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ESA5 > Neuro > Flashcards

Neuro Flashcards

1
Q

State the function of astrocytes

A

regulate the chemical content of the extracellular space

Envelope synaptic junctions in the brain.

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2
Q

State the function of oligodendrocytes

A

insulate axons within the CNS
Myelin speeds propagation of nerve impulses down axon
contribute to several axons

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3
Q

State the function of schwann cells

A

insulate axons in PNS
Myelin speeds propagation of nerve impulses down axon.
contribute to only one axon

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4
Q

State the function of microglia

A

remove debris left by dead or degenerating neurones and glial cells. Phagocytic.
Migrate into brain from the blood.
May be involved in remodelling synaptic connections.

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5
Q

Describe the structure of afferent neurones

A

from PNS to CNS

cell body in dorsal root ganglia

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6
Q

Describe the structure of efferent neurones

A

from CNS to PNS

cell bodies within the CNS derived from the ventral spinal cord

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7
Q

Describe the structure of interneurones

A

found exclusively within the CNS

Connection between afferent and efferent neurons. Form connections only with other neurons.

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8
Q

Which lobes of the brain does the central sulcus separate?

A

frontal

parietal

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9
Q

Which lobes of the brain does the lateral fissure separate?

A

frontal and parietal

temporal

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10
Q

Which lobes of the brain does the transverse fissure separate?

A

occipital

cerebellum

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11
Q

Which lobes of the brain does the longitudinal fissure separate?

A

right and left frontal and parietal

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12
Q

Where is the precentral gyrus found?

A

anterior to the central sulcus

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13
Q

Where is the postcentral gyrus found?

A

posterior to the central sulcus

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14
Q

Where is the parahippocampal gyrus found?

A

inferior to the hippocampus

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15
Q

where is the anterior commissure found?

A

inferior to the septum pellucidum

Superior to the hypothalamus

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16
Q

describe the location of the septum pellucidum

A

inferior to the corpus callosum

anterior and superior to the fornix

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17
Q

describe the location of the cingulate gyrus

A

superior to the corpus callosum

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18
Q

describe the location of the corpus callosum

A

inferior to cingulate gyrus

superior to fornix

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19
Q

describe the location of the fornix

A

surrounds thalamus

inferior to corpus callosum

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20
Q

describe the location of the hippocampus

A

inferior to fornix and thalamus
superior to parahippocampal gyrus and brain stem
Posterior to amygdala

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21
Q

describe the location of the thalamus

A

surrounded by fornix

superior to hippocampus

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22
Q

describe the location of the hypothalamus

A

anterior to fornix and thalamus

superior to pituitary gland

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23
Q

describe the location of the pituitary gland

A

inferior to hypothalamus

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24
Q

state the layers of the meninges

A 
periosteal dura
meningeal dura
arachnoid mater
(subarachnoid space)
pia mater
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25
Q

describe the location of the uncus

A

superior anterior to parahippocampal gyrus

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26
Q

describe the location of the calcarine sulcus

A

medial surface of the occipital lobe

divides the visual cortex (aka calcarine cortex) into two.

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27
Q

describe the location of the parieto-occipital sulcus

A

between parietal and occipital lobes of cortex

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28
Q

describe the location of the pineal gland

A

inferior to thalamus

superior to cerebellum and cerebral aqueduct

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29
Q

describe the location of the optic chiasm

A

superior to pituitary gland

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30
Q

where is the vermis found in the cerebellum?

A

centrally

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31
Q

where are the tonsils found in the cerebellum?

A

lateral to the inferior vermis

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32
Q

State where the spinal cord enlarges

A

cervical

lumbar

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33
Q

What is the conus medullaris?

A

lower end of the spinal cord

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34
Q

State the location of the conus medullaris?

A

L1/2

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35
Q

What is the cauda equina?

A

spinal nerves and nerve roots

L2-S5

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36
Q

What is the filum terminale?

A

connective tissue

stretches from apex of conus medullaris to the coccyx

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37
Q

What is the lumbar cistern?

A

subarachnoid space between the conus medullaris of spinal cord and inferior end of subarachnoid space and dura mater (about vertebral level S2);
occupied by the posterior and anterior roots constituting the cauda equina, the filum terminale, and cerebrospinal fluid;

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38
Q

What is the clinical significance of the lumbar cistern?

A

site for lumbar puncture and spinal anaesthesia

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39
Q

What is the notochord?

How is it formed?

A

solid rod of cells running down the midline

formed from prenotochordal cells migrating through primitive pit

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40
Q

How is neurulation initiated?

A

ectodermal cells above the notochord differentiate to become the neural plate

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41
Q

How is the neural tube formed?

A

neural plate thickens
lateral edges rise up
midline depresses (forms neural groove)
lateral edges fuse in midline

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42
Q

Where does fusion of the neural folds begin?

How does it spread?

A

cervical region

cephalo-caudally

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43
Q

Why are neuropores formed?

A

last parts of neural tube to fuse anteriorly and posteriorly

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44
Q

Which neuropore closes first?

A

anterior (day 25)

posterior (day 28)

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45
Q

What fails to develop in anencephaly?

What is the result?

A

failure of anterior neuropore closure

absence of cranial structures, including brain

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46
Q

What fails to develop in spina bifida?

A

failure of posterior neuropore to close
can occur anywhere from base of skull to sacrum
vertebral arch incompletely formed or absent

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47
Q

Where along the spine is spina bifida most common?

A

lumbosacral region

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48
Q

Describe spina bifida occulta

A

overlying skin intact
bony vertebral arch defect
no visible external overlying sac
no protusion of spinal cord or membranes

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49
Q

Describe spina bifida cystica

A

both vertebral defect and visible cystic mass

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50
Q

Describe a meningocoele

A

cystic swellng of dura and arachnoid mater
protrudes through vertebral arch defect
no spinal neural tissue present within sac

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51
Q

Describe myelomeningocoele

A

cystic swellng of dura and arachnoid mater
protrudes through vertebral arch defect
spinal neural tissue forms part of the sac

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52
Q

Describe rachischisis

A

cystic swellng of dura and arachnoid mater
spine lies widely open
neural plate has spread out on to the surface

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53
Q

Which form of spina bifida is most common?

A

spina bifida occulta

then myelomeningocoele

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54
Q

How can a neural tube defect be detected in a fetus?

A

raised maternal serum α-fetoprotein

USS

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55
Q

How can neural tube defects be prevented?

