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B&B Part 1 > B&B Week 3 > Flashcards

B&B Week 3 Flashcards

1
Q

list the ascending tracts of the brainstem

A

anterolateral system (spinothalamic)

dorsal column medial lemniscus system

spinocerebellar tracts

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2
Q

list the descending tracts of the brainstem

A

corticospinal tract

corticobulbar tract

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3
Q

what are the pontine nuclei?

A

connections from the brainstem to the cerebellum

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4
Q

name the three intrinsic systems of the brainstem

A
  1. reticular formation
  2. neurotransmitter systems
  3. central pattern generators
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5
Q

list the general components of the brainstem

A
  1. ascending and descending tracts
  2. cranial nerve nuclei
  3. connections to the cerebellum/pontine nuclei
  4. intrinsic systems
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6
Q

where are the cranial nerve nuclei found?

A

brainstem

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7
Q

describe the general organization of the brainstem

A

motor fibers are derived from the basal plate, located medially

sensory fibers are derived from the alar plate, located laterally

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8
Q

what fibers are derived form the brainstem basal plate?

A

motor

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9
Q

what fibers are derived from the brainstem alar plate?

A

sensory

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10
Q

what gross structures make up the brainstem?

A

midbrain

pons

medulla

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11
Q

what is the otic capsule?

A

The otic capsule refers to the dense osseous labyrinth of the inner ear that surrounds the cochlea, the vestibule and the semicircular canals. It is surrounded by the less dense / pneumatised petrous apex and mastoid part of the temporal bone.

in the petrous portion of temporal bone

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12
Q

describe the components of the membranous labyrinth contained within the otic capsule

A

3 semicircular canals, 2 otoliths (utricle and saccule)

the semicircular canals detect angular accelerations, and head rotations (are arranged orthagonally to each other)

otoliths sense body orientation and linear motion (utricle is detects horizontal and saccule detects sagittal)

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13
Q

what is the function of the semicircular canals in the vestibular system?

A

the semicircular canals detect angular accelerations, and head rotations (are arranged orthagonally to each other)

each canal is sensitive to head rotations in the plane of that canal

together, the 3 canals can specify the direction and amplitude of any head rotation

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14
Q

what is the function of the otoliths in the vestibular system?

A

otoliths sense body orientation and linear motion (utricle is detects horizontal and saccule detects sagittal)

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15
Q

name and describe the composition of the labyrinth fluids found in the vestibular system

A
  1. perilymph–> found between bony and membranous labyrinth
    - is similar to extracellular fluid and CSF
    - ultrafiltrate of CSF or blood
    - low K+, high Na+
  2. endolymph–> found inside the membranous labyrinth lumen
    - unique extracellular fluid as it is more similar to intracellular fluid (high K+ and low Na+)
    - produced by DARK cells of the sensory epithelium
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16
Q

describe the vestibular sensory epithelium

A

contains HAIR CELLS, which are receptor cells for detecting movement of endolymph by projecting into labyrinth lumen

60-100 stereocilia and ONE kinocilium per hair cell

supporting cells are microvilli

tight junctions

terminals of the vestibulocochlear nerve (VIII)

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17
Q

name the two otoliths

A

utricle

saccule

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18
Q

what does the utricle do?

A

detects body position and horizontal linear motion

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19
Q

what does the saccule do?

A

detects body position and sagittal linear motion

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20
Q

describe the pathway of the vestibulocochlear nerve (CN VIII)

A

follows internal auditory meatus with facial nerve (VII)

enters brainstem at pontine-medullary junction/the cerebellopontine angle

projects to vestibular nuclear complex, cerebellum

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21
Q

what are the 4 major functions of the vestibular system?

A
  1. it is a sensory organ that detects BODY POSITION relative to gravity and the MOTION of the body in space and the motion of the body in space
  2. maintains equilibrium–> balance, postural stability
  3. motor output–> reflex and controlled motor movements
  4. vision–> control of head and eye motion, stabilization of visual gaze during head, body movement
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22
Q

name the 3 semicircular ducts

A

anterior

horizontal

posterior

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23
Q

what are the 5 vestibular sensory organs?

A

3 semicircular canals

2 otoliths

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24
Q

what are otoliths?

A

2 sac like organs between the semicircular canals and the cochlea

sense body orientation and linear motion

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25
Q

how does perilymph drain?

A

via venules and middle ear mucosa

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26
Q

how does endolymph drain?

A

absorbed by endolymphatic sac

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27
Q

what are the types of sensory epithelia in the vestibular system?

A

5:

the cristae of the semicircular canals (3)

the maculae of the utricle and saccule (2)

sensory epithelia contain hair cells which are sensory cells that detect movement of the endolymph

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28
Q

how many stereocilia are there per hair cell?

A

60-100

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29
Q

how many kinocilia are there per hair cell

A

1

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30
Q

what neurotransmitter is released from the stereocilia and kinocilia of the hair cells in the vestibular system?

A

glutamate

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31
Q

how many hair cells do the utricles and saccules have?

A

about 35 000 hair cells

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32
Q

how many hair cells are in the ampulla of the semicircular canals?

A

about 8000

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33
Q

what is particularly important about the hair cells?

A

they are the terminals of the vestibulocochlear nerve (CN VIII)

afferent fibers send output to CNS

bipolar cells with cell bodies in the vestibular ganglia

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34
Q

what are the ampullae of the vestibular system?

A

swellings at the end of the semicircular canals

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35
Q

what are the cristae of the vestibular system?

A

hair cell sensory epithelium within the ampullae

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36
Q

what is the cupula of the vestibular system?

A

acellular, gelatinous mass

hinged gate spanning the ampulla lumen

hair cell cilia embedded in the cupula project into the endolymph

ALL hair cells in the ampulla are oriented in the same direction, with the kinocilium closest to the utricle

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37
Q

describe the functional planes and pairings of the semicircular canals

A

arranged in three functional planes with right-left pairing

  1. right anterior // left posterior
  2. right posterior //left anterior
  3. right horizontal // left horizontal
    * pairs of cristae are arranged as mirror opposites
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38
Q

describe how the semicircular canals would detect a head turn to the left

A

turning of the head to the left causes fluid motion in the canals and a change in the axis of the hair cells

on the left, afferent fibers of CN VIII increase firing while the afferent fibers of the right side decrease firing

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39
Q

what is the otolithic membrane?

A

acellular gelatinous mass

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40
Q

what are otoconia?

A

calcium carbonate crystals that sit on top of the otolithic membrane

**pressure of otoconia deflects hair cell cilium

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41
Q

what is another name for the vestibular ganglion?

A

scarpa’s ganglion

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42
Q

where is the vestibular nuclear complex found?

A

in the dorsal pons and medulla beneath the 4th ventricle

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43
Q

list the vestibular nuclei

A
  1. lateral vestibular nucleus
  2. medial vestibular nucleus
  3. superior vestibular nucleus
  4. lateral vestibular nucleus
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44
Q

what is the function of the lateral vestibular nucleus in the vestibular nuclear complex?

A

aka Deiter’s nucleus

innervates gravity-opposing muscles of limbs to MAINTAIN POSTURE

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45
Q

what is the function of the medial vestibular nucleus in the vestibular nuclear complex?

A

reflex adjustment of the head and trunk muscles to restore head position after disturbance

stabilizes head in space

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46
Q

what is the function of the superior and medial vestibular nuclei in the vestibular nuclear complex?

A

eye movements

vestibulo-ocular reflex (VOR)

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47
Q

what is the function of the inferior vestibular nucleus in the vestibular nuclear complex?

A

integrates multi-sensory input and the cerebellum to regulate VOR gain

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48
Q

what are the inputs to the lateral vestibular nucleus?

A

utricle, saccule, semicircular canals

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49
Q

what is the pathway of the lateral vestibulospinal tract?

A

from the lateral vestibular nucleus

descends entire spinal cord

UNCROSSED (ipsilateral)

runs in the white matter in the anterior of the spinal cord (ventral horn)

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50
Q

what is the target of the lateral vestibulospinal tract?

A

ventral horn alpha and gamma motor neurons that innervate gravity opposing muscles of limbs

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51
Q

what is the input to the medial vestibular nucleus?

A

primarily the semicircular canals

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52
Q

what is the pathway of the medical vestibulospinal tract?

A

it becomes the descending medial longitudinal fasciculus (MLF)

it is bilateral (but the ipsilateral projection is more dense)

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53
Q

what is the target of the medical vestibulospinal tract?

A

cervical and upper thoracic spinal cord

motor neurons innervating the neck musculature

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54
Q

what vestibular nuclei are responsible for the VOR?

A

superior and medial

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55
Q

what is the function of the superior and medial vestibular nuclei (combined)? input?

A

VOR–> reflex to stabilize image in response to head turn

*input is semicircular canals

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56
Q

what is the pathway of the superior and medial vestibular nuclei/VOR fibres?

