neuro block 2
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1. _____ are the only means by which the nervous system canexercise control over body movements, whether voluntary or involuntary.
Lower motor neuronsaka Alpha motor neurons
A # of different parts & pathways of the nervous system caninfluence these lower motor neurons but they alone can elicitmuscle contraction.
Destruction of the lower motor neurons suppling a muscle orinterruption of their axons causes complete paralysis of that muscle
2. ______ & _____ are always medial to the internal capsuleand
______ & _____ are always lateral to the internal capsule
Thalamus and Caudate nucleus = Medial
Globus pallidus & putamen = Lateral
The internal capsule looks like arrowheads or 2 letter Vs with theirpoints facing inward
3. _______ is continuous with the spinal cord. The medulla
The medulla is the last section and is just caudal to the pons andcontinuous with the spinal cord.
4. _______ is required for myelin formation
What happens if we are lacking it?
NUTRITIONAL DEFICIENCY
Vitamin B12 - required for myelin formation
(lack of cobalamin (not found in fruit or vegetables) causesPernicious Anemia and degeneration of myelin), Vitamin E.
Lack of intrinsic factor (produced in stomach and used in smallintestine to absorb cobalamin) causes tingling and numbness
(paresthesias) of hands and feet.
Degeneration of myelin in the dorsal columns is greater thandegeneration in corticospinal tract.
Dementia can occur with degeneration of cerebral white matter.
5. ________ looks like a dohnut in cross ection The Nucleus Solitarius
The tracts are in the middle and the Nucleus surrounds it
6. _________ is the point where the lower motor neurons forthe ipsi lateral half of the face (CN 7) wrap around theabducens nucleus (CN 6).
Internal genu of the facial nerve - (facial colliculus)
7. _________ process and coordinate eye movements. Superior coll iculi
Inferior colliculi process auditory information received bilaterally
from the cochlear nuclei from the lateral lemniscus.
Neuro ~ Block 2Study online at quizlet.com/_7e8o3
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8. _________ process auditory information received bilaterally from the cochlear nuclei from the lateral lemniscus.
Inferior colliculi
(Note: Superior colliculi process and coordinate eyemovements.
Remember eyes before hearing
9. _________ provide an appropriate pattern of musclecontractions about one or more joints
An Efferent set of motor neurons will provide an appropriatepattern of muscle contractions about one or more joints.
10. _________ will divide and create a tumor Glia will divide and create a tumorthere is a high probability
Axons won' t divide
11. __________ can lead to Inhibition of motor neurons Muscle Tension can lead to Inhibition of motor neurons
12. ____________ can occur with degeneration of cerebral whitematter.
Dementia can occur with degeneration of cerebral white matter.
(Nutritional Deficiencies)
13. ______________contains interneurons involved in thepupi llary light reflex.
What are the sensory and motor components of this reflex?
What does bright light do to the eye
Pretectal region contains interneurons involved in the pupillary light reflex.
RememberCN 2 = sensoryCN 3 = motor
Bright light constricts the eye - miosis
14. ____________overlie the cerebral aqueduct. Inferior and superior colliculi overlie the cerebral aqueduct.
Midbrain
Inferior colliculi process auditory information received bilaterally from the cochlear nuclei from the lateral lemniscus.
Superior colliculi process and coordinate eye movements.
15. ___________is the most ventral part of the brain stem
Where is it seen? Where is it not seen?
basis -most ventral part of the brain stem
(pons and midbrain only, not seen in medulla)
- location of large collection of fibers and tracts: corticospinal,corticobulbar, and corticopontine tracts.
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21. A disease of the central part of the spinal cord in which a tube like enlargement of the central canaldevelops, typically at a lower cervical or upperthoracic level.
Syringomyelia
As the syrinx enlarges, surrounding neural tissue is destroyed.
The 1st damage is to fibers crossing through the limited available areaaround the central canal.
The next area damanged is usually the anterior horn
The result is a distinct combination loss of pain & temp sensation bilaterally over the arms and shoulders ( as a result of damage to crossing fibers) &
weakness and atrophy of the muscles of the hand ( as a result oof anteriorhorn damage)
Of course if the syrinx occured at a different spinal level, the symptoms would be referred to a different part of the body
22. A distinct region of grey matter that caps theposterior horn
The substantia gelatinosa
In myelin stained preparations this region looks pale compared to the rest of the grey matter b/c it deals mostly with finely myelinated and unmyelinated
sensory fibers that carry pain & temp information
23. A lateral spina l cord lesion will cause Loss of contralateral pain and temperature starting a few segments below the level of the lesion
24. A lesion causing drooping =
What system gets damaged?
Ptosis;
Horner's Syndrome (Loss of Sympathetic)
25. A lesion of the abducens nerve will cause diplopia (CN VI palsy ipsilateral).
A lesion of the abducens nucleus will cause ipsila teral, lateral gaze palsy.
A lesion of the abducens nucleus AND ipsilateral MLF will cause ipsilateral,lateral gaze palsy AND an internuclear ophthalmoplegia (INO). "one and a
half syndrome."
A lesion of the cerebral hemisphere will cause gaze to the side of the lesion.
26. A lesion of the abducens nucleus AND ipsilateralMLF will cause
ipsilateral, lateral gaze palsy AND an internuclear ophthalmoplegia (INO)."one and a half syndrome."
A lesion of the abducens nerve will cause diplopia (CN VI palsy ipsilateral).
A lesion of the abducens nucleus will cause ipsila teral, lateral gaze palsy.
A lesion of the cerebral hemisphere will cause gaze to the side of the lesion.
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27. A lesion of the abducens nucleus will cause ipsilateral, lateral gaze palsy.
A lesion of the abducens nerve will cause diplopia (CN VI palsy ipsilateral).
A lesion of the abducens nucleus AND ipsilateral MLF will ca use ipsilateral, lateralgaze palsy AND an internuclear ophthalmoplegia (INO). "one and a half syndrome."
A lesion of the cerebral hemisphere will cause gaze to the side of the lesion.
28. A lesion of the cerebral hemisphere willcause gaze to the side of the lesion.
A lesion of the abducens nerve will cause diplopia (CN VI palsy ipsilateral).d. A lesion of the abducens nucleus will cause ipsilateral, lateral gaze palsy.e. A lesion of the abducens nucleus AND ipsilateral MLF will cause ipsilateral,lateral gaze palsy AND an internuclear ophthalmoplegia (INO). "one and a half syndrome."
29. A lesion of the Vagus will cause: Lesion of the vagus causes dysphagia (difficulty swallowing with nasal regurgitationof food), loss of gag reflex, and cough, dysarthria with hoarseness with fixed vocalcord.
a) Bilateral lesion of the vagus (rare) is fatal with complete laryngeal paralysis(aphonia, dyspnea and aphagia).
30. A lesion of what blood supply would knock out the upper motor neuron of Cranialnerve 7?
Middle Cerebral Artery could knock it out
31. A motor disease that attacks the motorneurons of the anterior horn
Poliomyelitis
32. A patient has an right UMN lesion of thefacial nerve ... what do we expect to see
Inability to move the lower left portion of the face
The upper portion of the face ha s bilateral innervation
The lower has unilateral innervation therefore with a Corticobulbar lesion (UMN) - will cause only lower face palsy contralateral to the lesion.
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33. A patient has been told they were in a knife fight, in whichthey were stabbed on the left hand side with a knife
Ultimately they suffered from Brown sequard.
What effects should we anticipate?
Hemi section = Brown sequard syndrome
1) A Small band of loss of total sensation roughly at the level of the lesion (left) bc the dorsal horn has been damage
2) We will have a loss of pain and a loss of fine touch of Alternating symptoms
Left side we will have a loss of fine touch, vibration &proprioception (ipsilateral)
Right side we will have a loss of pain and temp. (Contralateral)
2 totally different losses = a spinal cord lesion
34. A patient has Horner's Syndrome
How will we know what eye?
The pinpoint eye is always the side of the lesion ...IPSILATERAL
The classic signs of Horner's Syndrome are: MIOSIS - decreased pupil size (dilator muscle not innervated)
(Normally NEpi is released)
PTOSIS - drooping upper eyelid (Muller's smooth muscle notinnervated).
ANHIDROSIS - lack of sweating on the face and neck.
35. A patient is in somnolence
What do you suspect has undergone ischemia?
Somnolence = unconsciousness = coma
Pontomesencephalic reticular formation or bila teral tha lami(bilateral thalamus)
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36. A patient presents unable to move her upper andlower face
What has she damaged?
LMN lesion
Bells Palsy (herpetic facial paralysis) - facial nerve lesion (LMN) will causeipsilateral total (upper and lower) face paralysis.
If the upper face isn't working then we know we have damaged CN7 and wego to the pons to find out why.. . we won't be able to CLOSE the eye
Bells palsy is Ipsi
37. A patient presents unable to move the lower leftportion of her mouth - what has she damaged?
UMN lesion on the RIGHT side
Corticobulbar lesion (UMN) - will cause only lower face palsy contralateralto the lesion.
38. A patient presents with an unsteady gait
What do you suspect has undergone ischemia?
Cerebellar pathwaysLong sensory = Medial LemniscusCorticospina l tracts
39. A patient presents with blurred vision
What do you suspect has undergone ischemia?
Eye movement pathways or visual cortex
3,4,6
40. A patient presents with diplopia and adysconjugate gaze
What do you suspect has undergone ischemia?
Supranuclear or infranuclear eye movement pathways
3,4,6
41. A patient presents with dysarthria and dysphagia
What do you suspect has undergone ischemia?
