B&B 3 Brainstem Flashcards Preview

Brain & Behavior > B&B 3 Brainstem > Flashcards

Flashcards in B&B 3 Brainstem Deck (126):
0

How many people in BC have MS?

About 10,000

1

MS

Etiology

● autoimmune disease → inflammation causes demyelination →destroys oligodendrocytes
● viral infection, vitamin D def, environmental triggers

● Precipitating factors for acute attacks =
– infection
– trauma
– pregnancy

2

MS

Role of Genetics

NOT INHERITED ... but risk is inherited

Usual risk: 0.1%

Risk if parents affected: 2-3%

The only consistent MS associated gene is HLA-DRB1 gene on chromosome 6p21 accounting for 16-60% of genetic susceptibility in MS

3

What is the effect of geographical location on MS?

Prevalence increases with increasing latitude

Several studies have revealed that people who migrate from a high-risk, temperate zone to a low-risk, equatorial zone carry with them part of the risk from their country of origin if the migration occurs after 14 years of age but early-life migration reduces risk

4

Who gets MS?

• Primarily a disease of young adults
• 2/3 of cases presenting between 20-40 years of age
• about 10,000 in BC have it

• 2:1 women to men

5

T1 vs T2

MRI
►T1-weighted
– best anatomical detail
– gadolinium can be used as contrast

►T2-weighted
– usually most sensitive for pathological lesions
– water is white (WW2)

6

MS

What does we see on T2-weighted MRI?

Numerous areas of increased signal indicating extensive disease

7

Relapsing-Remitting MS

What is the pathophysiology?

– As the autoimmune attack induces demyelination and axonal damage nerve conduction will be slowed down or blocked

– Remyelination can occur with the surviving and proliferating oligodendrocytes when inflammation subsides leading to some remission

Eventually ... demyelination wins out

8

MS

Clinical Tests?

►MRI
– lesions via T2

►CSF
– mononuclear cell pleocytosis
– normal or slightly ↑protein
– ↑level of intrathecally synthesized IgG

►Evoked Potentials
– investigate demyleination

9

MS

Does it kill?

• Mortality as a direct consequence of MS is uncommon (which occurs during an acute MS attack)

• Death occurs as complication from MS (e.g. pneumonia in a debilitated person) and from suicide

10

MS

Prognosis?

– progressive neurologic disability
– 15 years after onset, only 20% have no functional limitation with between 1/3 and 1⁄2 progressing to secondary progressive MS and will require assistance with ambulation
– 25 years after onset ~80% of MS patients will have reached their level of disability

►However, we can treat well if diagnosed early

►Although the prognosis for disability is grave for the average patient, the prognosis in an individual is hard to establish

11

MS

What happens during pregnancy?

MS tends to improve during pregnancy

BUT ... increased risk of exacerbations up to twofold in the first few months postpartum

12

MS

Tx for Acute Attacks?

IV methylprednisolone

1000mg daily for 3 days

13

MS

Management of Sx?

►oxybutynin
→ bladder frequency and urgency


►baclofen
→ pain and spasms

►tricyclic antidepressants
→ emotional lability

►amantadine
→ fatigue

14

Types of MS

►Progressive-relapsing MS
(PRMS)
5%

►Primary Progressive MS
(PPMS)
10%

►Relapsing Remitting MS
(RRMS) - our PBL pt
85% .... about 80% of cases will progress to SPMS

►Secondary Progressive MS
(SPMS)

15

Which drugs are used to treat RRMS?

►Interferon β
►glatiramer acetate
– Reduce relapses
– decrease MRI activity
– possibly slow progression of permanent neurological disability

16

►Interferon β
►glatiramer acetate

MOA?

►IFN β
– anti-inflammatory effects decreases Ag presentation, apoptosis, and entry of immune cells into the CNS
– neutralizes ABs

►glatiramer acetate
– polymer of aa's that were designed to mimic myelin basic protein (MBP), a major component of CNS myelin → reduces Ag presentation and stimulates T cells secretion of cytokines associated with anti-inflammatory or Th2 actions

17

►Interferon β
►glatiramer acetate

S/E?