A

pathway is a 3 neuron arc

  1. bipolar neurons
  2. medial and superior vestibular nuclei
  3. motor neurons in the abducens nucleus (VI) and the oculomotor nuclei (III) that innervate oculomotor muscles
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57
Q

what muscles are coordinated by the horizontal VOR?

A

4 muscles:

left and right lateral recti

left and right medial recti

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58
Q

describe the basic neural mechanisms of the VOR based on a head turn to the right

A

if you turn your head to the right, but keep your eyes forward and want the image to be stable, your eyes need to remain pointing forwards

thus, if you turn your head to the right, the VOR causes excitatory signals to be sent to the lateral rectus muscle of the left eye and the medial rectus muscle of the right eye

the excitatory signal that goes to the lateral rectus of the left eye and the medial rectus of the right eye comes from the right semicircular canals, crossing over after the vestibular nucleus

at the same time, inhibitory signals are being sent to the lateral rectus of the right eye and the medial rectus of the left eye from the left semicircular canals

the excitatory and inhibitory signals synapse at the abducens nucleus and then at the oculomotor nucleus

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59
Q

what does the inferior vestibular nucleus do?

A

adjust the VOR

receives feedback from eyes and can then modulate the vestibular nerve to modulate the VOR

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60
Q

what is nystagmus?

A

rhythmic alteration of slow and fast eye movements during VOR

VOR –> slow

saccade–> fast

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61
Q

how can you induce a saccade?

A

by introducing warm or cold water to the ear canal

fast phase direction of the nystagmus: COWS

cold–opposite
warm–same

i.e if you introduce warm water to the right ear, the fast phase of the nystagmus will be towards the right (opposite for cold)

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62
Q

define benign paroxysmal positional vertigo (BPPV)

A

vestibular disorder

displaced otoconia lodged in the semicircular canals

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63
Q

define meniere’s disease (endolymphatic hydrops)

A

vestibular disorder

increased endolymph in the inner ear

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64
Q

define vestibular neuritis

A

vestibular disorder

viral infection of the vertibulo-cochlear nerve

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65
Q

define perilymph fistula

A

vestibular disorder

breach in the oval and/or round window

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66
Q

define ototoxicity

A

vestibular disorder

toxicity induced death of hair cells

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67
Q

define mal de debarquement

A

vestibular disorder

failure of CNS system plasticity to respond to prolonged movement

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68
Q

how do aging, dizziness and balance relate?

A

as we age we get visual and motor deficits, BPPV and gradual hair cell loss

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69
Q

when would you get bilateral vestibular dysfunction? how does it present?

A

occurs with toxicity–i.e aminoglycosides

slow onset of loss of vestibular function

instability of eyes with head movements

instability when walking in the dark (without visual input)

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70
Q

how does unilateral vestibular dysfunction present? what might cause it?

A

severe acute symptoms

extreme dizziness, nausea, vomiting

deviation towards the side of the lesion when walking

abnormal nystagmus

displaced otoconia, viral infection may cause it

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71
Q

how might the body adapt to unilateral vestibular dysfunction?

A

gradual recovery from unilateral lesions

learning induced changes to central circuits

vestibular inputs become ignored in favor of vision and proprioception

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72
Q

what can happen when there is a mismatch between vestibular and visual inputs?

A

dizziness

i.e rotation induced, optical illusions, motion sickness, alcohol (bed spins)

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73
Q

where do general somatic efferents (GSEs) go?

give examples of GSEs

A

to skeletal muscle

cranial nerves:
III
IV
VI
XII
XI
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74
Q

here do general visceral efferents go?

give examples of GVEs

A

these are the parasympathetics

cranial nerves:
III
VII
IX
X
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75
Q

where do special visceral efferents (SVEs) go?

give examples of SVEs

A

to skeletal muscle (pharyngeal arches)

cranial nerves:
V
VII
IX
X
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76
Q

what do general visceral afferents sense?

give examples of GVAs

A

visceral sensory

cranial nerves:
IX
X

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77
Q

what do special visceral afferents (SVAs) sense?

give examples of SVAs

A

taste

cranial nerves:
VII
IX
X

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78
Q

what do general somatic afferents (GSAs) sense?

give examples of GSAs

A

general sensory

cranial nerves:
V
IX
X

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79
Q

what so special somatic afferents (SSAs) sense?

give examples of SSAs

A

hearing and balance

cranial nerve VIII

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80
Q

how are the afferent and efferent nuclei generally arranged in the brain stem?

A

lateral (alar plate)–> from lateral towards the sulcus limitans
SSA–> GSA–> SVA–> GVA–> sulcus limitans

medial (basal plate)–> from sulcus limitans towards the midline
GVE–> SVE–> GSE

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81
Q

what nerve innervates the following extra-ocular muscles:

  1. superior rectus
  2. inferior rectus
  3. medial rectus
  4. inferior oblique
  5. superior oblique
  6. lateral rectus
A

1-4–> innervated by CN III (oculomotor)

5–> innervated by CN IV (trochlear)

6–> innervated by CN VI (abducens)

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82
Q

what nerve innervates the lateral rectus muscle of the eye?

A

CN VI (abducens)

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83
Q

what nerve innervated the superior oblique muscle of the eye?

A

CN IV (trochlear)

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84
Q

what nerve innervates the superior rectus muscle of the eye?

A

CN III (oculomotor)

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85
Q

what does the MLF do?

A

connects the abducens (VI) nucleus to the oculomotor nucleus (III)

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86
Q

define gaze

A

the coordinated, synergistic movement of both eyes to a target

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87
Q

define saccadic eye movements

A

rapid eye movements to redirect gaze to an object of importance, generated by the FRONTAL EYE FIELDS int he CORTEX

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88
Q

how do the pathways of the impulses that control reflexive saccades and volitional saccades differ?

A

REFLEXIVE saccades go through the superior coliculus

VOLITIONAL saccades BYPASS the superior colliculus

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89
Q

list and describe the types of volitional saccades

A
  1. anti-saccades –> away from stimulus
  2. predictive saccades–> towards where stimulus is expected to be
  3. memory saccades –> to where the stimulus was
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90
Q

define smooth pursuit

A

tracks a slowly moving object

keep object on fovea (the area of highest visual acuity)

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91
Q

what controls vertical gaze?

A

vertical gaze center

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92
Q

what is disconjugate gaze?

A

failure of eyes to turn together in the same direction

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93
Q

how do eyes converge? why?

A

eyes converge through adduction by both medial rectus muscles to focus on a NEAR object

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94
Q

how do eyes diverge? why?

A

eyes diverge through abduction by both lateral rectus muscles

this shifts the focus from the near object to a farther away object

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95
Q

how many layers make up the retina?

A

3

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96
Q

list the layers of the retina

A
  1. photoreceptors–rods (ro-sco-no) and far fewer cones (co-pho-co)
  2. bipolar cells–many rods to one bipolar, few cones to one bipolar
  3. retinal ganglion cells are designated as M cells or P cells
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97
Q

what is the nerve-chiasma tract of the visual system?

A

the optic nerve fibres from the nasal hemiretina cross over at the chiasma to the contralateral optic tract

optic nerve fibers from the temporal hemiretina do not cross over and reach the thalamus by the ipsilateral optic tract

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98
Q

describe the structure of the lateral genticulate nucleus (LGN) of the visual system, and state what types of cells are found there

A

2 lamina–> M cells from ipsilateral eye

most ventral:
#1 lamina --> M cells from the contralateral eye 
most dorsal:
#6 lamina--> P cells from contralateral eye
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99
Q

what are M cells?

A

ganglion cells of the visual system that generate APs

“magnocellular” cells

mostly rods tuned to movement

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100
Q

what are P cells?

A

ganglion cells of the visual system that generate APs

“parvocellular cells”

mostly cones tuned to fine detail

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101
Q

once the impulses from the optic nerve reach the LGN, what happens to them?

A

leaving the LGN, fibres fan out in a wide band to reach the visual cortex in the occipital lobe

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102
Q

where is the visual cortex?

A

in the occipital lobe

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103
Q

where is the LGN?

A

thalamus

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104
Q

what are optic radiations?

A

superior optic radiations are fibers that reach the visual cortex from above, via the PARIETAL lobe–> carry information from the INFERIOR retina

inferior optic radiations (Meyer’s) are fibres that reach teh visual cortex from below, via the TEMPORAL lobe–> carry information from the SUPERIOR retina

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105
Q

what is monocular scotoma?

A

loss of vision in the center of the visual field of one eye

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106
Q

what is the lesion behind monocular scotoma in the right eye?

A

damage to right retina, partial damage to right optic nerve

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107
Q

what is the lesion behind monocular vision loss in the right eye?

A

entire right retina or right optic nerve complete lesion

a lesion to the optic nerve of one eye will lead to loss of the complete visual field in that eye

the other eye can still perceive the entire visual field

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108
Q

what can cause the lesions that lead to monocular scotoma or monocular vision loss?