Corticobulbar pathways or brainstem cranial nerve nuclei
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42. A patient presents with Horners on her right side and can still feelpain felt on her left side ... we know she must have damaged _____
She damaged somewhere in the PNS system ... Outsidethe CNS
43. A patient presents with Horners on her right side and no pain felt onher left side ... we know she must have damaged _____
Somewhere in the CNS : Brainstem or Spinal cord
44. A patient presents with numbness and tingling particularly bilateralor perioral
What do you suspect has undergone ischemia?
Long somatosensory pathways or
Trigeminal system
45. A posterior spina l artery defect would result in what kind of Motorand Sensory problems
- Account for all tracts
Dorsal column medial leminsucs will be the mosteffected (posterior columns)
46. A somatotopic representation is located in the corticospinal tract
Fiber controlling upper extremities are located :
Upper extremities are located medial to thosecontrolling lower extremities
47. A speech disorder characterized by difficulty speaking properly, dueto paralysis of the muscles of speech.
Dysarthria
48. A woman has a stroke and damages her Lateral Corticospina l tract... why do we put her into physical therapy immediately?
We want Rubrospinal tract to pick up the slack
49. Acetylcholine has 2 types of receptors Nicotinic and Muscarinic acetylcholine receptors
Nicotinic receptors are ionotropic receptors, transmittergated ion channels that mediate fast EPSPs
Muscarinic receptors are metabotropic receptors, Gprotein coupled receptors that mediate a variety of 2ndmessenger effects
Nicotinic a re more common in the PNS
Muscarinic receptors are more common in the CNS
50. ALS lesions are always ________ Contralateral - no matter whether the lesion is in the
brain or spinal cord
This is called Alternating Symptoms
Loss of Pain in the Spinal cord = ContralateralSymptoms
Loss of Pain in the Brain stem = ContralateralSymptoms
51. Alternating symptoms in which long tracts symptoms are referred toone side and cranial nerve symptoms are referred to another side arehallmark of
Brainstem lesions
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52. An acute inflammatory demyelinating polyneuropathy (AIDP)
An immune mediated demyelination of peripheral nerves
When does it typically present?
Guillain-Barr Syndrome
(usually 1-2 weeks following viral illness.)
53. An acute polyneuropathy disorder affecting the peripheral nervoussystem.
Ascending paralysis, weakness beginning in the feet and hands andmigrating towards the trunk.
Some subtypes cause change in sensation or pain as well asdysfunction of the autonomic nervous system.
It can cause life-threatening complications, in particular if the breathing muscles are affected or if there is autonomic nervoussystem involvement.
The disease is usually triggered by an infection.
Guillain-Barr syndrome (GBS)
54. An anterior spina l artery defect would result in what kind of Motorand Sensory problems
- Account for all tracts
An anterior spinal artery infarct can damage theanterolateral pathways (no pain and temperature below
the lesion bilaterally).
Motor signs include:
upper motor neuron (corticospinal tract) spastic paralysis below lesion and
ventral horn cells ( lower motor neuron signs a t the levelof the lesion - "Al" is down) flaccid paralysis.
(the distal musculature & trunk will be effected )
Incontinence is common as descending pathways tend to be more ventral in the spinal cord.
(Note we lose everything except for the Dorsal columns -fine touch & proprioception will be ok )
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55. An upper motor neuron lesion caused by corticospinaldamage has very different effects from thoes of a lower motorneuron lesion
Charcateristically the muscle involved show hyperactivereflexes.
The resting tension is increased (they are hypertonic) & there isparalysis or weakness (paresis) particularly of fine voluntary movements.
This complex of symptoms is referred to as spastic paralysis
A # of pathological reflexes are associated w/ upper motorneuron lesions.
The best known is Babinski's sign
56. Approximately 15% of the corticospinal cord fibers continueinto the spinal cord with out crossing.
What are these fibers called & where do they go?
Anterior Corticospinal tract ...
they enter the spinal cord ipsila terally w/out crossing & enterthe anterior white matter columns to form the anteriorcorticospinal tract.
57. Are there more nuclear bag fibers or nuclear chain fibers in amuscle spindle?
More nuclear chain fibers
Most muscle spindles contain 2 or 3 nuclear bag fibers and atleast twice that many nuclear chain fibers
58. arises from "top of the basilar artery" at level of rostral pons
supplies superior cerebellum and bit of rostral laterodorsalpons
SCA (superior cerebellar artery)
59. arises from basilar artery (just after vertebrals fuse) at levelof caudal pons
supplies lateral caudal pons and a small portion of cerebellum
AICA (anterior inferior cerebellar artery)
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60. arises from vertebral artery at level of medulla
supplies lateral medulla and inferior cerebellum
PICA (posterior inferior cerebellar artery)
PICA : will be on the upper portion of the butterfly Vertebral arteries wil l be on the lower portion
61. Arousal & Awareness of pain ... think Spinoreticular tract
Spinoreticular release Glutamate to the reticular formation
The Ret thalamic activates the panic button to the ILN which notifies the
cortex -> for arousal62. As the nerve enters the dorsal horn of the spinal
cord, it eventually synapses and has to releaseglutamate?
What process allows for Glutamates release?
In the CNS we have voltage gated channels (Thus we have to be able togeneral an action potential via voltage gated sodium and potassiumchannels.
We need the voltage in order to open the voltage ga ted calcium channel in thedorsal horn.
Once this Calcium channel opens the calcium comes in and binds toSynaptotagmin "tag your it" & allows for the fusion of vessels and the releaseof GLUTAMATE
Then the 2nd neuron / projection neuron carries on i t's way to the thalamus.
(Note these Voltage gated channels are normally closed 24/7)
63. As you look at the brainstem from a Ventral pointof view - What features should immediately standout?
Cranial Nerves Arteries - especially the Basilar artery (It is bringing oxygen and glucose tothe middle of the pons)
64. At the level of the pons what cortico fiber will go both Ipsi and Contra lateral
CN 7Ipsi & contra for Upper face
Contralateral for lower face
65. At what location is the first synapse for the DC-ML
pathway?
The 1st neuron always connects with the 2nd neuron on the same side.
There is an ipsilateral kiss and it's at the CAUDAL MEDULLA
66. Atrophy ... we need to be thinking A lower motor neuron lesion
Look at C8 or C7 and one of the fingers may be skinnier
(yes you can have a little atrophy with a UMN but it would be from disuse... if we baby our patients their muscles wil l atrophy from disuse)
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67. Automatic posture and gait movements = What tract
Reticulospinal tracts (2) #3 in pic
(3a) One origina tes in pontine reticular formation = medialreticulospinal tract.
(3b) Other originates in the medullary reticular formation =lateral reticulospinal tract
(medial motor system)
68. axons project to effector organs
Give ganglion and nerve
Vagus (CN X) various TERMINAL ganglia
Ex. of effector organs to lungs , heart GI tract).
69. axons project to lacrimal glands and nasal mucosa.
Give ganglion and nerve
Facial nerve (CN VII) sphenopalatine gang lion
70. axons project to submandibular and submaxillary salivary glands.
Give ganglion and nerve
Facial nerve (CN VII)
submandibular ganglion
71. axons project to the eye ciliary muscle and constr ictor(sphincter) muscle of the iris
Give ganglion and nerve
Occulomotor nerve (CN III)
ciliary ganglion
72. axons project to the parotid gland.
Give ganglion and nerve
Glossopharyngeal (CN IX) otic ganglion
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73. Axons will synapse with projection neuron cell bodies in thenucleus and cross over here as the internal arcuate fibers to
become the medial lemniscus.
Fasciculus and Nucleus Cuneatus(Axons from the dorsal column that cross over and enter
the triangle thing in the middle till it builds up & becomesthe medial lemniscus)
(In the caudal medulla but a little bit up from theSpinomedullary Junction)
Note the CST (2 balls on the bottom) haven't crossed yet ...it's cell bodies are still on the ipsi side
74. Bilateral control of axia l and girdle muscles = what tract?
Anterior (ventral) corticospina l tract (doesn't cross themidline)
(medial motor system)#1
75. Blink to Threat reflex
What nerve is sensory? What nerve is motor?
Sensory - CN 2 (vision)
Motor - CN 7 (7 closes the eye)
76. Blood supply to the anterior 2/3rds of the spinal cord, includingthe anterior horns and anterior lateral white matter columns
Anterior spinal artery
supplies the gray sections
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77. Blood supply to the posterior column and partof the posterior horns
Posterior spinal arteries
78. Brain stem lesions producing ipsilateralHorner's Syndrome may also result in : (think other tracts affected)
Why?
Contralateral loss of pain and temperature sensations from the limbs and body.
The reason being b/c the descending fibers of the Corticospinal Tract &Hypothalamospinal SNS Fibers travel with the ascending spinothalamic fibers(ALS) in the lateral part of the brain stem.
ALS is always CONTRA
79. Brainstem losses are always _________ Contralateral
Whether its the ALS tract or DC-ML tract .. b/c we are dealing w/ Projectionneurons
80. C7
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81. C7
Extension of ElbowFlexion of wrist (median / ulnar nerve)
Extension wrist (Radial nerve)
C7 = Middle fingerC7 = Dorsal portion of hand
Palm of Hand (note hand is C5 - C8)
C6= Thumb & IndexC8 = Ring finger & pinky
82. Causes one or more joints toflex.
Flexion reflexes
83. Cell body for the body resides=
Dorsal root ganglion
This is in the PNS (outside the CNS)
84. Cell body for the face resides = Trigeminal Ganglion (CN V)
It's a ganglion so it's still in the PNS
85. Central 7 means what?
Where is our lesion?