– require IM or SC injections which can produce many SEs including flu-like symptoms, dermal rections, and in
the case of IFNβ, neutralizing antibodies

18

The MS patient fails with IFNβ and GA. A more aggressive Tx is required.

What drug now?

MOA?

Natalizumab (Tysabri)

– MAB specific for α4 integrins

– suppresses the binding of leukocytes to vascular endothelia (a critical step for immune cell entry into CNS)

19

Natalizumab (Tysabri)

A/E?

PML
– rare and most often fatal virus induced demyelinating disease of immunocompromised individuals
– caused by JC virus which almost everyone already has → JC virus can get unleashed when drug causes severe immune suppression

20

What are other Immunosuppressive drugs?

azathioprine

cyclophosphamide

methotrexate

21

►Alemtuzumab



MOA?

►Alemtuzumab
– MAB targeting CD52 antigens expressed on T and B cells to reduce circulating numbers

►Rituximab
– MAB against CD20 lymphocytes

22

How does CN 8 originate?

CN VIII (vestibulocochlear nerve)

originates as two separate nuclei
(cochlear and vestibular nerve)
→ fibers from both nerves join to form single trunk
→ enter opening of internal acoustic meatus located near the posterior surface of petrous bone

23

Where are the 3 ear bones located?

Otic capsule located in petrous portion of temporal bone

24

Bony Labyrinth

What does it contain?

three parts:
1. vestibule
2. semicircular canals
3. cochlea

● have hollow cavities containing a clear
fluid, the perilymph (low K, high Na), in which the membranous labyrinth is situated

25

Membranous labyrinth

What does it contain?

● Endolymph
(high K and low Na)

● contains 5 sensory organs:
– 3 semicircular canals
– 2 otoliths: Utricle / horizontal & Saccule / sagittal (sense body orientation and linear motion)

26

Perilymph
...vs...
Endolymph

►Perilymph
–high Na / low K (similar to CSF)
–"peri has low potassium"
– ultrafiltrate of CSF
– Drains via venules and middle ear mucosa

►Endolymph
– low Na / high K
– unique extra-cellular fluid
– similar to intracellular fluid

27

Semicircular canals

3 canals arranged orthogonally (at right angles) to each other
►anterior (superior)
►posterior
►horizontal (lateral)

Fx: detect angular acceleration (head rotations); specify direction and amplitude of any head rotation

29

Which as high Na?

Perilymph
... or ...
Endolymph

Perilymph

"peri has low potassium"

30

What are the 2 otolithic organs?

►utricle
– horizontal plane

►saccule
– sagittal plane

30

Within the sensory epithelia what are the hair cells suspended in?

Suspended in ...
►Otothilic membrane (acellular gelatinous mass)

►calcium carbonate crystals called otoconia sitting on top of the otolithic membrane

NOTE: Pressure of otoconia deflects hair cell cilium that will either produce an excitatory or inhibitory signal

31

What happens when hair is moved in the Excitatory direction?

Excitatory Direction:
stretch receptors activated → open up K channels → allow K influx → depolarization → increased Ca → increase glutamate release → increased impulse frequency

32

How do sensory epithelia receptor cells detect endolymph movement?

HAIR CELLS
►Stereocilia
– 60-100/hair cell

►Kinocilium
– 1/hair cell
– tallest one of all the hairs

►Cupulla:
– supporting microvilli suspended in a gelatinous
mass called cupulla

33

What happens when hair is moved in the Inhibitory direction?

inhibitory direction:
Less K influx → hyperpolarization → decreased Ca → decrease glutamate release → decreased impulse frequency

34

SUMMARY:

How does brain know when head is being turned?

When head is rotated to a certain direction there would be increased firing at a semicircular canal from one ear and decreased firing at another semicircular canal from the other ear → brain will interpret that as head turning to one side

36

Where does CN 8 enter the brainstem?

Junction of pons and medulla

(cerebello-pontine angle)

Fx = sense body orientation (i.e. head tilt) and linear motion (i.e. acceleration / deceleration)

37

Where are the 4 vestibular nuclei (VN)?

Where are they located?

►Lateral VN (Deiter’s nucleus)
►Medial VN
►Superior & Medial VN
►Inferior VN

– Located in dorsal pons and medulla beneath the 4th ventricle

38

►Lateral VN (Deiter’s nucleus)

Fx?

