March 18th, 2010 - Answers to Review Questions at the End of the Handout on Neurohistology
1a. retrograde filling of cells in locations 4,6
anterograde filling of terminals at locations 3,4
Note: location 2 would not be labelled because the terminals from cell 2 are not visible in this plane.
1b. retrograde filling of cells in location 6
anterograde filling of terminals at locations 3
2a. anterograde labelling of terminals in location 3
2b. anterograde labelling of terminals in locations 3,4
3. chromatolysis at location 1,3 and 4
axonal degeneration at location 2,4
4. labelling in locations 3,4
5. symptoms ipsilaterally, because none of the neurons injured cross the midline.
6. sensory symptoms would be ipsilateral loss of light touch and contralateral loss of pain and temperature
7. stimulate appropriate dermatomes with a) pin prick for pain and b) wisp of cotton for light touch or tuning fork for vibration.
Gross Brain Practical (Friday March 26th, at 9:15am)
This Practical Exam will cover the Gross Brain lab as well as integrative material from the Introduction to Nervous System, Development of the Nervous System, and Blood Brain Barrier lectures. There will be a mix of identification-type questions (1 point) and integrative questions (2 points). All questions will use slides (usually, but not necessarily ones that you've seen before) and be in multiple choice format.
The standard timing for the practical exam will be 45 sec/question for #1-10 and 90 sec/question for #11-15. We then repeat the slides at 10 sec/question and allow 5 min at the end to be sure of your answers. Thus, the total time for this practical is 22.5 min. Subsequent practicals will contain more integrative questions.
Dear Students,
We have changed the start time for the Gross Brain Practical from 8:30am to 9:15am on Friday 3/26.
Best of luck to everyone!
Jed Shumsky, PhD
Course Director, Medical Neuroscience
IFM Medical Neuroscience Gross Brain Practical Exam
Asnwer Key – 03/26/10
1. D
2. D
3. B
4. A
5. D
6. B
7. D
8. E
9. E
10. D
11. D
12. B
13. D
14. E
15. C
April 19: ANSWERS TO SPINAL CORD LAB QUESTIONS
-- H1:
Medial
a) dorsal column, clarke's, lamina VII lamina V/VI, lamina IX
b) clarke's, lamina VII lamina III/IV proprius V/VI, lamina IX
c) Proprioception and fine touch
d) Ia monosynaptic stretch, Ia and Ib inhibitory, II tonic stretch
e) Dorsal column to DCN to medial lemniscus
Lateral
a) Lissauer's tract
b) lamina 1 II, dendrites of V
c) pain and temperature
d) protective flexion, scratch
e) spinothalamic ALS
-- H2: e
-- H3: crushing of anterior white commissure and medial alpha motoneurons by
syrinx
-- H4: b, e, g
-- H5: LCST,MRST, RuST, PRST, VST, VCST
-- H6: STT, ALS, Fasciculus Gracilis
-- H7: No, not present
-- H8 Horner's syndrome results, ptosis, miosis and anhydrosis due to sympathetic
losses
-- H9: Control of trunk and posture uses VST
CASES
-- I1: Poliomyelitis : MN loss
-- I2: Brown sequard: lesion at L2 on the left
-- I3: The Medial part of fasciculus gracilis on the right is spared, everything else is gone as a result of the injury.
IFM MEDICAL NEUROSCIENCE
GUNSHOT WOUND MODULE PRACTICAL EXAM
ANSWER KEY – 04/21/10
IFM MEDICAL NEUROSCIENCE
GUNSHOT WOUND MODULE WRITTEN EXAM
ANSWER KEY – 04/21/10
33. A
34. C
35. E
36. A
37. A
38. E
39. D
40. E
41. B
42. A
43. D
44. D
45. D
46. B
47. B
48. D
49. B
50. D
51. A
52. D
53. A
54. E
55. E
56. A
57. A
58. A
59. B
60. D
61. A
62. E
63. C
64. C
65. E
66. C
67. C
68. A
69. C
70. D
71. E
72. C
73. D
74. A
75. D
76. A
77. D
78. D
79. A
80. C
81. C
82. A
83. C
84. D
85. E
86. B
87. A
88. D
89. D
90. C
91. D
92. B
93. E
94. B
95. C
96. C
97. E
IFM Brainstem Practical (Monday May 3rd, at 9:00am)
This Practical Exam will cover the Brainstem lab as well as integrative material from the Brainstem 1-3 and Reticular Formation lectures. There will be a mix of identification-type questions (1 point) and integrative questions (2 points). We recommend reviewing the Pathways, Brainstem Anatomy, and Brainstem Cranial Nerves Tutorials (we may include some structure-function questions regarding lesions, but we will be saving the majority of Brainstem Vascular Lesions for the Mid Module Exam). All questions will use slides (usually, but not necessarily ones that you've seen before) and be in multiple choice format.