The upper face was sparred - so we know we have an UMN lesion coming down onto lower CN 7
If the upper face is working then we know CN7 is working fine ... we will only lose the bottom half of the face
(Remember the CN is a LMN )
Our lesion is on the Contralateral side ... go look at the pons
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86. CNX
Sensory functions:Motor functions:
Sensory = Thoracic and Abdominal viscera
Motor = Speech, swallowing, thoracic & abdominal viscera(parasympathetic )
87. Compare the crossing of the DC-ML and the crossing of theCorticospinal tract
The DC-ML crosses just a tad rostral to the pyramidaldecussation
88. Contains the autonomic centers for respi ratory,cardiovascular, and gastrointestinal control.
Medulla
If we compress the medulla its a medical emergency
89. Contains the caudal portion of the Trigeminal Nuclei (spinalnucleus of CN 5) and caudal parts of two of the four VestibularNuclei (CN 8).
Medulla
90. Contrast how we can tell the difference (using eyes) betweenHorner's and Ocular motor nerve damage
Horners = ptosis is on the same side as the nonfunctionalpupillary dilator - on the s ame side as the SMALLER pupil(pblm w/ sympathetic)
3rd CN = ptosis caused by CN3 damage is on the same side asthe nonfunctional pupillary sphincter therefore on the sameside as the DILATED / LARGER pupil- also the ptosis is more pronounced & is usually accompanied
by defective eye movements and lateral strabismus
91. Control the proximal axial and girdle muscles involved inpostural tone, balance, orienting movements of the head & neck, automatic gait related movements
The 4 medial motor systems
Anterior Cortiospinal (the 10% that doesn't cross) VestibulospinalReticulospinalTectospinal
92. Controls bilateral axial and gridle muscles Anterior corticospinal tract
Note this never crosses - it's the 10% that goes straight downfrom the primary motor cortex and never crosses at thedecussation
93. Controls muscles for swallowing (gag reflex) and phonation.
State Nerve and Nuclei
Nucleus Ambiguus
CN X Vagus - motor
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94. Corneal reflex
What nerve is sensory? What nerve is motor?
Sensory - CN 5
Motor - CN 7
95. Cut the spinal thalamic tract in thepons on the right side what am Igoing to lose?
SensoryPain, temp and itchIt will be a contralateral loss
Remember - Brains tem is ALWAYS contralateral
96. Damage the LMN of the corticospinaltract.
What will happen & where?
Motor Weakness/paralysis ipsilateral to the lesion
97. Damage the UMN in the spinal cordof the corticospinal tract.
What will happen & where?
Motor Weakness/paralysis ipsilateral to the lesion
(note bc we have already crossed in the medulla)
98. Damage to cranial nerves and nuclei will result in lesions where?
What type of loss?
ipsilateral head sensory and / or motor deficits.
99. Damage to the ocular motor nerve willcause what findings in the eye
(List what we will see)
The eye ipsilateral to the lesion w ill deviate laterally bc the medial rectus will be paralyzedand the la teral rectus will be unopposed(Lateral strabismus)
Diplopia (double vision) & is unable to move the affected eye medially
verticle movements are also impaired bc of paralysis of the superior and inferior recti andinferior oblique
Ipsilateral levator palpebrae superioris is paralyzed so ptosis occurs
Pupillary sphincter & ciliary muscles are unfunctionalThe pupil on the effected side will be DILATED / mydriasis as a result of the now unopposed pupillary dilator muscle & it won't constrict in response to light, the lens can't
be focused for near vision
100. Damage to the pons of thecorticospinal tract.
What will happen & where?
How could a lesion in the pons occur?
Motor Weakness/ paralysis contralateral to the lesion
(note b/c we haven't crossed yet)
ex. Problem with the Basilar artery
101. DC-LM
Lesion in the Brainstem producesloss on what side?
Loss of Fine touch, proprioception in the Brain stem = CONTRALATERAL Symptoms
BRAINSTEM LOSSES ARE ALWAYS CONTRALATERAL
Loss of Fine touch, proprioception in the Spinal cord = Ipsilateral Symptoms
102. DC-LM
Lesion in the Spinal Cord producesloss on what side?
Loss of Fine touch, proprioception in the Spinal cord = IPSILATERAL Symptoms
Loss of Fine touch, proprioception in the Brain stem = Contralateral Symptoms
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103. DCML
At each successive spinal level, fibers entering the posteriorcolumns add on laterally to thoes already present.
As lamination results, w/ layers of fibers from sacral levelsmost ____ and layers from cervical layers most ____
Sacral levels will be medial andcervical levels will be lateral
This sort of arrangement is somatotopic organization
104. Degeneration of myelin in ____________ is greater thandegeneration in ___________
Degeneration of myelin in the dorsal columns is greater thandegeneration in corticospinal tract.
(Due to Nutritional Deficiencies)
105. DEGENERATIVE / DEVELOPMENTAL -
spina bifida, syringomyelia, amyotrophic lateral sclerosis(ALS)
(Lou Gehrig's disease - motor neuron disease.)
Upper motor neurons or lower motor neurons or BOTH can be involved.
Note in Pic LMN and UMN knocked out
Corticospina l tract and ALS track both wiped out
Weakness for suresome muscles may have atropy and fasciculations and others may
not.
We may see a Babinski relfex
It's not always bilateral - these are ugly , slow progressive deathsenstences & the one thing we are worried about is the diaphram
b/c they won't be able to breathe
106. Dermatomes overlap substantially so that injury to anindividual dorsal root does not lead to complete loss of sensation in the relevant skin region.
Is the overlap more extensive for :touch, pressure and vibration orfor pain and temperature?
The overlap is more extensive for sensations of touch, pressureand vibration than for pain and temperature.
Thus testing for pain sensation provides a more preciseassessment of a segmental nerve injury than does testingresponses to touch, pressure or vibration.
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107. Describe aPseudounipolar cell and
where they can be found
DC-MLOur Primary neuron has no free nerve endings : it's a PSEUDOUNIPOLAR CELL
The same cell -PSEUDOUNIPOLAR CELL goes from our foot all the way up to the medulla and it'smyelinated by 2 different types of glial cells
CNS = oligodendrocytes &PNS = Schwann cells
Its' one huge long a xon.
It's a "peripheral process "in the beginning & has been myelinated by Schwann cells
The same neuron - as soon as it gets to the CNS, we call it a "central process" which hasoligodendrocytes myelinating it
108. Describe Syringeomeylina
What do you "lose" What can you tell yourpatient about this lesion?
We were in some type of an accident - typically an accident, in which we suffered from whiplash.
We didn't damage the tract - just the fiber
The lesion will cause BILATERAL symptoms
For just the bilateral dermatomes (2or 3 segments below the black hole b/c it takes the ventral whitecommissure fibers time to rise before it joins the ALS)
Class ically A "Cape like" pattern of loss of Pain, you take your sharp needle and they cant feel pain, tempor itch
- it's a growing cylinder - it can grow all around- Each year you'll note on the chart that it is growing and keeps going out
- all you can do is correctly diagnose - there isn't much that you can do- the projection fibers are al l squashing to go thru to the ALS
- its going to grow out to the ventral horn a nd eventually cause motor problems of weakness / paralysis
109. Describe the Accomodation sequence... what happens when weContract the ciliary muscle?
Normally :ciliary muscles (which control the shape and therefore the refractive power of the lens)
Signals from the Edinger-Westphal nuclei travel via the ipsi lateral oculomotor nerve to reach the cil iary and cons trictor pupillae muscles of the eye. Contraction of the cilia ry muscle causes the lens to increaseits curvature / gets rounder (and thus its refractive power), while contraction of the constrictor pupillaereduces the size of the pupillary aperture.
Signals from the oculomotor nuclei travel via the ipsila teral oculomotor nerve to the medial rectusmuscles causing them to contract and resulting in convergence of the eyes on the object of interest.
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110. Describe theCorneal reflex (ex.pain on sclera)
Be sure to listsensory and motorcomponents
Is this amonosynapticresponse orpolysynaptic?
Sensory CN 5 (Trigeminal) comes in and transduces pain from the sclera
It goes to the reticular formation and activates it
The RF will then activate CN7 (Facial) which will allow us to close the eye.
The reticular formation helps us do the bilateral response
Polysynaptic
111. Describe theLateralCorticospinalTracts pathway:
(aka the Pyramidal tract)
~Its fibers origina te in the cerebral cortex (in the precentral gyrus)
~descend thru the cerebral peduncle, basal pons & medullary pyramid
~decussa te at the spinomedullary junction (pyramidal decussation) and
~end in the anterior horn or the intermediate gray matter
They terminate on the motor neurons of the anterior horn or more often on smaller interneurns that in turnsynapse on these motor neurons.
112. Describe thepathway of theSpinal TrigeminalTract?
Primary sensory axons from ipsilateral face (tract) provide pain, temperature, i tch, and crude touch sensation forthe face, mouth, anterior 2/3 of the tongue, nasal sinuses, and supratentorial dura, (CN 5) as well as encoding
pain and temperature from the outer ear on cranial nerves 7, 9 and 10.
They travel past the Trigeminal ganglion enter the pons but then travels downwards to the spinal cord where itsynapses at the Spinal trigeminal nucleus .
(At the Spinal Trigeminal Nucleus) - projection neuron cell bodies in the nucleus send axons which cross themidline to travel in the trigeminothalamic tract and synapse in the VPM nucleus of the thalamus.