A

retinal infarct

hemorrhage

infection

trauma

glaucoma

schwannoma

elevated ICP

neuropathy

several diseases of the eye

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109
Q

what is bitemporal hemianopsia?

A

vision loss in the lateral/temporal fields of both eyes

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110
Q

what is the lesion that leads to bitemporal hemianopsia?

A

damage to OPTIC CHIASM (often not perfect symmetry)

a lesion to the optic chiasm leads to loss of the nasal retinal fibers from both eyes–> these nasal retinal fibers carry information about the temporal visual field and thus a lesion to the optic chiasm (where the nasal fibers cross) leads to the loss of the temporal visual field in both sides

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111
Q

what can cause the lesions (damage to the optic chiasm) that lead to bitemporal hemianopsia?

A

pituitary adenoma

lesions

meningioma

hypothalamic glioma

craniopharyngioma

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112
Q

what is contralateral homonymous hemianopia?

A

loss of the temporal visual field in one eye, and the nasal field in the other (i.e both right or both left visual fields are gone)

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113
Q

what is the lesion that leads to contralateral homonymous hemianopia?

A

lesion in the contralateral optic tract or LGN

i.e if both left visual fields were gone, lesion would be in the right optic tract or LGN/occipital lobe

a lesion to the optic tract will affect the nasal (crossed) fibres from the contralateral eye and the temporal fibres from the ipsilateral eye

these fibers carry information from the contralateral visual field

**in addition, a lesion of the entire primary visual cortex on one side will lead to the loss the contralateral visual field from both eyes

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114
Q

what can cause lesions to the optic tracts etc leading to contralateral homonymous hemianopia?

A

infarct

bleeding

tumour

demyelination

infection (i.e toxoplasmosis)

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115
Q

what is contralateral superior quadrantanopia?

A

loss of vision in the upper quadrant of the visual field in both eyes (i.e both upper left quadrants)

“pie in the sky”

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116
Q

what lesion causes contralateral superior quadrantanopia?

A

lesion of the contralateral temporal lobe, lower bank (meyer’s loop)

a lesion to the Meyer loop will affect the fibers from the upper portion of the contralateral visual field in both eyes

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117
Q

what causes the lesion (lesion of the contralateral temporal lobe) that causes contralateral superior quadrantanopia?

A

MCA inferior division infarct (“pie in the sky”), tumour, demyelination

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118
Q

what is contralateral inferior quadrantinopia?

A

loss of the lower quandrants on the same side of the visual field

“pie on the floor”

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119
Q

what lesion causes contralateral inferior quadrantinopia?

A

lesion of parietal lobe or upper bank of calcarine fissure

a partial lesion of the optic radiations before they are joined by fibres from meyers loop will affect fibres from the lower portion of the contralateral visual field from both eyes

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120
Q

what causes the lesion (lesion of parietal lobe or upper bank of calcarine fissure) that causes contralateral inferior quadrantinopia?

A

MCA superior division infarct, bleed, trauma, tumour

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121
Q

how do you test the functioning of the extraocular muscles?

A

H test

also tests all cranial nerves that innervate these muscles

NOTE: the H test does NOT test all the extraocular muscles, but it does test all the CRANIAL nerves that innervate these muscles

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122
Q

how does the H test test each cranial nerve that innervates the ocular muscles?

A
  1. the patient is asked to look laterally (i.e left)
  2. the left eye ABDUCTS through the action of the lateral rectus muscle innervated by CN VI
  3. abduction of the eye aligns the axis of the eyeball with the axis of the orbit and the muscles attaching to the tendinous ring
  4. when the eye is abducted, the patient is asked to look UP–> this tests the superior rectus, innervated by CN III

the action of the superior rectus can only be isolated when the patient has already abducted their eye

  1. patient is then asked to look to the right, ADDUCTING the eye being examined–> tests the medial rectus muscle (CN III)
  2. with the eye adducted, the patient is asked to look DOWN—> a downward movement will isolate the action of the superior oblique muscle (CN IV)

same movements are repeated for each eye

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123
Q

how do you isolate the function of the eye’s superior rectus muscle, clinically?

A

abduct the eye and then look up

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124
Q

how do you isolate the function of the eye’s superior oblique muscle, clinically?

A

adduct the eye, and then look down

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125
Q

what is the sensory innervation of the lacrimal gland?

A

sensory neurons from the lacrimal gland return to the CNS thru the lacrimal branch of the ophthalmic nerve (V1)

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126
Q

what is the secretomotor/parasympathetic innervation of the lacrimal gland?

A

secretomotor fibres from the parasympathetic part of the autonomic division of the PNS stimulate fluid secretion from the lacrimal gland

these preganglionic parasympathetic neurons leave the CNS in the FACIAL nerve (CN VII), enter the GREATER PETROSAL nerve (a branch of the facial nerve VII) and continue with the greater petrosal nerve until it becomes the nerve of the PTERYGOID CANAL

the nerve of the pterygoid canal then eventually enters the PTERYOPALATINE GANGLION where the preganglionic parasympathetic neurons synapse on postganglionic parasympathetic neurons

the postganglionic neurons join the MAXILLARY nerve (V2) and continue with it until the ZYGOMATIC nerve branches from it and travel with the zygomatic nerve until it gives off the ZYGOMATICOTEMPORAL nerve, which eventually distributes postganglionic parasympathetic fibers in a small branch that joins the lacrimal nerve

the lacrimal nerve passes to the lacrimal gland

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127
Q

what happens if the BBB is breaches by infectious diseases?

A

increased protein and water permeation–> edema, accumulation of inflammatory cells to inflammation sites and increased adhesion molecules (ICAM, VCAM)

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128
Q

list 4 of the major bacterial infections of the CNS

A
  1. bacterial meningitis
  2. brain abscess
  3. tuberculous meningitis
  4. syphilis
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129
Q

what happens in bacterial meningitis?

A

inflammatory reaction in SUBARACHNOID space with lots of PMNs and other WBCs

acute inflammation of walls of arteries and veins, may lead to INFARCT over several days

commonly see EPENDYMITIS (inflammation of ventricles)

persistent meningitis causes brain damage from vasculitis, brain infection, fibrosis in subarachnoid space, cranial nerve damage and obstruction of CSF space

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130
Q

what organisms commonly cause bacterial meningitis?

A

H. influenza

pneumococcus

meningococcus

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131
Q

how would you develop a brain abscess?

A

bacteria reach CNS via blood from an infection outside the CNS (i.e an ear infection)

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132
Q

what is the causative agent in tuberculous meningitis?

A

secondary to TB infection elsewhere in the body

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133
Q

what are the characteristics of tuberculous meningitis?

A

characterized by meningitis, vasculitis, cranial inflammation, tuberculomas

multinucleated giant cells are frequent

tubercles consist of central area of caseous necrosis with epithelioid cells and lymphocytes around

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134
Q

how does syphilis affect the brain? (i.e paretic vs. tabetic vs. meningovascular)

A

brain disease is a tertiary manifestation of the disease

paretic neurosyphillis–> progressive dementia and death; nerve cell destruction; microglia proliferation; WBC inflammatory response

tabetic neurosyphillis–> spinal and cranial nerves exclusively affected, especially lumbar region

meningovascular neurosyphillis–> vasculitis, chroic meningitis with lymphocytes, plasma cells

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135
Q

list 7 viruses that can cause CNS infection

A
  1. acute –> poliomyelitis or smallpox
  2. herpes simplex/zoster
  3. subacute sclerosing panencephalitis
  4. progressive multifocal leukoencephalopathy
  5. rubella
  6. cytomegalic inclusion disease
  7. HIV
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136
Q

how would poliomyelitis or smallpox affect the brain?

A

elicit inflammatory response

recovery is common

microglial and WBC response concentrated in the PERIVASCULAR spaces

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137
Q

how does herpes simplex/zoster affect the brain?

A

acute infection that is followed by recovery with relapses later in life

virus is not killed by the immune system and it lives on in the dorsal root ganglion (usually of CN V)

herpes encephalitis –> uncommon, acute, hemorrhagic, necrotizing, usually fatal

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138
Q

what cranial nerve root often harbours herpes virus?

A

CN V

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139
Q

what is subacute sclerosing panencephalitis?

A

a rare, chronic destructive disease of the brain

caused by MEASLES

WBC response with intranuclear viral inclusions

microglial proliferation

140
Q

what is the causative agent behind subacute sclerosing panencephalitis?

A

measles

141
Q

what is progressive multifocal leukencephalopathy and how does it affect the brain?

A

mainly seen in IMMUNOCOMPROMISED patients

patchy destruction of gray and white matter with some demyelination, astrocytes are formed

caused by JC virus

142
Q

what is the causative agent behind progressive multifocal leukencephalopathy?

A

JC virus

143
Q

how does rubella affect the brain?

A

rubella is often a mild disease unless onset in the fetus

meningoencephalitis with WBC response and continued brain destruction

infests endothelial cells leading to vascular damage and ischemia in developing brain

144
Q

how does cytomegalic inclusion disease affect the brain?

