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ESA 5 > Neuro > Flashcards

Neuro Flashcards

1
Q

How many neuones in somatic vs autonomic pathways

A

2 vs 3

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2
Q

What are the emergent properties of the brain?

A

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

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3
Q

What is a Brodmann area?

A

Area of cortex classificed on histological appearence and subsequently function

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4
Q

Explain rostral caudal in CNS

A

Different for brain stem and cerebrum

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5
Q

Explain evolution of brain - out to in

A

Neocotex - complex function

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

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6
Q

What structure separates the anterior lateral ventricles?

A

Septum pellucidum

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7
Q

What is the fornix

A

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

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8
Q

Where is the calcarine sulcus?

A

Sagital view- occipital lobe

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9
Q

Where is the lateral fissure/ sulcus

A

Between temporal and frontal/ parietal lobes

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10
Q

What is the insula?

A

Infolding of brian deep

Responsible for consciousness, emotion and homeostasis

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11
Q

What is the corona radiata

A

Neural traffic from cerebral cortex

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12
Q

What is the caudate nucleus

A

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

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13
Q

What is the lenticular nucleus

A

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

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14
Q

What is the corpus striatum?

A

striatum plus globus pallidus/ caudate + lenticular

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15
Q

What is the (neo)striatum?

A

Caudate nucleus and the putamen.

Responsible for reward, motivation, motor and action planning

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16
Q

What composes the basal ganglia

A

Corpus striatum, substantia nigra and subthalamic nucleus

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17
Q

What are the cerebellar peduncles

A

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

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18
Q

Briefly explain drainage on the brain

A

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

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19
Q

What is the conus medullaris

A

Tapering end of spinal cord T12-L1

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20
Q

What is the filum terminale

A

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

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21
Q

What are the denticulate ligaments?

A

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

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22
Q

Describe lumbar puncture

A

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

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23
Q

Safe Lumbar puncture in kids?

A

L5/S1

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24
Q

Where is the substantia gelatinosa and what is found there?

A

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.

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25
Q

Where is the substantia nigra and what is found there?

A

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.

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26
Q

Difference between ataxia and apraxia

A 
Apraxia = inability to perform complex movements despite having the capability to bring about movement
Ataxia = a loss of full control of body movements
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27
Q

Aphasia vs aphonia vs dysarthria

A

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

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28
Q

What is paraplegia

A

Loss of sensory and motor functions of lower limbs

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29
Q

What is Chorea

A

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

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30
Q

Describe features of spasticity

A

hypertonia, hyperreflexia and paralysis

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31
Q

What is a neuropore

A

End of neral tube as it fuses away from cervical region

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32
Q

How can spina bifida be detected before birth?

A

alpha-fetoprotein in blood test or amniocentesis

USS

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33
Q

Types of spina bifidal

A

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

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34
Q

Symtoms of spina bifida

A

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

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35
Q

Neural tube defect cranially

A

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

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36
Q

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

A

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

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37
Q

Describe the dilations/ development of brain

A

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)

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38
Q

Location of ventricles in respect to enbryology

A

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

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39
Q

Describe the flexures of the CNS

A

Cervical at spinal cord/ medulla juntion

Cephalic at midbrain

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40
Q

Describe the growth of the neural tube into CNS structures

A

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

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41
Q

Descrbe neural crest cells in CNS developemtn

A 
Migrate
Undergo epithial to mesenchyme tranisition.
Include:
Cranial nerve ganglia
Spinal/ dorsal root ganglia
Sympathetic ganglia
Schwanne cells
Leptomeninges
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42
Q

How can alcohol affect developing CNS?

A

Neural crest cell migration

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43
Q

What is Hirschsprung’s disease

A

Aganglion megacolon - failure of migration

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44
Q

Describe the functions of astrocytes

A

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

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45
Q

Describe the functions of microglia

A

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.

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46
Q

Describe components of the BBB

A

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

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47
Q

Types of neurotranmittors

A

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

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48
Q

Describe Glutamate as a neurotransmittor

A

70% of all synapses. Excitatory.

Ionotropic or metabotropic

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49
Q

Explain ionotropic glutamate receptors

A

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

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50
Q

Explain metabotropic glutamate receptors

A

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

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51
Q

Upregulation of Glutamate receptors? Signidicance?

A

From NMDA and mGluRs upreg AMPA.

Long term potentiation. Ca through NMDA is important however too much can lead to excitotoxicity

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52
Q

Decribe GABA and glycine and their receptors

A

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

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53
Q

General action of biogenic amines and Ach

A

Mostly neuromodulators confined to specific pathways.