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113. Describe the RECIPROCAL INHIBITIONreflex
RECIPROCAL INHIBITION: Ia afferent fibers synapse (release Glutamate) on asingle inhibitory spinal INTERNEURON which produces inhibitory synapticpotentials (release GABA or Glycine) in lower motor neurons innervating theantagonist muscles
1) Excitation of motor neurons with the simultaneous inhibition of their antagonistmotor neurons causes one group of muscles to be excited while their antagonists areinhibited. (the antagonistic muscle DO NOT CONTRACT)
2) The neuronal circuit that causes this reciprocal relation is called reciprocalinnervation same as feed forward inhibition.
114. Describe the Reflex arc: polysynaptic - withdrawal reflex (step on a tack)
Increased firing of afferent sensory fibers from CUTANEOUS receptors /nociceptors (diverse group of fibers A transmitting extreme pain, temperature etc):
1) Stimulates the excitatory interneurons in the spinal cord to activate the alphamotor neurons that supply flexor muscles in the ipsilateral limb (We activate theFLEXOR MUSCLE by releaseing ACh)
a) Reverberating circuits of interneurons w ithin the spinal cord cause prolongedcontraction of the flexor muscles.
2) Stimulates inhibitory interneurons in the spinal cord to prevent the activation of alpha motor neurons that supply the ipsila teral extensor muscles. (We don't releaseanything to the MUSCLE b/c we released GLYCINE to the alpha motor neuron)
Crossed extension reflex - part of the withdrawal reflex.
1) Commissural interneurons evoke the opposite pattern of activity in thecontralateral side of the spinal cord.
2) Contralateral effect helps to maintain balance.
115. Describe the tract that leaves the
hypothalamus
The sympathetic nervous system (SNS) innervates the eye, face, and scalp.
Descending tract from the hypothalamus DOES NOT CROSS the midline as i tdescends through the brain stem and spinal cord to innervate the preganglionicSNS neurons.
116. Despite the somatotopic arrangement, thefibers of the internal capsule are compactenought that lesions at this level generally produce
Weakness of the entire contralateral body (face, arm and leg)
However occasionally capsular lesions can also produce more selective motordeficits
117. Destruction of the lower motor neuronssuppling a muscle or interruption of theiraxons causes :
complete paralysis of that muscle
Lower motor neuron lesions cause flaccid paralysis, indicating that the muscle islimp and uncontracted.
Reflex contractions can no longer be elicited and the muscle slowly atrophies thisoccurs in poliomyelitis ( a viral disease tha t attacks the motor neurons of theanterior horn) and in injuries in which the ventral roots are damaged
118. di- means
Ex.
both sides of the body are equally affected
ex. facial diplegiasymmetrical facial weakness
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119. Discuss the medial lemniscusaxons transition as it worksits way up the spinal cord.
The medial lemniscal axons carrying info from the lower limbs are located ventrally, where as theaxons related to the upper limbs are located dorsally. As the medial lemniscus ascends through the
pons & midbrain, it rotates 90 degrees laterally so that the fibers representing the upper body areeventually located in the medial portion if the tract & those representing the lower body are in the
lateral portion.
120. Do ALS neurons REALLY
cross Immediately?
After the kiss the projection neuron do start crossing however
It takes the projection neuron 2-3 segments to cross over to the ALS tract from there, once it crosses,it goes straight up to the ipsiside thalamus (VPL)
This is clinically relevant b/c when we have a lesion such as a Hemi section of the spinal cord
We won't feel the loss of pain until 2-3 spinal cord segments BELOW the cut/ lesion b/c the tractsare all ascending up at an angle
121. Do neurons divide andregenerate?
No but Glia cells do
Thus an axon in the white matter of the CNS can't grow back
122. Dominated by the 'dynamic'subtype of nuclear bag fiber
whose biochemical propertiesemphasize the 'velocity' of fiber stretch
Group Ia afferents
123. Ends at cervical cord level:controls head and neck muscles.
medial VST #2
( Vestibulospinal tracts (VSTs) of the medial motor system)
124. Facial (CN VII)
Where is the nuclei?Be specific
Facial (CN VII) - Superior salivatory nucleus (PONS).
The PNS PREganglionic neuron cell body is located in specific brain stem nuclei.
125. Fasciculations ... we need to bethinking
Lower motor neuron lesion
Involuntary twitchings
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126. Fasciculus and Nucleus Cuneatusaxons will synapse with projection neuron cell bodies in thenucleus and cross over as theinternal arcuate fibers to become ______________
The medial lemniscus.
Note this picture is the rostral medulla - the MedialLemniscus tract has been formed and is in the center of the
picture (praying hands)
Note the Corticospinal tract hasn' t crossed yet
127. Fast excitatory transmitter in the CNS Glutamate
128. Fast excitatory transmitter in the PNS Acetycholine
129. Fast inhibitory transmitter in the brain GABA (GABA - A receptors are mostly int he brain)
130. Fast inhibitory transmitter in the spinal cord Glycine - mostly in the spinal cord
131. Fine touch & dental pressure for CNV will synapse at whatnuclei?
Chief nucleus
aka major trigeminal sensory nucleus
(Paccinian corpusle)
132. First-order neuron axon fiber tract that carries informationabout fine touch, proprioception, pressure and vibration from
the legs and lower trunk.
Fasciculus gracilis
(T6 and below)133. First-order neuron axon fiber tract that carries information
about fine touch, proprioception, pressure and vibration fromthe upper trunk (above T6) and arms and neck.
Fasciculus cuneatus
more lateral to gracile(above T6)
134. First-order sensory neurons always ___________with secondorder neurons first then the axons of the second-order neurons
________ the midline.
First-order sensory neurons always SYNAPSE with secondorder neurons first (On the same side) then the axons of thesecond-order neurons CROSS the midline.
Synapse then Cross!!!
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135. Flexed Upper arms and Extendedlower extremities ... this i s classic for
what kind of lesion?
An UMN loss of the Lateral CorticoSpinal Tract
All that we have left is the Rubrospinal cord tract
Rubrospinal causes flexion of the upper extremities - normally this is offset w/ the Lateralcortical spinal tract & we get the normal angles ... obv when the Lat. Cotical spinal is out- we will only see the flexion
The vestibulospinal senses the change and tells the leg muscles to extend
136. Flexion of Upper Arms
What tract?
Rubrospinal
137. Force with which a muscle resists being lengthened
Tone ( stiffness of a muscle)
Think of the stretch reflex
138. Function = Movement of contra laterallimbs what tracts should I be thinking
Lateral corticospinal tract
Rubrospinal tract
(Lateral Motor Systems)139. GABA receptors are _______ gated Transmitter/ ligand gated
When they open they are permeable to Cl- ions
140. Ganglia reside in the ______
the exception to this is :
Ganglia reside in the PNS
The exception to this is the Basal Ganglia : Cuneate, Putamen and Globus Pallidus whichresides in the CNS
141. Genitals - describe it's position in thehumunculus
The genitals are only included in the Sensory (Postcentral Gyrus)
They are not part of the motor cortex
(note we have a total of 4 humunculi)
142. Glossopharyngeal (CN IX)
Where is the nuclei?Be specific
Glossopharyngeal (CN IX) - Inferior salivatory nucleus (MEDULLA).
The PNS PREganglionic neuron cell body is located in specific brain stem nuclei.
143. Glossopharyngeal is a mixed sensory and motor nerve.
What does it's "motor" componentcontrol?
State the nucleus involved
Motor.... No general somatic skeletal muscle innervation.
1) Innervation of s tylopharyngeus muscle.a) Nucleus Ambiguus.
b) Elevates the pharynx during talking and swallowing (part of gag reflex with vagus).
2) Parasympathetic innervation of parotid gland.a) Inferior Salivatory Nucleus.
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144. Glossopharyngeal is a mixedsensory and motor nerve.
What does it's "sensory"component control?
State the nucleus involved
1) Special Visceral Sensory - taste from posterior 1/3 of tongue.~Rostral Solitarius "gustatory" nucleus with vagus.
2) General Visceral Sensory - Carotid body and sinus: chemo- and baro- receptors.~Caudal Solitarius "cardiorespiratory" nucleus with X.
3) General somatic sensa tion from middle ear, outer ear, pharynx a nd posterior 1/3 of the tongue.
~Primary sensory neuron in the superior glossopharyngeal ganglion.~Spinal Trigeminal Nuclei - second order sensory neuron wi th X.
c. Lesion of the glossopharyngeal nerve causes loss of gag reflex with CN X.
145. Golgi tendon organs fiber = _____It regulates:
Ib fiber
regulates tension
It is thought that Golgi tendon organs contribute to fine adjustments in the force of musclecontraction during ordinary motor activities & tha t other receptors initiate additional forms of autogenic inhibition at higher tension levels
146. HEMI SECTION OF THESPINAL CORD LESION onthe Right side.
What getting cut? What will we lose feeling of? Where?
2 Tracts get cut!
ALS & DC-LM
We cut thru the ALS but we won't feel the loss of pain until like 2-3 spinal cord segments below thecut/lesion b/c the tracts are all ascending up at an angle: Contralateral side
The DCLM also got damaged!!!DC are also going upDorsal columns are axons of the FIRST neuron (central process) on the ipsilateral side
If we damage the hemisection, we cut the pain & temp on the CONTRALATERAL side and we cut thrudorsal column but here it is IPSILATERAL
So for instance, we will have a Loss vibration on the right but lost pain on the left
If a patient has lost pain on one side and vibration on the other side we know we have damaged thespinal cord
If they are both on the same side we have a lesion of the brain s tem
147. hemi- means
Ex.
one side of the body
ex. hemiplegia
no movement of one side of the body
148. hemiparesis weakness of one side of the body
149. hemiplegia no movement on one side of the body.
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154. How are the nuclei of the cranial nerves arranged?
How are the nuclei in the spinal cord arranged?