A

usually only in IMMUNOCOMPROMISED

brain malformation, multiple gyri with distorted architecture and calcific deposits in ependyma

145
Q

how does HIV affect the brain?

A

encephalitis and HIV-associated dementia complex are common complications of the disease

146
Q

list two fungal infections that can affect the brain

A
  1. mucormycosis

2. cryptococcosis

147
Q

how does mucormycosis affect the brain?

A

propagates in blood vessel walls, leading to thrombosis

148
Q

how does cryptococcosis affect the brain?

A

granulomatous reaction with giant cells–> may have no inflammation–> widely disseminated

149
Q

name two inflammatory diseases of the CNS

A

MS

primary CNS angiitis

150
Q

name a class of transmissible CNS diseases

A

prion diseases

i.e creutzfeldt-jacob

151
Q

what is creutzfeldt-jacob disease and how does it affect the brain?

A

prion disease

no immune response, no inclusion bodies, incubation can be very long

prions are normal cell membrane proteins found in nerve cells

conformational changes convert normal prions into pathological ones

accumulation of mutant prions causes neuropathology

progressive destruction of brain with loss of function, vegetative state and death

152
Q

what is the corona radiata?

A

sheet of white matter that continues caudally to become the internal capsule

153
Q

what does the corticobulbar tract arise from? what is its pathway?

A

corticobulbar tract arises primarily from areas of the motor cortex related to the HEAD and FACE and descends through the corona radiata

fibers converge in the genu of the internal capsule from where they then descend together with corticospinal fibers

154
Q

where do the corticobulbar fibers terminate?

A

motor nuclei of the brainstem

155
Q

what is the internal capsule?

A

The internal capsule is a white matter structure situated in the inferomedial part of each cerebral hemisphere of the brain. It carries information past the basal ganglia, separating the caudate nucleus and the thalamus from the putamen and the globus pallidus.

156
Q

what is the nucleus ambiguus?

A

cell bodies of IX, X, XI (cranial root)

receives bilateral innervation

The nucleus ambiguus (literally “ambiguous nucleus”) is a group of large motor neurons, situated deep in the medullary reticular formation. The nucleus ambiguus contains the cell bodies of nerves that innervate the muscles of the soft palate, pharynx, and larynx which are strongly associated with speech and swallowing.

It is a region of histologically disparate cells located just dorsal (posterior) to the inferior olivary nucleus in the lateral portion of the upper (rostral) medulla. It receives upper motor neuron innervation directly via the corticobulbar tract.

The nucleus ambiguus controls the motor innervation of ipsilateral muscles of the soft palate, pharynx, larynx and upper esophagus. Lesions of nucleus ambiguus results in nasal speech, dysphagia, dysphonia, and deviation of the uvula toward the contralateral side.

157
Q

what is the trigeminal motor nucleus responsible for?

A

The trigeminal motor nucleus contains motor neurons that innervate muscles of the first branchial arch, namely the muscles of mastication, the tensor tympani, tensor veli palatini, mylohyoid, and anterior belly of the digastric. This nucleus is located in the mid-pons (i.e. in the center of the pons going inferior to superior)

receives bilateral innervation

158
Q

what is the spinal accessory nucleus (IX) responsible for?

A

receives IPSILATERAL projecttions for the sternomastoid

mostly CONTRALATERAL projections for the trapezius

159
Q

where does the spinal accessory nucleus lie?

A

in the cervical spinal cord

160
Q

what is the function of the hypoglossal nucleus?

A

ipsilateral tongue muscle control (XII)

receives bilateral projections but crosses to genioglossus

161
Q

what is unique about the innervation to the facial motor nucleus (VII)?

A

there is bilateral innervation to the rostral part of the nucleus –> control UPPER face muscles

contralateral innervation to the caudal part of the nucleus–> controls LOWER face muscles

162
Q

what cranial nerve nuclei does the corticobulbar tract innervate?

A

motor nucleus of V

motor nucleus of VII

nucleus ambiguus (IX, X, XI)

hypoglossal nucleus

spinal accessory nucleus

163
Q

where in the motor cortex does the corticobulbar tract originate from?

A

precentral gyrus

164
Q

describe the innervation from the corticobulbar tract to the motor nucleus of V

A

bilateral

165
Q

describe the innervation from the corticobulbar tract to the motor nucleus of VII

A

bilateral for upper face

crossed (contralateral) for lower face –> ie innervation to upper face comes from both sides but innervation to lower face comes from the contralateral side

166
Q

describe the innervation from the corticobulbar tract to the nucleus ambiguus (IX, X, XI)

A

all bilateral, except crossed to UVULA

167
Q

what is the genioglossus?

A

muscle that runs from chin to tongue–> responsible for action of sticking out your tongue

168
Q

describe the innervation from the corticobulbar tract to the hypoglossal nucleus (XII)

A

all bilateral except crossed to GENIOGLOSSUS

169
Q

describe the innervation from the corticobulbar tract to the spinal accessory nucleus (XI)

A

ipsilateral to sternocleidomastoid

contralateral to trapezius

170
Q

what cranial nerves carry the GSA modality

A

V

IX

X

171
Q

what cranial nerves carry the SSA modality

A

VIII

172
Q

what cranial nerves carry the SVA modality

A

VII

IX

X

173
Q

what cranial nerves carry the GVA modality

A

IX

X

174
Q

what cranial nerves carry the GVE modality

A

III

VII

IX

X

175
Q

what cranial nerves carry the SVE modality

A

V

VII

IX

X

176
Q

what cranial nerves carry theGSE modality

A

III

IV

VI

XII

XI

177
Q

what modalities does the following cranial nerve carry?

III

A

GVE and GSE

178
Q

what modalities does the following cranial nerve carry?

IV

A

GSE

179
Q

what modalities does the following cranial nerve carry?

V

A

GSA and SVE

180
Q

what modalities does the following cranial nerve carry?

VI

A

GSE

181
Q

what modalities does the following cranial nerve carry?

VII

A

SVA, GVE, and SVE

182
Q

what modalities does the following cranial nerve carry?

VIII

A

SSA

183
Q

what modalities does the following cranial nerve carry?

IX

A

GSA, SVA, GVA, GVE, SVE

184
Q

what modalities does the following cranial nerve carry?

X

A

GSA, SVA, GVA, GVE, SVE

185
Q

what modalities does the following cranial nerve carry?

XII

A

GSE

186
Q

what modalities does the following cranial nerve carry?

XI

A

GSE

187
Q

name the following cranial nerve and state what it does

I

A

olfactory

The functional components of the olfactory nerve include SVA, special visceral afferent, which carries the modality of smell.

contains the afferent nerve fibers of the olfactory receptor neurons, transmitting nerve impulses about odors to the central nervous system

188
Q

name the following cranial nerve and state what it does

II

A

optic

paired nerve that transmits visual information from the retina to the brain

189
Q

name the following cranial nerve and state what it does

III

A

oculomotor

innervates 4/6 eye muscles

enters the orbit via the superior orbital fissure and innervates muscles that enable most movements of the eye and that raise the eyelid

contains fibers that innervate the muscles that enable pupillary constriction and accommodation (ability to focus on near objects as in reading)

190
Q

name the following cranial nerve and state what it does

IV

A

trochlear

motor nerve (a somatic efferent nerve) that innervates only a single muscle: the superior oblique muscle of the eye, which operates through the pulley-like trochlea…on the opposite side (contralateral) from its origin

191
Q

name the following cranial nerve and state what it does

V

A

trigeminal

nerve responsible for sensation in the face and motor functions such as biting and chewing

each trigeminal nerve (one on each side of the pons) has three major branches: the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3)

192
Q

name the following cranial nerve and state what it does

VI

A

abducens

is a somatic efferent nerve that, in humans, controls the movement of a single muscle, the lateral rectus muscle of the eye.

The abducens nerve carries axons of type GSE, general somatic efferent, which innervate skeletal muscle of the lateral rectus

193
Q

name the following cranial nerve and state what it does

VII

A

facial

controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue and oral cavity. It also supplies preganglionic parasympathetic fibers to several head and neck ganglia.

194
Q

name the following cranial nerve and state what it does

VIII

A

vestibulocochlear

transmits sound and equilibrium (balance) information from the inner ear to the brain

consists of the cochlear nerve, carrying information about hearing, and the vestibular nerve, carrying information about balance

The vestibulocochlear nerve carries axons of type SSA, special somatic afferent, which carry the modalities of hearing and equilibrium

195
Q

name the following cranial nerve and state what it does

IX

A

glossopharyngeal

mixed nerve that carries afferent sensory and efferent motor information

It receives general somatic sensory fibers (ventral trigeminothalamic tract) from the tonsils, the pharynx, the middle ear and the posterior 1/3 of the tongue.

It receives special visceral sensory fibers (taste) from the posterior one-third of the tongue.

