurotransmitter, but it also makes the neuropeptide, Substance P (SP), as well as the neuropeptide dynorphin. Usually, SP neurons project from the striatum to the globus pallidus internal
232
Where do SP neurons of the striatum project?
SP neurons project from the striatum to the GPi, the pars compact of the substantia nigra (where dopaminergic neurons also reside) and the pars reticulate of the substantia nigra. These are actually all different types of striatal neurons; thus, there are three types of SP neurons in total.
233
Are SP and ENK neurons intermingled or separated in the striatum?
They are intermingled.
234
Taking into consideration the projection targets of the ENK and SP striatal neurons, what are the types of striatal projection neurons?
Striato-GPe with neuropeptide ENK
Striato-GPi with neuropeptides SP/DYN
Striato-SNr with neuropeptides SP/DYN
Striato-SNe with neuropeptides SP/DYN
235
What is the receptor type of Striato-GPe neurons?
D2
236
What is the receptor type of Striato-GPi, Striato-SNr, and Striato-SNe neurons?
D1
237
What do striato-GPe neurons do?
They inhibit movement that might conflict with intended movement
238
What do striato-GPi neurons do?
They initiate limb movement
239
What do striato-SNr neurons do?
They initiate head and eye movement
240
What do striato-SNc neurons do?
They regulate dopamine neurons.
241
What are the four types of interneurons in the striatum?
Cholinergic interneuron
Parvalbuminergic interneuron
Somatostatinergic interneuron
Calretinergic interneuron
242
Describe the cholinergic striatal interneuron
Large cell body
Ach is neurotransmitter
Project to spiny projection neurons
Modulates PNs to oppose DA action
Survive in Huntington's Disease
243
Describe the parvalbuminergic striatal interneuron
Large cell body
GABA is neurotransmitter
Project to spiny projection neurons
Inhibit PNs to sharpen activity
Die in Huntington's Disease
244
Describe the somatostatinergic striatal interneuron
Medium-sized cell body
GABA and NO are neurotransmitters
Somatostatin and NPY are neuropeptides
Survive in Huntington's Disease - NPY cells are impervious to HD
245
Describe the calretinergic striatal interneuron
Medium-sized cell body
GABA is neurotransmitter
Survive in Huntington's Disease
246
Which striatal interneurons survive in Huntington's Disease?
Cholinergic, Somatostatinergic, and calretinergic striatal interneurons.
247
In a study illustrating striatal interneuron survival in Huntington's Disease, which neurons were impervious to Huntington's Disease?
NPY interneurons, which survived, unlike the spiny neurons.
Other interneurons are impervious, but the slide specifically mentioned NPY interneurons, which I think are also somatostatinergic interneurons that make NPY as a neuropeptide
248
What type of neuron is located in the globus pallidus?
Large, aspiny neurons
Long dendritic trees arranged in the vertical access of the GPe and GPi.
Globus pallidus neurons integrate information from striatal neurons that project to them.
At the same time, GPe and GPi neurons send their axons to the subthalamic nucleus and the motor thalamus respectively.
GPe and GPi neurons use GABA as their neurotransmitter
249
Where do GPe neurons project?
They project to the subthalamic neurons. The subthalamic nucleus then mainly projects back to GPi, wrapping around the smooth dendrites of smooth GPi neurons, which also receive terminals from striatal SP neurons.
250
Where do GPi neurons project?
They project to the motor thalamus, specifically to the ventral anterior nucleus and the ventral lateral nucleus
251
What two nuclei comprise the motor thalamus?
The ventral anterior nucleus (VA) and the ventral lateral nucleus (VL).
The ventral lateral nucleus has two parts - Caudalis (C) and Oralis (O)
252
In addition to the GPi neurons that project to the motor thalamus, neurons from what other area also project there?
The substantia nigra pars reticulata also projects to the motor thalamus.
253
The GPi and substantia nigra pars reticulata neurons project to the motor thalamus, but to where does the motor thalamus project?
The motor thalamus projects to the cortex.
The ventral anterior nucleus projects to area 6, the pre-motor cortex
The ventral lateral nucleus projects to area 4, the motor cortex
254
What are the inputs TO the striatum?
The cerebral cortex is a major input modality to the striatum, as almost all of the cerebral cortex projects there. The Layer 5 pyramidal neurons specifically are the neurons that project to the striatum.
The dopaminergic input from the substantia nigra pars compact is another major source of information sent to the striatum.
A part of the thalamus called the intralaminar thalamus contains a cell group called Centre Median. These project to the striatum, but not much is known, so it is less important than the first two.
255
What cortical neurons project to the striatum?
Layer 5 pyramidal neurons.
These also send motor commands to the spinal cord and pre-motor neurons of the hindbrain.
256
What neurotransmitter do Layer 5 pyramidal cells use when they project to the tips of the dendritic spines of the striatal spiny neurons?
Glutamate
257
What neurotransmitter do substantia nigra dopaminergic cells use when they project to the sides of the dendritic spines of the striatal spiny neurons?
Dopamine
258
Can dopaminergic input to striatal spiny neurons modulate the cortical input to said neurons?
