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Flashcards in Neuro Deck (278):
1

How many neuones in somatic vs autonomic pathways

2 vs 3

2

What are the emergent properties of the brain?

Properties the whole system has but individual components do not. e.g. consciousness, sensory awareness, thought process, sensory attention

3

What is a Brodmann area?

Area of cortex classificed on histological appearence and subsequently function

4

Explain rostral caudal in CNS

Different for brain stem and cerebrum

5

Explain evolution of brain - out to in

Neocotex - complex function
Paleocortex - memory and emotion e.g. cingulate gyrus, archicortex e.g. brainstem, olfaction

6

What structure separates the anterior lateral ventricles?

Septum pellucidum

7

What is the fornix

Band of nerve fibres within the limbic system which connects the hippocampus, mammillary bodies and the anterior nuclei of the thalamus

8

Where is the calcarine sulcus?

Sagital view- occipital lobe

9

Where is the lateral fissure/ sulcus

Between temporal and frontal/ parietal lobes

10

What is the insula?

Infolding of brian deep
Responsible for consciousness, emotion and homeostasis

11

What is the corona radiata

Neural traffic from cerebral cortex

12

What is the caudate nucleus

Part of basal ganglia.
Involved in voluntary movement.
Loops around the putamen/ globus palidus, lateral to thalamus and medial to insula

13

What is the lenticular nucleus

Lens shaped, formed from the putamen and globus pallidus (medial).

14

What is the corpus striatum?

striatum plus globus pallidus/ caudate + lenticular

15

What is the (neo)striatum?

Caudate nucleus and the putamen.
Responsible for reward, motivation, motor and action planning

16

What composes the basal ganglia

Corpus striatum, substantia nigra and subthalamic nucleus

17

What are the cerebellar peduncles

Fibres from cerebellum to brain stem. L and R sup, mid and inf (6)

18

Briefly explain drainage on the brain

Centrally via the superior and inferior sagittal sinuses. Into confluence with occipital.
Transverse sinuses to sigmoid to IJV

19

What is the conus medullaris

Tapering end of spinal cord T12-L1

20

What is the filum terminale

Delicate strand of fibrous tissue from apex of conus medullaris - continuation of pia. Travels within a dural sac before adhering to the dural and then fusing to the coccyx

21

What are the denticulate ligaments?

Ligaments either side of the spinal cord which attach to the arachnoid and dura maters to provide support (between them) extension of Pia.

22

Describe lumbar puncture

L3/4 by finding the PSIS and going medially- feel above and below for largest space

23

Safe Lumbar puncture in kids?

L5/S1

24

Where is the substantia gelatinosa and what is found there?

Rexed lamina 2. Part of spinothalamic trunk. C fibres pain gate control theory of pain. Fibres from Lissauer's synapse here. 2nd order neuones then deccusate in the anterior white commissure.

25

Where is the substantia nigra and what is found there?

Parts of rexed lamina III-V form. Pain and temperature from spinthalamic. Fibres from Lissauer's synapse here. 2nd order neuones then deccusate in the anterior white commissure.

26

Difference between ataxia and apraxia

Apraxia = inability to perform complex movements despite having the capability to bring about movement
Ataxia = a loss of full control of body movements

27

Aphasia vs aphonia vs dysarthria

aphasia = speech and language disorder
aphone = pysical inability to produce sound e.g. bilateral recurrent laryngeal nerve damage
Disarthria - disruption of articulation of speech e.g. movement of tongue

28

What is paraplegia

Loss of sensory and motor functions of lower limbs

29

What is Chorea

Involuntary jerky movements of hips shoulders face e.g. Huntington's

30

Describe features of spasticity

hypertonia, hyperreflexia and paralysis

31

What is a neuropore

End of neral tube as it fuses away from cervical region

32

How can spina bifida be detected before birth?

alpha-fetoprotein in blood test or amniocentesis
USS

33

Types of spina bifidal

Occulta - just vertebrae affected often asymptomatic
meningocoele - meningeal involvement
Myelomeningocoele - neural tissue outside the body

34

Symtoms of spina bifida

Anywhere along length of cord by normally lumbosacral.
Weakness in lower limbs.
Blader control
Orthopaedic problems
Pressure sores
Hydrocephalus
Neurological development - behaviour, problem solving and memory

35

Neural tube defect cranially

Anencephaly
Rachischisis - failure of neural fold elevations = motor and sensory deficits, chronic infections, and disturbances in bladder function or anencephaly

36

How can hydrocephalus be treated? What happens if no treatment?

Peritoneal/ jugular shunt
causing convulsion, tunnel vision, and mental disability.
headaches, vomiting, nausea, papilledema, sleepiness or coma

37

Describe the dilations/ development of brain

3 cranial dilations in neural nube.
Prosencephalon becomes telencephalon (cerebrum) and diencephalon (thalamus).
Mesencephalon becomes mesencephalon (midbrain).
Rhombencephalon becomes metencephalon (pons) and myelencephalon (medulla oblongata)

38

Location of ventricles in respect to enbryology

Lateral in tele
third in Di
Aqueduct in mes
Forth in Met/ myel

39

Describe the flexures of the CNS

Cervical at spinal cord/ medulla juntion
Cephalic at midbrain

40

Describe the growth of the neural tube into CNS structures

Thickening around central canal = neuroepitheal layer
Mantal around that into dorsal/ alar (sensory) and ventral/ basal plates being motor. Around that is marginal layer which is white matter

41

Descrbe neural crest cells in CNS developemtn

Migrate
Undergo epithial to mesenchyme tranisition.
Include:
Cranial nerve ganglia
Spinal/ dorsal root ganglia
Sympathetic ganglia
Schwanne cells
Leptomeninges

42

How can alcohol affect developing CNS?

