Neuro 3 - special senses

Question 1

Auditory system qualities

Answer 1

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

Question 2

What is sound?

Answer 2

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

Question 3

Audiometric curve of human hearing

Answer 3

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

Question 4

Anatomy of human ear

Answer 4

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

Question 5

Function of middle ear

Answer 5

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

Question 6

Ossicular reflex in middle ear

Answer 6

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

Question 7

Cochlea spiral structure

Answer 7

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

Question 8

Chambers of cochlea

Answer 8

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

Compartmentalisation is essential to keep fluid apart

Question 9

Scala media contents

Answer 9

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

Question 10

Cochlear fluids

Answer 10

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

Question 11

Properties of inner and outer hair cells

Answer 11

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

Question 12

Properties of inner hair cells

Answer 12

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

Question 13

Properties of outer hair cells

Answer 13

~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

Question 14

When sound enters the ear…

Answer 14

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

Question 15

Stereocilia response to movement

Answer 15

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

Question 16

Phase locking

Answer 16

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

Question 17

Tonotropy

Answer 17

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

Question 18

OHCs role in hearing

Answer 18

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

Question 19

How do OHCs amplify

Answer 19

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

Question 20

Otoacoustic emissions

Answer 20

Sounds produced by ear

Send click sound in, hear click back

Question 21

Neural encoding of loudness in IHCs

Answer 21

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

Question 22

Cochlea to brain main pathway

Answer 22

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

Question 23

Function of vestibular system

Answer 23

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

Question 24

Anatomy of vestibular labyrinth

Answer 24

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

Question 25

Vestibular hair cells

Answer 25

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

Question 26

Transduction and encoding in vestibular hair cells

Answer 26

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

Question 27

Stimulation of macula

Answer 27

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

Question 28

Hair cell orientation in vestibular apparatus

Answer 28

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

Question 29

Peripheral vestibular pathologies

Answer 29

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

Question 30

Hearing loss

Answer 30

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)

Question 31

Conductive hearing loss

Answer 31

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)

Question 32

Sensorineural hearing defects causes

Answer 32

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

Question 33

Drug induced sensorineural hearing loss

Answer 33

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

Question 34

Acoustic trauma -> hair cell defects

Answer 34

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

Question 35

Genetic hearing loss

Answer 35

-> 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

Question 36

Presbycusis

Answer 36

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

Question 37

Tinnitus

Answer 37

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

Question 38

Cochlear implant

Answer 38

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

Question 39

Candidacy for cochlear implant

Answer 39

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

Question 40

Properties of light

Answer 40

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

Question 41

Anatomy of eye

Answer 41

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

Question 42

Incident light

Answer 42

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.

Question 43

Retinal landmarks

Answer 43

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

Question 44

Image on retina

Answer 44

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

Question 45

Retinal disease

Answer 45

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

Question 46

Aqueous humour

Answer 46

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

Question 47

Pupillary light reflex

Answer 47

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

Question 48

Light enters eye, pupillary reflex

Answer 48

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

Question 49

Lens

Answer 49

Transparent, bioconvex Behind iris Held by suspensory ligaments Thickens throughout life In cataracts - lens becomes opaque, accumulation of metabolic products

Question 50

Accomodation reflex

Answer 50

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

Question 51

Photoreceptors

Answer 51

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

Question 52

Rod photoreceptors

Answer 52

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

Question 53

Cone photoreceptors

Answer 53

``` 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!

Question 54

Adaptation to light

Answer 54

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)

Question 55

Visual pigments

Answer 55

Rods - rhodopsin (similar to vitamin A) Cones - iodopsin Inside discs From dark to light - conformational change in structure of pigment

Question 56

Colour-deficient vision

Answer 56

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

Question 57

Photoreceptors transducing stimulus

Answer 57

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 ```

Question 58

Light adaptation

Answer 58

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

Question 59

Glutamate action

Answer 59

Product of postsynaptic receptor, not neurotransmitter In visual system, glutamate is inhibitory!

Question 60

Retinal map of rods and cones

Answer 60

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

Question 61

Receptive fields

Answer 61

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

Question 62

Bipolar cells

Answer 62

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.

Question 63

ON system

Answer 63

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.

Question 64

Ganglion cell receptive fields

Answer 64

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

Question 65

Lateral Geniculate Nucleus

Answer 65

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

Question 66

Primary visual cortex

Answer 66

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

Question 67

Simple cells in visual cortex

Answer 67

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

Question 68

Complex cells in visual cortex

Answer 68

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

Question 69

Anatomical pathway of light detection

Answer 69

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

Question 70

Lesions in visual pathway

Answer 70

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

Question 71

Substance abuse

Answer 71

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

Question 72

Tolerance and dependence

Answer 72

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

Question 73

Drug addiction reward pathways

Answer 73

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

Question 74

Neurotransmitter/neuromodulatory systems

Answer 74

``` 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

Question 75

Meningitis definition

Answer 75

``` 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 ```

Question 76

Causative agents of meningitis

Answer 76

Mainly bacteria – S. pneumoniae, N. meningitidis Virus Fungus Parasites

Question 77

How does meningitis get into brain?

Answer 77

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

Question 78

Pathogenesis of meningitis (once in meninges)

Answer 78

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

Question 79

Predisposing factors for bacterial meningitis

Answer 79

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

Question 80

Symptoms of meningitis

Answer 80

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)

Question 81

CSF findings in meningitis

Answer 81

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

Question 82

When to not do lumbar puncture

Answer 82

``` 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 ```

Question 83

Complications of bacterial meningitis

Answer 83

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

Question 84

Managing meningitis

Answer 84

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.)

Question 85

CSF penetration antibiotics

Answer 85

GOOD Penicillin, Ceftriaxone, Meropenem, Chloramphenicol BAD Vanomycin, Gentamicin