Neuro 3 - special senses Flashcards

1
Q

Auditory system qualities

A

Mechanical to electrical transduction
Very rapid, works at extremes of physiology
Very small movements transduced
- 70% of over 60s have hearing impairment
- 840 babies born each year with bilateral impairment

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2
Q

What is sound?

A

Noise generated, then compress and rarefy air as sound wave
Amplitude (peak to trough distance) - loudness - decibels - Db
Frequency (no. of cycles passing point in time) - pitch - Hertz - Hz

But sound is very complex, use Fourier analysis to study tones in a complex sound
- peripheral auditory system is doing this, breaking down complex sounds and encoding to nervous system

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3
Q

Audiometric curve of human hearing

A

Total area inside curve = area of auditory perception, around 20Hz - 20kHz, 0Db - 120Db
Bottom line = threshold for hearing, lowest intensity (differs at different frequencies)
Top line = level of feeling and pain, sounds too intense and damaging to auditory system

Conversation area in middle, so speak at the most sensitive frequencies

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4
Q

Anatomy of human ear

A

OUTER - pinna, to funnel sound along external auditory canal
(divided by tympanic membrane)
MIDDLE - ossicles, eustachian tube
INNER - cochlea coil, vestibular system

Outer + middle = conductive part
Inner = sensory-neural part, for transduction

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5
Q

Function of middle ear

A

Impedence matching:

  • airwaves cause tympanic membrane to vibrate
  • lever action of ossicle (moving through air)
  • stapes moves against oval window, to move fluid

More energy needed to move fluid than air
Hence why oval window very small, energy concentrated to very small area, so 20x increase in pressure
- necessary to move fluid, otherwise not much energy would transfer

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6
Q

Ossicular reflex in middle ear

A

To protect against intense sounds (= attenuation reflex), reduce damage to ear
2 muscles, stapedius and tensor tympani are attached to ossicles and the bony part of ear
- if muscles tense, bones can’t move freely, stiffens lever action, so decreases energy conduction

BUT

  • must be continuous loud sounds, ineffective for impulse noise
  • doesn’t work at very high frequency sounds - though can help discrimination of low, so can understand high pitch
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7
Q

Cochlea spiral structure

A

35mm long when uncoiled
Structure formed by 10 weeks gestation, functional by 20 weeks
Compartmentalised into series of chambers

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8
Q

Chambers of cochlea

A

Three chambers in a section:
Scala vestibuli + scala tympani - perilymph
Scala media - endolymph, + organs of hearing

Compartmentalisation is essential to keep fluid apart

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9
Q

Scala media contents

A

Stria vascularis – maintains ion composition of fluid (Na+/K+)
Tectorial membrane – gelatinous membrane overlying organ of Corti

Organ of Corti:

  • on flexible basilar membrane
  • inner and outer sensory hair cells
  • spiral ganglion nerve cells
  • associated supporting, non-sensory cells to hold hairs rigidly
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10
Q

Cochlear fluids

A
PERILYMPH
- in scala vestibuli and scala tympani
- resembles CSF
- to bathe cell bodies of organ of Corti
- 0mV potential
ENDOLYMPH
- in scala media
- resembled intracellular fluid
- sealed in tight compartment
- to bathe surface of organ of Corti
- maintained by stria vascularis
- +80mV potential
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11
Q

Properties of inner and outer hair cells

A

Stereocilia (hair-like) projecting from apical surface
Mechano to electrical transduction
Transduction channels in hair bundles
Outward K+ channels in basolateral membrane
Sensitive to damage and disease

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12
Q

Properties of inner hair cells

A
~3500, one row
Flask shaped
Hair bundle flat
Afferent innervation mainly
10-20 afferent terminals per cell
Inward Ca2+ channels
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13
Q

Properties of outer hair cells

A

~1200, three rows
Columnar shape
Hair bundle in V or W shape
Mainly efferent innervation
(small afferent – one neurone to many cells)
Prestin motor protein in lateral membranes

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14
Q

When sound enters the ear…

A
Along external auditory canal
Vibrates tympanic membrane
Moves ossicles in lever action
Stapes displaces fluid in scala vestibuli
Travelling wave
Displace basilar membrane up and down
Sensory hair cells contact tectorial membrane, so stereocilia displace membrane
-> Travelling wave
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15
Q