Neural crest cell migration

43

What is Hirschsprung's disease

Aganglion megacolon - failure of migration

44

Describe the functions of astrocytes

Provides structural support
Provides blood brain barrier
Removes (uptakes) neurotransmittors
Provides nutrient to neurones e.g. glucose-lactate shuttle as no glycogen store
Maintains ionic environment e.g. buffers K

45

Describe the functions of microglia

Phagocytose foreign material and debris - becomes activated. Can APC and activate t cells although inflam is limited as CNS is immune privileged (not to raise ICP). Immune privileged means they can tolerate antigens without an inflam response.

46

Describe components of the BBB

Tight endothelial cell junctions, basement membrane and astrocyte foot processes.

47

Types of neurotranmittors

Amino acids e.g. GABA, glycine, glutamate. Biogenic amine e.g. dopamine, na, 5HT, histamine. Peptides e.g. dynorphin, somatostatin, CCK. Others e.g. purines

48

Describe Glutamate as a neurotransmittor

70% of all synapses. Excitatory.
Ionotropic or metabotropic

49

Explain ionotropic glutamate receptors

AMPA -fast K Na
Kainate- K Na
NMDA - slow K Na Ca (glycine also agonises) Causes depoalrisation EPSP

50

Explain metabotropic glutamate receptors

G protein coupled, linked to IP3/ Ca/ cAMP. known as mGluRs. Can upregulate AMPA

51

Upregulation of Glutamate receptors? Signidicance?

From NMDA and mGluRs upreg AMPA.
Long term potentiation. Ca through NMDA is important however too much can lead to excitotoxicity

52

Decribe GABA and glycine and their receptors

Inhibitory (IPSP).
Binding to receptors with integral Cl- causes hyperpolarisation.
GABA can also bind to modulatory GPCRs.
GABA is main ihibitory. Barbiturates and Benzos work here.
Glycine mostly in the spinal cord and brainstem - inhibitory interneurones in reflex pathways

53

General action of biogenic amines and Ach

Mostly neuromodulators confined to specific pathways.

54

Describe Ach neurotransmission effects and clin sig

Autonomic functions
Mostly excitatory
Often present on pre synaptic terminal to enhance the release of other transmitters.
Also nicotinic and muscurinic in CNS.
Neurones originate in basal forefrain and brainstem spread diffusely to cortex and hippocampus (hence learning and memory).
Within the corpus striatum.
Degen in Alzheimers

55

Dopamine pathways

Nigrostriatal = motor control (parkinsons)
Mesolimbic (psychotic treatment in schitzo D2) and mesocortical = mood, arousal and reward
tuberoinfundiblar = prolactin release and endocrine function

56

Describe Na pathways

Brainstem = neurone bodies.Most from locus coeruleus in pons.
Release of Na throughou cortex, hyothalamus, amygdala and cerebellum.
Inactive during sleep and increases with arousal.
Deficiency linked with depression

57

Describe 5HT pathways

Similar to NA.
From Raphe nuclei also in pons.
Functions:
Sleep
Wakefullness
Mood
Vomiting centre

58

Origin of superior cerebellar artery

Basilar artery just posterior to superior cerebellar artery

59

Origin of inferior cerebellar artery

Lateral off vertebral artery

60

Origin of anterior spinal artery

Anastomosis between vertebral arteries

61

Origin of pontine arteries

Basillar artery

62

Origin of opthalmic arteries

ICA just before it becomes middle

63

Describe blood supply to the spinal cord

Ant and 2 post in SAS. From anastomostes with segmental medulary arteries.
Radicular and intercostal arteries from abdominal aorta. Disruption of artery of Adamkiewicz can cause infarction e.g. AAA surgery

64

Supply of anterior posterior and middle cerebral arteries

Medially - mostly anterior (almost all of cingulate gyrus and corpus callosum) the posterior for occipital lobe.
Middle = lateral surface (not feet of precentral gyrus.
Middle and posterir share temporal lobe

65

How does CSF cushion brain?

Isotonic

66

Causes of subarachnoid

Berry aneurysm

67

How does CSF get removed and where?

Arachnoid granulations at superior sagittal sinus

68

CSF from forth to subarachnoid space via?

foramen magendie

69

What drives flow of CSF

Pressure and chorid epithelia villi

70

What causes a communicating hydrocephalus

Factors external to ventricular system e.g. scarring of meninges at arachnoid granulations

71

How is CSF different from blood?

