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Year 2 - Semester 1 > Neuro- week 5 > Flashcards

Neuro- week 5 Flashcards

1
Q

What is Uhthoff’s phenomenon?

A

heating up a patient can cause them to decompensate and their symptoms worsen

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2
Q

what can diffuse inflammation affecting the CNS cause?

A

delerium

old age can cause a leaky BBB which can cause a UTI to lead to delerium

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3
Q

what is MS and what characterises it?

A

Chronic inflammatory and degenerative disease of the central nervous system

Characterised pathologically by:
• Inflammation
• Demyelination ± variable extent of remyelination
• Neuroaxonal injury/loss
• Astrogliosis
o Scarring due to proliferation of astrocytes

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4
Q

what is the incidence like for MS?

A

Incidence increases the further from the equator you get – hypothesis is lower aggregate sunshine exposure
In Scotland there is a latitudinal and longitudinal trend – more in north and west
Female 3:1 male - peak incidence 40.8 years

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5
Q

what is heritability like for MS

A

Heritability (identical twin) is 30% - overall children have 1/40 chance

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6
Q

what contributes to risk for MS?

A 
Contribution of risk from genes and environmental factors
	Vitamin D
	Smoking
	EBV
	Obesity
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7
Q

what is the hypothesis for viruses causing MS

A

Molecular mimicry – immune system fight off pathogen which looks like host antigens in the CNS – EBV and other pathogens?

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8
Q

what is thought to be required along with risk and a trigger which contributes to MS

A

an amplifying step - possibly something to do with the gut biome

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9
Q

what proportion of patients have the different types of MS

A

85% start with relapsing-remitting stage
As they progress they get relapses with persistent deficits and then secondary progressive MS
Around 15% don’t get relapses and just progress from the start – primary progressive MS

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10
Q

what does the diagnosis of MS involve

A

Diagnosis involves exclusion
History/examination – dissemination in space and time
MRI and lumbar puncture

If the patient has oligoclonal bands in the CSF but not the serum then the immune system must be active in the CNS

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11
Q

what are the treatments for MS

A

In relapses we have immunomodulating and immunosuppressive drugs which we call disease modifying drugs

“resetting” immune system by wiping out immune system and giving them stem cells in hope that the immune system is unreactive when it comes back – 80% 5 year survival but obviously very risky

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12
Q

what controls the sleep wake cycle

A 
•	Circadian rhythm
       o	C process
       o	Suprachiasmatic nucleus
       o	Influence of light
       o	Melatonin (pineal gland)
       o	Cortisol
       o	Body temp
•	Homeostasis	
       o	S process
       o	Urge to sleep increases the longer you 
                 haven’t
       o	Unknown mechanism

• Cognitive pressure
o Top down influence from cognitive and
emotional state

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13
Q

what area of the brain is involved with waking up

A

tuberomammillary nucleus : histamine

posterior lateral hypothalamus : orexin (aka hypocretin)

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14
Q

what area of the brain is involved with going to sleep

A

ventrolateral pre-optic area

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15
Q

what is narcolepsy

A

low levels of CSF orexin

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16
Q

sleep architechture

A

4 stages
each lasts around 90 mins
REM sleep increases in proportion the longer we sleep

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17
Q

describe NREM parasomnia

A

stage 3 and 4

sleepwalking, confusional arousals, night terrors

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18
Q

describe REM parasomnia

A

strongly predictable of alpha-synucleinopathies

isolated sleep paralysis - failure of CST inhibition to be switched off when waking

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19
Q

what is involved in arousal

A
  • Posterolateral hypothalamus (“wake up switch”) - diencephalon
  • Reticular activating system (Ach – nicotinic) -brainstem
  • VTA (ventral tegmental area) (mesolimbic and mesocortical dopamine) - brainstem
  • Both thalami intact – bilateral thalamus
  • Neocortex intact - global cortex
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20
Q

what can cause unconsciousness

A

Brain without fuel
• Glucose
• Oxygen
• need a BP high enough to overcome gravity, pumping blood through the brain and back to the heart

Brain with a problem
•	Metabolic/toxic
•	BS/thalamic stroke
•	Raised ICP that compromises perfusion
•	Electrical failure (post seizure)
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21
Q

where are vision nuclei and where do the axons run?

A

in the brainstem, and axons run through cranial nerves 3, 4 & 6

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22
Q

what is the visual field

A 
•	FROM VERTICAL MERIDIAN:
       o	 ~60° NASALLY,
       o	 ~100° TEMPORALLY
•	FROM HORIZONTAL MERIDIAN:
       o	~60° ABOVE
       o	~75° BELOW
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23
Q

how does the visual field change?