Stereocilia response to movement

A

Arranged in rows, with tallest at back
Tip links between ends of tall and short stereocilia
Movement of the cilia opens ion channels, so K+ rush in – driving force for K+ from endolymph into cell 135mV
- sensitive to very small movements
⇒ depolarisation of hair cell
Voltage gated Ca2+ open, Ca2+ in
Neurotransmitter release, increased firing of nerve cell

After stimulus gone, return to upright position

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16
Q

Phase locking

A

At rest – some trickle of transducer current (K+ movement)
Positive stimulus – push towards tallest cilia - increase current up to a maximum point
Negative stimulus – push towards smallest cilia – switch off current

Activity in hair cell -> receptor potential -> nerve activity

  • only encodes 1-4kHz, we can hear up to 20, so other mechanism also
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17
Q

Tonotropy

A

For hearing 4+ kHz
Maximum displacement of basilar membrane occurs at different positions – regional variations in fibrous structure
Depends on frequency of sound
In low freq – displacement close to apex
In high freq – displacement close to base of basilar membrane
Tonotopic map in brain so can understand, auditory nerves end at different points on cochlear nucleus (isofrequency bands)
PASSIVE MECHANISM

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18
Q

OHCs role in hearing

A

Cochlear amplifier - amplification and tuning of IHC stimuli

Tonotopy is passive
Must be active component, otherwise would dissipate and lose energy by end of basilar membrane
Only occurs in live cochlea, by OHCs
- drugs can reduce this

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19
Q

How do OHCs amplify

A

Depolarisation -> activates prestin (motor protein) -> cells shorten rapidly
Rigidly held cells contract, so amplify basilar membrane movements
Gain (size change) modulated by efferent system

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20
Q

Otoacoustic emissions

A

Sounds produced by ear

Send click sound in, hear click back

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21
Q

Neural encoding of loudness in IHCs

A

Louder sounds, larger stimulus
IHCs have numerous (10-20) synaptic contacts with different nerve types:

High spontaneous rate fibres – easily excited at low sound levels, soon saturated
Medium spontaneous rate fibres – excited at medium sound levels, will saturate
Low spontaneous rate fibres – not excited until sound loud, saturate slowly – good for detecting changes in sound at very high sound levels
- sound encoded by activation of populations of neurones

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22
Q

Cochlea to brain main pathway

A

Cell bodies of afferent nerve terminals in spiral ganglion
Ventral cochlear nucleus
Superior olive – ipsi + contralateral input from both ears, important for localisation of sound. Then carried parallel bilaterally.
Inferior colliculus
Medial geniculate nucleus
Auditory cortex

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23
Q

Function of vestibular system

A

Report on position and movement of head
Give sense of balance and equilibrium
Coordination and posture adjustment, with cerebellum
- disorders – feels like vertigo - nausea, disequilibrium, nystagmus

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24
Q

Anatomy of vestibular labyrinth

A

Three semicircular canals – crista
- sensitive to head rotation and angular acceleration
- have sensory hair cells
Otolithic organs – saccule and utricle
- sensitive to gravity, linear acceleration
- have sensory hair cells

Hair cells the same, though for different functions, due to structures they sit in

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25
Q

Vestibular hair cells

A

Kinocilium are tallest cilia
Type I and II
Afferent and efferent innervation
Transduction similar to IHCs

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26
Q

Transduction and encoding in vestibular hair cells

A

Positive direction – towards tallest (kinocilium) – depolarisation – excitation

Negative direction – away from kinocilium – hyperpolarisation – inhibition

But, high resting rate of nerve fibres, firing even when hairs vertical, so high sensitivity to direction

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27
Q

Stimulation of macula

A

Macula = sensory epithelium of the otolithic organs
- saccule and utricle

Otoliths are crystals of calcium carbonate, lie over:
Gelatinous cap, coating hair cells

When head moves, otoliths (high density) lean
Moves gelatinous cap
Deflects stereocilia
Transduction

Positive direction is head to chest
Negative is head back

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28
Q

Hair cell orientation in vestibular apparatus

A

Many hair cells oriented in different directions:

Saccule and utricle have positive direction facing outwards and inwards respectively
- and organ is curved, so get wide range, have all cell orientations necessary

Semicircular canals also are at 90degrees to each other, so can respond to rotation in any given direction

  • hair cells oriented one way in each ampulla
  • adaptation after 15-30s as fluid catches up
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29
Q