Lower conc of glucose, Ca, protein, K but higher Na, Mg and Cl. Very low immune cells

72

State the foramen of the cranial nerves as they leave the skull base

1 Cribiform plate
2 Optic canal
3 Superior orbital fissure
4 Superior orbital fissure
5i Superior orbital fissure
5ii Foramen rotundum
5iii Foramen ovale (post sphenoid) and foramen spinosum just lateral to in
6 Superior orbital fissure
7 Facial canal (internal acoustic meatus then stylomastoid foramen)
8 Internal acoustic meatus
9 Jugular foramen
10 Jugular foramen
11 Jugular foramen
12 Hypoglossal canal

73

Describe sensory neuones

Free nerve endings in temp
Encapsulated for pressure
Specialised cell cuch as pacinian corpuscle for pressure and vibration

74

What is a quality

Subset of a modality e.g. salt, sweet, sour

75

Types of receptors found in muscle

Proprioceptors in muscle spindle = length
Golgi tendon organ = tension

76

Are receptors specific to one modality

Generally yes but punch in the eye

77

How are stronger stimuli recognised?

More AP frequency
Neibouring cells activated

78

Whats the difference between tonic and phasic receptors

Tonic - slowly adapting, continually firign
Phasic - raidly adapting, respond maximally and briefly to a stimulus

79

How is sensory acuity achieved? What is it?

Precision by which a stimulus can be located
Laterally inhibiting interneurones
2 point discrimination
Synaptic convergence (decrease) and divergence (increase

80

What is two point discrimination and what factors influence it?

Minimum distance required to percieve two simultaneously applied skin indentations.
Dependant on size of receptive field and density of sensory receptors.

81

How is the percieved loaction of a stimulation based on?

Crude thalamic localisation. Proetion into cortex.
Somatosensory cortex sharply localises the stimulus. Somatotropic representation.
Relays to other cortical and sub-cortical areas to chose how to respond

82

What is perception?

Ability to sense stimuli and discriminate between different types

83

What is the result of a lesion of the sensory cortex?

Epleptic events, loss of two point discrim, astereognosis (3D) touch

84

L and R of the spinal cord are divided by what?

Dorsal median sulcus and the ventral median fissure

85

What fibres do the dorsal columns carry

Light touch and proprioception

86

Describe the fasciculi of the dorsal column

Gracile = medial (thinner) above T6
Cuneate lateral below T6

87

Describe the two corticospinal tracts' modalities

Lateral = limb
Ventral = axial
motor descending

88

Describe the spinothalamic tracts' modalities

Lateral = pain and temp
Anterior = crude touch

89

Describe the Medial lemniscus pathway

=Dorsal column.
1st ganglion = dorsal root ganglion.
Secondary neurones in the cuneate and gracile nuclei in the medulla.
Decussate to become the internal arcuate fibres to become the medial lemniscus pathway in the Pons and midbrain.
Terminate in Ventral posterolateral nucleus in the thalamus 3rd.
THese terminate in the post centra gyrus (proproception in the sensory-motor cerebral cortex).

90

Describe the spinothalamic tract pathway

Lissauer's fasciculus for 1-3 levels. 1st cell body = dorsal root.
Terminate in dorsal horn in Sub gel or nucleus proprius
Deccussate in same level.
Ascends to thalamus at the ventra posteriolateral nucleus.
Tertiary to post central gyrus via internal capsule.
Ascend somatotropically Caudal = dorsolateral.

91

What is Syringomyelia?

cyst (syrinx) in spinal cord from rugby/ spinal injury e.g. high tackles. Causes pain, paralysis, weakness, loss of temp sensation.
Filled with CSF into spinal cord

92

Describe Brown- Sequard syndrome

Hemisection of the spinal cord. Loss of ipselateral dorsal column = ipsilateral proprioception and fine touch.
Couterlateral = temp and pain.
(spinothalamic)
Causes include tumour, trauma, ischemia, infection and inflammation

93

B12 deficiency neuro?
Also B6 -pyroxidine

Dorsal root column degeneration

94

Effect of syphillis on spinal cord?

Tabes dorsalis.
Demyelination of dorsal column

95

What is Freidrich's ataxia?

Heridatary.
Sclerosis and degeneration of dorsal root ganglion, spinocerebellar tracts, lateral corticospinal tracts, and posterior columns.
5-15

96

Describe Shingles pathology

Reactivation. Dormant in dorsal root ganglion. Infects PNS neurones.
Increased sensitivity and rash.
Postherapeutic neuralgia = chronic pain

97

Explain conscious and unconscious proprioception pathways

Concious = Dorsal column spinal tract.
Unconscious = Dorsal and ventra spinocerebellar tracts and the Cuneo-cerebellar tract.

98

Describe the Spinocerebellar tracts

1st order from muscles terminate in Clarke's nucleus/ column. Cell body in dorsal root ganglion.
2nd order trvel in lateral funiculus 3.
Dorsal remains ipsilateral.
Anterior decussates in the cord but the recrosses in the cerebellum and is ipsilateral

99

Direct of fall in cerebellar damage

= ipsilateral fall and coordination
Vermis damage = fall backwards

100

Define a motorneuone

A somatic efferent that displaces limbs and sets muscle tone.
Upper and lower motor neuone

101

Upper motor neurone lesion signs.

Hyper reflexia
Hyper tonia
Hypokinesia (regidity)
Spastic Paralysis
Chorea if extrapyradimal
Pyradimal = Babinski

102

Lower motor neurone lesion signs

Paralysis
Flaccid weakness
Hypotonia or atone
Hyporeflexia or areflexia
Atrophy
Fasciculations

103

Origin of LMN?