A

Increased folic acid intake pre-conceptually (3 months) and in first trimester

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56
Q

State in general terms how the neuroectoderm tube forms the developed neural tissues

A

lumen = ventricular system
cranial dilations = brain
caudal tail = spinal cord

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57
Q

Why does the cauda equina form?

A

at 3 months of fetal development, the spinal cord and vertebral column are the same length
but after this, the spinal column grows faster
the spinal roots need to elongate to exit at their original intervertebral foramina

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58
Q

What are the three primary brain regions?

A
  • forebrain (prosencephalon),
  • midbrain (mesencephalon)
  • hindbrain (rhombencephalom)
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59
Q

In what week do the three primary brain regions form?

A

week 4

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60
Q

In what week do the five secondary brain regions form?

A

week 5

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61
Q

State which primary brain region each of the secondary brain regions developed from

A

prosencephalon -> telencephalon and diencephalon

mesencephalon -> mesencephalon

rhombencephalon -> metencephalon and myelencephalon

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62
Q

What does the telencephalon develop into?

A

cerebral hemispheres

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63
Q

What does the diencephalon develop into?

A

thalamus

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64
Q

What does the mesencephalon develop into?

A

midbrain

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65
Q

What does the metencephalon develop into?

A

pons

cerebellum

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66
Q

What does the myelencephalon develop into?

A

medulla oblongata

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67
Q

Why do flexures form in the neural tube?

A

cranial end of the neural tube develops rapidly
exceeds available space
folds up

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68
Q

Where is the cervical flexure found?

A

spinal cord hindbrain junction

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69
Q

Where is the cephalic flexure found?

A

in the midbrain region

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70
Q

Which secondary brain region lumen does the lateral ventricle develop from?

A

telencephalon

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71
Q

Which secondary brain region lumen does the third ventricle develop from?

A

diencephalon

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72
Q

Which secondary brain region lumen does the cerebral aqueduct develop from?

A

mesencephalon

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73
Q

Which secondary brain region lumen does the fourth ventricle develop from?

A

metencephlon and myelencephalon

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74
Q

How does hydrocephalus develop in newborns?

A

blockage of ventriular system

impaired absorption of CSF

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75
Q

What are the symptoms of hydrocephalus?

What are the signs?

A

irritability
vomiting
impaired conscious level

dis-junction of sutures
dilated veins
rapid increase in head circumference

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76
Q

How is hydrocephalus treated?

A

shunt

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77
Q

Describe the organisation of the neural tube from inside to out

A

neuroepithelial layer
intermediate layer = neuroblasts
marginal layer = processes

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78
Q

How is dorsal and ventral patterning of the neural tube achieved?

A

roof and floor plates

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79
Q

State the dorsal and ventral patterns of the neural tube

A

roof = alar plate = sensory

floor = basal plate = motor

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80
Q

Where do the neural crest cells originate from?

A

lateral border of the neuroectoderm tube

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81
Q

What transition do the neural crest cells undergo?

A

displaced and enter mesoderm

epithelial to mesenchymal transisition

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82
Q

Give examples of where the neural crest cells are used in development

A

adrenal medulla
schwann cells
c cells
thyroid gland

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83
Q

Why are the neural crest cells vulnerable to environmental insults such as alcohol?

A

complex migratory pattern

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84
Q

What is Hirschprung’s Disease?

A

failure of neural crest cells to migrate to intestine
affected segment of colon fails to relax
obstruction occurs

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85
Q

State the functions of an anstrovyte

A 
structural support
provide nutrition for neurones
remove neurotransmitters
maintain ionic environment
help form BBB
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86
Q

Why do neurones require a constant source of glucose?

A

cannot store or produce glycogen

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87
Q

Describe how astrocytes provide a direct source of glucose or lactate to neurones

A

glycogen in astrocyte converted to lactate
transport of lactate from astrocyte to neuron via MCT1 and MCT2 lactate transporters across interstitial space
lactate converted to pyruvate
used in respiration

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88
Q

Why do astrocytes have transporters specific for neurotransmitters?

A

remove neurotransmitter after an action potential
extracellular conc remain low
prevents toxicity of neurotransmitter
prevents spread of neurotransmitter to other receptors

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89
Q

Why do astrocytes have a very negative resting membrane potential?

A

high intracellular K+ conc

due to removal of K+ after an action potential

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90
Q

What is the function of oligodendrocytes?

A

myelination in CNS

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91
Q

What is the function of microglia?

A

immune system
APC
phagocytosis

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92
Q

Where to microglial cells originate from?

Why is this important?

A

mesoderm

other glial cell are ectodermal

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93
Q

why is the CNS described as immune privileged?

A

specialised immune function

regulated inflammatory response
T cells are able to enter CNS but their inflammatory response is limited
so that inflammatory expansion is limited (rigidity of skull)

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94
Q

What forms the BBB?

A

tight junctions between endothelial cells
basement membrane surrounding capillaries
end feet of astrocyte processes

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95
Q

Describe the structure and action of the tight junction of the BBB

A

bound by clodin and occluding proteins

prevent hydrophilic molecules from entering the CSF

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96
Q

State the main categories of neurotransmitter, giving examples

A

amino acids - glutamate, GABA
biogenic amines - NA, ACh
peptides - somatostatin, neuropeptide P

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97
Q

What is the main excitatory amino acid?

A

glutamate

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98
Q

State the three main types of ionotropic glutamate receptors

A

AMPA
NMDA
kainate

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99
Q

What change does glutamate binding to AMPA receptors cause?

A

increases Na+ and K+ permeability

initial fast DEPOLARISATION

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100
Q

What change does glutamate binding to NMDA receptors cause?

A

increases Na+, K+ and Ca2+ permeability

DEPOLARISATION

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101
Q

How do ionotropic glutamate receptors allow more APs to fire?

A

depolarisation

EPSP

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102
Q

Why does the cell membrane need to be depolarised in order for the NMDA receptor to open?

A

at resting potential the channel is blocked by an Mg2+ ion

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103
Q

What needs to occur for the NMDA channel to open?

A

glutamate binds
depolarisation of membrane
glycine binds as co-agonist

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104
Q

What is Long Term Potentiation?

A

increased synaptic strength in the long term

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105
Q

What causes long term potentiation?

A

activation of NMDA receptors
Ca2+ entry
phosphorylation and insertion of additional AMPA receptors in postsynaptic membrane

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106
Q

What is the main inhibitory neurotransmitter in the brain?

A

GABA

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107
Q

What is the main inhibitory neurotransmitter in the brainstem and spinal cord?