In discrete, discontinuous cell columns
The cell columns in the spinal cord are continuous
155. How can Muscle cramp can be inhibited?
This is an ex of:
Muscle cramp can be inhibited by contracting the antagonist of thecramped muscle.
Ex. of Reciprocal Inhibition
156. How can we tell if we are looking at a cervical fromlumbar section of the spinal cord?
There is less white further down the spinal cord bc many of the fibertracts have already been given off
So in a lumbar section we see a BIG grey matter/ cell bodies section("butterfly") and not as much white axons
157. How do nuclear bag fibers & nuclear chain fibersdiffer?
The 2 classes differ in
~the arrangement of their nuclei
~the intrinsic architecture of their myofibrils &
~their dynamic sensitivity to stretch
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158. How do the medial motor systemsdescend?
They descend ipsilaterally OR bilaterally
They tend to terminate on interneurons tha t projectto both sides of the spinal cord,controlling movements that involve multiple bilateral spinal segments
Thus unila teral lesions of the medial motor system produce no obvious deficits.
159. How do watershed infarcts produceman in a barrel syndrome?
Explain how our patient will present
b/c regions of the homunculus involved often include trunk and proximal l imbs
Thus these watershed infarcts can produce proximal arm and leg weakness
160. How does Guillain-Barr syndrome(GBS) present?
How do we treat it ?
An acute polyneuropathy disorder affecting the peripheral nervous system.
***Ascending paralysis, weakness beginning in the feet and hands and migratingtowards the trunk.
Some subtypes cause change in sensation or pain as well as dysfunction of theautonomic nervous system.
It can cause life-threatening complications, in particular if the breathing muscles areaffected or if there is autonomic nervous system involvement.
If it affects the diaphram we wil l put them on a breathing machine for a period of time.
The Schwann cells in the PNS are regenerative ... so the peripheral myelin will grow back
161. How does the 3rd order neuron send itsaxons to the postcentral gyrus orparacentral lobule?
What is the name for the 3rd orderneuron?
The third order neurons in the thalamus send their axons to the postcentral gyrus orparacentral lobule (primary sensory cortex) in the cerebral cortex by way of thePOSTERIOR limb of the internal capsule.
Thalamocortical fiber/ axon/tract ... just can't be a nerve
162. How is the medulla connected to the
cerebellum ?
Inferior cerebellar peduncle connects medulla to the cerebellum.
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163. How many skeletal eye muscles do we have?
List them:
Which ones are associated w/ CN 3
12 total : 6 on each side
1. Inferior rectus (3)2. Inferior Oblique (3)3. Superior Rectus (3)4. Medial Rectus *** (3)5. Lateral Rectus 6.Trochlear (4)
7.Abducens (6) Levator Palpebrae Superioris (is also innervated by 3 These muscles elevate the eylids)
Smooth muscle Parasympathetic N.S innervation of constrictorpupillae & ciliary muscles(3)
164. How many spinal segments does i t take for the 2nd orderneurons fibers to cross?
It takes 2-3 spinal s egments for the fibers to cross
165. How many synapses does the Lower motor neuron have? ThousandsIts the Final Common Pathway
Everybody has to synapse on the cell body in order for themuscle to contract
Sensory
166. Ia fiber comes from A muscle spindle primary endingIt transduces LENGTH
167. Ib fiber comes from a Golgi tendon organ
Stimualtion has an effect that varies depending on the position& activity of the limb at the time of stimualtion
It sometimes has an effect opposite that of stimualting a Iafiber: the alpha motor neuron that innervate the muscle
connected to that tendon organ a re inhibited
This effect is a form of autogenic inhibition & involves aninhibitory interneuron between the afferent and afferent fibers
168. If a disturbance causes the muscle length to increase , thespindle increases its firing rate causinf the motor neuron tofire and the muscle to ________
Shorten
Decreases in muscle length produce the opposite effect
The system corrects for deversions from the desired musclelength
169. If a patient has lost pain & vibration on the same side weknow we have damaged ________
The brain stem
If a patient has lost pain on one side and vibration on the otherside we know we have damaged the spinal cord
170. If a patient has lost pain on one side and vibration on theother side we know we have damaged ________
The spinal cord
If they are both on the same side we have a lesion of the brainstem
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171. If I step in glass with my right foot
What part of my parietalcortex will light up?
What artery supplies thisarea?
The left side of my paracentral lobule
(remember the humunculus... leg and foot is paracentral lobule)
The Anterior CerebralArtery supplies this area (blue)
172. If our patient is in a state of complete extension whatdo we know for sure ISINTACT?
EXTENSION = Vestibulospinal tracts are important mediators of postural adjustments and headmovements
Ex if the room is tilting
173. If there is a DC-ML lesion what functions are lostcompletely
Complex discrimination tasks are more severely affected than simple detection of s timuli.
Damage would cause impairment but not aboli tion of tactile perception
PROPRIOCEPTION & KINESTHESIA are cla ssically considered to be totally lost a fter posterior columdestruction. This results in a type of ATAXIA (Incoordination of movement); the brain is unable todirect motor activity properly w/out sensory feedback about the current position of parts of the body.This ataxia is particularly pronounced when the pts. eyes are closed, preventing visual compensation.
174. If we damage the motortract what will oursymptoms be?
If we damage the motor tract what wil l our symptoms be?
Motor - the symptoms will be paralysis / weakness
175. If we damage thesympathetic hypothalamic
fibers where will we see thesymptoms?
descending sympathetic hypothalamic fibers -
lesion always results in a Horner's Syndrome ipsilateral to the side of the lesion in the brain stem.
176. If we had a lesion of theBasilar artery whatstructure will not bereceiving adequate bloodsupply?
GO thru the tracts - where will we see the
ALS
Pons
ALS = contralateral loss of pain and tempML= contra loss
Motor- Body(We haven't crossed yet) so we will see our symptoms contrala teral to the lesion
Motor - FaceCranial nerves are all secondary - ipsi symptoms
Note alternating symptoms for motor
177. If we have a berry aneurysm impinging on theeye - we will loseparasympathetic ... what
will the eye look like?
We will have a large pupil bc we will LOSE Parasympathetic .. .
Normally :ciliary muscles (which control the shape and therefore the refractive power of the lens)
the constrictor pupillae muscle of the iris (which constricts the pupil).
Due to the bilateral projections from the pretectal nuclei to the Edinger-Westphal nuclei, ligh t shinedinto one eye produces pupillary constriction in both eyes.
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178. If we have a Berry anyeurysm of the leftPosterior cerebral artery that isimpinging on the ocular motor nerve
What kind of problems can we expect?
we will have problems with motor of the eye on the left
Cranial nerves that are Motor will all be "ALs"Lower Motor Neurons . .. they innervate ipsilaterally
Note if we had a berry aneurysm in which we were inpinging on CN3, ourparasympathetic nerve fibers would go down 1st b/c they form a sheath on the outside of CN3
179. If we have a capsular stroke and lesionthe Lateral Corticospinal cord, how willour patient present?
Their UPPER EXTREMITIES would be constantly FLEXED
Normally we maintain a normal joint angle due to the Lateral corticospinal tract &Rubrospinal tract dual actions on eachother.
A lesion in which we damage the lateral corticospinal tract would allow us to have solerubrospinal action ... which would lead to constant flexion of the UPPER
EXTREMITIES
180. If we have a lesion and burn out the VPM where will we see symptoms?
VPM is the face
Pain, Temp, Itch and Fine touch, Vibration all go thru there. By the time the tracts getthe the VPM they have already crossed thus we wil l see symptoms on the CONTRA
lateral side of the face ... it's the secondary neurons that are on their way to the VPM181. If we have a loss of pain due to a spinal
cord injury... were will our symptoms be?
Contralateral to the lesion
A Lose of pain in the spinal cord the symptoms will be on the other side
182. If we have a patient in the ER and all wesee is their legs and arms fully extended... what tract do we know is INTACT?
VestibuloSpinal
Note - if you took an unconscious patient and yanked their hair ... really hard and yougot a response - you would also know that the vestibulospinal tract was working ... (atthe cervical cord level this tract control the head and neck muscles)
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183. If we have an ALS lesion of the sp inal cord what will we loseand where ?
We lose Projection neurons (#2)
we'll have contralateral loss of pain, temp and itch
184. If we knock out a UMN will we have flaccidity or spastici ty? Spasticity
185. If we lesion one of the extraocular muscles of the eye with alesion of CN3 what can we expect to see?
Occulomotor Nerve CN III - Motor (somatic and parasympathetic).
The CN 3 innervates the inferior oblique and inferior, superior, andmedial recti extraocular muscles.
Lesion causes diagonal diplopia, loss of horizontal gaze.
186. If we lose our primary sensory neuron will we see a motorresponse?
NO
If we lose the afferent sensory coming in we won't be able togenerate an efferent
187. If we see Babinski sign on the ri ght we know we havedamaged...
UMN
(of the left side - b/c we are high in the cortex and we prob haven'tcrosses yet)
(Hyper-reflexia and Increased muscle tone = UMN)
188. Immediate loss of all reflex activity below the point of transsection of the spinal cord.
Spinal shock - immediate loss of all reflex activity below the pointof transsection of the spinal cord.
189. IMPRECISE term
Give ex.
Palsy
Imprecise term for weakness or no movement
ex. facial palsy weakness or no movement of the face muscles.
190. In order to have our 1st synapse ...
What ion must come in to the axon terminal to causefusion of the vesicle with the terminal end of the neuronmembrane?
Then what happens?