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54
Q

Describe Ach neurotransmission effects and clin sig

A

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

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55
Q

Dopamine pathways

A

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

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56
Q

Describe Na pathways

A

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

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57
Q

Describe 5HT pathways

A 
Similar to NA.
From Raphe nuclei also in pons.
Functions:
Sleep
Wakefullness
Mood
Vomiting centre
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58
Q

Origin of superior cerebellar artery

A

Basilar artery just posterior to superior cerebellar artery

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59
Q

Origin of inferior cerebellar artery

A

Lateral off vertebral artery

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60
Q

Origin of anterior spinal artery

A

Anastomosis between vertebral arteries

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61
Q

Origin of pontine arteries

A

Basillar artery

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62
Q

Origin of opthalmic arteries

A

ICA just before it becomes middle

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63
Q

Describe blood supply to the spinal cord

A

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

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64
Q

Supply of anterior posterior and middle cerebral arteries

A

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

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65
Q

How does CSF cushion brain?

A

Isotonic

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66
Q

Causes of subarachnoid

A

Berry aneurysm

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67
Q

How does CSF get removed and where?

A

Arachnoid granulations at superior sagittal sinus

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68
Q

CSF from forth to subarachnoid space via?

A

foramen magendie

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69
Q

What drives flow of CSF

A

Pressure and chorid epithelia villi

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70
Q

What causes a communicating hydrocephalus

A

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

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71
Q

How is CSF different from blood?

A

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

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72
Q

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

A 
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
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73
Q

Describe sensory neuones

A

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

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74
Q

What is a quality

A

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

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75
Q

Types of receptors found in muscle

A

Proprioceptors in muscle spindle = length

Golgi tendon organ = tension

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76
Q

Are receptors specific to one modality

A

Generally yes but punch in the eye

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77
Q

How are stronger stimuli recognised?

A

More AP frequency

Neibouring cells activated

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78
Q

Whats the difference between tonic and phasic receptors

A

Tonic - slowly adapting, continually firign

Phasic - raidly adapting, respond maximally and briefly to a stimulus

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79
Q

How is sensory acuity achieved? What is it?

A 
Precision by which a stimulus can be located
Laterally inhibiting interneurones
2 point discrimination
Synaptic convergence (decrease) and divergence (increase
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80
Q

What is two point discrimination and what factors influence it?

A

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

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81
Q

How is the percieved loaction of a stimulation based on?

A

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

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82
Q

What is perception?

A

Ability to sense stimuli and discriminate between different types

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83
Q

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

A

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

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84
Q

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

A

Dorsal median sulcus and the ventral median fissure

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85
Q

What fibres do the dorsal columns carry

A

Light touch and proprioception

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86
Q

Describe the fasciculi of the dorsal column

A

Gracile = medial (thinner) above T6

Cuneate lateral below T6

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87
Q

Describe the two corticospinal tracts’ modalities

A

Lateral = limb
Ventral = axial
motor descending

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88
Q

Describe the spinothalamic tracts’ modalities

A 
Lateral = pain and temp
Anterior = crude touch
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89
Q

Describe the Medial lemniscus pathway

A

=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).

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90
Q

Describe the spinothalamic tract pathway

A

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.

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91
Q

What is Syringomyelia?

A

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

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92
Q

Describe Brown- Sequard syndrome

A

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

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93
Q

B12 deficiency neuro?

Also B6 -pyroxidine

A

Dorsal root column degeneration

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94
Q

Effect of syphillis on spinal cord?

A

Tabes dorsalis.

Demyelination of dorsal column

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95
Q

What is Freidrich’s ataxia?

A

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

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96
Q

Describe Shingles pathology

A

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

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97
Q

Explain conscious and unconscious proprioception pathways

A 
Concious = Dorsal column spinal tract.
Unconscious = Dorsal and ventra spinocerebellar tracts and the Cuneo-cerebellar tract.
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98
Q

Describe the Spinocerebellar tracts

A

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

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99
Q

Direct of fall in cerebellar damage

A

= ipsilateral fall and coordination

Vermis damage = fall backwards

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100
Q

Define a motorneuone

A

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

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101
Q

Upper motor neurone lesion signs.

A 
Hyper reflexia
Hyper tonia
Hypokinesia (regidity)
Spastic Paralysis
Chorea if extrapyradimal
Pyradimal = Babinski
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102
Q

Lower motor neurone lesion signs

A 
Paralysis
Flaccid weakness
Hypotonia or atone
Hyporeflexia or areflexia
Atrophy
Fasciculations
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103
Q

Origin of LMN?