Peripheral vestibular pathologies

A

Kinetosis (motion sickness)
Lesions/irritations – usually unilateral
Meniere’s disease – excessive fluid pressure
Benign paroxysmal positional vertigo – otoliths dislodged from utricle

When chronic, can compensate using visual stimuli, proprioceptors

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30
Q

Hearing loss

A

MILD – difficulty following speech in noisy situations, 25-39dB quietest sounds heard
MODERATE – difficulty following speech without hearing aid, 40-69dB quietest sounds heard
SEVERE – rely on lipreading, even with hearing aid, 70-94dB quietest sounds heard, signing maybe preferred language
PROFOUND – 95dB+ only, signing or lipreading

  • conductive hearing loss (damage/blockage to outer or middle ear) or sensorineural hearing loss (damage/loss of sensory hair cells or neurones)
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31
Q

Conductive hearing loss

A

Damage/blockage to outer or middle ear

Outer – obstructions (eg wax), tympanic membrane rupture (from infection, foreign object, barotrauma)

Middle – otosclerosis (overgrowth of stapes so not proper lever action), glue ear (chronic fluid build up), otitis media (acute inflammation, redness, pain)

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32
Q

Sensorineural hearing defects causes

A
  • drug induced
  • genetic defects
  • acoustic trauma to hair cells and neurones, acute and chronic
  • presbycusis - age related
  • infectious disease
  • tinnitus
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33
Q

Drug induced sensorineural hearing loss

A

eg Aminoglycoside antibiotics
- ototoxic, so only used when necessary

LOSS OF OHCS

  • dose dependent
  • > partial deafness, poor frequency discrimination
  • hearing aid helps intensity only, as lost cochlear amplification and tuning

progresses to… (with higher dose/longer treatment)
LOSS OF IHCS AND OHCS
- complete deafness
- need cochlear implant

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34
Q

Acoustic trauma -> hair cell defects

A

If mild, up to 90dB

  • disruption of hair bundle, breakage of tip links
  • may be reparable
  • temporary threshold shift, eg after club night

Severe, more than 130dB (or quieter but sustained)

  • complete loss of area of hair cells
  • scar formation fills void

Due to:

  • metabolic exhaustion
  • physical disruption of hair bundle
  • excitotoxicity, damage at synapse
  • build up of toxic metabolites
  • hole in reticular lamina
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35
Q

Genetic hearing loss

A

-> most childhood deafness
also -> predisposition to traumatic, ototoxic, age-related hearing loss

  • K⁺ channels, for repolarizing hair cell
  • Structural components in stereocilia and tiplinks
  • Collagens and connexins in connective molecules
36
Q

Presbycusis

A

Deafness of ageing
70% of 70+ yos
Starts in high frequencies, loss of hair cells at base of cochlear coil, progresses to lower frequencies with age
Hearing aid to treat

Increased by exposure to:

  • drugs
  • age
  • noise
  • genetic predisposition
37
Q

Tinnitus

A

Auditory perception without sound stimulus
10-15% adults
Hearing loss main risk factor

Often not originating in cochlear, can cut cochlea nerve and still experience
Less activity in cochlear nerve downregulates inhibitory processes in cortex

No effective drug therapy
Sound therapy and cognitive behaviour therapy

38
Q

Cochlear implant

A

Only treatment for severe/profound hearing loss

External speech processor captures sound, converts to digital signals
Sent to internal implant
Implant converts to electrical energy, send to array inside cochlea
Electrodes stimulate auditory nerve - bypass damaged hair cells
Brain hears sound, frequency coding stimulates spiral ganglion neurones in correct position

39
Q

Candidacy for cochlear implant

A

EITHER
Postlingually deafened adults
OR
Prelingually/congenitally deaf children

Only in bilateral severe or profound deafness
Need residual neurones - must be put in fast, or neurones connecting to dead hair cells will die
Need normal inner ear anatomy to allow surgery
Auditory cortex not fully developed until age 6, so implant before then

40
Q

Properties of light

A

Visible light only narrow band of electromagnetic radiation
- higher wave energy - blue
- lower wave energy - red
Only know colours because of perception, interpretations different

Travels in straight line in vacuum
We see waves, reflected and scattered from objects