– innervates gravity opposing muscles of limbs to maintain posture

– Receives input from utricle, saccule and semicircular canals then exerts its efferent effect via lateral vestibulospinal tract which descends the spinal cord ipsilateral to ventral horn alpha and gamma motor neurons innervating gravity opposing muscles of limbs

39

►Medial VN

Fx?

– reflex adjustments of neck and trunk muscles to restore head position after disturbance

– Receives input primarily via semicircular canals then exert its efferent effect via medial vestibulospinal tract (descending medial longitudinal fasciculus) bilaterally

– Targets cervical and upper thoracic spinal cord motor neurons innervating neck musculature

40

►Superior VN
...and...
►Medial VN

Fx?

● Eye movements to stabilize visual image in head turn; vestibulo-ocular reflex (VOR)

● Receives input via semicircular canals then exert its efferent effect via 3 neuron arc:
– Bipolar neurons
– Medial and superior VN
– Motor neurons in the abducens nucleus (VI) and the oculomotor nuclei (III) that innervate oculomotor muscles

41

Inferior Vn

Fx?

Integrates multi-sensory input and cerebellum to regulate VOR gain; adjust VOR

VOR = vestibulo-ocular reflex

42

There are a number of disorders that can affect the vestibular system?

Quick list ...

►BPPV
►Meniere’s disease
►Vestibular neuritis
►Perilymph fistula
►Ototoxicity
►Mal de Debarquement
►Aging, Dizziness & Balance

43

►BPPV

►Benign paroxysmal positional vertigo
(BPPV)

– displaced otoconia lodged in the semicircular canals

– uncommon, but devastating: dizziness & vomiting

44

►Meniere’s disease

►Meniere’s disease
(endolymphatic hydrops)

– increased endolymph in inner ear causing dizziness

45

►Vestibular neuritis

►Vestibular neuritis

– viral infection of vestibule-cochlear nerve
– rather common, unilateral damage organ

46

►Perilymph fistula

►Perilymph fistula

– breach in the oval and/or the round window

– opposite of Meniere’s

47

►Ototoxicity

►Ototoxicity

Induced death of hair cells caused by aminoglycoside ABX:
– Gentamicin
– Streptomicin
– Kanamicin
– Neomicin

48

►Mal de Debarquement

►Mal de Debarquement

– failure of CNS plasticity to respond to prolonged movement

49

►Aging, Dizziness & Balance

►Aging, Dizziness & Balance

visual and motor deficits, BPPV, and gradual hair cell loss

50

What muscles opens eyelid?

Levator palpebrae superiorus

51

Which muscle of the eye runs through the trochlea?

Which nerve?

Superior oblique

CN 4 abducens

(SO4, LR6)

52

Nystagmus:

What is it?

rhythmic alteration of slow and fast eye movements during VOR

53

What is the mechanism of rotational induced dizziness?

(eg) merry go round

When you start to spin, endolymph stays in the same spot. But, once you are spinning long enough the endolymph starts moving to. When you stop spinnng, the physical structures are now stationary but the the endolymph is continues to slosh around

54

Superior / Inferior Rectus?

Which nerve?

Which nerve?

CN III

– first abduct each eye to put it in orbital axis of testing then look up/down

55

Superior Oblique

Which nerve?

How to test?

CN IV
(1) adduct each eye to put it in axis of testing
(2) then look DOWN

56

Inferior Oblique

Which nerve?

How to test?

CN III
(1) adduct each eye to put it in axis of testing
(2) then look UP

57

Describe the parasympathetic innervation of the lacrimal gland

Originate from lacrimal nucleus of facial nerve (CN VII) in pons → go through pterygoid canal to pterygopalatine ganglion → synapse then the postganglionic fibers join fibers of maxillary nerve through inferior orbital fissure → join lacrimal branch of ophthalmic division of CN V (V2)

58

Horizontal Eye Movement

How/Where is it controlled?

►Horizontal gaze centre
PPRF: "paramedian pontine reticular formation"
– gives input to abducens nucleus to direct gaze at ipsilateral side → signal to lateral rectus on ipsilateral side via CN VI & signal to contralateral
– oculomotor nucleus via medial longitudinal fasiculus (MLF)

59

Vertical Eye Movement

How / Where is it controlled?