It receives visceral sensory fibers from the carotid bodies, carotid sinus.

It supplies parasympathetic fibers to the parotid gland via the otic ganglion.

It supplies motor fibers to stylopharyngeus muscle, the only motor component of this cranial nerve.

It contributes to the pharyngeal plexus.

196
Q

name the following cranial nerve and state what it does

X

A

vagus

vagus nerve supplies motor parasympathetic fibers to all the organs except the suprarenal (adrenal) glands, from the neck down to the second segment of the transverse colon. The vagus also controls a few skeletal muscles

197
Q

name the following cranial nerve and state what it does

XI

A

spinal accessory

controls the sternocleidomastoid and trapezius muscles

198
Q

name the following cranial nerve and state what it does

XII

A

hypoglossal

innervates muscles of the tongue

199
Q

name the branches of the trigeminal nerve

A

V1–ophthalmic nerve

V2–maxillary nerve

V3–mandibular nerve

200
Q

what does the oculomotor nucleus (III) innervate?

A

somatic motor to inferior, superior and medial rectus muscles of the eye, and to the inferior oblique muscle of the eye as well as the levator palpebrae superioris

visceral motor to the ciliary and constrictor papillae muscles (parasympathetic)

201
Q

where is the main oculomotor nucleus located?

A

rostral midbrain

in anterior part of the periaqueductal gray

efferent fibers pass anteriorly through the red nucleus and emerge from the midbrain in the interpeduncular fossa on the medial surface of the cerebral peduncle

202
Q

where is the parasympathetic nucleus (edinger-westphal nucleus) of the oculomotor nucleus found?

A

located posterior to the main oculomotor nucleus in the periaqueductal gray

efferent fibers run with other oculomotor fibres and synapse in the ciliary ganglion

203
Q

what does the trochlear nucleus innervate?

A

CN IV

somatic motor to the superior oblique muscle

204
Q

where is the trochlear (IV) nucleus located?

A

caudal midbrain, in anterior part of periaqueductal gray

efferent fibres pass POSTERIORLY around the central gray

fibers decussate in superior medullary velum and emerge caudal to the inferior colliculus

this is the ONLY cranial nerve to emerge from the POSTERIOR aspect of the brainstem

205
Q

what does the abducens nucleus (VI) innervate?

A

somatic motor to the lateral rectus muscle

206
Q

where is the abducens nucleus (VI) located?

A

posterior part of the caudal pons, beneath the floor of the 4th ventricle, near the midline

efferent fibers pass ANTERIORLY through the pons and emerge in the pontomedullary junction

207
Q

through what fissure does the abducens nerve run?

A

superior orbital fissure

208
Q

what innervates the following muscle and what does the muscle do?

levator palpebrae muscle

A

superior branch of oculomotor nerve (CN III)

elevation of upper eyelid

209
Q

what innervates the following muscle and what does the muscle do?

medial rectus muscle

A

inferior branch of oculomotor nerve (CN III)

adduction of eyeball

210
Q

what innervates the following muscle and what does the muscle do?

lateral rectus muscle

A

abducens nerve (CN VI)

abduction of eyeball

211
Q

what innervates the following muscle and what does the muscle do?

superior rectus muscle

A

superior branch of oculomotor nerve (CN III)

elevation, adduction, medial rotation of the eyeball

212
Q

what innervates the following muscle and what does the muscle do?

inferior rectus muscle

A

inferior branch of oculomotor nerve (CN III)

depression, adduction and lateral rotation of the eyeball

213
Q

what innervates the following muscle and what does the muscle do?

inferior oblique muscle

A

lower division of oculomotor nerve (CN III)

elevation, abduction, lateral rotation of eyeball

214
Q

what innervates the following muscle and what does the muscle do?

superior oblique muscle

A

trochlear nerve (CN IV)

depression when eye is in adduction

medial rotation of eyeball (intorsion) when eye is abducted

215
Q

list the major nerve of the orbit

A

CN II–optic

CN V1–frontal + branches and nasociliary + branches

CN III–oculomotor

CN IV–trochlear

CN VI–abducens

216
Q

what are the two major branches of V1 in the orbit?

A

frontal nerve and nasociliary nerve

217
Q

what are the branches of the frontal nerve (branch of V1) in the orbit and what do they do?

A
  1. supratrochlear nerve–> conjunctiva, eyelid, lower medial forehead
  2. supraorbital nerve–> conjunctiva, eyelid, forehead (can extend all the way to mid-scalp
218
Q

what are the branches of the nasociliary nerve (branch of V1) in the orbit and what do they do?

A
  1. long ciliary nerve–> carries afferent info from eyeball
  2. short ciliary nerve–> carry parasympathetic innervation for CN III (sphincter pupillae muscle and ciliary muscle)
  3. anterior ethmoidal nerve–> sensory from anterior cranial fossa, nasal cavity, skin of lower half of nose
  4. infratrochlear nerve–> sensory from eyelids, lacrimal sac, skin of upper half of nose
219
Q

what type of pathway is the dorsal column medial lemniscus pathway?

A

ascending

220
Q

what kind of information is transmitted by the dorsal column medial lemniscus pathway?

A

role in discriminative touch, vibration, pressure, conscious proprioception

221
Q

what kind of deficits would arise in response to a lesion in the dorsal column medial lemniscus pathway?

A

if in spinal cord, would result in deficits in discriminative touch, vibration, pressure or conscious proprioception on the IPSILATERAL side of the lesion

if it is in the caudal medulla, (i.e nucleus gracilis or cuneatus) or above,, deficits will be on the CONTRALATERAL side

222
Q

what is a “pyramidal pattern of weakness”?

A

results from UMN lesions

the pattern results in the flexors of the upper limbs being stronger (more spastic) than the extensors, and the opposite (extensors being stronger than the flexors) in the lower limb

WYSIWIS–> “what you see is what is strong”

so you see people with this pattern of symptoms with their arms flexed against their chests and their legs “too long” (ie straight with foot plantar flexed) which affects their gate

223
Q

what is the Romberg test?

A

test used in a neuro exam and also as a test for drunk driving

exam based on the premise that a person requires at least two of the three following senses to maintain balance while standing:

  • proprioception (body position in space)
  • vestibular function (one’s head position in space)
  • vision (can be used to monitor and adjust for changes in body position)
224
Q

what senses do you need to maintain balance?

A

2/3:

  • proprioception (body position in space)
  • vestibular function (one’s head position in space)
  • vision (can be used to monitor and adjust for changes in body position)
225
Q

how do you perform the romberg test?

A

ask subject to stand erect with feet together and eyes closed

stand close by as a precaution in order to stop the person from falling

watch the movement of the body in relation to a perpendicular object behind the subject (i.e door)

a positive romberg sign is noted when a swaying, sometimes irregular swaying and even a toppling over occurs

essential feature is the patient becomes unsteady with eyes closed

226
Q

how do you interpret the romberg test?

A

used to investigate the loss of motor coordination (ataxia)

a positive romberg test suggests that the ataxia is SENSORY in nature (i.e loss of proprioception in pathologies affecting the PCML or peripheral sensory neurons)

this is NOT a test of cerebellar function–> patients with cerebellar ataxis will generally be unable to balance even with eyes open

227
Q

why must the eyes be closed in the romberg test?

A

basis of test is that balance come from the combination of several neuro systems, namely proprioception, vestibular input, and vision

if any two of these systems are working the person should be able to demonstrate a fair degree of balance

the key to the test is that vision is taken away by asking the patient to close their eyes

this leaves only two of the three systems available and if there is either a vestibular or sensory/proprioception disorder then the patient will become much more imbalanced

228
Q

where is the optic disc located?

A

region of the eye where axons of the ganglion cell layer gathers to form the optic nerve

lies 15 degrees medial (nasal) to the fovea

*it is also the entry point for the central artery and vein–supply and drain the inner retina

229
Q

why is there a blind spot on the optic disc?

A

there are no photoreceptors (rods or cones) over the optic disc and thus it is a blind spot for each eye (15 degrees lateral and slightly inferior to the central fixation point for each eye)

230
Q

what is the swinging light test?

A

shows abnormal light response of the affected eye (initial dilation followed by restriction)

i.e if the left eye were abnormal, both pupils constrict when the light is shown into the right eye but when the light is swung to the left eye, both pupils dilate–> when the light is swung back to the right, both pupils again constrict

this reaction indicates a defect in the afferent pupillary fibers from the left eye(the near reflex is normal)

231
Q

what is marcus gunn pupil?

A

relative afferent pupillary defect

medical sign noted during the swinging light test

most common of marcus gunn pupil is a lesion of the optic nerve proximal to the optic chiasm or severe retinal disease

232
Q

how do you do the swinging light test?

A

for an adequate test, vision must not be entirely lost

in dim room light, the examiner notes the size of the pupils

patient asked to gaze into the distance, and the examiner swings a beam of a penlight back and forth from one pupil to another and observes the size of pupils and reaction in the eye that is lit

233
Q

how do you interpret the swinging light test?