The standard timing for the practical exam will be 45 sec/question for #1-10 and 90 sec/question for #11-20. We then repeat the slides at 10 sec/question and allow 5 min at the end to be sure of your answers. Thus, the total time for this practical is 31 min.
Best of luck to everyone!
Jed Shumsky, PhD
Course Director, Medical Neuroscience
May 4th - Answers to questions in Medical Neuroscience Lab Manual (pp42-45)
REVIEW QUESTIONS FOR CRANIAL NERVES (Lab Manual pp45):
1. If the Xllth nerve were destroyed by a vascular lesion:
a) What blood vessel would probably be responsible?
ANTERIOR SPINAL ARTERY
b) What other major structure would be likely to be destroyed concomitantly?
MEDULLARY PYRAMID CONTAINING CORTICOSPINAL FIBERS
c) If this patient showed paralysis of the tongue and of the body would the 2 paralyses be on the same side or on opposite sides?
OPPOSITE SIDES
d) If the patient died 10-14 days later, how would you expect the cells of the hypoglossal nucleus to look?
CHROMATOLYTIC
2. How would you examine a patient to test for possible damage to the Xl nerve?
SHRUG SHOULDERS/ TURN HEAD TO OPPOSITE SIDE
3. If a patient had decreased pain and temperature sensation on one side of the face and some difficulty in speaking (phonation) and in swallowing, where would you expect the lesion to be?
LATERAL MEDULLA AT EXIT POINT OF VAGUS NERVE INCLUDING SPINAL NUCLEUS OF V (and ALS)
4. If a patient underwent thyroidectomy and, due to inadvertent damage suffered from permanent hoarseness, what nerve will have been involved?
RECURRENT LARYNGEAL OF X
What cranial nerve nucleus would show retrograde chromatolysis?
NUCLEUS AMBIGUUS
5. If a patient showed paralysis of the left side of the body but couldn't look to the right with the right eye, where would his\her lesion be?
CORTICOSPINAL TRACT RIGHT SIDE AND EXITING FIBERS OF RIGHT ABDUCENS NERVE VENTROMEDIAL CAUDAL PONS
6. What lesion would cause, on one side, a facial paralysis with auditory and vestibular symptoms and loss of taste in the anterior 2/3 of the tongue, plus loss of pain and temperature on the opposite side of the body?
POINT OF EXIT OF VII AND VIII AT PONS MEDULLARY JUNCTION. FACIAL NERVE (TOTAL PARALYSIS INCLUDING LOSS OF TASTE)
HEARING/BALANCE PROBLEMS (VIII) AND ANTEROLATERAL SYSTEM NEARBY INVOLVED.
7. If a patient showed a paralysis on the left side of the face, and an inability to look to the left with the left eye, where would the lesion be?
There might be symptoms of cerebellar dysfunction-too - Why?
LEFT GENU OF FACIAL NERVE AND LEFT ABDUCENS NUCLEUS IN FLOOR OF FOURTH VENTRICLE.
INFERIOR CEREBELLAR PEDUNCLE MIGHT ALSO BE AFFECTED WITH VESTIBULAR NUCLEI
8. What sort of lesion would cause a disturbance in eye movements, of both eyes and in all directions?
ONE IN THE MLF- THE VESTIBULO-OCULAR EXPRESSWAY
9. If a patient with a brainstem lesion complained of double vision (diplopia) when looking down to the right, in what nucleus and on which side of the brain would the lesion be found?
SUPERIOR OBLIQUE CAUSES THE EYE TO LOOK DOWN AND OUT; IT DEPRESSES AND ABDUCTS THE EYE.
DIPLOPIA LOOKING DOWN AND TO THE RIGHT INVOLVES THE RIGHT SUPERIOR OBLIQUE OF THE RIGHT EYE AND THE RIGHT TROCHLEAR NERVE.
AND IF THE LESION WERE IN THE MIDBRAIN, THE LEFT TROCHLEAR NUCLEUS BECAUSE IV IS THE ONLY COMPLETELY CROSSED CRANIAL NERVE
PATIENT COMPLAINS OF DIFFICULTY GOING DOWN STAIRS.
10. What lesion would cause a paralysis of left medial eye movement, an enlargement of the left pupil (mydriasis) and a drooping of the left eyelid? If there was also para!ysis of the right side of the body as well, where would the lesion be?