►Vertical gaze centre
– rMLF (reticular MLF)
– pretectal area

60

Saccadic Movement

There are two types:
►Reflexive Saccade
►Volitional Saccade

Describe Reflexive Saccade...

Retina → visual layer in superior colliculus → motor layer in superior colliculus → gaze centers (PPRF for horizontal movements and rMLF for vertical movements) → saccade to object of interest → retina

61

►Volitional Saccade

What are the 3 types?

►Anti-saccade
= eyes averted from stimulus (e.g. do not look at the red block)

►Memory saccade
= eyes go back to a stimulus despite it already being removed while person shuts the eye

►Predictive saccade
= eyes go where a stimulus is predicted to be (e.g. catching a ball thrown at you)

62

Pursuit movements
– keep object of interest on fovea (follow an object of focus as it moves)

What is required?

Need integration of...
►Cortical information (primary visual cortex – the object & frontal eye fields – move eyes)

►Cerebellar info (how am I moving in environment)

►Vestibular info (where am I in the environment)

►CN VI and III nuclei to achieve synergistic eye movement

63

Can someone with PPRF lesions still have normal pursuit movements?

YES

Pursuit movement relies on vestibular nucleus
and is independent of PPRF

64

Disconjugate Gaze occurs whenever the eyes don't track together. This occurs physiologically when looking at something close

Explain

CONVERGENCE
– both eyes move medially when focusing on something near
– Eyes converge through vergence centre sending signals to both CN III nucleus leading to adduction of both eyes

65

Disconjugate gaze ALSO occurs physiologically when looking at something from a distance

Explain

DIVERGENCE
– Eyes diverge through vergence centre sending signals to both CN VI nucleus leading to abduction of both eyes

66

What is VOR?

Vestibulo-ocular reflex
– adjust EMs to head movements to keep image stable on retina despite our movement
– VOR is much faster than the tracking movement of slow pursuit

67

How does the VOR work?

– Head movements are detected by the vestibular organ in the inner ear

– Acceleration in any given plane will activate extraocular muscles to counteract this movement

Sample: rotation sensed by vestibular organ → vestibular ganglion → vestibular nuclei → abducens nucleus → move L or R depending on the movement sensed

68

Describe the major regions of the eyeball

►OUTER LAYER
– sclera
– anteriorly covered by conjunctiva

►MIDDLE LAYER
– uvea: contains the choroid layer (pigmented to reduce light scattering); ciliary body, suspensory ligament; lens;
iris/pupil

►INNER LAYER
– Retina:
(1) RPE - outer
• absorbs light & prevents light scatter
• role in photoreceptor regeneration
(2) Neural Layer - inner
• Photoreceptors (rods & cons)
• Neurons (bipolar, amacrine, horizontal & ganglion cells)

69

Cornea

What actually is it?

transparent layer in front of the iris/pupil

70

Conjunctivitis
...vs...
Uveitis

is more serious often associated with systemic diseases (sarcoidosis, rheumatoid arthritis, MS, AIDS, tumors or
infections)

►Conjunctivitis
(outer layer)
– commonly viral (infectious) event that is benign

►Uveitis
(middle layer)
– more serious
– often associated with systemic diseases (sarcoidosis, RA, MS, AIDS, tumors or infections)

71

Blood Supply of Eye

Internal carotid → opathalmic artery → branches:

►Posterior ciliary arteries supply...
– choroid
– outer retina
– optic disc

►Central retinal artery supplies...
– inner retina

72

Rods
...vs...
Cones

►RODS
– for dim light (grey scale)
– uses rhodopsin as the pigment
– highest in density at ~20 degrees eccentrically then decline more peripherally

►CONES
– for bright colour vision
three types of cones: red (long), green (middle), blue (short)
– responsible for high resolution central vision
– highest in density centrally

73

Optic Disk
...vs...
Macula
...vs...
Fovea

►Optic Disk
– Physiological blindspot; aka "punctum caecum"
– no photoreceptors
– location where retinal ganglion cells gather to form the optic nerve

►Macula surrounds fovea

74

How do photoreceptors work?