A

glycine

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108
Q

How do GABA(A) and glycine receptors cause inhibition?

A

integral Cl- ion channels
HYPERPOLARISATION
IPSP
decreased AP firing

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109
Q

What is the mechanism of action of barbiturates and benzodiazepines?

A

bind to GABA(A) receptors
enhance inhibitory response

leads to sedation and anti-anxiety actions

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110
Q

What is the role of GABA(B) receptors?

A

modulation

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111
Q

State the major biogenic amines

A

ACh
dopamine
NA
serotonin (5-HT)

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112
Q

State the main action of ACh in the CNS

A

excitatory neurotransmitter at nicotinic and muscarinic receptors
present on presynaptic terminals to enhance the release of other neurotransmitters

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113
Q

Where do ACh neurones originate?

A

basal forebrain

pontomesencephalotegmental cholinergic complex

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114
Q

Which areas of the brain do ACh neurones originating in the basal forebrain innervate?

A

hippocampus

neocortex

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115
Q

Which areas of the brain do ACh neurones originating in the pontomesencephalotegmental cholinergic complex innervate?

A

dorsal thalamus

parts of forebrain

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116
Q

What actions are ACh receptors involved in?

A

arousal
memory
learning
motor control

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117
Q

Describe the link between cholinergic neurons and Alzheimer’s disease

A

degeneration of cholinergic neurones in the nucleus basalis is associated with Alzheimer’s disease.

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118
Q

Which areas of the brain have a high concentration of dopamine receptors?

A

substantia nigra in midbrain

ventral tegmental area of midbrain

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119
Q

Where do the dopaminergic neurons of the substantia nigra project axons into?

What is their function?

A

striatum

initiating voluntary movement

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120
Q

What causes Parkinson’s disease?

A

degeneration of dopaminergic neurons that being in the substantia nigra

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121
Q

What disorder can too much dopamine in the CNS lead to?

A

schizophrenia

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122
Q

Which neurotransmitters does amphetamine cause the release of?

A

dopamine

noradrenaline

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123
Q

How is Parkinson’s treated?

A

L-DOPA
crosses BBB
aromatic amino acid decarboxylase (AADC) converts L-DOPA to dopamine

Carbidopa given at same time
inhibits AADC so conversion does not occur in periphery

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124
Q

Where are noradrenaline containing neurones found in the brain?

A

locus coeruleus in brainstem

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125
Q

Where in the brain do noradrenaline containing neurones innervate?

A 
cerebral cortex,
thalamus 
hypothalamus, 
olfactory bulb, 
cerebellum, 
midbrain 
spinal cord
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126
Q

What is the function of noradrenaline containing neurones?

A

behavioural arousal

mood

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127
Q

Where are serotonin containing neurones found in the brain?

A

raphe nuclei in the midline of the brainstem

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128
Q

What is are dopamine containing neurones involved in the control of?

A

sleep/wakefulness

mood

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129
Q

How is knowledge of serotonin used in treatment of depression and anxiety disorders?

A

SSRIs (Serotonin Selective Reuptake Inhibitors)

increases serotonin at synapse

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130
Q

Which paired arteries supply the brain?

A

vertebral arteries

internal carotids

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131
Q

Where do the internal carotid arteries arise?

A

bifurcation of common carotid

C4

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132
Q

Describe the course of the carotid arteries

A

carotid sheath
enter brain via carotid canal of temporal bone
pass anteriorly through cavernous sinus

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133
Q

State the branches that the internal carotid arteries give rise to distal to the cavernous sinus

What does the ICA then continue as?

A

ophthalmic artery
posterior communicating artery
anterior cerebral

middle cerebral artery

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134
Q

What structures does the anterior cerebral artery supply?

A

medial surfaces of frontal and parietal lobes

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135
Q

What structures does the middle cerebral artery supply?

A

lateral portions of cerebrum

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136
Q

Describe the course of the vertebral arteries

A

arise from subclavian arteries medial to anterior scalene
ascends through transverse foramen of cervical vertebrae
enter cranium via foramen magnum

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137
Q

State the branches of the vertebral artery within the cranial vault

A

meningeal branch
anterior spinal arteries
posterior spinal arteries
posterior inferior cerebellar

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138
Q

How do the vertebral arteries terminate?

A

converge

form basilar artery

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139
Q

How does the basilar artery terminate?

A

bifurcates

forms posterior cerebral arteries

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140
Q

What structures does the posterior cerebral artery supply?

A

inferior surface of brain

occipital lobes

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141
Q

State the components of the circle of willis

A 
anterior cerebral arteries
anterior communicating artery 
internal carotid arteries
posterior communicating arteries
posterior cerebral arteries
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142
Q

In disease states, what is the benefit of the circle of willis?

A

anastomoses can provide collateral circulation
if arteries have become progressively blocked

however, if the block happens suddenly, collateral supply would be inadequate

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143
Q

Describe the blood supply of the spinal cord

A

anterior spinal artery - formed from branches of the vertebral arteries

two posterior spinal arteries - arise from the vertebral artery

lower than cervical: extra support from segmental and radicular arteries

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144
Q

What is a stroke?

A

acute development of a neurological deficit,

due to a disturbance in the blood supply of the brain.

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145
Q

What are the main causes of cerebrovascular accident?

A

thrombosis
embolism
hypoperfusion (due to systemically low BP)
haemorrhage - accumulation of blood within cranial cavity

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146
Q

What is an aneurysm?

A

dilation of an artery, which is greater than 50% of the normal diameter

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147
Q

What is spinal cord infarction?

A

the death of nervous tissue in the spinal cord

resulting from an interruption of the arterial supply.

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148
Q

What are the causes of spinal cord infarction?

A 
vertebral fractures
vertebral dislocations
vascular disease
atheroma
external compression (eg. abdominal tumour)
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149
Q

What are the signs and symptoms of spinal cord infarction?

A

muscle weakness
paralysis
loss of relfeces

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150
Q

Where are the dural venous sinuses found?

A

between the periosteal and meningeal layers of the dura mater

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151
Q

Where do the dural venous sinuses drain into?

A

internal jugular vein

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152
Q

Which dural sinuses are found in the flax cerebri?

Where do they meet?

A

straight
superior
inferior

confluence of sinuses (posterior)

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153
Q

Describe the course of the venous blood from the confluence of sinuses

A

transverse sinuses continue bilaterally
curves into sigmoid sinus
joins to internal jugular vein

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154
Q

how does blood enter the cavernous sinus?