Calcium comes into the axons & it binds to synaptotagmin
As the glutamate is released it DIFFUSES to neuron #2 from high [] when the vesicle fused to low [ ] of the cell body / dendrite of
vesicle #2
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191. In order to lift my right foot what do I need to do to my muscles
In order to lift my right foot I need to flex it-> stimulate flexors by releasing ACh
-> inhibit the extensor muscle (they will have no action potentials b/cthey didn't get any neurotransmitter)
(Flexion reflex)
In the left foot I do the opposite!Left foot I stimulate the extensor and I inhibit the flexor (crossed
extension)
192. In reference to the Internal Capsule ... Where does theCorticospinal tract lie?
The corticospinal tract lies in the POSTERIOR LIMB of the internalcapsule
193. In the ALS system, what does the 1st neuron release atthe first synapse?
Gluatmate
The EPSP gives the right voltage to open up the voltage ga ted channels.
Then a little further down on the neuron, we can get an action potential,it's at the axon hillock bc that's where the voltage gated sodium and
potassium channels are.
We only have the voltage gated channels at the axon hillock - we don'thave it on the cell bodies.
The axon potential moves along the projection neuron straight up rightthru to the 3rd and depending on what part of the body we then take i tright to the cortex.
194. In the DC-ML pathway our sensory neuron enters thespinal cord, goes to the medulla and synapses.
At that point in time what are our fibers called?
On the ipsilateral side we have Internal Arcuate Fibers
then they cross (in the medulla) and then we cal l the fibers MedialLemniscus
195. In the hospital you give a woman a drink with a straw,however she is unable to drink from it but rather itgoes up her nose.
What do you think she has lesioned?
Where is the cell body for it?
Nasal regurg
CN 10 (and 9 as well)
We have trouble in our medulla
Cell body for 10 = Innervation of skeletal pharyngeal and laryngealmuscles (old gill arches).
*Nucleus Ambiguus *
Controls muscles for swallowing (gag reflex) and phonation.
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196. In the monosynaptic reflex arc what happens tothe synergist?
We want it to Contract and help to close the joint angle
(the synergistic Lower motor neuron goes to this)
197. In the Posterior Column - Medial LemniscalPathway
What happens after the initial synapse in thecaudal medulla?
The axons of the second-order neurons immediately cross over (decussa te)as the internal arcuate fibers and then form the medial lemniscus (ML) fiber
tract.
The second synapse occurs in the thalamus (VPL.)
The axons of the third-order neuron travel from the thalamus to the primary somatosensory cortex (they synapse in layer 4 of the neocortex) by way of
the POSTERIOR limb of the internal capsule
198. In the Posterior Column - Medial LemniscalPathway
Where do the axons of the third-order neurontravel to?
Be specific as to how they get there
The axons of the third-order neuron travel from the thalamus to the primary somatosensory cortex (they synapse in layer 4 of the neocortex) by way of the POSTERIOR limb of the internal capsule
199. In the stretch reflex, what happens then there is aSudden unloading of a skeletal muscle
the muscle is inhibited from contracting.
200. Increased muscle tone and abnormal reflexes seen below the point of transection about two weeksafter a spinal cord transection.
Spasticity
Ex. Babinski 's sign
201. Influence axial musculature bilaterally.
MEDIAL motor systems
Anterior Cortiospinal (the 10% that doesn't cross) Vestibulospinal
ReticulospinalTectospinal
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202. Information that reaches the cerebellum is used in the ____________; we arenot consciously aware of cerebellar activity
Used in the regulation of movements
203. Information that reaches the thalamus is relayed to the cerebral cortex andpreceived ______
Information that reaches the thalamus isrelayed to the cerebral cortex and preceived"Consciously"
204. Inhibitory reflex, provides negative feedback to prevent development of toomuch tension in a muscle.
Inverse myotatic reflex
205. Innervate static nuclear bag fibers & the nuclear chain fibers, signal the level of 'sustained' fiber stretch by firing tonically at a frequency in proportion to thedegree of stretch w/ little dynamic sensitivity
Group II afferents
206. Integrates somatic sensory information with vision and hearing to help orient body and head to stimuli.
midbrain tectum
(Spinomesencephalic (spinotectal) tract )
207. Involved in postural tone, balance, orienting movements of the head and neck,automatic gait-related movements.
MEDIAL motor systems
Anterior Cortiospinal (the 10% that doesn'tcross)
Vestibulospinal
ReticulospinalTectospinal
208. Is Corticobulbar innervation of the LMN in cranial nerves
UNILATERAL or BILATERAL.
BILATERAL
Each LMN of the brain stem receives inputfrom axons arising from both the right andleft cerebral motor cortex.
EXCEPTION: CN 7 - facial nerve LMN tothe lower face receives only contralateralUMN innervation.
209. Is there a synapse in the DRG? No there is no synapse in the DRGThere are no neurotransmitters thereeither. It's just a bunch of cell bodies :
There are cell bodies in there for everybody - ALS tract, DCML tract etc
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210. Jaw Jerk reflex
Where does it happen?Sensory receptor =The action potentials encode =
Motor
Brainstem ... sometimes called a 55
Afferent Sensory 1st : The stretch receptor is the muscle spindle.Ia is the fiberThe action potentials encode muscle stretch/ length
CN 5 for the face(Note CN 1 for the back of the head )
Motor :CN5 motor divisionthe alpha fiber lower motor neuron, innervatesmuscle of mastication.It's cell body will be medial & in the pons
211. Knocking out what Ganglion will lead to Hornerssyndrome?
Knocking out the superior Cervical Ganglion
212. L5
Big ToeHamstrings - Flexion
(Lower leg - right above the knee)213. Lack of intrinsic factor (produced in stomach and
used in small intestine to absorb cobalamin)causes :
Lack of intrinsic factor (produced in stomach and used in small intestine toabsorb cobalamin) causes tingling and numbness (paresthesias) of handsand feet.
(Due to Nutritional Deficiencies)
214. Lamina X corresponds to The zone of gray matter surrounding the central canal
215. Large diameter sensory axons are coiled aroundthe central part of each class of intrafusal fiberforming
so called "annulospiral" primary endings(group Ia afferents)
216. Lateral corticospinal tract
Site of origin?
Site of decussation?
Level of Termination?
Function:
Origin =
Primary motor cortex ( Precentral Gyrus) and other frontal & parietal areas
Decussation = primary decussation at the cervicomedullary junction
Termination = Entire cord (predominatly a t cervical & lumbosacralenlargements)
Function = Movement of contra lateral limbs
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217. Lateral Medullary Syndrome (WallenburgSyndrome)
could occur with loss of what bloodsupply?
What symptoms will be seen?
Whats the prognosis?
vertebral artery more common than PICA
Pica will be on both sides of the upper part of the butterfly ... this is the posteriorportion
inferior cerebellar peduncle: ipsilateral ataxia vestibular nuclei: vertigo, nausea, nystagmus
CN V (spinal trigeminal tract and nucleus): ipsilateral facial loss pain and temperaturenucleus ambiguus: hoarseness, dysphagia
nucleus solitarius: ipsi lateral decreased tastedescending sympathetic fibers***: ipsilateral Horner's Syndrome
spinothalamic tract (ALS)***: contralateral body, decreased pain and temperature
Lateral tegmentum involved, not too much motor affected and prognosis is good
218. leg para lysis no movement of the leg
219. Lesion of _____ will cause the gag reflex Lesion of the glossopharyngeal nerve causes loss of gag reflex with CN X.
(both are in the medulla)
220. LESION OF THE ALS
Damage the right side of the SPINALCORD
What will we lose & where ?
We damaged the PROJECTION neuron (#2) and we got loss of pain, temp and touchCONTRALATERAL to the lesion
ALS LESIONS ARE ALWAYS CONTRALATERAL
221. LESION of the ALS in the brainstem(Right medulla)
What will we lose & where ?
We damage just the ALS tract inSensory deficit & CONTRALATERAL symptoms
If we mess w/ Brainstem or Spinal cord lesions in the ALS symptoms will ALWAYS BECONTRALATERAL
Cuz pain can't wait ... it synapses immediately and sends it's axons up to the thalamuscontralaterally
222. LESION of the DCML to the Gracilis tractof the spinal cord
What will we lose (be specific)& where ?
Note we Damage the PRIMARY central process in the central column (not theprojection neuron as in the ALS system)
For ex. we Damage the Gracilis tract ... Just that location - it will prob never happenclinically but w/e
What happens?Sensory deficit
The sensory lost is fine touch, vibration and proprioception and it's going to be on thesame side "ipsilateral" to the lesion
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223. LESION of the DCML to the right side of the medullain the brain stem:
What will we lose & where ?
We damaged Right medial lemniscus (this is our projection neuron / #2 )
Sensory loss : Proprioception, Fine touch & vibrationContral lateral loss
BRAINSTEM LOSSES ARE ALWAYS CONTRALATERAL
224. Lesions in the brain stem to ________ (list) _________ tracts willresult in a body contralateral deficit.
Lesions in the brain stem to any of the long tracts will result in a body contralateral deficit.
corticospinal tractspinothalamic tractmedial lemniscus
there are exceptions
EXCEPT! descending sympathetic hypothalamic fibers -lesion always results in a Horner's Syndrome ipsilateral to the side of thelesion in the brain stem.
EXCEPT! cerebellar peduncle damage will result in ipsi lateral motorataxia.
EXCEPT! damage to cranial nerves and nuclei will result in ipsilateral headsensory and / or motor deficits.