A

normally, each illuminated eye looks or promptly becomes constricted with the opposite eye constricting consensually

when ocular disease (cataracts) impairs vision, the pupils still respond normally

when the optic nerve is damaged, the sensory stimulus sent to the midbrain is reduced and thus the pupil, responding less vigorously to the stimulus, dilates from its prior constricted state

this response is an afferent pupillary defect (marcus gunn pupil)

234
Q

why do we use the swinging light test?

A

allows the examiner to observe the relative defect in an eye by using the normal eye as a control

235
Q

what is conjugate gaze?

A

motion of both eyes in the same direction at the same time

236
Q

how are saccadic eye movements controlled to allow for conjugate gaze?

A

ascending MLF connects CN VI on one side with CN III on the opposite side –> driven by the PPRF area in the pons

the ipsilateral visual field–> contralateral frontal eye field in the cortex (area 8)–> stimulate PPRF–> activate ipsilateral VI nucleus and ipsilateral lateral rectus–> MLF contralateral–> contralateral CN III nucleus and contralateral medial rectus

237
Q

how are pursuit eye movements controlled to allow for conjugate gaze?

A

stabilizes image on fovea during slow movement of object or during locomotion

input from primary visual cortex, frontal eye fields in cortex, cerebellum, and vestibular nuclei to relay center in CN VI–> results in coordinated movements by connecting VI and III

238
Q

how is the VOR controlled to allow for conjugate gaze?

A

adjust eye movements to head movements–image stable on retina

if head rotates to the right, endolymph flows in the opposite direction–> project to ipsilateral vestibular nuclei–> contralateral CN VI nucleus AND ipsilateral CN III–> eyes move to right

239
Q

what is nystagmus?

A

rapid back and forth rhythmic eye movements

rapid component (flick) in one direction and slow component in the opposite

named for the RAPID component (i.e L nystagmus is rapid to the left)

240
Q

what can cause physiological nystagmus?

A

physiologically by stimulation of the vestibular system or by visual stimuli

241
Q

what causes physiological vestibular nystagmus?

A

when head rotation is greater than what can be compensated for by the VOR, the eyes reset with a rapid movement in the same direction as rotation, and then the compensatory movement of the VOR can happen again

the VOR usually moves the eyes opposite to the movement of the head to maintain fixation on the visual stimulus or object–> ie if head moves left, eyes move right, vision stays straight ahead

if you move your head too far to the left then you will get eyes slowly moving right as part of VOR, then the rapid movement will be the “reset” to the left–> nystagmus

242
Q

how does a rapidly moving object cause nystagmus?

A

as the eyes follow the moving object in the field of view then rapidly shift focus to the next object in the field of view (i.e tracking a train as it moves by, passing rapidly by power poles as you look out the window of a car)

243
Q

list 5 mechanisms/problems that can result in a disruption of horizontal conjugate gaze that can lead to double vision

A
  1. right abducens nerve palsy
  2. right abducens nucleus damage
  3. right PPRF problem
  4. left MLF damage (INO)
  5. left MLK and left abducens nucleus damage
244
Q

how would the following problem disrupt horizontal conjugate gaze and cause double vision?

right abducens nerve palsy

A

no transmission thru to the right eye, therefore cannot abduct the right eye

245
Q

how would the following problem disrupt horizontal conjugate gaze and cause double vision?

right abducens nucleus damage

A

the nucleus synapse is dysfunctional therefore right eye cannot abduct and left eye cannot adduct (because this nucleus tell the contralateral eye when it needs to adduct along with the ipsilateral side abducting)

246
Q

how would the following problem disrupt horizontal conjugate gaze and cause double vision?

right PPRF problem

A

results in the same dysfunction as the right abducens nucleus damage

right eye cannot abduct and left eye cannot adduct

247
Q

the nucleus synapse is dysfunctional therefore right eye cannot abduct and left eye cannot adduct

left MLF damage (INO)

A

cannot adduct the left eye

nystagmus is also produced in the right eye as it abducts–> theory is that maybe the left eye feels it needs to adduct, and the only other way to do this is through disconjugate conversion of both eyes–> causes right eye to experience nystagmus

248
Q

the nucleus synapse is dysfunctional therefore right eye cannot abduct and left eye cannot adduct

left MLF and left abducens nucleus damage

A

same situation as with left MLF damage except now the eyes cannot deviate to the left when attempting to look at something in the left visual field

249
Q

what is the medial longitudinal fasciculus? (MLF)

A

fibre tract that interconnects CN III, IV and VI nuclei to each other and to the vestibular nuclei, thus allowing synergistic or coordinated movements of the two eyes and adjustments of eye position in response to movements of the head

facilitates conjugate gaze

250
Q

where does the MLF originate from?

A

originates from the vestibular nuclei in the ROSTRAL MEDULLA/CAUDAL PONS and has both descending and ascending components

251
Q

describe the pathway and function of the ascending part of the MLF

A

arises from the medial vestibular nuclei, with some input from the superior vestibular nuclei

responsible for the coordination and synchronization of all major classes of eye movements

appears as a small pair of heavily myelinated tracts near the midline, just anterior to the 4th ventricle in the medulla and pons and anterior to the cerebellar aqueduct in the midbrain

252
Q

what is internuclear ophthalmoplagia? (INO)

A

lesion of the MLF which interrupts the input to the MEDIAL RECTUS muscle

the eye ipsilateral to the lesion does not fully adduct on attempted horizontal gaze

the eye contralateral to the lesion experiences nystagmus, possible because of mechanisms trying to bring the eyes back into alignment (towards the midline)

  • the side of the INO is the side with the lesion
  • -> since the ascending MLF crossed almost immediately after leaving the abducens nucleus, the side of the INO is also the side on which the eye adduction is weak (i.e the lesion would never occur before the nerve crosses)
253
Q

why is the eye with the impairment with adduction with horizontal gaze (in INO) usually spared during convergence?

A

efferent signal for this travels in a tract separate from the ascending MLF

254
Q

what are some common causes of INO?

A

MS

pontine infarcts

neoplasms involving the MLF

255
Q

list peripheral causes of diplopia

A

extraocular muscle damage

lens abnormalities (cataracts, opacities, following lens implant, problems with implant)

256
Q

list central causes of diplopia

A

cranial nerve dysfunction (CN III/IV/VI)

myasthenia gravis

disorders of the neuromuscular junction between the cranial nerves and the extraocular muscles

retinal dysfunction (detachment, central retinal venous occlusion)

INO

257
Q

what does it indicate if the diplopia is persistent with one eye covered?

A

this is monocular diplopia stemming from intrinsic eye problems (corneal abrasions, uncorrected refractive error, cataract, foveal traction)

258
Q

what does it indicate if the diplopia disappears with one eye covered?

A

this is binocular diplopia caused by disruption of ocular alignment

259
Q

how is MS diagnosed?

A

mostly a CLINICAL diagnosis

clinical evidence of lesions in the CNS that are DISSEMINATED in TIME and SPACE

diagnosis cannot be made unless evidence of TWO or MORE different regions in central white matter have been affected at different times

260
Q

what are some clinical symptoms of MS used in diagnosis?

A

clinical symptoms vary widely, depending on where the pathology occurs in the CNS

  1. motor–> weakness, spasticity, brisk reflexes
  2. sensory deficits, cerebellar (ataxia, tremor, nystagmus, dysarthria)
  3. cranial nerve/brainstem (i.e vision, ocular disturbance)
  4. autonomic (bowel, bladder, sexual)
  5. psychiatric (depression, euphoria, cognitive)
  6. fatigue
261
Q

what imaging is used in the diagnosis of MS?

A

T1 weighted images (fat is bright)–> show hypointense black holes which are areas of permanent axonal damage

T2 weighted images (water is white)–> bright areas which are demyelinated plaques located in white matter

262
Q

what lab tests can be done to help diagnose MS?

A

oligoclonal bands in CSF

these arise from the synthesis of large amounts of homogenous immunoglobins by individual plasma cell clones in CSF

sensitivity –80%
specificity– 92%

263
Q

how good are MRIs at helping to diagnose MS?

A

highly sensitive, with abnormalities detected in 90% of MS patients

detects clinically silent AND overt lesions

BUT many infectious, inflammatory, neoplastic and ischemic illnesses can present with T2 weighted abnormalities as well

can be used to monitor disease activity more than clinical exam

264
Q

how helpful are CSF tests in diagnosing MS?

A

may help to exclude neoplasm and infection (thus is complementary to MRI)

abnormal findings in 85-95% of patients with MS, but may be normal in early stages

look for: abnormal oligoclonal banding, abnormal leukocytic pleocytosis (elevated CNS leukocytes with lymphocytic predominance)

good specificity but not perfect–> infections and inflammatory processes may have similar findings in CSF)

265
Q

how helpful are evoked potential tests in diagnosing MS?