►Photo energy is transformed into nerve signals by photoreceptors:

►Photopigment = opsin combined with retinal (vitamin A)

►When light strikes photopigment → transform from cis to trans-retinal → amplifying cascade via G protein transducin → reduction in cGMP closes Na channels  hyperpolarization → reduction in glutamate release

75

What causes different types of congential colour blindness?

Opsin mutations

X-linked (occurs mainly in men)

76

Cone dystrophy, macular degeneration

central scotoma (depressed vision) with poor central daytime vision

►Cone dystrophy
– inherited ocular disorder characterized by the loss of cone cells, the photoreceptors responsible for both central and color vision.

►macular degeneration
– affects older adults
– results in a loss of vision in the center of the visual field (the macula) because of damage to the retina

77

Retinitis pigmentosa

What is it?

Retinitis pigmentosa
"disease of rods"
– causes ring scotomata (circular area of depressed vision surrounding point of fixation) and nyctalopia (night blindness)

78

Bipolar Cells

Bipolar cells get glutamate stimulation from photoreceptors:

►ON cells are inhibited by glutamate → if there is light to reduce photoreceptor glutamate release → ON cells activate

►OFF cells are excited by presence of glutamate → more glutamate when photoreceptors not excited by light

79

Horizontal Cells

What is the role?

Horizontal cells: connected laterally to many rods, cones, and bipolar cells

ROLE: inhibit activity of neighbouring less illuminated photoreceptors (lateral inhibition) to increase acuity of sensory signals
→ only signal from well lit photoreceptors reach ganglion cells to improve contrast and definition of visual stimulus

80

Bipolar cells convey signal to several different types of retinal ganglion cells (RGCs)

The two most numerous RGCs are ...

►Parvocellular RGCs
– small receptive fields
– sustained response
– high spatial but low temporal resolution
– colour opponency

►Magnocellular RGCs
– large receptive fields
– transient responses
– low spatial but high temporal resolution

81

Describe the spatial arrangement of the RGC axons

►Papillomacular bundle
– large bundle from fovea and macula to optic disc

►Temporal raphe
– divides fibers from upper and lower temporal retina (nasal visual field) as they must curve around papillomacular bundle in their way

►Fibers from nasal retina
(temporal visual field)
– head straight to the optic disc

82

Clinical points:
field defects from optic neuropathy reflect the anatomy of the nerve fiber layer

Examples ...

►Central / cecocentral scotoma
(e.g. optic neuritis)

►Nasal arcuate defect
(e.g. glaucoma)

►Monocular altitudinal defects
(e.g. anterior ischemic optic neuropathy)

►Temporal wedge defect (rare)

NOTE: With time lesions of the optic nerve cause disc to turn pale: “optic atrophy”

83

Where do the axons of the RGCs gather?

Gather to form optic nerve at optic disk

Optic nerve is actually a CNS component → myelinated by oligodendrocytes rather than Schwann cells (like other CNs)

84

Optic nerve passes into cranium via optic canal → converges above pituitary gland at optic chiasm → axons from nasal half of each retina (temporal hemifield) decussate in this structure

After the optic chiasm, where does the optic tract go?

Optic tract continues from optic chiasm → terminates in the LGN (in thalamus)

"lateral geniculate nucleus"

85

What do Lesions of the optic chiasm cause?

bitemporal hemianopia
(loss of temporal zones)

(eg) pituitary tumor

86

What do Lesions of the optic tract cause?

homonymous hemianopia

usually partial and usually incongruous
(differing in extent between the two eyes)

87

Lateral geniculate bodies constitute important relay nuclei within the thalamus

What are the 6 layers?

►2 where magnocellular RGC axons terminate (these layers have larger cells) one for each eye

►4 where parvocellular RGC axons terminate (these layers have smaller cells) two for each eye in alteration

88

What is optic radiation?

aka. "geniculo-calcarine tract"

– axons from the neurons in the lateral geniculate nucleus (LGN) to the primary visual cortex.

– receives blood through deep branches of the middle cerebral artery and posterior cerebral artery.

– carry visual info through two divisions (called Upper and Lower division) to the visual cortex (aka striate cortex) along the calcarine fissure

Lesion results in Quadrantanopia

89

Where does the fibres of the Optic Tract terminate?