225. List 3 groups of cell bodies ...aka "nuclei" found i nthe reticular formation
Locus Ceruleus (aka Blue Spot)
Raphe Nucleus
Substantia Nigra
226. List some signs of dysfunction that would bepresent w/ a Medulla lesion
Medulla - signs of dysfunction
respiratory arrest vertigoataxianausea
vomitingautonomic instability hiccups
227. List the components in the Anterolateral System(ALS system)
Spinalthalamic ***SpinoreticularSpinomesencephalic (spinotectal)
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228. List the Humunculus starting laterally
(Genital) Sensory only (Scalp goes where?)ToeLeg
KneeHip
Trunk Shoulder
ArmElbow WristHand
FingersTHUMB
Neck BrowEyeFaceLipsJaw
TongueSwallowing
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229. List the Posterior Column - Medial LemniscalPathway
What does this pathway mediate?
fine touch, proprioception, pressure and vibration
The FIRST-order neurons in the fasciculus gracilis and fasciculus cuneatus enterthe spinal cord and travel on the same side up the spinal cord.
They synapse ipsilaterally onto SECOND-order neurons in the nucleus gracilisand nucleus cuneatus respectively in the caudal medulla.
The axons of the second-order neurons immediately cross over (decussa te) as theinternal arcuate fibers and then form the medial lemniscus (ML) fiber tract.
The second synapse occurs in the thalamus (VPL.)
The axons of the third-order neuron travel from the thalamus to the primary somatosensory cortex (they synapse in layer 4 of the neocortex) by way of the
POSTERIOR limb of the internal capsule
230. LMN are located where 1) In the Spinal cord in the Ventral/ Anterior hornThere is somatotopy there:The more lateral neurins in the ventral horn will run the fingers and wrist; themore medial ones will run the trunk
2) Brainstem
231. Location of pain ... think Spinalthalamic tract
232. Locus Ceruleus:
Aka =
Where is it found & what does it do
aka Blue Spot
Found in the reticular formation of the brains tem.
It makes & delivers NorEpi with every single action potential
233. Looking at the brainstem dorsally - we take off
the cerebellum ... what i s the major thing that we are looking at?
4th ventricle!
As soon as we take the cerebellum off thats all we can see.
234. Main job of CN IX Glossopharyngeal IX = conveyor of taste and pharyngeal sensations
235. Main job of CN V Trigeminal nerve = general sensory for the head
236. Main job of CN VII Facia l Nerve = Motor nerve for facial expression
237. Main job of CN X Vagus = carries parsympathetic outflow to the thoracic and abdominal viscera
238. Major Anterior circulation to the brain isfrom :
Internal Carotid
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250. Nociceptors:
What are they? Where are their cells bodies located?
Pain, temp and crude touch sensory neurons
For the body = In the dorsal root ganglia
For the face = In the Trigeminal Ganglia
Note they have free nerve endings!
251. Normal muscle tone (stiffness or tension in the muscle) can befelt or judged by:
simple passive stretch of the muscle
252. Normally only _____ have a powerful enough influence tocause a reflex withdrawl
Nociceptors
aka flexor reflex
253. Normally our Lower motor neurons are hovering at whatmembrane potential?
We are normally hovering around -67, -68 .. . right nearthreshold.
We are at this "chronically depolarized" level b/c we have lotsof descending info coming down from the supraspinalsections releasing Glutamate onto our LMN which isdepolarizing the membrane
IF we had a lesion we become HYPERPOLARIZED and go back to a level around -70 b/c we no longer have thedescending depolarizations
254. Nuclear bag fibers can be further subdivided into subclasses: Dynamic & Static
255. Occulomotor nerve (CN III)
Where is the nuclei?Be specific
Occulomotor nerve (CN III) - Edinger-Westphal nucleus(MIDBRAIN).
The PNS PREganglionic neuron cell body is located inspecific brain s tem nuclei.
256. Once we are in the brainstem ... what type of neurons are we
dealing with?
Nuclei (secondary - projection neuron cell bodies) are seen at
ALL brainstem levels.
The one exception = Mesencephalic of CN5 which is aprimary neuron
257. Pacinian corpuscles, Merkel's Disks, muscle spindles mediate _________
Conscious proprioception,fine touch,
vibration &pressure
258. Pain and temp afferents for the right side og the face come intothe middle cerebral peduncle of the pons and headsdownwards toward the spinal cord (Primary neuron axon of Spinal trigeminal tract)
It synapses on the ipsi side of the spinal cord, crosses(secondary neuron / Trigeminalthalamic tract) and heads
________
to the VPM Ventral posteromedial nucleus (VPM) of the thalamus
259. Pain modulation / Endogenous relief ... think Spinomesencephalic tract
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260. Pain, temp and itch, crude touch for CNV will synapse at what nuclei?
Spinal trigeminal nucleus
Pain leaves the free nerve fibers - goes past the Trigeminal g anglion enter the pons but travels downwards to the spinal cord where it synapses at the Spinal trigeminal
nucleus .
Then a 2ndary neuron wil l cross the midline to travel in the trigeminothalamic tract
& synapse in the VPM of the thalamus
261. Painful stimuli elicits ________ Painful stimuli elici ts coordinated withdrawl reflexes
262. para- means
Ex.
both legs
Ex. paraparesis
weakness in both legs
263. Participates in central modulation of pain midbrain periaqueductal gray (PAG)
(Spinomesencephalic (spinotectal) tract )
264. Pin point pupi l eye symptoms on the sameside as the lesion =
...
265. Provide the predominant autonomic toneto the head and thoracoabdominal visceraabove the splenic flexure.
The crania l nerves associated with the parasympathetic nervous system (PNS)(CN 3, 7, 9, and 10).
Note we are talking Postganglionic neurons
266. Provides coordination of head and eyemovements
Tectospinal tract - Ends in the cervical cord.
(medial motor system)
267. quadri- or tetra means
Ex.
all four limbs
ex. quadriplgia
tetraplegia
paralysis of all 4 limbs
268. Raphe Nucleus
Where is it found & what does it do?
Found in the reticular formation
these neurons release serotonin 5- HT
The cell bodies are in a nucleus specifically with axons that go throughout thecerebrum & if they have an action potential they will secrete Serotonin in the postsynaptic membrane to be spread throughout the cortex
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269. Reflex arc: polysynaptic
Contraction of a muscle ?????
Contraction of a muscle increased muscle tension.
Ib afferent is our fiber
(Inverse myotatic reflex)
Too much tension causes the muscle to stop contracting!
270. Reflexes ~
Length to muscle use :
Too much tension use
Pain use:
Length to muscle use : Stretch reflex
Too much tension use: inverse myotatic reflex
Pain use: Flexion / With-drawl
271. Respond to small stretches Group Ia afferents
This is bc the Ia afferent activity is dominated by the 'dynamic'subtype of nuclear bag fiber whose biochemical properties
emphas ize the 'velocity' of fiber stretch272. Responsible for the transmission of tactile, proprioceptive,
pain, temp info from the head to the cerebral cortex,cerebellum and reticular formation
CN V Trigeminal system
273. Runs length of the spinal cord: controls extensor tone.
lateral VST #2
( Vestibulospinal tracts (VSTs) of the medial motor system)
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274. S1
275. Scalp - describe it's position in the humunculus
Be specific
The scalp is only included in the Sensory (Postcentral Gyrus)
It is not part of the motor cortex
C1 level
(note we have a total of 4 humunculi)
276. Sensory and motor loss due to high blood pressure in the Lenticulostriate CAPSULAR STROKE
(the Lenticulostriate supply the blood forthe Internal Capsule ... they come off theMiddle Cerebral Artery )
277. Sensory cranial Nerves Sensory 1, 2, and 8**
* #8 is in the brainstem : tegmentum of the pons; it's lateral b/c its sensory
278. Sensory neurons from the vestibular portion of the membranous labyrinthencoding acceleration go to _______ nuclei located in the _______
CN 8
Vestibular Nuclei - located in the pons
279. Simplest and fastest (< 1 msec) of all reflexes monosynaptic reflex arc.
280. SNS innervation of this muscle keeps the eye open Mullers smooth muscle
(Nor Epi is released)
sanneapanam
281. Spinal Trigeminal Nucleus - projection neuron cell bodies in the nucleus sendaxons which cross the midline to travel in the trigeminothalamic tract andsynapse in the VPM nucleus of the thalamus.
What location?
Spinomedullary Junction Motor (centralcanal)
Note the corticospinal tract crossing
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282. State Nerve
Motor for muscles of facialexpression
CN 7
283. State nerve
Motor for muscles of mastication
CN 5
284. State Nerve
Motor for palate, pharynx andlarynx
CN 10
285. State nerve
Motor for sternocleidomastoidand trapezius muscles
CN 11
286. State Nerve
Motor for Tongue
CN 12
287. State the Functional importanceof the stretch reflex: (4) 1. The steady (tonic) afferent information from the stretch reflex is important for maintainingposture and the position of the limb when a load is applied or removed.
2. Provides recovery of original length (posture) from any displacement.
(e.g. riding a bus - muscles contract to prevent falling a fter muscle stretch.)
3. Provides muscle tone (stiffness of muscle = force with which a muscle resists beinglengthened).
4. Regulates smooth motor movements.
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288. State the pathway for the Spinothalamictract:
"Pain can't wait"
Free nerve endings ...
1. The first-order neuron (nociceptor) transduces information about pain andtemperature sense (passes the DRG)
enters the spinal cord & immediately synapses in the dorsal horn (lamina I and V.)GLUATMATE @synapse
2. The axons from the 2nd order neuron CROSS immediately in the white ventralcommissure (takes 2-3 spinal s egments for the fibers to cross.)
3. The axons from the 2nd-order neuron synapse with neurons in thethalamus VPL nuclei (spinotha lamic tract), brains tem reticular formation
(spinoreticular tract), andmidbrain (spinomesencephalic tract).