41
Q

Anatomy of eye

A

Extraocular muscles - to move eyeball in bony orbits of skull

  • oculomotor
  • trochlear - superior oblique
  • abducens - lateral rectus

Pupil - allows light into eye

Iris - muscles to control size of pupil

Lens - curved structure, parasympathetic of oculomotor (ciliary ganglion) control shape

42
Q

Incident light

A

Choroid layer - vascular layer with connective tissue

  • between retina and sclera
  • dark melanin choroid pigment absorbs stray light, limits uncontrolled reflection -> crisp image
  • in night animals (reflective eyes), melanin partly absent, have tapetum lucidum to collect as much light as possible, but with less visual acuity.
43
Q

Retinal landmarks

A

Optic disk - blind spot
- axons of ganglion to optic nerve

Fovea - depression directly behind pupil - to allow clear path for light to photoreceptors

Macula - yellow disk around fovea
- greatest visual acuity - look straight better than periphery

Foveola - centre of fovea
- contains only cone receptors

44
Q

Image on retina

A

Light bends at cornea and lens to form crisp image on back of retina

-> image flipped 180^, back to front and upside down - inverted
Info leaves retina in optic nerve
- some crossing over
- nasal and temporal retina of each eye on same side, forms optic tract

Nasal info crosses, temporal info stays same side

45
Q

Retinal disease

A

Macula degeneration - lose central vision, maintain peripheral - problem in targeting image
- mainly in older age

Retinitis pigmentosa - degeneration in periphery - tunnel vision

  • heritable
  • > night vision and peripheral vision problems
46
Q

Aqueous humour

A

To nourish lens, iris, cornea - have no blood supply
Replaced every hour
Produced in posterior chamber by ciliary process

Excess production -> glaucoma, pressure to damage structures
- treat with carbonic anhydrase inhibitor

47
Q

Pupillary light reflex

A

Undilated pupil - focus most light into fovea
DIlated pupil - light across retina
(also dilate in response to eg fear)

Direct and consensual reflex - direct for same eye, consensual for other also
- as info from pre-tectal area splits, to Edinger-Westphal on other side

48
Q

Light enters eye, pupillary reflex

A

Info along optic nerve
To pre-tectal area (split, also to other side)
To Edinger Westphal nucleus
Info back down pathway on occulomotor nerve via ciliary ganglion, synapse
Short ciliary fibres -> pupillary constriction

49
Q

Lens

A

Transparent, bioconvex
Behind iris
Held by suspensory ligaments
Thickens throughout life

In cataracts - lens becomes opaque, accumulation of metabolic products

50
Q

Accomodation reflex

A

Ability to look at close objects, switch from far

  • ciliary muscles contract - reduce pressure on fibres suspending lens, allows to become convex
  • increase refractive power, direct onto retina

Also need convergence:

  • need image on fovea of both eyes
  • if not, diplopia, double vision

Also need pupillary reflex:
- constrict pupil size, improve focus of light so not scattered - reduces abberation, increased depth of focus

51
Q

Photoreceptors

A

Two types, specialised to function - rods and cones, inner segments same

  • light sensitive part is outer segment
  • light needs to pass through retina before detection
  • not barrier to light as retina is transparent and thin

LIght for VISION, not circadian rhythms

52
Q

Rod photoreceptors

A

For low levels of light - scotopic
Don’t detect colour
Can detect single photon of light (but won’t percieve light here)
Easily saturated
Discs in outer segment, organised to capture photons
Mostly in periphery - none in foveola
Convergence - info from many rods comes together in CNS - less acuity as from number of receptors

53
Q

Cone photoreceptors

A
High levels light - photopic
Less easily saturated
Mostly in fovea
Little convergence - need precise info - single cone to single ganglion cell
No discs, membrane folds

3 types - blue (short wavelength), green (medium), red (long)
To detect especially at specific wavelengths (can alos detect at others, overlap to allow brain to create spectrum)
- no blue cones in foveola!