How does blood drain from the cavernous sinus?

A

from ophthalmic veins

via the superior or inferior petrosal sinuses to the internal jugular vein

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155
Q

What is Cerebral venous sinus thrombosis?

A

presence of a thrombus within one of the dural venous sinuses
occludes venous return
deoxygenated blood accumulates in brain parenchyma
venous infarction

also CSF accumulates as it can no longer drain

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156
Q

What are the symptoms of Cerebral venous sinus thrombosis?

A

headache
nausea
vomiting
neurological defects

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157
Q

How is a Cerebral venous sinus thrombosis treated?

A

anticoagulation

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158
Q

What is the role of the veins of the cerebrum?

A

carrying blood from the brain tissue

depositing it in the dural venous sinuses

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159
Q

How are cerebral veins divided into superficial and deep groups?

A 
deep = emerge from transverse fissure
superficial = in subarachnoid space. pierce meninges to drain blood into venous sinuses
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160
Q

state the three layers of the meninges

A

dura mater
arachnoid mater
pia mater

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161
Q

Describe the dura mater

A

lies directly beneath the skull
thick, tough, inextensible

periosteal layer
meningeal layer

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162
Q

What is a dural reflection?

A

meningeal layer of the dura mater folds inwards

partitions the brain, and divide the cranial cavity into several compartments

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163
Q

Describe the blood supply and innervation of the dura mater

A

middle meningeal artery and vein

trigeminal nerve

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164
Q

What is an extradural haematoma?

What is the common cause?

A

Arterial blood collects between the skull and periosteal layer of the dura.

The causative vessel is usually the middle meningeal artery, tearing as a consequence of brain trauma

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165
Q

What is a subdural haematoma?

What is the common cause?

A

Venous blood collects between the dura and the arachnoid mater.

damage to cerebral veins as they empty into the dural venous sinuses.

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166
Q

Describe the arachnoid mater

A

middle layer of the meninges,
lies directly underneath the dura mate
consists of layers of connective tissue
avascular.

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167
Q

What does the subarachnoid space contain?

A

CSF

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168
Q

How does CSF re-enter the circulation from the subarachnoid space?

A

arachnoid granulations = projections of arachnoid mater into the dura
enters dural venous sinuses

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169
Q

Meningitis causes cerebral oedema, raising ICP.

What are the life-threatening effects of this?

A

cranial herniation = parts of the brain forced out of the cranial cavity

reduced cerebral perfusion

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170
Q

How does a fracture of the skull vault lead to a haematoma formation?

A

disruption of dura and blood vessels

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171
Q

Why does CSF rhioorrhoea occur?

What is a complication of this?

A

fracture of frontal sinus or cribriform plate
dura (normally adheres to periosteum) tears
CSF leaks out

infections

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172
Q

What are the functions of CSF?

A

protection - cushions the brain
bouyancy
chemical stability

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173
Q

Where is CSF produced?

A

ependymal cells of choroid plexus in ventricles

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174
Q

What is the embryological derivative of the ventricles?

A

neural tube

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175
Q

Name the paired ventricles

A

left ad right lateral ventricles

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176
Q

How are the lateral ventricles connected to the third ventricle?

A

foramen Monro

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177
Q

Describe the location and anterior projections of the third ventricle

A

between the left and right thalamus

supra-optic recess - above optic chiasm
infundibular recess - above optic stalk

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178
Q

How is the third ventricle connected to the fourth ventricle?

A

cerebral aqueduct

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179
Q

Describe the location of the fourth ventricle

A

within the brainstem

a the junction between the pons and medulla

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180
Q

Where does the fluid drain into from the fourth ventricle?

A

central spinal canal - bathes the spinal cord

subarachnoid cisterns - bathes the brain. between arachnoid mater and pia mater.

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181
Q

How is the chemical composition of the CSF controlled?

A

plasma is filtered by the epithelial cells of the choroid plexus

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182
Q

What is hydrocephalus?

A

abnormal collection of CSF within the vetricles

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183
Q

Describe communicating non-obstructive hydrocephalus and what causes it

A

Abnormal collection of CSF in the absence of any flow obstruction in the ventricles

functional impairment of the arachnoid granulations, such as fibrosis of the subarachnoid space following a haemorrhage

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184
Q

Describe non-communicating obstructive hydrocephalus and what causes it

A

Abnormal collection of CSF, with flow obstructed within the ventricular system.

The most common site of obstruction is the cerebral aqueduct, connecting the third and fourth ventricles.

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185
Q

Describe hydrocephalus ex vacuo and what causes it

A

ventricular expansion, secondary to brain atrophy.

neurodegenerative conditions, such as Alzheimer’s disease.

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186
Q

How is hydrocephalus treated?

A

reversal of cause

shunt, draining fluid into right atrium or peritoneum

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187
Q

Describe the features of first order sensory neurons

A

sensory receptors in dermis

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188
Q

How many neurones make up the somatosensory ascending tracts?

A

three:
primary - sensory receptors
secondary
tertiary

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189
Q

What modality do Merkel discs detect?

A

vibration
pressure
texture

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190
Q

What modality do Mesissner’s Corpuscles detect?

A

light touch

vibration

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191
Q

What modality do Riffini Corpuscles detect?

A

temperature

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192
Q

What modality do Pacinian Corpuscles detect?

A

vibration

pressure

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193
Q

How is information about the intensity and duration of a stimulus encoded by the primary afferent?

A

frequency - faster rate of action potential = stronger stimulus
activation of neighbouring cells - activation of neighbouring cells = stronger stimulus

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194
Q

Describe the difference between tonic and phasic receptors

A

tonic = respond continuously in presence of adequate stimulus

phasic = adapt to stimulus, so action potential frequency decreases during a maintained stimulus

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195
Q

What is acuity?1

A

the precision by which a stimulus can be located

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196
Q

What determines acuity?

A

size of the receptive field
lateral inhibition
convergence and divergence

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197
Q

What is a receptive field?

A

area of receptors innervated by the same sensory neuron.

small receptive field = greater acuity

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198
Q

Describe lateral inhibition

A

primary afferent neurones (with receptive field centre closest to point of stimulation) synapse with inhibitory interneurons in the spinal cord

inhibition of adjacent second order neurons

action potential from second order neurons whose receptive fields are to the periphery of the stimulus are more strongly inhibited

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199
Q

What is two point discrimination?

A

minimal distance required to perceive two simultaneously applied skin indentations

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200
Q

What is two point discrimination determined by?