A

enlarges with distance

changes with object size and colour

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24
Q

what defects can cause a change in visual field

A

major visual field defects

constriction of visual field

enlarged blind spots

scomata - holes in visual field

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25
Q

describe some major visual field defects

A

 Pre chiasmal
• Uni ocular visual loss

 Chiasmal
• Bi temporal hemianopia (outsides of vision)
• Can be caused by pituitary tumours

 Post chiasmal
• Homonymous hemianopia
o Temporal on one side and nasal on the
other
• Quadrantanopia
o Optic radiation lesion
o Affects just upper left quadrants for
example

 Also altitudinal (upper field of vision)

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26
Q

describe visual acuity

A

• Measure of clarity of vision

• Can be affected by
o Light being impaired getting through the eye
 Lens
 Cornea
 Vitreous humour
 Glasses or contact lenses etc
o Neurological problem
 Not fixable with glasses

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27
Q

describe colour vision defects

A
  • Defects may be congenital or acquired

* Acquired are of neurological interest (optic neuritis)

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28
Q

where does the visual pathway start

A

the conjunctiva

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29
Q

describe rods

A

o Function mainly in dim light
o Black and white
o 120 million

30
Q

describe cones

A

o Function in bright light
o Colour vision
o 3 cones, red, green and blue
o 6-7 million

31
Q

describe photosensitive ganglion cells

A

o Important for reflex responses to light

o Quite rare

32
Q

describe the retina

A
  • Layers of neuronal cells connected by synapses
  • Rods
  • Rods and cones are beneath a few layers of cells and have a pigmented layer underneath them
  • Signals from rods and cones are processed by other retinal neurones – axons from the retinal ganglia cells form the optic nerve
33
Q

describe the macula

A
  • Yellow oval spot
  • 6mm diameter
  • Specialised for high acuity vision
34
Q

descibe the fovea

A
  • 1.5mm pit in the macula centre
  • The area of greatest visual acuity and best colour vision
  • 0.01% of the visual field
  • 10% of axons
35
Q

what does an enlarged blind spot mean?

A

reflects optic nerve size which can be enlarged by optic neuritis or papilloedema

36
Q

which side of the brain does nasal light travel

A

crosses over to contralateral side

temporal light remains ipsilateral

37
Q

what comes after the optic chiasm and before the visual cortex

A

the optic tract, then the lateral geniculate of the thalamus, then the optic radiations to the visual cortex

38
Q

3rd cranial nerve and what it innervates

A

oculomotor nerve

superior, medial and inferior rectus
inferior oblique
(everything other than lateral rectus and superior oblique)

eyelid
pupil

39
Q

4th cranial nerve innervates

A

trochlear

superior oblique

40
Q

6th cranial nerve innervates

A

abducens

lateral rectus

41
Q

why are obliques called such

A

because they don’t do what you expect
inferior makes it go UP and outward
superior makes it go DOWN and outward

42
Q

what are ocular palsies

A

the eye takes up an abnormal position due to unopposed action of remaining muscles

43
Q

diplopia

A
  • Failure to align eyes
  • Double vision
  • Does it resolve if you close one eye? – if it does then its diplopia
44
Q

describe vestibular function

A

– perception of position and motion

o Static gravitational orientation
 Perception of relationship to gravitational field
o Motion in space – essentially acceleration
 Relative to environment
 Rotation
 Linear translations

45
Q

which cranial is for hearing and vestibular function

A

8th

vestibulocochlear

46
Q

where are receptors for the vestibulocochlear nerve

A

these receptors are in the membranous labyrinth part of the bony labyrinth located in the temporal bone

47
Q

what are the three parts of the human ear

A

• The outer ear
o The pinna (what you can see)
o The auditory canal
o The tympanic membrane

• The middle ear
o A small air filled chamber
o 3 small bones (ossicles)

• The inner ear
o The bony labyrinth of the temporal bone

48
Q

what fluids do the bony labyrinth and membranous labyrinth contain

A

the bony labyrinth contains perilymph

the membranous labyrinth contains endolymph

49
Q

what does the inner ear contain

A
  • the vestibule: a large central area
  • the utricle & saccule: adjacent to the vestibule
  • the cochlea: on one side
  • the semicircular canals: on other side
50
Q

how is sound heard?

A

the tympanic membrane receives pressure waves from the auditory canal and vibrates accordingly. This vibration is transmitted to the ossicles. The ossicles transmit the signals to the oval window of the vestibule. Then into the fluid in the membranous labyrinth and into the cochlea. Cells in the cochlea convert the vibrations into electrical signals. These then transmit along the axons of the 8th cranial nerve towards the brainstem around where the medulla meets the pons to the cochlear nuclei (ventral and dorsal cochlear nuclei). Then ascends to the thalamus and cerebral cortex.