A

brain electrical responses to visual, auditory and somatosensory stimuli are recorded and time averaged by neurologist

evaluates multiple areas of CNS

abnormal tests correlate with CNS demyelination, which is sensitive but not specific for MS

266
Q

what are the lesions associated with MS? how do they occur? what do they do?

A

plaques generate in the nervous system

majority of lesions are in the white area near the cerebellum, the spinal cord, the brain stem and the optic nerve

when MS lesions are present, neurons cannot transmit impulses efficiently –> the disease destroys the myelin covering the nervous systems fibers –> results in diminishing or complete disappearance of myelin

a partial restorative process (remyelination) occurs at thea early stages of the disease but as the cells myelin cover cannot completely be rebuilt and there is continued attack against the myelin this leads to fewer successful remyelinations and thus the formation of lesions

267
Q

what role do T cells play in MS pathology?

A

in MS T cells infiltrate into the brain via the BBB which is both a physical barrier and a system of cellular transport

this barrier is not normally accessible to T cells unless the CNS is affected by a virus which reduces the strength of the junctions that form the barrier

T cells then remain locked in the brain, wrongly perceiving myelin as an alien agent and attacking it as if it were a virus

this generates an inflammatory process and further damages the CNS via swelling and activation of other immune cells and antibodies

268
Q

what is the etiology of MS?

A

MS is a demyelinating, autoimmune disease which affects the CNS

research seems to implicate a small or incomplete slow-growing virus as the causative agent

the measles virus has been suspected because of high titers of measles antibodies in MS patients serum and CSF

an immunological deficiency in MS patients may be linked to genetic factors such as HLA tissues types and histocompatability antigens

genetics and socioeconomic conditions may also result in the distinct geographical pattern of MS distribution globally

269
Q

describe the course of MS

A

MS is a PROGRESSIVE autoimmune disease characterized by the presence of acute, focal inflammatory demyelination

generally occurs in the second and third decades of life and it affects women more than men (3:2)

course is unpredictable and induces a wide spectrum of symptoms as lesions can occur anywhere in the CNS

commonly affected sites include the optic nerve, periventricular areas, corpus callosum, brainstem and spinal cord

however, there are still a number of common patterns of initial presentation

270
Q

what are some commonly affected areas in MS?

A

optic nerve, periventricular areas, corpus callosum, brainstem and spinal cord

271
Q

what is l’hermitte’s symptom?

A

sensation of electric shock down the back and limbs upon neck flexion

can occur in MS

272
Q

what is uhthoff’s phenomenon?

A

increased symptoms due to heat (i.e after a hot bath or exercise), altering the conduction of nerves

can occur in MS

273
Q

what is ephatic transmission?

A

transmission of charge between neighboring axons resulting in paroxysmal symptoms

can occur in MS

274
Q

what is the prognosis of MS?

A

there are 3 general types of MS

80% of people affected initially present with a relapsing/remitting form–> women more than men–> many of these patient experience phases of relapse followed by full recovery until they can no longer recover from relapses (this is secondary progression)

20% of people affected experience primary progression–> there are no relapses and the disease progresses from the onset

25% of patients never experience significant adverse effects upon their daily activities, while another 15% are significantly disabled

275
Q

what is usually the cause of death in a patient with MS?

A

most patients die from other reasons and lire expectancy is about 25-30 years after disease onset

276
Q

what are the 4 major aims of medical tx for MS?

A
  1. reduce relapse rates
  2. prevent permanent disability
  3. manage permanent disability
  4. prevent disability due to progressive disease
277
Q

what are some non-medical aspects to MS tx?

A

people with MS generally require patient education and counseling

may benefit from physio, support groups, OT, social work, nutrition counseling and other supports

278
Q

list disease suppressing agents that can help reduce relapse rates in patients with MS

A

beta interferons

beta 1b–> betaseron can decrease relapse rate and progressive disease

beta 1a–> avonex can decrease relapse rates

copolymer can also decrease relapse rates

279
Q

what is used to prevent disability in patients with MS (i.e acute tx during relapse)?

A

corticosteroids–> given as IV methyl prednisone over 3-5 days

since administered in response to a relapse (damage to axons has already occurred) they merely shorten the duration of the relapse without decreasing morbidity

there is evidence that regularly administered or “pulsed” corticosteroids can decrease this morbidity

280
Q

how is permanent disability managed in MS?

A

requires the services of an interprofessional team, as well as tx of individual sx

spasticity is effectively treated with baclofen or tizanidine

bladder problems due to a failure to empty can be treated with self catheterization

if the bladder is unable to store well, then the detrusor can be inhibited with an anti-cholinergic such as oxybutinin

pain can be treated with TCA or carbamazepine

erectile impotence can be treated with sildenafil citrate

there has been some success treating fatigue with adamantine and modafanil

depression can be treated with SSRIs

281
Q

how is spasticity treated in MS?

A

with baclofen or tizanidine

282
Q

how might an overactive bladder be treated in MS?

A

with an anti-cholinergic like oxybutinin

283
Q

what might you use to treat pain in MS?

A

TCA or carbamazepine

284
Q

what might be used to treat erectile impotence in MS?

A

sildenafil citrate

285
Q

how might you treat fatigue in an MS patient?

A

adamantine and modafanil

286
Q

what symptoms of MS tend to indicate a more benign future course? what about a more difficult course?

A

patients that present with sensory sx (blurred vision, paresthesias) tend to have a more benign course

patients that present with pressure sores, intractable spasticity with contractures, and recurrent UTIs tend to have a more severe disease progression with little likelihood of significant recovery

287
Q

function of sclera?

A

protects eye and anchors muscles

288
Q

function of cornea?

A

transparent window

pain nerve endings

289
Q

function of the pupil?

A

regulates amount of light entering

290
Q

function of the ciliary body?

A

ring of smooth muscle

controls lens shape via suspensory ligament

291
Q

what are the two layers of the retina? what is their function?

A
  1. outer PIGMENTED layer (RPE)
    - absorbs light and prevents light scatter
    - plays role in photoreceptor regeneration
  2. inner NEURAL layer
    - photoreceptors (rods and cones)
    - neurons (bipolar, amacrine, horizontal and ganglion cells)
292
Q

what is the function of rods?

A

responsible for “scotopic vision” –> high sensitivity in dark, saturate as light increases

low spatial resolution–> input from many rods is summated by one bipolar cell

293
Q

what is the function of cones?

A

“photoptic vision” –> best in bright light

“colour vision”–> 3 types of cones, which reflect the type of photopigment (opsin)

R–> long
G–> medium
B–>short

HIGH spatial resolution–> only a few cones converge on one bipolar cell

294
Q

how doe the phototransduction cascade occur?

A

photopigments = opsin + retinal (which is a vitamin A derived molecule)

1 photon converts 11-cis-retinal to all-trans-retinal–> this changes the shape of the photopigment

this activates hundreds of G protein TRANSDUCIN–> this activates a cyclic GMP phosphodiesterase–> each of these breaks down thousands of cyclic GMP–> decreased cGMP concentration closes Na+ channels in the membrane–> leads to hyperpolarization

295
Q

what area of the retina has the highest resolution?

A

fovea–> only cones

296
Q

if you have a central scotoma, what types of photoreceptors are likely affected?

A

cones

297
Q

what does the bipolar cell do in the eye?

A

relays from photoreceptor to retinal ganglion cell

there are separate bipolars for rods and cones

ON/OFF bipolar cells

bipolar cells receive inputs from horizontal and amacrine cells–> this creates lateral inhibition by light in neighbouring regions of the retina, giving rise to “center-surround” receptive field organization

298
Q

what are the two types of retinal ganglion cells?

A

magnocellular RGCs and parvocellular RGCs

299
Q

what is the function of magnocellular RGCs?

A

large cell bodies, long dendrites, large receptive fields–> low spatial resolution

respond transiently to onset/offset of light–> high TEMPORAL resolution

300
Q

what is the function of parvocellular RGCs?

A

small cell bodies, short dendrites, small receptive fields–> high SPATIAL resolution

sustained responses to onset of light–> low temporal resolution

“colour opponency”

301
Q

what is optic atrophy?

A

lesions of the axons of the retinal ganglion cells, anywhere from the outer retinal layer to the intracranial optic nerve, eventually causing pallor of the optic disc

302
Q

what is the blood supply to the eye?

A

from the internal carotid artery

the ophthalmic artery has 2 end divisions–> posterior ciliary arteries (choroid, outer retina, optic disc) and the central retinal artery (inner retina)

303
Q

what visual hemifield is carried in the left optic tract?

A

the right visual hemifield

the visual input from the nasal hemiretinas (temporal visual field) decussates at the optic chiasm–> thus the left optic tract represents the left hemiretina which is the right visual hemifield of each eye

304
Q

where do the axons of the retinal ganglion cells (the optic tracts) project?