A

density of receptors

size of neuronal receptive field

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201
Q

What is convergence between primary and secondary neurons?

How does this affect acuity?

A

when multiple primary afferents synapse onto one secondary neuron

decreases acuity

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202
Q

What is divergence between primary and secondary neurons?

How does this affect acuity?

A

one primary neuron splits to synapse with multiple secondary neurons

causes amplification

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203
Q

What modalities does the DCML ascending tract carry?

A

fine touch

conscious proprioception

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204
Q

In the DCML ascending tract, where are the cell bodies of primary neurons found?

A

dorsal root ganglion

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205
Q

In the DCML ascending tract, where are the cell bodies of tertiary neurons found?

A

thalamus

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206
Q

In the DCML ascending tract, where does decussation occur?

A

medulla

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207
Q

Where does the DCML ascending tract terminate?

A

sensory cortex

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208
Q

In the DCML ascending tract, describe the route of the first order neurones

A

neurons from lower limb travel in the fasciculus gracilis (medial part of dorsal column)

neurons from upper limb travel in fasciculus cuneatus (lateral part of dorsal column)

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209
Q

In the DCML ascending tract, describe the route of the secondary neurones

A

travel from medulla oblongata in contralateral medial lemniscus to the thalamus

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210
Q

In the DCML ascending tract, describe the route of the tertiary neurones

A

from the ventral posterolateral nucleus of the thalamus
through the internal capsule
to the sensory cortex

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211
Q

What can cause a spinal cord lesion affecting the DCML?

A 
vitamin 12 deficiency
tabes dorsalis (syphilis)
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212
Q

What modalities does the lateral spinothalamic tract carry?

A

pain

temperature

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213
Q

What modalities does the anterior spinothalamic tract carry?

A

crude touch

pressure

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214
Q

In the spinothalamic tracts, where are the cell bodies of primary neurons found?

A

dorsal root ganglion

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215
Q

In the spinothalamic tracts, where are the cell bodies of secondary neurons found?

A

dorsal horn - substantia gelatinosa

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216
Q

In the spinothalamic tracts, where are the cell bodies of tertiary neurons found?

A

thalamus

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217
Q

In the spinothalamic tracts, where does decussation occur?

A

spinal cord - via the vental white commissure

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218
Q

In the spinothalamic tracts, where does the tertiary neuron terminate?

A

sensory cortex

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219
Q

In the spinothalamic tracts, describe the route of the secondary neurones

A 
from substantia gelatinosa
decussate via ventral white commissure
ascend in contralatrral anerior or lateral spinothalamic tract depending on modality 
medial to lateral = C,T,L,S
synapse at thalamus
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220
Q

In the spinothalamic tracts, describe the route of the tertiary neurones

A

from the ventral posterolateral nucleus of the thalamus,
through the internal capsule,
terminating at the sensory cortex.

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221
Q

What will damage to the lateral spinothalamic tract in the spinal cord cause?

A

complete loss of pain and temperature sensation on opposite side

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222
Q

How does sacral sparing of sensation occur?

A

sacral and lumbar fibres lie dorsolateral to the thoracic and cervical fibres in the spinothalamic tract
so an expanding tumour or lesion in the grey matter will affect the thoracic and cervical fibres first
so the sacral and lumbar fibres have intact pain and temperature still present initially,

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223
Q

What is Brown-Séquard syndrome?

A

(one sided lesion) of the spinal cord
involves both the anterolateral system and the DCML pathway:
• DCML pathway – ipsilateral loss of tactile sensation and proprioception
• Anterolateral system – contralateral loss of pain and temperature sensation.

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224
Q

Where are the cell bodies of primary neurons of the pathways of unconscious sensation found?

A

dorsal root ganglion

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225
Q

Where are the cell bodies of secondary neurons of the pathways of unconscious sensation found?

A 
spinocerebellar = spinal grey matter
cuneocerebellar = accessory cuneate nucleus in brainstem
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226
Q

Describe the tertiary neuron of the pathways of unconscious sensation

A

there are none!!!

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227
Q

Describe the decussation of the pathways of unconscious sensation

A

anterior spinocerebellar decussates once in cord and again in pons

posterior spinocerebellar and cuneocerebellar DO NOT

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228
Q

Describe the course of the second order neurons of the spinocerebellar tracts

A

anterior = Decussate in spinal cord, travel in anterior spinocerebellar tract on CONTRALATERAL side, decussate in pons to terminate in the cerebellum

posterior = ascend on IPSILATERAL side in posterior spinocerebellar tract. terminate in the cerebellum

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229
Q

If the anterior spinocerebellar tract is damaged in the spinal cord, what will happen?

A

loss of proprioception and co-ordination in the contralateral side

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230
Q

If the posterior spinocerebellar tract is damaged in the spinal cord, what will happen?

A

in loss of proprioception and co-ordinated movement on the ipsilateral side.

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231
Q

Describe the course of the first order neurons of the cuneocerebellar tract

A

cell body in dorsal root ganglion
ascend on ipsilateral side in the fasciculus cuneatus
synapse in brain stem in accessory cuneate nucleus

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232
Q

Describe the course of the second order neurons of the cuneocerebellar tract

A

begin in accessory cuneate nucleus
travel in the cuneocerebellar tract
terminate in the cerebellum.

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233
Q

Describe the ascending tract from the trigeminal nerve of the face

A

Cell bodies from the first order neurones lie in the trigeminal ganglion
their central processes synapse in the trigeminal nucleus of the pons.
Second order neurones can then ascend to the thalamus
third order neurons ascend to the cerebral cortex.

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234
Q

What is a nociceptor?

A

free dendritic nerve endings that respond to noxious stimuli which would cause injury if they persisted

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235
Q

Describe nociceptive afferent C-fibres

A

Small in diameter
Unmyelinated with slow conduction
Associated with dull, aching pain
Activated by all three noxious stimuli, so are polymodal

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236
Q

Describe nociceptive afferent Aδ-fibres

A 
Myelinated so faster conduction velocity
Larger diameter
Associated with sharp pain
Mechano-heat fibres
activated by chemical stimuli
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237
Q

What are the three noxious modalities?

A

chemical
mechanical
temperature

238
Q

Where do first order nociceptive afferent fibres terminate?

A

dorsal horn of spinal cord

A delta fibres in lamina I and V
C fibres in lamina II

239
Q

Where do first order nociceptive afferent fibres synapse with second order nociceptive afferent fibres?