Rexed laminae VIII and IX. Cranial nerve motor nucleus = CNVII not in spinal cord?

104

What is a motor unit?

A-motorneurone and all the mucle fibres it supplies = minimal functional unit.

105

What is a strecthc relfex

An involuntary, unlearned, repeatable, automatic reaction to a specific stimulus that does not require the brain intact.

106

Name the 5 components to a strectch relex

A stretch receptor (e.g. golgi organ or muscle spindle)
Afferent fibre
Integration cetre
An efferent fibre
An effector

107

What is a myotatic reflex?

Monosynaptic stretch reflex. Sets motor tone

108

Muscle tone in utero and new born?

Low in utero and supressed in new born and returns within months

109

Muscle tone during sleep and exceptions?

Increased inhibition during sleep apart from resp, extraocular muscles and sphincters.

110

What do gamma motor neuones do?

Adjust sensitivity of muscle spindles, allow a motorneurones to continue to discharge

111

Signs of an extra pyradimal lesion e.g. cerebellum or basal ganglia

Tardive dyskinesia, parkinsonism (tremor, rigidity, dyskinesia), akathisia (muscle restlessness), dytonia e.g. spasms
Corticospinal = fine movements.
Extra pyradimal = way they are carried out

112

Two pyradimal tracts?

Corticobulbar and corticospinal tract

113

Describe the cortico-bulbar tract

Fibres from Motor cortex/ pre centra gyrus to nuclei of motor cranial nerves - 5, 7, 9,10,12 (not Occulomotor).

114

Descrube the corticospinal tract

Pre central gyrus (primary motor cortex).
Through internal capsule to brain stem.
Travels in anterior medulla in medullary pyramids.
Limb motor fibres deccasate at bottom of medulla and become lateral corticospinal tract.
Synapse directly in ipsilateral anterior horn (VIII, IX).
Ant = axial, no decussation in anterior white commissure then synapse in ant horn also.

115

Describe the non-cortical/ extrapyradimal descending tracts

Rubero = voluntary skeletal contraction e.g. hand.
Reticulospinal = Autonomic control, posture and locomotion, modulation pain
Tectospinal = automatic reactions to visual and auditory stimuli (cervical)
Vestibularspinal = Posture maintainance, damage = loss of righting reflex, ataxia of gait and postural instability

116

Decorticate appearence

Flexors- Cs = spinal tract or cerebral. Relative strength of flexors and extensors

117

Decerebrate appearence

Extensors Es = pons or midbrain e.g. reticulospinal

118

Why do you get fasciculations?

Upregulation of Ach receptors. Ach remnants in the blood.

119

What is spinal shock?

Damage to descending tracts.
Areflexia and flaccid.
Gradually turns to UMN signs.

120

Explain the functional zones of the cerebellum

Vestibulocerebellum (archicerebellum): balance and ocular relfexes
Spinocerebellum (Paleocerebellum)- error correction (recieves proprioceptive and visual imputs
Cerebrocerebellum (neocerebellum) - motor planning, memory and coordination

121

Signs of Cerebellar dysfunction

Dysdiadochokinesia, Dysmetria (past pointing)
Ataxia
Nystagmus
Intention tremor
Scanning dysarthia (monotone)
Hypotonia

No atrophy or weakness

122

Positive Romberg test and uses?

Causes of gate-
ataxia = sensory
Suggests cerebellar damage

123

Causes of Cerebellar dysfunction?

Tumour, stroke, genetic e.g. friedreich's ataxia

124

Briefly explain the direct, indirect and hypodirect pathways throught the basal ganglia

Direct = Cerebral cortex - striatum, inhibits GPi/ SNr, activates thalamus. - more movement. (Dopamine from SNc increases).
Indirect - striatum inhibits GPe, inhibits STN, activates GPi/ SNr, inhibits thalamus- acts to dampen direct and give finer control. (Dopamine inhibits)
Hypodirect - Cerebral cortex activates STN - activates GPi/ SNreticulata, inhibits thalamus. = breaks

125

Explain pathophysiology of parkinsons

Progressive degeneration of dopaminergic neurones of the substantia nigra/ nigrostriatal pathway.
Less contol of movements

126

Describe signs and symotoms of Parkinson's

Tremor at rest reduced by movement and increased by distraction 'pill roll'
Hypertonia - lead pipe/ cog wheel rigidity
Bradykinesia
PD gait - small shuffle, pedestal turn, tremor only in upper body

127

Define pain

An unpleasant and emotional experience involving actual or potential tissue damage.
Has autonomic, somatic, endocrine and emotional responses

128

What is nociception and some things that can affect it

The perception of physical pain
Modified by experience, expectation, immediate context, culture

129

Threshold and tolerance to pain.

Threshold is all the same
Tolerance is our variable reaction to a painful stimulum. Increases with age, placebo effect, ongoing pain ect.