A

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

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104
Q

What is a motor unit?

A

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

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105
Q

What is a strecthc relfex

A

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

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106
Q

Name the 5 components to a strectch relex

A 
A stretch receptor (e.g. golgi organ or muscle spindle)
Afferent fibre
Integration cetre
An efferent fibre
An effector
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107
Q

What is a myotatic reflex?

A

Monosynaptic stretch reflex. Sets motor tone

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108
Q

Muscle tone in utero and new born?

A

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

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109
Q

Muscle tone during sleep and exceptions?

A

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

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110
Q

What do gamma motor neuones do?

A

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

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111
Q

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

A

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

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112
Q

Two pyradimal tracts?

A

Corticobulbar and corticospinal tract

113
Q

Describe the cortico-bulbar tract

A

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

114
Q

Descrube the corticospinal tract

A

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
Q

Describe the non-cortical/ extrapyradimal descending tracts

A 
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
Q

Decorticate appearence

A

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

117
Q

Decerebrate appearence

A

Extensors Es = pons or midbrain e.g. reticulospinal

118
Q

Why do you get fasciculations?

A

Upregulation of Ach receptors. Ach remnants in the blood.

119
Q

What is spinal shock?

A

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

120
Q

Explain the functional zones of the cerebellum

A

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

121
Q

Signs of Cerebellar dysfunction

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

No atrophy or weakness

122
Q

Positive Romberg test and uses?

A

Causes of gate-
ataxia = sensory
Suggests cerebellar damage

123
Q

Causes of Cerebellar dysfunction?

A

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

124
Q

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

A

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
Q

Explain pathophysiology of parkinsons

A

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

126
Q

Describe signs and symotoms of Parkinson’s

A

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
Q

Define pain

A

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

128
Q

What is nociception and some things that can affect it

A

The perception of physical pain

Modified by experience, expectation, immediate context, culture

129
Q

Threshold and tolerance to pain.

A

Threshold is all the same

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

130
Q

Difference between direct and indirect lateral STT

A

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
Q

Describe the stages of nociception

A

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

132
Q

Difference in stimulation of Adelta and C fibres

A 
Ad = mechanical
C = mechanical, thermal, chemical (polymodal)
133
Q

Perception of Ad, C and visceral fibres?

A

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
Q

Rexed lamina of Ad, C and cisceral fibres

A 
Ad = I, V
C = Substantia gel (i, II) and V.
Visceral = V
135
Q

Describe transduction of pain

A

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
Q

Actionn of drugs on transduction

A

NSAIDS -prostaglandin

Steroids - IL

137
Q

How can transmission be blocked

A

Local anaesthetic e.g. lignocaine, inhibits VGSC

138
Q

What is analgesia and what can cause it?

A

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

139
Q

Describe pain modulation in spinal cord

A

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
Q

Why does rubbing help?

A

Stimulates cutaneous inhibition which increases descending inhibition

141
Q

Describe perception of pain

A 
Thalamus and the cortex
Varies hugely
Thalamocortical projection = info about pain.
Emotional via limbic
Stress via hypo
142
Q

What is chronic pain

A

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

143
Q

Describe the gate control theory of pain

A

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

144
Q

What is hyperalgesia

A

Increased pain at a normal threshold stimulation.

Results from peripheral and central sensitisation

145
Q

What is allodynia

A

Pain from stimuli not normally painfull.

Also from an area not stimulated (not referred)

146
Q

Signs of pain

A

Brow lowers, lids tighten, nose wrinkles, lips tighten

147
Q

Describe ‘winding up’

A

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
Q

Types of chronic pain

A

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

149
Q

Explain nocicpetive chronic pain e.g. RA

A 
Wind up
Inflam
Synovia damage
C and A delta
Hyperalgesia
150
Q

Explain neuropathic pain

A

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
Q

Describe complex regional pain syndrome types

A

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
Q

What is RSD/ CRPS symptoms

A

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

153
Q

Stages of CRPS

A

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

154
Q

Opiod receptor info

A

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

155
Q

Opioids and their receptors

A

Endomorphins = MOP
Dynorphins = KOP
Enkephalns =DOP

156
Q

Give common weak opiods

A

Codeine

157
Q

Give strong opiod examples

A

Morphine, Fentanyl

158
Q

Who analgesic ladder

A

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

159
Q

Definition of adjuvants and examples

A

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
Q

Central pain and opiods?