54
Q

Adaptation to light

A

Dark to light - quickly adjust (light adaptation)
Light to dark - slowly adjust (dark adaptation), as rods previously saturated, unable to respond until have regenerated photopigment

  • pupillary reflex to reduce/increase amount of light in
  • changes in conc of visual pigment
  • changes in numbers of available light activated channels (Ca2+ conc)
55
Q

Visual pigments

A

Rods - rhodopsin (similar to vitamin A)
Cones - iodopsin

Inside discs
From dark to light - conformational change in structure of pigment

56
Q

Colour-deficient vision

A

9% males, 0.5% females

  • due to absence of a cone type - usually green (deuteranopia) or red (protanopia)
  • if blue, rare (tritanopia)

Sex linked recessive, on X chromosome (so more common in men)

Ishihara plates to test
Colour should be constant for everyone - weird dress is photo taken in fluorescent lighting, brain not adapted to understand - PERCEPTION

57
Q

Photoreceptors transducing stimulus

A

Photopigment sits in membrane
Coupled to G protein

DARK
Pigment in cis form
G protein inactive
Ion channels open, as coupled to cGMP, mainly Na+ enters cell = DARK CURRENT
-> photoreceptor depolarised (-30mV) - glutamate continuously released, bipolar cell inhibited

LIGHT
Pigment activated, conformational change
G protein activated
Removal of cGMP from ion channel
Ion channel shuts, no +ve ions in
-> cell hyperpolarised (-60mV) - no glutamate release, bipolar cell can transmit signal
58
Q

Light adaptation

A

Ca2+ enters in dark also - levels higher than others
Inhibits cGMP synthesis
Long term light, Ca2+ levels fall, some synthesis cGMP allowed
Some dark current flow
Can re-respond
- why get small depolarisation in long term light

59
Q

Glutamate action

A

Product of postsynaptic receptor, not neurotransmitter

In visual system, glutamate is inhibitory!

60
Q

Retinal map of rods and cones

A

At 0°, fovea
Cones concentrated here
Optic nerve is blind spot
Many rods in periphery, absent in centre of fovea

61
Q

Receptive fields

A

Centre (direct to bipolar cell) of receptive field and surround (to horizontal cell) on retina
Directly underneath centre, horizontal and bipolar cell
Fields overlap

62
Q

Bipolar cells

A

ON
- depolarise when no/less glutamate - light on, on

OFF
- depolarise where more glutamate - light off, on

Can have opposite reactions - focus to ON system.

63
Q

ON system

A

Transmitter released from rods/cones is glutamate
Inhibition of bipolar cells, excitation of horizontal cells

Light -> less release glutamate, depolarise bipolar cells, hyperpolarise horizontal cells

On centre, off surround -> centre illumination
If shine light in centre, on response
If shine in surround, off response

Or can be off centre, on surround.

64
Q

Ganglion cell receptive fields

A

Good for detecting changes in light levels
Some on, some off in static light

If suddenly lights on - more signalling from on centre, firing in ganglion cells (no change in surround)
If lights more - on centre and off surround (change across whole receptive field), and change in firing rate

-> good edge detection, to see where light changes, interpret outlines of objects

65
Q

Lateral Geniculate Nucleus

A

Information - from rod/cone, left/right eye - remains separate in magnovellular (M) and parvovellular (P) pathways to LGN - no crossing of info other than nasal
Stay separate in LGN, recombine in visual cortex

Therefore, visual receptive fields of LGN identical to ganglion cells

66
Q

Primary visual cortex

A

V1
Brodmann’s area 17
Most connections to layer 4 of cortex
Cells respond to bars of light of particular orientation - orientation selectivity
Most respond to info from both eyes - binocularly driven
Not colour sensitive (most)
Simple and complex cells

67
Q

Simple cells in visual cortex

A

Respond best to specific orientation of stimulus bar in receptive field - not at all in some directions

Brain can then analyse best vs worst response, determine orientation of bar
Edge detection

68
Q

Complex cells in visual cortex

A

Some respond to edge (light/dark border) crossing receptive field

  • sensitive to orientation (like simple)
  • insensitive to position (unlike simple)

Will show either on or off firing, no inbetween

69
Q

Anatomical pathway of light detection

A
Rods and cones
Bipolar cells in retina
Ganglion cells in retina
- optic nerve -
Lateral geniculate nucleus
- optic radiation -
Primary visual cortex
70
Q

Lesions in visual pathway

A

Right optic nerve - none right, all left
Optic chiasm - no lateral info
Right optic tract - no peripheral in left, no medial in right

If before LGN, lose in quarters
If in visual cortex, retain central (cutout), lose elsewhere

Because image inverted - peripheral to nasal

71
Q

Substance abuse

A

Drug abuse – taking of drugs for non-medicinal reasons
Drug addiction – chronic, relapsing brain disease with compulsive drug seeking and use, despite harmful consequences. Psychological craving, physical withdrawal symptoms.
⇒ negative health consequences