Yes, because the cortex neurons synapse on the tips of the dendritic spines, whereas the dopaminergic neurons synapse on the sides of the dendritic spines.
259
Describe the input for GPi paladin neurons
The GPi receives both projections from the subthalamic nucleus and from the striatum.
The spiny striatal projections and the neurons from the subthalamic nucleus interweave on dendrites of neurons of the internal pallidal segment (GPi).
Remember this order of projections: GPe projects --> subthalamic nucleus projects --> GPi.
260
What thalamic structures are important for peripheral sensory function?
Ventral posterior lateral nucleus
Ventral posterior medial nucleus
Dorsal medial nucleus
Centromedian nucleus
Parafascicular nucleus
261
What substances are released when tissue injury occurs, and what do they do?
Hydrogen ion, 5-HT, bradykinin, ATP, and prostaglandins
They activate nociceptive receptors, which are free nerve endings that fire an AP back to the dorsal horn neuron.
262
Activation of nociceptive receptors at the injury site causes local release of substance P and calcitonin gene-related peptide, or CGRP. What do these molecules do?
They trigger a release of histamine from mast cells and cause vasodilation.
263
What happens to the free nerve ending of a proprioceptive receptor when substance P, CGRP, and histamine are released? And inflammatory chemical milieu are added to the mix?
The free nerve ending is sensitized so that their threshold for activation is lowered
264
Describe the neo-spinothalamic pathway
This pathway encodes for the intensity, location, and quality of pain. It mediates fast pain, which is sharp and well-localized and relayed rapidly to the somatosensory cortex.
The first order neuron cell bodies are in the DRG if the pain is coming from the body; they are in the trigeminal nuclei if coming from the face.
They first synapse in Rexed Layer 1 of the dorsal horn, then decussate and ascend to either the VPL or VPM of the thalamus and finally, on to the cortex.
265
Describe the paleo-spinothalamic tract
The pathway encodes for the emotional and visceral responses to pain and also influences the descending pathways from the brain stem that modulate pain. It mediates dull, throbbing, and poorly localized pain.
The first order neuron cell bodies are located in the DRG and synapse in Rexed Layer II, the substantia gelatinosa. The second order neuron synapse in Rexed Layers 4-8. From there, the fibers take a variety of different pathways to reach their intended target.
266
Which thalamic nucleus receives protopathic and epicritic sensory information from the limbs and body?
The VPL
267
Which thalamic nucleus receives protopathic and epicritic sensory information from the face?
The VPM
268
The VPL and VPM receive pain fibers from which tract?
The neo-spinothalamic tract, relayed on the lateral pain system.
269
The dorsal medial nucleus (DPM), the centromedian nucleus (CM), and the parafascicular (PF) nucleus all receive fibers from which tract?
The paleo-spinothalamic tract, relayed on the medial pain system.
270
Pain sensors are free nerve endings that deal with various sensations, including temperature. What are the two temperature receptors we need to know?
Temperature is sensed by Transient Receptor Potential Channels, of which we must know two types.
The TRPV1, or transient receptor potential vanilloid, is sensitive to temperature > 43 degrees Celsius, as well as capsaicin.
The TRPM8, or transient receptor potential melastatin, is sensitive to temperatures
271
Pain sensors are free nerve endings that deal with various sensations. Name three main sensations
Temperature, mechanical, and chemical sensations
272
Adelta fibers transduce what kind of sensations?
These are thinly myelinated fibers that transmit temperature and mechanical pain.
They transmit fast, sharp pain and provide discrete location information.
273
What kind of fiber transmits information about fast, sharp, mechanical or temperature-mediated pain that is discretely localized?
Adelta fibers
274
C-Fibers transmit what kind of sensations?
These are unmyelinated fibers that transmit temperature, mechanical, and chemical pain, so they are considered to be polymodal.
The transmit slow, diffuse pain.
275
Which pain fibers are polymodal?
C-fibers
276
Do C-fibers transmit slow, diffuse pain, or fast, sharp, discretely localized pain?
Slow, diffuse pain
277
Where are the cell bodies of Adelta and C-fibers located?
The dorsal root ganglia
278
What neurotransmitters are used by Adelta and C-fibers?
glutamate, substance P, and CGRP, which can be released either from the dorsal horn or from the periphery (skin/organs)
279
What are nociceptive specific neurons?
These are neurons in the laminae I and II of the dorsal horn that respond only to Adelta and C-fibers, and encode only pain
280
What kind of neurons in the laminae of the dorsal horn respond only to Adelta and C-fibers?
Nociceptive specific neurons
281
Want are wide dynamic range neurons?
These are neurons in laminae V of the dorsal horn that respond to a variety of synaptic input - that is, pain and non-pain stimuli.
They are also responsible for Wind Up
282
How do WDRNs (wide dynamic range neurons) determine the frequency at which they send APs?