51
Q

what are the three bones in the ear called

A

the malleus, the incus and the stapes.

52
Q

describe the ventral cochlear nucleus

A
  • Concerned with minute differences in the timing and loudness of the sound in each ear in order to localize sound
  • axons go to superior olive then to inferior colliculus then medial geniculate body and finally cerebral cortex
53
Q

describe the dorsal cochlear nucleus

A
  • Concerned with the quality of sound, picking apart the tiny frequency differences which allow differentiation of similar sounds
  • axons go directly to inferior colliculus then medial geniculate body and cerebral cortex
54
Q

how does information travel from the cochlear nuclei to the cortex

A

as they go up they form a particular tract in the lateral lemniscus
information from each cochlea goes to both sides of the brain.
There are also efferent pathways which go down to influence hearing

55
Q

how do vibrations travel through the cochlea

A

stapes transmit vibration to the scala vestibuli. the scala vestibuli abuts the oval window. it then travels through the scala vestibuli, then through the scala tympani and out the round window

56
Q

what is the scala media

A

the cochlear duct
membranous labyrinth
contains endolymph which moves in response to perilymph moving

57
Q

what separates the cochlear duct from the scala vestibuli

A

Reissner’s membrane

the tectorial membrane

58
Q

what separates the cochlear duct from the scala tympani?

A

the basilar membrane

59
Q

what does the basilar membrane do

A

stiff and supports the organ of corti which determines the mechanical wave propagation properties of the cochlea

60
Q

describe the organ of corti

A
  • A sensory epithelium
  • A cellular layer lying on the basilar membrane
  • Hair like structures which are moved by vibrations which produces electrical responses
61
Q

how does the basilar membrane change

A

the stiffness & width of the bm varies along the cochlea, stiffest near start at oval window
this allows different parts of bm to respond to different frequencies
coiling also enhances low freq waves as they travel along cochlea
highest freq near oval window, lowest freq near other end

62
Q

what makes up static gravitational orientation and perception of movement

A
  • Visual – you can see where you are
  • Vestibular function
  • Somatosensory - proprioception from limbs
  • These three come together to keep you upright etc
63
Q

what helps with vestibular function

A 
the semicircular canals (rotation)
the otiliths  (linear translations)
64
Q

describe the semicircular canals

A

three canals

horizontal canal - rotation of head around a vertical axis

2 vertical canals

   - anterior (or superior) 
   - posterior (or inferior)

rotations of head in the sagittal plane
rotations of head in the frontal plane

the canals:
 a continuous endolymph-filled hoop
 special hair cells sit in a small swelling called the ampula
 the hair cells project into a gelatinous mass: the cupula.
 Movement in the plane of the canal causes movement of the fluid and therefore movement of the hairs – causes cells to change activity
 movement one way: inhibition on one side, excitation on the other

65
Q

describe the otiliths

A

o the utricle & saccule have a sheet of hair cells: the macula
o the macula have cilia embedded in a gelatinous mass
o embedded in this gel: small crystals (otoliths)
o the otoliths provide inertia

o hair cells are arrayed in different directions to cover different directions of movement
 utricle: horizontal
 saccule: sagittal (up/down, forward/back)

66
Q

what are the connections with the vestibular nuclei

A

cerebellum

spinal cord (vestibulo-spinal tract)

cerebral cortex

eye movement motor nuclei
- vestibulo-ocular reflex
 Keeps eyes still in space while your
head moves
 Inhibits one side of eye and excites the
other to turn eyes in opposite way of
head rotation

67
Q

describe vertigo

A

One, or more, of the following:
• A distortion of static gravitational orientation
• An erroneous perception of movement of the sufferer
• An erroneous perception of movement of the environment

Results from:
• Unusual stimulation of intact systems
• (Motion sickness)
• Pathological dysfunction of those systems

68
Q

what does disturbance of the vestibular system lead to?

A
  • Ataxia
  • Falls
  • Vertigo
  • Nystagmus
  • Nausea
  • Vomiting
  • Sweating
  • Anxiety and avoidance behaviour – not very nice at all
69
Q

describe Benign paroxysmal positional vertigo (BPPV)

A 
•	Parts of the otoliths break off and get lodged in parts of the vestibular system
•	One of the commonest causes of vertigo in clinical practice
•	Attacks of rotational vertigo
•	Provoked by positional change such as
o	Lying down or sitting up
o	Turning over in bed
o	Looking up or bending forward
•	40% due to head injury
•	60% no obvious cause (age is a factor)
70
Q

what is nystagmus a clinical feature of

A

Nystagmus clinical feature of ear or brainstem disease

71
Q

why is the vestibulo-ocular reflex useful for

A

part of brain stem death criteria

Year 2 - Semester 1 (13 decks)

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