Cross fibers → terminate within laminas 1, 4, 6
(contralateral)

Uncrossed fibers → terminate in laminas 2, 3, 5
(ipsilateral)

90

Describe the

Optic nerve → optic chiasm → optic tract → LGN → optic radiation → striate cortex

91

Bitemporal hemianopia

two halves lost are on the outside of each eye’s peripheral vision

optic chiasm

92

Homonymous hemianopia

two halves lost are on the corresponding area of visual field in both eyes (i.e. either left or right
half of the visual field)

93

CNS Infection

Generalized Sx
...vs...
Focal Sx

►Generalized Sx
– fever, headache, neck stiffness
– confusion
– seizures

►Focal Sx
– seizures, numbness, weakness
– visual changes
– ataxia, dizziness, memory loss
– related to part of brain involved

94

Neuro Exam

What are the 5 Signs?

1. Mental Status
2. CNs
3. Sensation
4. Motor Strength
5. Reflexes, Coordination, Gait

95

CNS Infection Localization

ALL OF THESE ARE MEDICAL EMERGENCIES!

►Epidural
Abscess → enclosed collection of pus

►Subdural
Empyema → collection of pus in a cavity

►Subarachnoid
Meningititis → Inflammation of the meninges

►Parenchymal
●Diffuse → Encephalitis → inflammation of the brain
●Focal → Brain Abscess → enclosed collection of pus

►Venous
Septic Thrombophlebitis → infected venous clot

96

What causes the infection in each of the various locations?

►Meningitis → bacteria, virus

►Abscess → bacteria, parasite, fungus

►Empyema → bacteria

►Encephalitis → virus

►Thrombophlebitis → bacteria

97

Meningitis

Sx?

What causes it?

►Subarachnoid
Meningititis → Inflammation of the meninges

Sx:
–Fever, headache, stiff neck

Caused by:
►BACERIAL
– change in LOC
– Emergency!

►VIRAL
– non change in LOC (should be alert, wide awake)
– self-limiting

98

Meningitis

How do we use imaging?

Imaging will be NORMAL

Therefore, we use it to rule OUT other pathology

99

Meningitis

What do we see in CSF?

►BACERIAL
↑↑↑ WBC (in 1000s)
↑ Neutrophils
↓ Glucose
↑ protein

►VIRAL
↑ WBC (100s)
– normal glucose

100

Again, how many WBC should there be in CSF?

When do we see elevations?

►Normal CSF
<5

►Bacterial
1000s

►Viral, Fungal, FB
100s

101

Bacterial Meningitis

What organisims?

►NEWBORN
– GBS
– E. Coli
– Listeria

►INFANT/ CHILDREN
– GBS
– Haemophilus
– Neissaria

►ADULT
– Pneumococcus
– Meningococcus
– Haemophilus
– Listeria
– Staphylococcus

102

Viral Meningitis
(actually quite common!)

What organisims?

– Enteroviruses – echo & coxsackie
– HSV, Varicella, HIV, Mumps
– Lymphocytic choriomeningitis
– Adeno, CMV,...

Altered LOC??
→ HSV ... medical emergency!

103

Brain Abscess

What causes it?

►Immunocompetent Pop
BACTERIAL → trauma, emboli, osteomyelitis
• Strep anginosus
• Anaerobes
• S. aureus
• Gram neg organisms

►Immunocompromised
PARASITE:
• Parasite (Toxoplasma gondii)
FUNGAL:
• Cryptococcus neoformans
• Mycobacterial (tuberculosis)

104

Brain Abscess

Sx?

• Headaches
• Fevers
• Focal Neurological Deficits (depends on location within the brain
• Mental Status Changes
• Seizures
• Nausea & Vomiting
• Nuchal Rigidity

105

Subdural Empyema

What causes it?

BACTERIAL
– often S. Aureus
– via trauma, surgery, sinus disease

Tx:
surgical drainage & antibiotics

106

Enchephalitis

Sx?