130

Difference between direct and indirect lateral STT

Fasts vs Slow
Intensity loation, quality (somatotopic) vs affective e.g. arousal, emotion
no synapse vs synapse in BS
Corical target vs hypothalamus, RF, Limbic, autonomic centres

131

Describe the stages of nociception

Transduction - activation of nociceptors
Transmission - replay of action pertentials along nociceptive fibres to CNS
Modulation - By other peripheral nerves or CNS
Perception - Interpretation

132

Difference in stimulation of Adelta and C fibres

Ad = mechanical
C = mechanical, thermal, chemical (polymodal)

133

Perception of Ad, C and visceral fibres?

Ad = stabbing sharp, ow, well localised, first pain, lower threshold, withdrawral reflex
C = Dull throbbing 'ooh', poorly localised, second pain, higher threshold, tissue damage occuring.
Visceral fibres share somatic nociceptive fibres

134

Rexed lamina of Ad, C and cisceral fibres

Ad = I, V
C = Substantia gel (i, II) and V.
Visceral = V

135

Describe transduction of pain

Lesion = K, prostaglandins, 5HT, bradykinin which activate.
AP fired and substance P released from nerve endings.
P increases cap permeability and contributes to inflam.
P (and CGRP - calcitonin gene replated peptide) causes rast cells to release histamine (further nociceptive activation).

136

Actionn of drugs on transduction

NSAIDS -prostaglandin
Steroids - IL

137

How can transmission be blocked

Local anaesthetic e.g. lignocaine, inhibits VGSC

138

What is analgesia and what can cause it?

Inability to perceive pain when tissue damage is occurring. Hypnosis, morphine, TENS (transcutaneous electrical nerve stimulation), natural childbirth techniques and placbos

139

Describe pain modulation in spinal cord

Exogenous methods e.g. analgesics.
Gate control theory
Endogenousour opioid peptide analgesics (and others) from centtral and decending spinal systems.
Mediated by the periaqueductal grey matter (PAG) in midbrain via feedback from thalamus, cortex, hypothalamus.
Act on nucleus raphe magnus

140

Why does rubbing help?

Stimulates cutaneous inhibition which increases descending inhibition

141

Describe perception of pain

Thalamus and the cortex
Varies hugely
Thalamocortical projection = info about pain.
Emotional via limbic
Stress via hypo

142

What is chronic pain

Pain >3 months. Unknown cause/ underlying problem or pain disorder.

143

Describe the gate control theory of pain

Between SG (via interneuones) around the synapse of C/A fibres in dorsal horn

144

What is hyperalgesia

Increased pain at a normal threshold stimulation.
Results from peripheral and central sensitisation

145

What is allodynia

Pain from stimuli not normally painfull.
Also from an area not stimulated (not referred)

146

Signs of pain

Brow lowers, lids tighten, nose wrinkles, lips tighten

147

Describe 'winding up'

Tissue injury causes nerve damage and pain
Repeated C stimulus
Excess Glutamate and NMDA.
Upregulation so these neurones become hyperexcitable (lower threshold) and hyperalgesia.
Can lead to receptive field expansion or allodynia.
Pain decreases after stimulus but does not reach zero before another (same stimulus).
Changes in somatosensory mapping

148

Types of chronic pain

Nocicpetive, Neuropathic (central and peripheral), Visceral (organ disease inflam), mixed e.g. cancer, lower back, FMS (fibromyalgia)

149

Explain nocicpetive chronic pain e.g. RA

Wind up
Inflam
Synovia damage
C and A delta
Hyperalgesia

150

Explain neuropathic pain

Neuronal origin
Not explained by a single location/ disease.
Central e.g. thalamic lesion presenting as somatic sensation, not responsive to opioids.
May be burning, shooting, pins and needles.
Causes usual decreased in thrshold, increased fields, prolonged stimulus (hyperpathia).
Spontaneous activity.
Includes hantom limb pain

151

Describe complex regional pain syndrome types

Type 1 - no lesion but after illness e.g. RSD (reflex sympathetic dystrophy)
Type 2 - identifiable nerve lesion e.g. causalgia - burning in limb caused by peripheral nerve lesion

152

What is RSD/ CRPS symptoms

Reflex sympathetic dystrophy
Sensory - severe, continuous burning pain, hyperalgesia,
Vasomotor -
Sudomotor/oedema
Motor/ trophic - decreased range of motion, dysfunction, trophic (skin) changes

153

Stages of CRPS

1 - acute
II dystrophic - thickening of skin, muscle wasting, oedema
III atrophic - limitation of movement, contractures, waxy skin

154

Opiod receptor info

GPCRs, close VOCC, open K, inhibit cAMP and neurotransmittior release

155

Opioids and their receptors

Endomorphins = MOP
Dynorphins = KOP
Enkephalns =DOP

156

Give common weak opiods

Codeine

157

Give strong opiod examples

Morphine, Fentanyl

158

Who analgesic ladder

1 non opiod +/- adjuvant
2 weak opiod adjuvant
3 strong oioid adjuvant,
Non = Paracetamol, NSAID

159

Definition of adjuvants and examples

A pharmacological agent fiven to increase or aid a drug's effect. Not analgesics in their own right.
AEDs and Steroids e.g. prednisolone

160

Central pain and opiods?