A

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

161
Q

Describe the development of the ear

A

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
Q

Define placode

A

Thickened ectoderm patches on developing head

163
Q

Congenital causes of middle ear deafness?

A

Problems with 1/2 branches

164
Q

Causes of inner ear deafness

A

Tetratogenic agents and infection e.g. rubella

165
Q

Describe development of the eyes to shreks ear

A

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

166
Q

Whats inside the choroid fissure and its fate

A

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

167
Q

Fate of the optic cup?

A

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

168
Q

Where do muscles of the eye come from?

A

Preoptic myotomes from the surrounding region

169
Q

How does coloboma arise?

A

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

170
Q

Future pathology associated with the optic cup?

A

Retinal tear = separation of the layers

171
Q

What is the iris?

A

A contractile diaphragm with a central aperture

172
Q

Features of rubella?

A

Microcephaly, PDA, cataracts

173
Q

Where does the optic tract start and terminate?

A

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

174
Q

Temporal lobe optic rediation lesion = what?

A

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

175
Q

Where is Meyers loop?

A

Temporal optic radiation

176
Q

Describe differences in rods and cones

A

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

177
Q

Describe the three main functional classes of neurones

A

Photoreceptors
Interneurones
Ganglion cells

178
Q

Describe interneurones

A

Bipolar, horizontal and amacrine.

Combine photoreceptor signils

179
Q

Describe Magnocellular ganglion cell pathways

A

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
Q

dESCRIBE pARVOCELLULAR GANGLIIONIC CELLS

A

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
Q

Describe the primary visual cortex

A

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
Q

Explain the development of cones

A

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
Q

Sign of fovea hyperplasia?

A

Nystagmus

184
Q

What is ambyopia?

A

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

185
Q

Causes of ambyopia

A

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

186
Q

Types of anisometropia

A 
Emmetropia = normal
Myopia = infront of retina
Hyperopia = behind retina
187
Q

Types of Stabismus

A

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

188
Q

Treatment of ambyopia

A

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

189
Q

What is glaucoma

A

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

190
Q

Sympathetic innervation of eye pathway

A

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

191
Q

Abduction and adduction movements

A

SR and IR are opposite
SR and SO are inverse.

SO abduct = intorsion

192
Q

Appearance of VI nerve palsy

A

Esotropia

193
Q

IV nerve palsy

A

Hypertrophia

194
Q

III

A

Exotropia and hypotropic

Also ptosis and mydriasis

195
Q

Describe the properties of sound

A

Compressive wave, frequencey and amplitude

196
Q

Level of conversation and painful sound

A

60dB vs 120dB

197
Q

Describe the travelling wave theory

A

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

198
Q

What is Tonotopy

A

Place on basillar membrane = frequency

199
Q

Describe the structure of the basillar membrane

A

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

200
Q

Functions of inner and outer hair cells

A

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
Q

What is the tectorial membrane?

A

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

202
Q

Exlain How bending of stereocillia triggers a nerve AP

A

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

203
Q

What is the olivocochlear system?

A

Regulates OHC amplification via efferent feedback

204
Q

How are loud sounds interpreted and location

A

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.

205
Q

What constitutes the auditory brainstem?

A

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

206
Q

The auditory pathway

A 
Cochlear
SGN
Dorsal and ventral cochlear nuclei 
Suppeior olive
Inferior colliculus
Medial geniculate nucleus
The auditory cortex
207
Q

Causes of hearing impairment

A 
Age, presbyacusis
Infection
Congenital
Loud noises
Gentamicin
TraumA
208
Q

Explain the assessment of hearing

A

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

209
Q

Treatments fr hearing loss

A

Hearing aid
Cochlear implant
Cochlear nucleus
implant.

210
Q

Congenital causes of hearing loss

A

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

211
Q

Where do most strokes occur?

A

Middle cerebral artery

212
Q

Describe the vertebral arteries

A

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

213
Q

Describe the Basilar artery

A

Supplies most of brainstem. Located over pons.

Superior and anterior inferior cerebellar arteries. supplies most of PCA

214
Q

Describe PCA distribution

A

Occipital, midbrain, thalamus, half on temporal

215
Q

Define stroke

A

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

216
Q

Causes of cerebral infarct

A

Atheroma, embolism, idiopathic, arterititis, blood disorder

217
Q

Describe intracerebelar haemorrhage causes

A

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

218
Q

Define TIA

A

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

219
Q

Temporal lobe stroke signs

A

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

220
Q

Pariatal lesion

A

Primary sensory cortex
Neglect
Speech
Optic radiation either inferior or hemianopia

221
Q

Describe TACS - total anterior circulation stroke

A 
Proximal occlision
Contralateral hemiparesis/ hemianaesthesia
Higher dysfunction
Hemianopia
High mortality
222
Q

Describe PACs

A

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

223
Q

Describe LACS (lacunar stroke)

A

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

224
Q

Describe POCS

A

Brainstem, cerebellar or occipital involvement.

