neuro block 2

8/14/2019 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.



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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."


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


Cerebellar pathwaysLong sensory = Medial LemniscusCorticospina l tracts

39. A patient presents with blurred vision


Eye movement pathways or visual cortex

3,4,6

40. A patient presents with diplopia and adysconjugate gaze


Supranuclear or infranuclear eye movement pathways

3,4,6

41. A patient presents with dysarthria and dysphagia


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


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.


Facial nerve (CN VII) sphenopalatine gang lion

70. axons project to submandibular and submaxillary salivary glands.


Facial nerve (CN VII)

submandibular ganglion

71. axons project to the eye ciliary muscle and constr ictor(sphincter) muscle of the iris


Occulomotor nerve (CN III)

ciliary ganglion

72. axons project to the parotid gland.


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.


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.


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)


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)


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:


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)


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

neuro block 2

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