LEFT MEDIAL EYE MOVEMENT- LEFT EYE CANNOT BE ADDUCTED - IIIRD NERVE OR OCULOMOTOR NUCLEUS
DILATED PUPIL LEFT EYE- IIIRD NERVE OR EDINGER WESTPHAL NUCLEUS LEFT PTOSIS (EYELID DROOP)- IIIRD NERVE
LESION OF VENTRAL MIDBRAIN ON LEFT
Answers to Case Study questions on page 42 Medical Neuroscience Lab Manual
Acoustic Neuroma
Structures Involved:
1. LEFT TRIGEMINAL NERVE HYPESTHESIA MEANS REDUCED SENSATIONS- ALL SENSATIONS
2. BLINK REFLEX LOSS COULD BE LEFT V OR VII, BUT DRY AND RED EYE IMPLICATES VII
3. LEFT VII NERVE OR CORTICOBULBAR FIBERS?
4. LEFT VII NERVE
5. LEFT VIIITH NERVE OR COCHLEAR NUCLEUS
6. CEREBELLAR PEDUNCLE OR VIIITH NERVE
7. LEFT VTH NERVE
Brainstem Lab Review Quiz Answers (page 43):
1) Where are the cell bodies of the axons which terminate in the right nucleus gracilis?
Dorsal root ganglia from T6 down on the right
2) Will lesions to the right cuneate nucleus and right medial lemniscus produce symptoms on the same or opposite sides of the body?
Opposite
3) A lesion involving the left lower quadrant of the brainstem at the level of mid-medulla (slide 55), would cause motor symptoms.
a. Where?
Contralateral upper and lower limb
b. What Cranial nerves might be involved?
CN XII
c. What would happen if a person with such a lesion were asked to stick out his tongue, and raise both arms?
Tongue would deviate on protrusion toward the side of the lesion. One could only raise the arm ipsilateral to the side of the lesion.
4) Name some specific cranial nerve nuclei that contribute fibers to the MLF.
Vestibular nuclei, CN VI, CN IV, CN III
5) Name some of the ascending pathways that contribute to the inferior cerebellar peduncle.
Dorsal spinocerebellar tract, cuneocerebellar tract, olivocerebellar fibers, vestibulocerebellar fibers, reticulocerebellar fibers, trigeminocerebellar fibers
6) What would be a likely site of blockage giving rise to an enlargement of the IVth ventricle at the level of the open medulla?
A blockage of the foramen of Luschka or Magendie
What cranial nerves might be affected?
Any nucleus in the floor of the fourth ventricle e.g., Hypoglossal nucleus, Dorsal motor nucleus of X, Abducens nucleus, Genu of the facial nerve.
7) What symptoms would you expect from a lesion to the left facial genu?
Left side facial weakness, hyperacusis, but no sensory or parasympathetic signs.
8) After vascular damage in the region of the red nucleus, what cranial nerve would be likely to be affected at the same time?
CN III
9) Given a tumor in the cerebral aqueduct, expanding ventrally:
a. What structures would it involve (in order)?
MLF, then the trochlear nucleus in the mid midbrain, or the oculomotor nucleus and the nucleus of Edinger Westphal in the rostral midbrain.
b. What changes would you expect in the lateral and 3rd ventricles?
Enlargement; non-communicating hydrocephalus
10) Where are the cell bodies located whose axons comprise the mesencephalic tract?
In the mesencephalic nucleus
Are they considered primary or secondary afferents?
Primary
11) What symptoms would result from a unilateral lesion destroying the cerebral peduncle and IIIrd nerve?
Dilated pupil, external strabismus, ptosis, ipsilateral to the lesion side; contralateral lower face weakness and contralateral upper and lower limb spastic weakness
12) What sensory modality is served by the nucleus solitarius?
Taste from the entire tongue and chemo and baroreception from the carotid body and carotid sinus.
Which nerves send afferents to his nucleus?
CN's VII, IX, X
Would you expect the cells of the solitary nucleus to show chromatolysis following axotomy of the vagus nerve?
No, anterograde degeneration because it contains neurons that respond to sensation.
13) What muscle group does the main motor nucleus of V innervate?
Muscles of mastication (pharyngeal arch 1)
14) For what two parasympathetic functions of the eye is the Edinger-Westphal nucleus responsible?
Pupillary constriction and contraction of the ciliary muscle.
15) What sensory and motor impairments might follow section of the Vth nerve?
Anesthesia of the face, scalp, oral cavity including the anterior 2/3 of the tongue, and nasal cavity for touch, pain and temperature.
16) If you had a lesion on one side of the base of the pons, where would you find orthograde fiber degeneration?