A

most fibres are destined for the Lateral Geniculate Nucleus (LGN) which is the last neuron in the relay to the striate cortex

some fibres do project elsewhere:

  1. suprachiasmatic nucleus in the hypothalamus (sleep wake cycles)
  2. pretectal nucleus in the midbrain (input for pupil light reflex)
  3. midbrain ocular motor structures (i.e superior coliculus… mediates reflexive eye movements)
305
Q

what is the function of the suprachiasmatic nucleus in the hypothalamus?

A

regulates sleep wake cycles

306
Q

what is the function of the pretectal nucleus in the midbrain?

A

input for pupil light reflex

307
Q

what is the function of the midbrain ocular motor structures (i.e superior coliculus)?

A

mediates reflexive eye movements

308
Q

where do the inputs from the RGCs travel after they reach they LGN?

A

LGN relays info via its axons in the optic radiations to the striate cortex

some modulation by feedback from cortical regions occurs in the LGN

309
Q

what happens in the striate (V1) cortex? where is it located?

A

termination of the retino-geniculo-striate pathway

initial stage of cortical processing

information is still highly “retinotropic” (specific for the location on the retina)

instead of spots of light, information is represented as linear segments and boundaries–> cells prefer lines of a specific orientation and these are organized in a regular array of “orientation columns”

located in occipital lobe

310
Q

what happens in the extrastriate cortex?

A

beyond the striate (V1) cortex, information fans into a parallel distributed hierarchy of specialized modules

ascending the hierarchy, information is less concerned with retinotropic location and more concerned with specific stimulus properties

modules can be grouped into two streams: ventral (occipitotemporal stream)–> the WHAT; dorsal (occipitoparietal) stream–> the WHERE

311
Q

what processing is done in the ventral/occipitotemporal stream of the extrastriate cortex?

A

WHAT

color perception, form processing, object, face and word recognition

312
Q

what processing is done in the dorsal/occipitoparietal stream of the extrastriate cortex?

A

WHERE

motion perception, stereopsis, saccadic targeting, manual reaching

313
Q

list defects resulting from lesions in the ventral/occipitotemporal stream of the extrastriate cortex and what they are

A
  1. achromatopsia–> inability to perceive colors
  2. general visual agnosia–> inability to recognize objects by sight, though able to by touch or sound

selective agnosias:
3. pure alexia–> inability to read, though able to write, talk and comprehend speech

  1. prosopagnosia–> inability to recognize faces
314
Q

what is another name for the occipitotemporal gyrus (the WHAT of processing visual stimuli)?

A

fusiform gyrus

315
Q

list defects resulting from lesions in the dorsal/occipitoparietal stream of the extrastriate cortex and what they are

A

WHERE stream

  1. akinetopsia–> inability to perceive object motion
  2. hemineglect–> failure to attend to stimuli on the contralateral side
  3. astereopsis–> inability to perceive depth from binocular cues
  4. Balint’s syndrome–> triad of:
    - ocular motor apraxia (inability to make saccades accurately to visual targets)
    - optic ataxia (inability to reach accurately to visual targets)
    - simultanagnosia (inability to attend to more than one object at a time)
316
Q

what regions of the brain are involved in control of eye movements?

A

frontal, parietal, occipital cortical regions with connections thru the internal capsule to the gaze centers in the brain stem

brainstem structures from midbrain to medulla with cerebellar and vestibular system inputs are responsible for voluntary and reflex eye movements

317
Q

where is the vergence center?

A

midbrain

318
Q

where is the vertical gaze center?

A

midbrain

319
Q

where is the horizontal gaze center?

A

pons

320
Q

list the supranuclear regions that control eye movements

A
  1. frontal gaze center (voluntary movements)
  2. occipital gaze center (pursuit) center
  3. descending projections (internal capsule) to brainstem
  4. vergence center
  5. vertical gaze center
  6. horizontal gaze center
  7. MLF
321
Q

where is the voluntary gaze center?

A

frontal lobe

322
Q

where is the pursuit gaze center?

A

occipital lobe

323
Q

list the nuclear structures responsible for control of eye movement

A
  1. CN III nerve nuclear complex (including the edinger-westphal nucleus)
  2. CN IV nerve nucleus
  3. CN VI nerve nucleus (relationship to VII and PPRF)
324
Q

list the infranuclear structures responsible for control of eye movement

A
  1. CN III nerve–> intramedullary relationships include red nucleus (cerebellar connections) and cerebral peduncle (pyramidal tract); tentorium and MCA/PCom junction; cavernous sinus and pituitary; superior orbital fissure and orbit
  2. CN IV nerve–> long course from dorsum of brainstem; through cavernous sinus and adjacent to pituitary
  3. CN VI nerve–> over petrous ridge; through cavernous sinus and adjacent to pituitary
325
Q

why is the CN III intermedullary relationship with the red nucleus important?

A

cerebellar connection

326
Q

what is the fixation system?

A

supranuclear gaze system

poorly localized in cortex

micromovements to move the object of regard on the fovea

global confusional state and dementia

anxiety

sedative/tranquilizing drugs

327
Q

what is the saccadic system? and what are some common problems?

A

supranuclear gaze system

voluntary eye movements and fast eye movements

frontal eye fields crosses to brainstem gaze centers

unilateral–> horizontal gaze palsy

bilateral–> vertical gaze palsy

disorders commonly seen

328
Q

what is the pursuit system?

A

supranuclear gaze system

tracking of objects

slow eye movements

occipital-parietal localization

projects to brainstem gaze centers

“cogwheel” pursuits

329
Q

what is the vergence system?

A

supranuclear gaze system

slow eye movements

disconjugate

occipital-parietal to midbrain pre-tectum

allows focus on near

330
Q

what is the non-optic reflex system?

A

supranuclear gaze system

slow eye movements

brainstem vestibular system-labyrinthine and tonic neck receptor inputs

maintenance of fixation during head movement

331
Q

what are generalized symptoms of CNS infection?

A

fever, headache, neck stiffness, confusion, seizures

332
Q

what are focal symptoms of CNS infection?

A

seizures, numbness, weakness, visual changes, ataxia, dizziness, memory loss

related to the part of the brain involved

333
Q

in terms of CNS infection localization, name the type of syndrome that would present in each of the following “spaces”:

  1. epidural
  2. subdural
  3. subarachnoid
  4. parenchymal (focal vs. diffuse)
  5. venous
A
  1. abscess (enclosed collection of pus)
  2. empyema (collection of pus in a cavity)
  3. meningitis (inflammation of the meninges)
  4. diffuse–> encephalitis//focal–> brain abscess
  5. septic thrombophlebitis (infected venous clot)
334
Q

how seriously must you treat CNS infections?

A

they are all medical/surgical emergencies

335
Q

what are the two types of meningitis based on causative agent and how do their prognoses differ?

A

bacterial–> life threatening

viral–> self limited

336
Q

how can you distinguish bacterial from viral meningitis just based on symptoms?

A

both get fever, headache, stiff neck

bacterial–> get change in level of consciousness

viral–> no change in LOC

337
Q

how can you distinguish bacterial from viral meningitis just based on lab tests?

A

bacterial: +++ WBC, +++ CSF PMNs, low CSF glucose
viral: +/- WBC, + CSF lymph, normal CSF glucose

338
Q

what two factors in the pathogenesis of bacterial meningitis cause increased BBB permeability?

A

endothelial cell invasion (from bacteremia) and subarachnoid space inflammation (from meningeal inflammation)–> leads to vasogenic edema

339
Q

overall what causes death in bacterial meningitis?

A

disease progresses such that you get increased ICP and cerebral infarction and thus decreased cerebral blood flow

340
Q

what causes bacterial meningitis in the newborn?

A

group B strep

e coli

listeria

341
Q

what causes bacterial meningitis in an infant?

A

group B strep

haemophilus

neisseria

342
Q

what causes bacterial meningitis in an adult?

A

pneumococcus

meningococcus

haemophilus

listeria

staphylococcus

343
Q

how do you treat bacterial meningitis?

A

start appropriate antibiotics ASAP

if LP is going to be delayed by need for CT scan, obtain blood cultures and start Abs right away

empiric therapy:
ceftriaxone IV + vancomycin (for penicillin resistant S. pneumo) + ampicillin (for elderly, immunosuppressed, pregnant) + dexamethasone IV (corticosteroid…prior to or with first dose of Abs)

344
Q

how would you empirically treat a suspected brain abscess?

A

ceftriaxone + metronidazole +/- vancomycin

-OR-

neropenem +/- vancomycin

glucocorticoids when there is significant swelling (dexamethasone)

345
Q

how do you distinguish clinically between meningitis and encephalitis?

A

meningitis has intact brain function, whereas encephalitis does not

i.e in encephalitis you might get:
altered mental status
motor or sensory deficits
change in behavior/personality
speech or movement disorder
346
Q

what type of brain syndrome does rabies or west nile cause?

A

encephalitis

B&B Part 1 (4 decks)

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