Complex presentation

225
Q

Atypical symptoms of stroke

A

Delerium, confusion, collapse, incontinence

226
Q

Write note for telangiectasia

A

k

227
Q

Investigations for stroke

A 
BM
HAematology
Biochem
CT/ MRI
Carotid US
ECG
Echocardiogram
228
Q

Treatment for stroke

A

IV thrombolysis - alteplase
Early asprin
Acute stroke unit

229
Q

Damage to spinal cord blood supply

A 
Aortic damage
Vasculitis - giant cell arteritis
Sickle cell
Hypotension
Cardiac emboli
Disc Herniation
230
Q

Symptoms of spinal artery occlusion

A

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

231
Q

What is a flaccid bladder? (same as areflex)

A

Lesion at S2-4 lower motor neurone

232
Q

Describe reflex bladder

A

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

233
Q

Describe motor and sensory areflexic bladder

A

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

234
Q

Describe the management of head trauma

A

ABCD (disability)
History
Examination

235
Q

RAS control

A

dd

236
Q

What is a coup and contrecoup injury

A 
Coup = front
Contrecoup = rebound`
237
Q

What are contusions?

A

Damaged blood vessels around the brain (like bruising)

238
Q

Describe primary and secondary insult in brain

A 
Primary = haematoma, contusion, haemorrhage, diffuse axonal injury
Secondary = preventable, hypoxiam hypoperfusion, oedema, ICP.
239
Q

BBB disruption?

A

More permeable so vasogenic oedema.

240
Q

What is cytotoxic oedema?

A

Inflam mediatorys and oxiditive stress. NA retention

241
Q

ICP compensation?

A 
CPP = MAP-ICP.
Venous blood and CSF can move out of brain to lower ICP.
MAP increases (mean arterial pressure) via Cushings.
242
Q

Uses of propofol

A

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

243
Q

USe of Thiopentone (barbiturate)

A

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

244
Q

Describe use of opiods

A

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

245
Q

Benefits to ketamine? and disadvantages?

A

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

246
Q

Use of neuromuscular blocking agent

A

Need for intubation

247
Q

Use of mannitol

A

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

248
Q

Explain vasopressors

A

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

249
Q

MEasures in medically induced coma?

A

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

250
Q

Evidence and reasoning behind medically induced comas?

A

Relieve swelling and brain decrease brain damage.

Mixed evidence.`

251
Q

Describe the reticular formation

A

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

252
Q

Imputs on the reticular formation

A

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

253
Q

Outputs of RF

A

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

254
Q

RF in sleep

A

Ach silent.

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

255
Q

Describe EEG and waves

A

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
Q

Describe specific wave forms

A

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
Q

Describe locked in syndrome

A

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

258
Q

What is persistent vegative state?

A

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
Q

What is a coma?

A

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

260
Q

Describe the purpose of sleep

A

Allows CNS to reset and memories to process

261
Q

What controls the sleep wake cycle?

A

RF and hypothalamus (by inihibiting the RF)

262
Q

Describe a sleep cycle

A

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

263
Q

Describe REM sleep

A 
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
Q

Describe non REM sleep

A 
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
Q

Describe waking

A

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

266
Q

What is parasomnia

A

Sleep paralysis

267
Q

What is hypersomnia

A

Day time sleepiness e.g. OSA

268
Q

What is Narcolepsy

A

Disorder of arousal - constant hypersomnia

269
Q

Conditions that affect RAS?

A

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

270
Q

Loss of consciousness, where is damage?

A

Not cortex but RF

271
Q

Initial management of loss of consciousness?

A

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
Q

Treatment loss of consciousness

A

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

273
Q

Explain the Glasgow coma scale (not score)

A

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
Q

Extradural presentation

A

Trauma, torn MMA, slow onset, decline in GCS

275
Q

Subdural presentation

A

Trauma- brain move in skull/ (boxing).

Slower onset - days to weeks but can be acute, alcohol, age, atrophy of brain (dementia

276
Q

Subarachnoid presentation

A

Thunderclap - berry aneurysm

277
Q

Decorticate response in terms of RF

A

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

278
Q

Decerebrate response

A

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

ESA 5 (4 decks)

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