In the ipsilateral middle cerebellar peduncle because of damage to the trasnsverse pontine fibers; in the contralateral middle cerebellar peduncle because of damage to the pontinne nuclei; in the medullary pyramid; in addition if cranial nerve VIth or VIIth is damaged there will be degeneration in the periphery.
Answers for Brainstem Practical of 5/3/10
May 20th, 2010
Motor Systems Clinical Cases (from: Neuroscience lab manual)
Case 1
A 45 year old carpenter came to his physician with "a trembling right hand" ...
Answer: This lesion is in the lateral hemisphere of the posterior lobe of the cerebellum. [right side]
This lesion also includes the deep cerebellum nuclei, which is indicated by the presence of an intention tremor.
Case 2
A man was brought to the hospital after collapsing in the street...
Answer: This is a lesion that involves the posterior limb and genu of the internal capsule on the right side. The pathways damaged that result in the described deficits include
(1) corticospinal (paralysis, Babinski)
(2) corticoreticular (spasticity, increased deep tendon reflexes)
(3) corticobulbar (forehead wrinkled, but mouth drooped on left side) (4) thalamocortico (specifically from VP to parietal lobe).
Case 3
An elderly housewife went to her doctor complaining of involuntary movements in her right arm...
Answer: Hemiballism: This lesion is caused by damage to the subthalamic nucleus (left side).
Case 4
A 61 year old architect suddenly lost his ability to speak and within a few minutes he was unable to move his right arm...
Answer: This involves a lesion in the cortex on the left side. Specifically, motor and premotor cortex in the area to which the mouth and arm are somatotopically mapped. Sudden onset indicates a cerebrovascular accident or sudden trauma.
(1) Corticospinal (paralysis)
(2) Corticoreticular (spasticity)
(3) Corticobulbar (there is bilateral representation to upper part of facial motor nucleus which innervates upper 1/2 of face). Thus, forehead can wrinkle even if one side of cortex is damaged
May 20th, 2010
Motor Systems Review Question Answers
(Questions in Neuroscience Lab manual)
A. Spinal Cord
1 . Spasticity is an abnormality of muscle tone that results in a hyperactive stretch reflex.
a. Relax patient and apply a light stretch stimulus, e.g. tapping tendon with a percussing finger. If reflexes are hyperactive this is usually sufficient to induce it, therefore tendon reflexes are not normal.
b. With rapid passive displacement, resistance of muscle tone increases, then suddenly relaxes (clasp-knife phenomena).
c. Net overexcitation to reflex interneuron systems that in many cases influence gamma motor neurons.
d. Activating reciprocal inhibition systems via Ia muscle stretch to opposing muscle or Ib GTO reflexes with massage or vibration. Cutting the dorsal roots (deafferentation) removes the afferent limb of the stretch reflex. Administering intrathecal Baclofen (GABA agonist) to inhibit spinal reflexes can alleviate spasticity.
2. a. Clasp knife reflex describes the abrupt decrease in resistance to stretching of spastic muscles. As the resistance of a spastic muscle increases when passively stretched, the muscle will suddenly relax, correlated with a sudden loss of muscle tone.
b. Any injury that involves damage to the medullary reticulospinal pathway or its cortical control (i.e. corticoreticular) results in spasticity. Typically damage to the pyramidal system at a number of different levels causes spasticity since the LCST and corticoreticular are damaged concomitantly at rostral levels (e.g. internal capsule, basis peduncle) and at lower levels (e.g. spinal cord) the LCST and the MRST may be damaged concomitantly. Pure pyramidal lesions at the caudal medulla are the rare exception. At this level, all corticoreticular fibers have synapsed on MRST neurons and the MRST is traveling in the lateral medulla. A lesion here, therefore, that only damages LCST fibers, results in contralateral flaccid paralysis and a Babinski sign. Similarly, a small lesion in area 4 primary motor cortex, which gives rise to corticospinal but not corticoreticular fibers, results in contralateral flaccid paralysis of the area.
c. One mechanism for this may be subsequent to inhibitory impulses from the golgi tendon organs (protective mechanism prevents tearing of muscle) subsequent to stretch.
3. Rigidity is an increased muscle tone
a. In rigidity, tendon reflexes are normal or only slightly increased. In parkinsonism, rigidity is often termed cogwheel, indicating a ratcheting movement imposed on the rigid muscles. Rigidity affects all muscles equally and in all directions of movement. Spasticity is associated with the antigravity
muscles primarily. In spasticity, the resistance to stretch increases with increased stretch of the muscle. In rigidity, the increase is felt up to a certain point, but
then does not continue to increase.
b. overexcitation of alpha motor neurons
c. No. see #2 and #3a
d. Cut dorsal roots. If hypertonus is not diminished, assume rigidity is cause. Another way would be to inject a GABA agonist. Spasticity would be reduced, but not rigidity.