A

laminae I and V of the dorsal horn

240
Q

If nociceptive afferents synapse in lamina II of the dorsal horn (substantia gelatinosa), what occurs?

A

synapse onto cell bodies of inhibitory neurons
inhibitory neurons run into lamina I and V
inhibit transmission between first and second order nociceptive afferents

241
Q

How is output from the substantia gelatinosa regulated?

A

Gate Control Theory

non-noxious stimuli (from Aalpha and ABeta fibres) increase inhibitory output, reducing transmission between first and second order nociceptive afferents

Noxious stimuli cause decreased inhibitory output, increasing transmission between first and second order nociceptive afferents

242
Q

Describe the course of the nociceptive second order afferents

A

ascend the spinal cord in the anterior and lateral spinothalamic tracts
terminate in the thalamus, brain stem, limbic system and frontal cortex.

243
Q

Describe the course of the nociceptive third order afferents

A

from the thalamus, brain stem, limbic system and frontal cortex
to the cerebral cortex

244
Q

Describe descending inhibitory control of pain

A

cortical stimulation of periaqueductal grey area in midbrain
neurons in periaqueductal grey stimulate nucleus raphe magnus in the medulla
neurons from nucleus raphe magnus stimulate inhibitory interneurons in the substantia gelatinosa of the spinal cord
reduces transmission between primary and secondary afferent nociceptive neurons.

245
Q

Describe chronic pain

A

lasts for more than three months
persists after all possible healing has occurred
cause often unknown

246
Q

How does tissue damage lead to pain?

A

tissue damage leads to detruction of cells and local leakage of contents
attraction of immune cells
release of further chemical mediators

substance P and 5-HT cause pain directly
other mediators potentuate the actions of pain mediators, as well as sensitising nociceptors

247
Q

What is peripheral sensitisation?

A

noxious stimuli sensitise nervous system response by causing increased release of glutamate, excess NMDA receptor activation and increased second order neuron firing

at the same stimulus intensity, there is a greater pain intensity

nociceptive neurons have become hyperexcitable

248
Q

What is hyperalgesia?

A

There is increased pain at normal threshold stimulation.
nociceptive afferents respond at a lower stimulus activity
This is the result of peripheral and central sensitisation.

249
Q

What is allodynia?

A

pain is felt from stimuli which are not normally painful.

Pain which occurs at an area other than in the area stimulated.

250
Q

What is central sensitisation?

A

Repeated stimulation increases spinal processing

of the same stimulus intensity, there is a greater pain intensity

251
Q

What is neuropathic pain?

A

pain of neural origin

burning, tingling or shooting sensation

252
Q

What are the symptoms of a peripheral nociceptive nerve injury?

A

Decreased threshold of Nociceptor activation
Increased receptive field
allodynia
hyperalgesia
prolonged post-stimulus sensations = hyperpathia
emergence of spontaneous activity

253
Q

What is Complex Regional Pain Syndrome?

What is it caused by?

A

neuropathic disease of the extremities. diagnosis of exclusion

can be triggered by minor trauma, bone trauma, surgery, stroke or MI

254
Q

What are the symptoms of Complex Regional Pain Syndrome?

A
  • Continuous burning pain, hyperalgesia, allodynia
  • Temperature and skin colour asymmetry
  • Oedema, sweating changes
  • Decreased range of motion, motor dysfunction, trophic changes
255
Q

Describe the mechanism of action of opioids

A 
act on MOP, DOP and KOP GPCR dopamine receptors centrally and peripherally
close VOCC
opens potassium channels
inhibits cAMP formation
reduces neurotransmitter release
analgesia
256
Q

What are some of the effects of opioids?

A 
respiratory depression
nausea and vomiting
antitussive (preventing cough)
constipation, 
itching,
euphoria
257
Q

State the names of some weak opioids

A

codeine
tramadol

dihydrocodeine

258
Q

State the names of some strong opioids

A

morphine,
diamorphine

fentanyl,
oxycodone,
hydromorphone

259
Q

Describe the steps of the WHO analgesics ladder

A

step one = non-opioids
step two = incorporate weak opioids
step three = adding strong opioids

260
Q

What kind of pain are opioids poor at controlling?

A

neuropathic pain

261
Q

What are adjuvant analgesics?

A

drugs that increase or aid the effect of the analgesia already being used

262
Q

What is a lower motor neurone?

A

cell bodies in spinal cord or cranial nerve motor nuclei

act directly on muscle

263
Q

What is a motor unit?

A

group of muscle fibres innervated by one motor neuron.

The muscle fibres are not a discrete group, but are distributed at random.

264
Q

Describe S motor units

A 
o	Slow contracting
o	Very resistant to fatigue
o	Very small force
o	Oxidative metabolism
o	Well vascularised (so red)
265
Q

Describe FR motor units

A

o Faster contracting
o Fatigue resistant
o Low force
o Oxidative and glycolytic

266
Q

Describe FF motor units

A 
o	Fast contracting
o	Fast fatigue
o	High force
o	Glycolytic
o	Low vascularisation (so pale)
267
Q

What are S fibres used for?

A

maintaining posture

268
Q

What are FF fibres used for?

A

rapid motor movements

269
Q

What is the force of muscle contraction affected by?

A

frequency of activation of motor units

number and type of motor units activated

270
Q

What is a spinal reflex?

A

involuntary, unlearned, automatic reaction to a specific stimulus that does not require the brain,

271
Q

What are the components of a reflex arc?

A 
receptor
afferent fibre
integration centre (in spinal cord)
efferent fibre
effector
272
Q

Describe the structure of muscle spindle

A

made of intrafusal skeletal muscle fibres
serve as proprioceptors that detect the amount and rate of change in length of a muscle
innervated by one sensory and one motor axon

273
Q

Describe intrafusal fibres of muscle spindle

A

have contractile proteins (thick and thin filaments) at either end,
central region that is devoid of contractile proteins.
The central region is wrapped by the sensory dendrites of the muscle spindle afferent.

274
Q

How is an action potential triggered in the muscle spindle afferent?

A

muscle lengthens and the muscle spindle is stretched
opens mechanically-gated ion channels in the sensory dendrites,
receptor potential that triggers action potentials

275
Q

State the function of the two types of afferent fibre in the muscle spindle

A

The primary endings (1a)

  • respond to muscle speed and the size of a muscle length change.
  • fast conduction, because of their wide diameter and myelination.
  • contribute both to movement and the sense of limb position.