May be opiod insensitive so antidepressants, AEDs, local anaesthetics and opiod mixtures are given

161

Describe the development of the ear

Otic placodes arise laterally
Grow and invaginate
Pinch off to become auditory vesicle
Changes shape to form membranous labyrinth: Utricle and saccule/
Utricle becomes semi lunar canals and saccule become choclear. Ossicles from 1st and 2nd arches.
Pouch and cleft forms meatus.
Mandible grows and the ears ascend to be in line with eyes

162

Define placode

Thickened ectoderm patches on developing head

163

Congenital causes of middle ear deafness?

Problems with 1/2 branches

164

Causes of inner ear deafness

Tetratogenic agents and infection e.g. rubella

165

Describe development of the eyes to shreks ear

Lens placode invaginates and pinches off. Shreks ear. Choroid fissure in the middle.

166

Whats inside the choroid fissure and its fate

Hyaloid artery- degenerates distally to become the central artery of the retina

167

Fate of the optic cup?

Retina (pigment and sesnory/ neural) in to layers which fuse, iris and ciliary body (from the rim)

168

Where do muscles of the eye come from?

Preoptic myotomes from the surrounding region

169

How does coloboma arise?

Failure of fusion of the edges of the optic stalk around choroid fissure inferio-medially

170

Future pathology associated with the optic cup?

Retinal tear = separation of the layers

171

What is the iris?

A contractile diaphragm with a central aperture

172

Features of rubella?

Microcephaly, PDA, cataracts

173

Where does the optic tract start and terminate?

Starts at the optic chiasm and terminates at the lateral genicular nucleus

174

Temporal lobe optic rediation lesion = what?

Superior visual field defect (ST elevation) so an inferior retinal field problem.

175

Where is Meyers loop?

Temporal optic radiation

176

Describe differences in rods and cones

Not in fovea vs fovea
Photosensitive vs high acuity
Dark adapted vs day vision
Converge on bipolar cells vs blue, red and green.

177

Describe the three main functional classes of neurones

Photoreceptors
Interneurones
Ganglion cells

178

Describe interneurones

Bipolar, horizontal and amacrine.
Combine photoreceptor signils

179

Describe Magnocellular ganglion cell pathways

No sensitive to colour
Sesnsitive to luminescence contrast and fast motion. Magnum = fig e.g. foramne magnum - looks at big picture? Via the dorsal stream to the posterior parietal cortex

180

dESCRIBE pARVOCELLULAR GANGLIIONIC CELLS

bETTER AT COLOUR CONTRAST, NOT LUMINANCE AND FINE DETAIL HOWEVER LESS SENSITIVE TO MOTION.
Goes via the ventral stream to the inferior temporal cortex

181

Describe the primary visual cortex

Separated by the calcarine fissure
Occipital lobe
Each quarter of VF is represented, larger area for macula/ fovea.
Interpretation by cortex e.g. comparison of things so some may seem bigger.

182

Explain the development of cones

Take ages to mature.
Can be seen via Optical coherence tomography (OCT) - images the retina.
Can see development of the outer nuclear layer still at 5 years. Fovea only has an outer nuclear layer

183

Sign of fovea hyperplasia?

Nystagmus

184

What is ambyopia?

Diminished vision in one eye and a result of disuse in childhood.

185

Causes of ambyopia

Strabismus - inability to focus both eyes on one object = lazy eye
Anisometropia = refractive difference in botheyes
Deprivation e.g. congenital cataracts, ptosis, media opacies

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Types of anisometropia

Emmetropia = normal
Myopia = infront of retina
Hyperopia = behind retina

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Types of Stabismus

Esotropia = In
Exotropia = out
Left hypertropia = up
hypotropia = down

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Treatment of ambyopia

Glasses/ patch when yound due to brain plasticity but poor comliance

189

What is glaucoma

High intraocular pressure, damage to optic nerve, peripheral field defect which is often unnoticed and gradual

190

Sympathetic innervation of eye pathway

Hypothalamus to T1, To Superior cervical ganlion under SCA to dilator pupillae

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Abduction and adduction movements

SR and IR are opposite
SR and SO are inverse.

SO abduct = intorsion

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Appearance of VI nerve palsy

Esotropia

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IV nerve palsy

Hypertrophia

194

III

Exotropia and hypotropic
Also ptosis and mydriasis

195

Describe the properties of sound

Compressive wave, frequencey and amplitude

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Level of conversation and painful sound

60dB vs 120dB

197

Describe the travelling wave theory

Basillar membrane resonates and machanically amplifies sound with progressively lower frequencies along its length.

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What is Tonotopy

Place on basillar membrane = frequency

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Describe the structure of the basillar membrane

One row of inner hair cells and 3 rows of outer hair cells.

200

Functions of inner and outer hair cells

Inner sense sound
Outer amplify sound
Mechanically tuned by location and electrically tuned by expression of particular ion channels .
Both contain stereocillia to sense sound

201

What is the tectorial membrane?

attached to the hair bundles. Not sure of function. When basilar moves?

202

Exlain How bending of stereocillia triggers a nerve AP

Bending opens K channels = depolarisation as endolymph at high conc. Larger if more displacement.
Ca influx
Triggers transmitter release onto spiral ganglion neurones (SGN) - afferent axons of CNVIII

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What is the olivocochlear system?