  • to feel good, feel better, perform better, peer pressure
72
Q

Tolerance and dependence

A

Adaptive changes in response to the presence of the drug – acute -> desensitisation of receptor, chronic -> downregulation of receptor
Adaptive changes in pharmacokinetics – increased metabolism, enzyme induction

73
Q

Drug addiction reward pathways

A

Dopamine
Serotonin (5-hydroxytryptamine)
Glutamate

Ventral tegmental area (VTA) to nucleus accumbens
Increased dopamine with positive outcomes
⇒ learning

Faster onset = better rush – smoking drug best for fast effects

74
Q

Neurotransmitter/neuromodulatory systems

A
Dopamine
Noradrenaline
Serotonin (hallucinogens)
Glutamate
Acetylcholine (nicotine)
Adenosine (caffeine)
Endocannaboid (cannabis)
Opioid (heroin)

Endogenous targets and their receptors – upregulate transmitter or block breakdown of drug, remain in system longer – to have effects

75
Q

Meningitis definition

A
Inflammation of lepto-meningeal membranes (usually arachnoid and pia mater)
Due to
-	infection
-	inflammation
-	parameningeal foci (eg close septic foci (sphenoid sinusitis))
-	neoplastic or para-neoplastic
Rare, very serious – 10% mortality
⇒	disability
⇒	deafness
⇒	paralysis
⇒	speech problems
⇒	epilepsy
⇒	neuro-psychiatric problems
76
Q

Causative agents of meningitis

A

Mainly bacteria – S. pneumoniae, N. meningitidis

Virus
Fungus
Parasites

77
Q

How does meningitis get into brain?

A

Blood brain barrier prevents infection reaching brain – no lymphoid tissue – immunological sanctuary mostly
BUT
- bacteraemia/viraemia/parasitaemia mainly, esp choroid plexus, or where vulnerable capillaries
- direct spread – chronic infections in cranial bones, ears, sinuses, oral cavity, upper resp tract
- neuronal spread – infected peripheral neurones, cell-cell spread eg rabies

78
Q

Pathogenesis of meningitis (once in meninges)

A

Mucosal colonisation
Intravascular survival
Meningeal invasion
Survival in subarachnoid space
Inflammatory response, Increased BBB permeability, Cerebral vasculitis (as vessels clot and inflame)
Oedema, CSF flow disturbances
Increased ICP, Decreased cerebral blood flow
Loss of cerebro-vascular autoregulation -> coma, death

79
Q

Predisposing factors for bacterial meningitis

A
  • Extremes of age (newborns have underdeveloped BBB, elderly has degenerated)
  • Geography – crowded housing
  • Immunodeficiency
  • Trauma/post-neurosurgery
80
Q

Symptoms of meningitis

A

Fever
Neck stiffness
Headache
Altered mental status

Also more specific signs – if see is definitely meningitis, but only 5% will show these
- neck rigidity, Kernig’s sign, Brudzinski’s sign

(so diagnosis challenging – best test is lumbar puncture)

81
Q

CSF findings in meningitis

A

Do lumbar puncture, to subarachnoid space

  • measure pressure, cell count, protein, culture pathogens
  • should be clear, sterile, low lymphocytes

Also many extra tests in CSF – PCR, virology, antigens etc

82
Q

When to not do lumbar puncture

A
RAISED ICP
-	seizures
-	unconscious/low GCS
-	focal neurology
-	post trauma/neurosurgery
-	papilloedema
Need imaging first.
As if do LP with raised ICP, will get sudden drop in pressure, brain can herniate
83
Q

Complications of bacterial meningitis

A

Seizures
Transtentorial herniation
Infarcts -> focal neurological deficits, hemiplesia, paraplesia etc
Hydrocephalus (enlarged ventricles)

84
Q

Managing meningitis

A

SUPPORTIVE CARE
Specific antibiotic therapy – need to also consider CSF penetration (and route)
Steroids – unsure how helpful, but to bring down inflamed meninges
Surgical intervention - if complicated eg local antibiotics needed/hydrocephalus

(Prevent! Vaccines.)

85
Q

CSF penetration antibiotics

A

GOOD
Penicillin, Ceftriaxone, Meropenem, Chloramphenicol

BAD
Vanomycin, Gentamicin