Secondary endings (II)

  • only sensitive to length and not to velocity
  • contribute only to the sense of position.
  • smaller axons and thus slower conduction speed
276
Q

Describe the efferent innervation of the intrafusal fibres

A

the gamma motor neuron

When the extrafusal fibres have been stimulated to contract by alpha MN activation, the gamma MN is simultaneously excited.
This is known as alpha-gamma coactivation.
The gamma MN stimulates contraction in the two ends of the intrafusal fibre, readjusting its length and keeping the central region of the intrafusal fibre taut, to keep the muscle spindle afferent responsive.

277
Q

What is the role of the efferent innervation of intrafusal fibres

A

to maintain muscle spindle sensitivity, regardless of muscle length.

278
Q

What are Golgi tendon organs?

A

high-threshold receptors located at the junction of muscle and tendon
provide nformation about muscle tension.

279
Q

Describe the structure of Golgi tendon organs

A

bare nerve endings of group 1b axons that invest a collagen matrix
sit at the junction between a muscle fibre and the tendon

280
Q

How is an action potential triggered in the golgi tendon organ afferent?

A

When tension is created in the muscle, the collagen fibres distort and squeeze the mechanosensetive nerve endings, triggering an action potential.

281
Q

Describe the stretch reflex

A

primary receptor = muscle spindle, afferent neurone = group 1a afferents
synapse = group 1a afferents synapse directly with alpha-motor neurones in the spinal cord to innervate the extrafusal muscle fibres
efferent neruone = alpha-motor neurones effect = contraction of the same muscle

282
Q

Describe the inhibitory pathway in the stretch reflex

A

An excitatory synapse is also made with an inhibitory interneurone in the spinal cord,
this makes an inhibitory synapse with the alpha-motor neurones innervating the antagonistic muscle

283
Q

Describe the flexion reflex

A

primary receptor = nociceptor
afferent neuron = myelinated afferent fibres (group 3 fibres) and unmyelinated afferent fibres (group 4 fibres).
Synapse = directly synapse with alpha-motor neurones in the spinal cord (normally polysynaptic so 3 or 4 interneurones are involved),
efferent neuron = alpha-motor neurones effect = contraction of ipsilateral flexor muscles. The net result is to withdraw the limb in response to the noxious stimuli.

284
Q

Describe an alpha motor neuron

A

cell body in the ventral horn of the spinal cord
large diameter axon
Myelinated
60 m/s conduction velocity
innervate extrafusal fibres (the normal skeletal muscle fibres)

285
Q

Describe a gamma motor neuron

A
  • innervate the intrafusal fibres (found in muscle spindles)
  • small diameter axon
  • excitation leads to stimulation of intrafusal muscle fibres to contract in parallel with extrafusal fibres
286
Q

What is an upper motor neuron?

A
  • Cell body in cerebral cortex or brain stem

* Remain within CNS

287
Q

State the names of the pyramidal descending tracts

A

corticospinal

corticobulbar

288
Q

State the names of the extrapyramidal descending tracts

A
  • Vestibulospinal
  • Tectospinal
  • Reticulospial
  • Rubrospinal
  • Olivospinal
289
Q

State difference between the pyramidal and extrapyramidal descending tracts

A

pyramidal system has direct (monosynaptic) contact with lower motor neurones
pyramidal pass through the medullary pyramids
control voluntary movements

extra-pyramidal system has an indirect contact with the rest of the motor neurone pools.
do not pass through medullary pyramids

290
Q

What is the function of the corticospinal tract?

A

control of voluntary movements

291
Q

Where are the cell bodies of the upper motor neurons of the corticospinal motor tract found?

A

cerebral cortex

30% motor cortex,
30% premotor cortex and supplementary motor areas,
40% somatosensory cortex

292
Q

Describe the course of the upper motor neurons of the corticospinal tract

A

pass through internal capsule
descend through midbrain, pons and medulla
descend in spinal cord to ventral horn of spinal level

293
Q

State how fibres form either the lateral or anterior corticospinal tract and state their level of decussation

A

90% of fibres decussate to the contralateral side at the medulla = known as pyramidal decussation.
these fibres form the lateral corticospinal tract
terminate in the ventral horn

10% stay ipsilateral to form the anterior corticospinal tract
decussate in the spinal cord and then synapse with lower motor neurones

294
Q

What is the function of the corticobulbar tract?

A

controlling muscles of facial expression, extra-oculuar muscles etc
mainly BILATERAL innervation

295
Q

Where are the cell bodies of the upper motor neurons of the corticobulbar motor tract found?

A

cerebral cortex

30% motor cortex,
30% premotor cortex and supplementary motor areas,
40% somatosensory cortex

296
Q

Describe the course of the upper motor neurons of the corticobulbar tract

A

descends through the internal capsule to the brainstem
decussate in brainstem
terminate on CONTRALATERAL cranial nerve motor nuclei in the midbrain, pons, and medulla

297
Q

What is the function of the vestibulospinal tract?

A

balance and posture

298
Q

State the source, decussation and termination of the vestibulospinal tract

A

arises from the vestibular nucleus

the fibres DO NOT decussate.

termination in the spinal cord

299
Q

What is the function of the reticulospinal tract?

A

control of posture and rhythmic movements.

facilitate flexor and extensor spinal reflexes.

300
Q

State the source and decussation of the reticulospinal tract

A

The lateral reticulospinal tract fibres arise from the medulla
descend ipsilaterally to all levels of the spinal cord. DO NOT decussate
act to facilitate flexor spinal reflexes.

The medial reticulospinal tract fibres arise from the pons
descend ipsilaterally to all levels of the spinal cord. DO NOT decussate
They act to facilitate extensor spinal reflexes.

301
Q

What is the function of the tectospinal tract?

A

aids the directing of head movements in response to visual and auditory stimuli.

302
Q

State the source, decussation and termination of the tectospinal tract

A

arise from the tectum (superior and inferior colliculi) of the brainstem
DECUSSATE within the brainstem
terminate in neck and upper thoracic spinal cord

303
Q

What is the function of the rubrospinal and rubrobulbar tracts?

A

control flexor tone in distal muscles and also the tone of facial muscles.

304
Q

State the source, decussation and termination of the rubrospinal and rubrobulbar tracts

A

arise from neurones of the red nucleus, DECUSSATE in the midbrain
descend contralaterally in the spinal cord
terminate in contralateral spinal cord.

305
Q

What is Amyotrophic Lateral Sclerosis?

A

progressive degenerative disease
the corticospinal tracts and ventral horn cells degenerate
often beginning with the lower limbs

306
Q

What is Brown-Sequard Syndrome?