SICK & FEVER
• acute febrile illness
• convulsions, delirium, confusion, stupor or coma
• aphasia, hemiparesis
• involuntary movements, ataxia
• myoclonic jerks, nystagmus
• May have meningitic component

107

How to distinguish
Meningitis
...vs...
Encephalitis

Meningitis
– intact brain Fx

Encephalitis
– Abnormal Brain Fx

108

Encephalitis

What causes it?

VIRAL

HSV & HIV are the ones we treat

Rabies is usually fatal ...

109

Septic Thrombophlebitis

What causes it?

Sx?

Tx?

Bacterial
• Trauma, Surgery
• Facial Skin infection
• Sinusitis

Sx
• Headache (↑ICP)
• Obtundation (↓LOC)
• Seizures, venous infarctions

Tx:
Anticoagulants & ABX

110

Romberg Test

What does it rely on

MUST HAVE 2/3 TO BE NORMAL (neg Romberg)
• Intact Proprioception (PCML)
• Intact Vestibular function
• Vision

Having the patient close their eyes reveals whether proprioception / vestibular function are in tact.

111

What is RAPD?

Relative Afferent Pupillary Defect
• Assessed via Swinging light Test
• Aims to reveal any asymmetry of afferent input in the pupillary light reflex

NOTE: Presence of any efferent pupil defect precludes a meaningful application of the swinging light test

112

INO

What is it?

Internuclear opthalmoplegia
– Results from lesions of the MLF between the midpons and the oculomotor nerve nucleus resulting in disconnection of the abducens nerve nucleus from the contralateral oculomotor nucleus

113

What is a R INO?

Right side is affected

Remember: The site of INO is named according to the side on which oculomotor nerve is impaired

114

What is the most common cause of INO in adults or patients with bilateral involvement?

MS

115

Patient has isolated INO

What do we need to rule out?

Myasthenia gravis

-- can closely mimic a lesion of MLF

116

Patient is seeing double vision.

What is it?

How to approach it?

Diplopia

COVER ONE EYE ...
►Corrected?
• binocular diplopia → caused by disruption of ocular alignment

►Not Corrected?
• monocular diplopia stemming from intrinsic eye problems (corneal aberrations, uncorrected refractive error, cataract, or foveal traction)

117

Binocular Diplopia

What are causes?

occurs from a wide range of processes:
• infectious
• neoplastic
• metabolic
• degenerative
• inflammatory
• vascular

Need to decide if it is neurogenic in origin or due to restriction of globe rotation by local disease in orbit

118

herpes simplex encephalitis
(HSE)

What part of the brain is affected?

Adults & Kids >3 months
• localized to the temporal and frontal lobes
• caused by HSV-1

Neonates; < 3 months
• brain involvement is generalized
• HSV-2
• acquired at the time of delivery

119

herpes simplex encephalitis
(HSE)

Sx

• Fever (90%)
• Headache (81%)
• Psychiatric Sx(71%)
• Seizures (67%)
• Vomiting (46%)
• Focal weakness (33%)
• Memory loss (24%)

120

herpes simplex encephalitis
(HSE)

Pathogenesis

HSV-1 induces neuronal apoptosis

severe necrosis and inflammation in infected parts of the brain

CHARACTERISTICS:
• Temporal lobe most commonly involved.
• Intranuclear inclusion in neurons and glia
• Perivascular lymphocytic infiltrates

NOTE:
• No Abscess formation

121

HSV-1
vs
HSV-2

►HSV-1
– oral lesions
– can cause HSE in pts > 3months (kids & adults)

►HSV-2
– causes genital lesions
– can cause HSE in neonates < 2 months due to transmission at birth

122

Pupillary Light Reflex

How does it work?

Shine light in pupil → Retinal Ganglion Cells → CN2 → Pretectal Nucleus → CN 3 neurons exit to go to each eye → EW nucleus → Ciliary Ganglion → Sphincter Pupillae

123

What is the role of the MLF in the Pupillary Light Reflex?

NOTHING!

Think about it. The MLF is for moving the eyes together. This has NOTHING to do with eye movement!

124

tuberculous meningitis

S&S?

Fever
Headache

125

Prion Disease

What are pathogolical features?

Accumulation of prions in nerve cells

Neuronal loss

Gliosis

126

What is Optic neuritis?

What is the most common cause?

Inflammation of CN2

Most common cause is MS