4. a. Descending pathways (CST, rubrospinal, lateral vestibulospinal and reticulospinal) and medial division afferents.
b. Descending pathways (reticulospinal primarily) and medial division afferents
5. Spastic paralysis occurs. Following a period of spinal shock the Babinski sign emerges (loss of CST) and myotactic reflexes are exaggerated (loss of reticulospinals). Transection removes all descending systems and therefore the drives to motor neurons responsible for alpha motor neuron activation in "alpha" rigidity are absent.
B. Brainstem
1. Parkinson's is an example of a disease that results in rigidity. Removal of control of vestibular systems (vermal lesion of cerebellum) can cause increased vestibular drive (e.g. the LVST) to alpha motor neurons causing rigidity.
Strokes that affect descending suppresser effects on muscle stretch result in spasticity.
2. a. Increased muscle tone, primarily in extensors (Decerebrate Posturing).
b. Net inhibition is removed, resulting in unopposed facilitation of gamma motor neurons (either directly or indirectly via interneurons). Antigravity muscles demonstrate increased muscle tone.
c. Cut dorsal or ventral roots - use Baclofen-.
C. Cerebellum
1. Clarke's nucleus, accessory cuneate nucleus, fastigial nucleus, inferior olive, medial and inferior vestibular nuclei, and lateral reticular nucleus and some processes of Purkinje cells to vestibular nuclei.
3. lesion of fastigial nucleus - diffuse and bilateral projections... muscle tone is increased (net loss of inhibition over vestibulospinal tract, loss of excitation of medullary RF), trunk and neck muscles affected resulting in an ataxic gait and foot slapping, hypertonia from vermal lesion.
lesion of dentate/interpositus nuclei - muscle tone is decreased (net loss of excitation to rubrospinal, and less directly via VL of thalamus and intralaminar (CM) to corticospinal), limbs primarily affected resulting in intention tremor, ataxia, dysmetria.
4. Overlapping, see diagrams in lab manual and handouts. Polysensory and polymodality (many parts of cortex project to the cerebellum)
D. Basal Ganglia
3. Tremor at rest, flexor rigidity, cogwheel rigidity, postural instability (marche a petit pas). Dystonia (flexed posture) occurs. Tremor is lost eventually "lead pipe" rigidity ensues.
E. Cortex
1. Precentral - lose CST therefore lose tactile reflexes and ability to fixate limbs and perform fractionated movements, but do have sensation. Gain Babinski reflex. Contralateral paralysis of body and contralateral lower quadrant facial paralysis. Increased muscle tone. VL projects here.
Postcentral - loss of light touch and position sense contralateral to lesion, reflexes increased, ataxia. VP projects here. Loss of stereognosis. (Area 1,2,3).
2. Compare the following lesions:
Premotor Cortex lesion
a) hemiparesis
b) hypertonia
c) increased and brisk DTRs,
d) grasp reflex
e) movement organization in limb (fingers and toes) forehead
Internal Capsule lesion (posterior limb)
a) hemiparesis
b) hypertonia (spasticity)
c) increased
d) Babinski and grasp
e) contralateral body (not involving head unless genu is involved)
may have contralateral hemianesthesia if thalamcocortico fibers from VPL/VPM are involved.
may have a contralateral hemianopsia if retrolenticular portion of posterior limb is involved.
Pyramid (small lesion of corticospinal fibers only)
a) hemiparesis
b) normal tone
c) normal
d) babinski and grasp
e) contralateral (not involving head)
Pyramid (large lesion of corticospinal and reticulospinal fibers)
a) hemiparesis
b) hypertonia (spasticity)
c) increased
d) babinski and grasp
e) contralateral (not involving head)
May 25th
Notes for Dr. Giszter's Motor Systems Review lecture and Dr. Cunningham's Aging and AD lecture are available on the Supplemental Handout section of our course website.
May 26th
Answers to Cortex Lab Manual Cases pp 80-81.
1. Contralateral neglect
2. Gertsmann's syndrome
3. Narcolepsy
May 28th
Dear Students,
There was another problem with the Scantron machine this afternoon. We were able to score and hopefully release the Practical, but it failed in the midst of the Written. It should be fixed by early next week and after the scores are available, the Neuro faculty will meet to determine the cut-offs.
We apologize for the delay and wish everyone a pleasant summer!
Page maintained by: F. M. Sessler