Regulates OHC amplification via efferent feedback

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How are loud sounds interpreted and location

More APs from SGN, recruitment of neighbouring fibres. Goes to choclear nucleus in the auditory brainstem. Goes to Medial nucleus of trapezoid body on both sides. Delay allows left/ right and difference in volume/ amplitute.

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What constitutes the auditory brainstem?

Lateral and medial superior olives and the medial nucleus of the trapezoid body.

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The auditory pathway

Cochlear
SGN
Dorsal and ventral cochlear nuclei
Suppeior olive
Inferior colliculus
Medial geniculate nucleus
The auditory cortex

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Causes of hearing impairment

Age, presbyacusis
Infection
Congenital
Loud noises
Gentamicin
TraumA

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Explain the assessment of hearing

Otoscope
Audiograph - sensitivty against frequency (higher lost with age)
Otoacoustic emissions (sound generated by OHC - test in babies)
Auditory brainstem response - electrodes on the brain

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Treatments fr hearing loss

Hearing aid
Cochlear implant
Cochlear nucleus
implant.

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Congenital causes of hearing loss

DFN - X linked
DFN - AD
AFNB AR
Hair hells, tectorial ....

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Where do most strokes occur?

Middle cerebral artery

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Describe the vertebral arteries

Tortuous
Posterior ineferior cerebellar artery is the largest branch.
Also the spinal arteries

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Describe the Basilar artery

Supplies most of brainstem. Located over pons.
Superior and anterior inferior cerebellar arteries. supplies most of PCA

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Describe PCA distribution

Occipital, midbrain, thalamus, half on temporal

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Define stroke

Abrupt loss of brain function lasting more than 24 hours or causing death due to inadequate blood supply or spontaneous haemorrhage

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Causes of cerebral infarct

Atheroma, embolism, idiopathic, arterititis, blood disorder

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Describe intracerebelar haemorrhage causes

Primary or Secondary
Haemorrhagic transformation of infarct
Hypertensive, microaneurysms, lipophyalinosis (wall problem), AV or aneurysm, amyloid, haemostatic, cocain, amphetamines, tumour, venous thrombosis

218

Define TIA

Sudden focal disturbance of brain functioning (global or local) which resolves within 24 hours

219

Temporal lobe stroke signs

CNVIII, taste and smell
Wernicke's area
Memory
Optic radiation - superior quadrantanopia

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Pariatal lesion

Primary sensory cortex
Neglect
Speech
Optic radiation either inferior or hemianopia

221

Describe TACS - total anterior circulation stroke

Proximal occlision
Contralateral hemiparesis/ hemianaesthesia
Higher dysfunction
Hemianopia
High mortality

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Describe PACs

Occlusion of MCA or restricted infarct
2 signs from TACS or restricted motor deficit (one thing e.g. face) or isolated cortical signs
High early recurrence

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Describe LACS (lacunar stroke)

Single perforating artery in the basal ganglia or pons.
Pure motor, sensory, sensory motor, ataxic or hemiparesis.
Silent and underdiagnosed

224

Describe POCS

Brainstem, cerebellar or occipital involvement.
Complex presentation

225

Atypical symptoms of stroke

Delerium, confusion, collapse, incontinence

226

Write note for telangiectasia

k

227

Investigations for stroke

BM
HAematology
Biochem
CT/ MRI
Carotid US
ECG
Echocardiogram

228

Treatment for stroke

IV thrombolysis - alteplase
Early asprin
Acute stroke unit

229

Damage to spinal cord blood supply

Aortic damage
Vasculitis - giant cell arteritis
Sickle cell
Hypotension
Cardiac emboli
Disc Herniation

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Symptoms of spinal artery occlusion

Spinal shock. (seen in urinary spincter too)
Normal ant so dorsal is fine (proproception and touch)
Normally motor

231

What is a flaccid bladder? (same as areflex)

Lesion at S2-4 lower motor neurone

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Describe reflex bladder

UMN lesion.
Works fine but detrusor is more sensitive.
No control.
Increased muscle tone.

233

Describe motor and sensory areflexic bladder

Aware on unaware of filling - no release in response. Lesion of the sacral spinal cord or sensory nerve or detrusor

234

Describe the management of head trauma

ABCD (disability)
History
Examination

235

RAS control

dd

236

What is a coup and contrecoup injury

Coup = front
Contrecoup = rebound`

237

What are contusions?

Damaged blood vessels around the brain (like bruising)

238

Describe primary and secondary insult in brain

Primary = haematoma, contusion, haemorrhage, diffuse axonal injury
Secondary = preventable, hypoxiam hypoperfusion, oedema, ICP.

239

BBB disruption?

More permeable so vasogenic oedema.

240

What is cytotoxic oedema?

Inflam mediatorys and oxiditive stress. NA retention

241

ICP compensation?

CPP = MAP-ICP.
Venous blood and CSF can move out of brain to lower ICP.
MAP increases (mean arterial pressure) via Cushings.

242

Uses of propofol

Decreases Cerebral metabolic rate of O2 (CMRO2) like hibernation.
Dose dependent

243

USe of Thiopentone (barbiturate)

Decrease CMRO2
Hypotension
EEG monitoring - birst suppression.
Vary heavy = seizures- very bad as high O2 requirement

244

Describe use of opiods

Pain relief
Reduces stress response
Reduce cough so can intubate
Can exacerbate hypotension

245

Benefits to ketamine? and disadvantages?