These guys fire APs in a graded fashion depending on the stimulus intensity, so as intensity increases, so does the frequency of APs
283
What is Wind Up in regards to signal amplification?
channel blockade on the WDRN Wind up occurs because repetitive action potentials from C-fibers cause release of glutamate. Glutamate activates the wide dynamic range neurons (WDRN) AMPA receptors. Calcitonin gene-related peptide, or CGRP, activates wide dynamic range neuron (WDRN) CGRP receptors. Activation of these two receptors causes WDRN depolarization, which releases the Mg++-induced block of the NMDA, or N-methyl-D-aspartate channel. Calcium can now flow into the NMDA channel. Increased Ca++ causes both increased Na+ channel insertion into the WDRN membrane and blockade of K+ channels in the WDRN membrane.
To prolong WDRN depolarization, Substance P activates NK1, or neurokinin 1, receptors. This allows for continued calcium influx, as well as increased Na channel insertion and K membrane.
As you can see, three neurotransmitters, glutamate, CGRP, and substance P, all work together to reduce the threshold of WDRNs by increasing the number of Na+ channels in its membrane. A lowered threshold means increased firing of action potentials to the intended target.
284
The activation of what two receptors play an important role in initiating Wind Up?
1) Wide dynamic range neuron AMPA receptors by glutamate
| 2) WDRN Calcitonin gene-related peptide (CGRP) receptors by CGRP
285
What kind of pain fibers initiate wind up? How do they work?
C-fibers
C-fibers fire action potentials that cause the release of glutamate.
286
What neurotransmitters activate two different receptors on WDRNs during the initial steps of wind up?
Glutamate
CGRP, or calcitonin gene-related peptide
287
What occurs when WDRN AMPA and WDRN CGRP receptors are activated during the wind up process?
The WDRN membrane depolarizes, causing a calcium channel called NMDA that is blocked by Mg++ to become un-blocked.
288
What does Ca++ influx into the WDRN cause during wind up?
It increases Na+ channel insertion and effects blockage of K+ channels on the WDRN membrane
289
What neurotransmitter prolongs WDRN depolarization?
Substance P
290
What receptor does Substance P activate during wind up to prolong depolarization of the WDRN?
NK-1, or neurokinin-1 receptor
291
What is a functional consequence of wind up?
The consequence is that a relatively brief C-fiber stimulation of Wind Up can lead to long-lasting facilitation of the stimulated pain pathway. In other words, hyperalgesia, or abnormally heightened sensitivity to pain, as well as chronic pain, can result from C-fiber activation of Wind Up.
292
Describe three ways that central modulation of pain is achieved
Gate Control Mechanism, in which Abeta fibers activate dorsal column interneurons that inhibit WDRN - blunting their response to Adelta and C-fiber activity
Descending Pathways, in which the cortex, amygdala, and the hypothalamus all impinge on the periaqueductal gray and reticular formation neurons that then send neurons to modulate neurons in Lamina II of the dorsal horn. They can lead to either inhibition or facilitation of pain.
Endogenous Opioids, in which activation of opioid receptors block presynaptic voltage-gated Ca++ channels and open postsynaptic K+ channels, thus hyper polarizing the postsynaptic neuron to reduce APs.
293
Does Gate Control Mechanism result in decreased or increased pain pathway action? Why?
Decreased pain because WDRNs are inhibited.
294
Which fibers facilitate the Gate Control Mechanism? What kind of neuron do they have an effect on?
Abeta fibers facilitate the pathway; they ultimately blunt WDRNs via dorsal column interneurons.
295
Do Descending Pathways from central pain modulating centers inhibit or facilitate pain?
They can do either
296
Who are the main central players in the descending pathway that modulate pain?
The cortex, amygdala, and hypothalamus
297
What midbrain structures are essential to the Descending Pathway in pain modulation?
The periaqueductal gray and the reticular formation
The periaqueductal gray, through various and sundry steps, can eventually and ultimately inhibit pain via mu-opioid receptors.
The reticular formation can also block pain signals to the brain.
No idea how pain is facilitated by the descending pathway.
298
What receptors do endogenous opioids bind to? What channels are affected when they bind to their receptor?
Endogenous opioids bind to and activate opioid receptors.
Presynaptic voltage-gated Ca++ channels are blocked
Postsynaptic K+ channels are opened.
299
What occurs in the post-synaptic neuron when endogenous opioids bind to receptors on presynaptic membranes?
They are hyper-polarized because K+ channels are opened.
300
What is the end result when endogenous opioids bind to their receptors?
Reduced action potentials in the postsynaptic neuron.
301
Explain referred pain.
Common dermatome hypothesis: When pain is referred, it is usually to a structure that developed from the same embryonic segment or dermatome as the structure in which the pain originates. Radiating pain down the left arm is the result of a myocardial infarction, or pain originating from the shoulder (dermatomes 3-5).
Convergence and facilitation theories: Inputs from visceral and skin receptors converge on the same spinal cord neuron (i.e., viscerosomatic neurons). Therefore, visceral pain is referred to skin area because the nociceptors' terminals from the viscera terminate in the spinal cord on the same neurons that receive input from the skin.
302
How can intractable cancer pain be solved?
By causing a small, midline lesion of the dorsal column at the lower thoracic spinal cord.
303
At what age has a gyrencephalic brain developed?
9 months gestation/birth
304
How is the cerebral cortex divided?
It is divided into the frontal lobe, parietal lob, occipital lobe, and temporal lobe.