4. The 3rd order neuron then sends their axons to the postcentral gyrus or paracentral
lobule (primary sensory cortex) in the cerebral cortex by way of the POSTERIOR limb of the internal capsule.
289. State the pathway of the LateralCorticospinal tract (be sure to inculdestructures as landmarks)
Pyramidal cells Axons from the Cerebral Cortex descend downwards to the internalcapsule
Go thru the posterior limb of the internal capsule
go thru the 'ventral portion of the cerebral peduncles'
Descend thru the "ventral pons" where they form somewhat scattered fascicles
Collect in the ventral surface of the medulla to for the medullary pyramids
At the caudal portion of the medulla 85% of the pyramidal tract fibers cross at thepyramidal decussation to enter the * lateral white matter columns * of the spinal cordforming the lateral corticospinal tract.
Finally, the axons of the lateral corticospinal tract enter the spinal cord central gray matter to synapse on an terior horn cells.
Note a somatotopic representation is present in the lateral corticospinal tract w/ fiberscontrolling the upper extremities located medial to those controlling the lowerextremities
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290. State the Reflex Arc :MONOSYNAPTIC
1) Passive stretch of a muscle.
(e.g. lengthening of the rectus femoris muscle by tapping the patellar tendon - deep tendonreflex = stretch reflex).
2) Increase discharge from the afferent Ia sensory endings that innervate the muscle spindles.
3) Ia sensory ending synapses (monosynaptic) directly on the alpha motor neuron of its own
(homonymous) muscle and other synergistic muscles.
1) II sensory afferent fibers also excite alpha motor neurons (monosynaptically andpolysynaptically).
d. Ia and II sensory endings cause excitation of the motor neurons and stimulate contraction of the stretched muscle.
e. The synergistic muscles also contract resisting the lengthening of the stretched muscle.
291. State the steps of the Inversemyotatic reflex
Inverse myotatic reflex - inhibitory reflex, provides negative feedback to prevent development of too much tension in a muscle.
a. Contraction of a muscle increased muscle tension.
b. Increase discharge from the afferent Ib sensory endings in the Golgi tendon organ.
c. Afferent Ib fibers from the Golgi tendon organ make INHIBITORY synapses with theirhomonymous alpha motor neurons (via Ib inh ibitory spinal interneuron) and excitatory connections with the motor neurons of antagonist muscles.
For ex. we will inhibit our flexor and Contract our Extensor
292. State whether the sign will beIncreased or decreased in a UMNor LMN lesion or both.
Reflexes
UMN = Increased (with acute UMN lesions, & tone may be decreased due to acute spinalshock)~Hyper-reflexia after a period of time
LMN = Decreased
293. State whether the sign will beIncreased or decreased in a UMNor LMN lesion or both.
Tone
UMN = IncreasedMuscle tone of arm = flexedMuscle tone of leg = Extension
LMN = Decreased
294. State whether the sign will bepresent in UMN or LMN lesions or
both.
Atrophy
UMN = No ... (mild atrophy 'may' develop due to disuse)
LMN = Yes - look at C8 - the finger will look skinnier
295. State whether the sign will bepresent in UMN or LMN lesions or
both.
Fasciculations
UMN = No
LMN = Yes
fascicilations = abnormal muscle twitches caused by spontaneous activity in groups of musclecells.
Ex. of a benign fasciculation not associated w/ motor neuron damage is the eyelid twitchingoften experienced during periods of fatigue, caffeine excess & eye strain.
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296. State whether the sign will be present in UMN or LMN lesions or both.
Weakness
UMN = yes (Spasticity after some time)LMN = yes (Flaccid)
297. Stretch from the jaw jerk reflex / Proprioception for the face will synapseat what nuclei?
At the Mesencephalic trigeminal nucleus notethis is the exception: A primary nerve fiber travels
from the muscle spindle into the the nucleus
298. Stretch imposed on the muscle deforms the intrafusal muscle fibers, which in turn ini tiates action potentials by activating ______________gated ion channels in the afferent axons innervatingthe spindle.
Activating mechanica lly gated ion channels
299. Striking the patellar tendon activates muscle spindle primary endings , which then monosynaptically excite alpha motor neurons that innervatethe stretch muscle
Monosnaptic reflexMyotatic reflex
300. Striking the patellar tendon ini tiates a stretch reflex. It also causesinhibition, thru an i nterneuron of the motor neurons to the antagonisthamstring muscles.
This sequence of events is called:
Reciprocal Inhibition
301. Substantia Nigra
Where is it found and what does it do?
Found in the reticular formation
Substantia Nigra and the VTA (VentralTegmental area) release Dopamine
302. Sympathetic NS causes Muellers Muscle to release ________ to keep theeyelid open
NorEpi
303. Synapse late = dorsal column-medial lemniscus system
304. Synapse right away = anterolateral system (ALS)
Consists of 3 pathways:
Spinalthalamic ***SpinoreticularSpinomesencephalic (spinotectal)
"Pain cant wait"
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305. Syringomyelia usually happens at what location?
Ventral White Commissure
We'll have bilateral loss of pain, tempand itch
306. T/FIa afferent action potential alone is not enough to fire an action potential in an
alpha motor neuron.
True
307. T4
Nipples
308. T10
Umbilicus Belly button area
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309. The "Butterfly" cross section means we are where?
Rostral Medulla
The Curly Hair on top means Ventral & corresponds to The inferior Olivary nucleus
Aboe the curly hair - the "bow" is the Pyramid which houses theCorticalSpinalTract
310. The 1st order sensory neuron is ca lled a ________
What does it do?
A "tranducer" (ex nociceptor)It's a sensory neuron
The first order (aka Primary) neuron transduces environmental physical energy into electrochemical energy
Note this is a change in RECEPTOR (MEMBRANE) potential (NOT action
potential)
Electrotonic: small & can summate
311. The Abducens Nerve is also called :
What does it innervate?
The horizontal gaze center.Motor nerve
Innervates the lateral rectus muscle (abducts the eye) &internuclear neuron innervating the occulomotor nerve (CN III) via the MLF.
1) Keeps the two eyes yoked together for horizontal eye movements.
It's nuclei location is near the midline, in the floor of the fourth ventricle [just
lateral to the MLF (medial longitudinal fasciculus)].
312. The blood supply to the spinal cord arises from branches of _______ arteries
Branches of the vertebral arteries and spinal radicular arteries
The vertebral arteries give rise to the an terior spinal artery that runs along the ventral surface of the spinal cord
2 psterior spinal arteries a rise from the vertebral or posterior inferior cerebellararteries & supply the dorsal s urface of the cord
313. The Bouton Has main acesss to the axon hil lock
This is the
if we are going to have a short circuit - that says don't fire - we are going toactivate it from a higher center.
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314. The centrally projecting branch of the sensory neuron formsmonosynaptic excitatory connections with those alpha motor neurons inthe ventral horn of the spina l cord that i nnervate the same (homonymous)muscle &
via local circui t neurons forms inhibitory connections with those alphamotor neurons that innervate antagonistic (heteronymous) muscles
This is an ex of :
Reciprocal innervation & results in rapidcontraction of the s tretched muscle andsimultaneous relaxation of the antagonistmuscle
315. The classic signs of Horner's Syndrome are:
The classic signs of Horner's Syndrome are: MIOSIS - decreased pupil size (dilator musclenot innervated). Normally Nor Epi is released
PTOSIS - drooping upper eyelid (Muller'ssmooth muscle not innervated).
ANHIDROSIS - lack of sweating on the faceand neck.
Note Pts. Left eye
316. The clinical syndrome of bilateral upper extremity paresis with intactmotor functioning of the lower extremities, giving the appearance of beingconfined within a barrel.
What is the pathogenesis of this syndrome?
Man In Barrel Syndrome (MIBS) refers to
MIBS is believed to be cerebral hypoperfusionleading to border zone infarctions between theterritories of the anterior and middle cerebral
arteries.
"the watershed areas"
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317. The collapse of resistance seen when a spastic,hypertonic limb is forcibly flexed or extended
Clasp knife response
This exhibits autogenic inh ibition
In certain pathological conditions that follow damage to DESCENDING motorpathways the resisitance of muscles to manipulation is greatly increased. Thusone would have considerable difficulty flexing the leg of an individual w. such aconsition.
If sufficient force is applied however, the leg slowly flexes until at some pt. allresisitance suddenly disappears & the leg collpases in flexion, like a clasp knifesnapping shut
318. The coticobulbar / corticonucleasr tract lies in what limb of the internal capsule?
Genu of the internal capsule
The genu is at the transition between the anterior and posterior limbs, a t thelevel of the foramen Monro
319. The coticospinal tract goes thru what limb of the internal capsule?
Posterior limb
320. The cranial nerves are all lower motor neurons
... they are all "ALs"
What does this mean as far as innervationgoes?
They will all innervate skeletal muscle ipsilaterally
Motor neurons = 3,4,6, 11, 12
321. The cranial nerves associated with theparasympathetic nervous system (PNS) arelocated :
What nerves?
in the CNS brainstem andin the sacral S2-4 intermediate horn
(CN 3, 7, 9, and 10).
The PNS preganglionic neuron cell body is located in specific brain stem nuclei.
a. Occulomotor nerve (CN III) - Edinger-Westphal nucleus (MIDBRAIN).
b. Facia l (CN VII) - Superior salivatory nucleus (PONS).c. Glossopharyngeal (CN IX) - Inferior salivatory nucleus (MEDULLA).d. Vagus (CN X) - Dorsal motor nucleus of CN X (MEDULLA).
322. The DC- ML tract goes thru what limb of
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