No effect on BP
Predictable
No loss of airway relfexes, semi conscious, hallucinations/ terrors.

246

Use of neuromuscular blocking agent

Need for intubation

247

Use of mannitol

Potent osmotic diuretic to remove cererbral oedema but can worsen if passes the BBB

248

Explain vasopressors

Adjust BP
Invasive BP monitoring
given IV (impair venous drainage?)

249

MEasures in medically induced coma?

EEG
Bispectral index - depth of anaethesia 1 number from many imputs
ITU nurse and wakefullness

250

Evidence and reasoning behind medically induced comas?

Relieve swelling and brain decrease brain damage.
Mixed evidence.`

251

Describe the reticular formation

Central core of brain stem, includes raphe and nucleus coeruleus.
Sleep regulation
Motor control
Cardio/ Resp control
Autonomic functions
Motivation and rewards.
Ascending reticular activating system = consciousness

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Imputs on the reticular formation

Senses, hypothalamus, drugs and alcohol. Activate/ inhibit arousal/sleep.

253

Outputs of RF

Motor system (make more sensitive), autonomic, thalamus, cortex. Many different neurotransmittors. Ach sensitises thalamus to sensory stimuli but quiet during sleep.

254

RF in sleep

Ach silent.
Cortex can inhibit RF if wanting sleep- waves on EEG. e.g. whilst driving

255

Describe EEG and waves

Algebraic sum of electrical activity.
Less info when eyes are shut so higher amplitude and lower frequency. Hihger frequency when open and wavees cancel each other out.

256

Describe specific wave forms

Delta large - deep sleep and brain conditions
Theta intermediate Parietal and temporal children concentrating or meditating adults
Beta like theta but irregular = awake parietal and frontal
Alpha small = awake occipital

257

Describe locked in syndrome

Loss of RAS descending pathways e.g. lesion below the mid pons - patient is alert and aware but quadriplegic and mute.

258

What is persistent vegative state?

loss of cortex PVS different from coma as they show some signs of consciousness. Brain death is the irreversible loss of all features of the brain

259

What is a coma?

State of unconsciousness from which a patient cannot be roused using pain, sound, light. No voluntary movement.

260

Describe the purpose of sleep

Allows CNS to reset and memories to process

261

What controls the sleep wake cycle?

RF and hypothalamus (by inihibiting the RF)

262

Describe a sleep cycle

Quickly into stage 4 (1 hour), straight back to REM, then cycle between stage 3 and REM with progressively more REM

263

Describe REM sleep

Active brain, inactive body
EEG as if awake
Waves from pons to thalamus to occipital = dreaming
Difficult to disturb
Irregular HR and RR
Increased BMR
Descending inhibition of motorneurones
Penile erection
Reduced by alcohol
Na and 5HT inhibited - explains memory without emotion

264

Describe non REM sleep

Slow wave sleep
Active body, inactive brain
e.g. sleepwalking
3/4 stages
Waves decreasein amplitude to stage 3 then become delta waves- slows.
Restorative
Neuroendocrine
Decreased cerebral bloodflow, O2 consumption, temp, BP, RR, lower BMR

265

Describe waking

Na and 5HT start to be released. Ach from brainstem sensitises thalamus and allows wakefulness - thalamo-cortical neurones and communication

266

What is parasomnia

Sleep paralysis

267

What is hypersomnia

Day time sleepiness e.g. OSA

268

What is Narcolepsy

Disorder of arousal - constant hypersomnia

269

Conditions that affect RAS?

Parkinsons and Schizophrenia, PTSD, Depression(NA, 5HT), Alzheimers (Ach)

270

Loss of consciousness, where is damage?

Not cortex but RF

271

Initial management of loss of consciousness?

ABCD
Airway - jaw thrust- not neck extension. Nasopharyngeal better tolerated with suction in mouth. High conc O2
Breathing - mist mask, chest, breast sounds, indicator mask, assist e.g. bag valve mask (BVM) and intubation
Circulation - pulse, breathing effort, cough, movement, ETCO2 (end tidal vol) if ventilated, cap refill, IV access BM stix.
Disability - GCS
Monitor

272

Treatment loss of consciousness

High flow O2 if hypoxic
Hypoglycaemia - glucose IV
If fitting then Lorazepam IV

273

Explain the Glasgow coma scale (not score)

Eye 1-4:
None, pain, speech, spontaneous
Verbal 1-5
None, incomprehensible, inappropriate words, confused, orientated
Motor 1-6
None, extension pain, flexion, flexion pain, localise pain, obey command
Use to find pattern of change - if decreasing then bad..

274

Extradural presentation

Trauma, torn MMA, slow onset, decline in GCS

275

Subdural presentation

Trauma- brain move in skull/ (boxing).
Slower onset - days to weeks but can be acute, alcohol, age, atrophy of brain (dementia

276

Subarachnoid presentation

Thunderclap - berry aneurysm

277

Decorticate response in terms of RF

Intact. Thalamus and cortex connection lost. Unconscious but respond to pain.

278

Decerebrate response

Rigidity, lower brain/brainstem injury
Inhibition of RF on motor tracts removed
Relexive extension to pain