A

loss of sensation and motor function (paralysis and ataxia) that is caused by the lateral hemisection of the spinal cord.

presentation:
· Spastic paralysis of ipsilateral side (corticospinal tract)
· Loss of fine touch and proprioception to the ipsilateral side due to damage to fasciculus gracilis and cuneatus
· Loss of pain, temperature, and pressure sensation to the contralateral side due to damage to the spinothalamic tract.

307
Q

What is Anterior Spinal Artery Syndrome ?

A

motor paralysis and impaired pain and temperature sensation due to ischaemia affecting the spinal cord by the anterior spinal artery, affecting the corticospinal tracts

308
Q

What is Syringomyelia?

A

development of a cyst/cavity around central canal
this grows and spreads out over time, disrupting the spinothalamic tract as this decussates just ventral to central canal.

The result is reduced temperature and pain sensation at level of lesion, yet fine touch, proprioception and vibration are unaffected.
It can affect motor system as it extends

309
Q

What are the functions of the cerebellum?

A

coordination
precision and timing of movement
motor learning

310
Q

Name the anatomical lobes of the cerebellum

A

anterior lobe
posterior lobe
flocculonodular lobe

311
Q

State how the anatomical lobes of the cerebellum are divided

A

primary fissure divides anterior and posterior

posterolateral fissure divides posterior and flocculonodular loves

312
Q

Name the zones of the cerebellum

A

vermis
intermediate zone
lateral hemispheres

313
Q

Name the functional divisions of the cerebellum

what parts of the cerebellum are these formed from?

A

cerebrocerebellum - lateral hemispheres

spinocerebellum - vermis and intermediate zone

vestibulocerebellum - flocculonodular lobe

314
Q

What is the function of the cerebrocerebellum?

A

planning movements and motor learning

receives inputs from the cerebral cortex and pontine nuclei
sends outputs to the thalamus and red nucleus

regulates coordination of muscle activation

important in visually guided movements

315
Q

What is the function of the spinocerebellum?

A

regulating body movements by allowing for error correction.

receives proprioceptive information

316
Q

What is the function of the vestibulocerebellum?

A

controlling balance and ocular reflexes eg. fixation on a target.

receives inputs from vestibular system
sends outputs to the vestibular nuclei

317
Q

What are the causes of cerebellar dysfunction?

A

stroke
trauma
tumours
ageing

318
Q

What are the signs of cerebellar dysfunction

A 
ataxia
dysarthria
scanning speech
dysmetria (past-pointing)
dysdiadochokinesia
inability to learn new movements
nystagmus
abnormal gait
wide stance
loss of  balance
319
Q

Describe the function of the basal ganglia

A

regulate the amplitude and velocity of planned movement,

320
Q

Name the basal ganglia

A 
caudate nucleus
putamen
globus pallidus interna and externa
substantia nigra 
subthalamic nucleus
321
Q

Which structures together form the striatum?

A

caudate nucleus

putamen

322
Q

Which structures together form the lenticular nucleus

A

putamen

globus pallidus

323
Q

What is the effect on movement of the direct pathway through the basal ganglia?

A

acts to increase movement

324
Q

Describe the direct pathway

A
  1. Excitatory signals from the cerebral cortex act to increase the release of inhibitory signals from the striatum (caudate nucleus + putamen) to the globus pallidus
  2. This means that less inhibitory signals are released from the internal segment of the globus pallidus
  3. So there is less inhibition at the thalamus.

More excitatory signals are sent from the thalamus to the cortex.

This stimulates movement.

325
Q

How does the substantia nigra impact the direct pathway?

A

dopamine released
acts at D1 receptors

stimulates striatum

more inhibitory signals sent to globus pallidus interna

less inhibitory signals to thalamus

increased stimulation of cortex

stimulates movement

326
Q

What is the effect on movement of the indirect pathway through the basal ganglia?

A

acts to inhibit movement

327
Q

Describe the indirect pathway

A
  1. The cerebral cortex stimulates the striatum.
  2. This increases the inhibitory signals from the striatum, which act at the globus pallidus externa
  3. So less inhibitory signals are sent from the globus pallidus externa to the subthalamic nucleus.
  4. The decreased inhibition at the subthalamic nucleus leads to an increase in stimulatory signals sent to the globus pallidus interna from the subthalamic nucleus
  5. As the globus pallidus interna is stimulated, there are more inhibitory signals sent to the thalamus
  6. Less stimulation of the cerebral cortex.

so less movement

328
Q

How does the substantia nigra impact the indirect pathway?

A

dopamine released
acts at D2 receptor

inhibits striatum

less inhibition of globus pallidus externa

more inhibition of subthalamic nucleus

less excitation of globus pallidus interna

less inhibition at thalamus

increases movement

329
Q

Describe the pathogenesis of Parkinson’s disease?

A

degeneration of dopaminergic neurons of the substantia nigra, affecting the nigro-striatal pathway

330
Q

How does Parkinson’s disease affect the direct pathway?

A
  1. Decreased stimulation of the striatum (less activation of D1 receptors)
  2. Decreased inhibition at the globus pallidus interna
  3. Increased inhibition from the globus pallidus interna at the thalamus
  4. Less excitation of the cerebral cortex
331
Q

How does Parkinson’s disease affect the indirect pathway?

A
  1. Less inhibition at the striatum (less activation D2 receptors)
  2. Increased release of inhibitory signals from the striatum to the globus pallidus externa
  3. Decreased release of inhibitory signals from the globus pallidus externa to the subthalamic nucleus
  4. Increased excitatory signals sent from subthalamic nucleus to globus pallidus interna
  5. Increased inhibition from the globus pallidus interna at the thalamus
  6. Less excitation of the cerebral cortex
332
Q

Describe the signs seen in Parkinson’s disease?

A 
tremor at rest
increased tone
 - lead pipe or cog wheel rigidity (tremor imposed on hypertonia)
bradykinesia
festinating gait
taking more steps to turn
reduced arm swing
stooped posture
hypomimia
dysphonia
333
Q

What is muscle tone?

A

The minimal muscle power that allows us to maintain our posture and minimal stiffness in our muscles

334
Q

What creates muscle tone?

A

stretch reflex
when a muscle is stretched, muscle spindle afferent detect it
reflex contraction of muscles

335
Q

What are some causes of LMN lesions?

A

peripheral neuropathy
radiculopathy
anterior horn cell damage

336
Q

What causes peripheral neuropathy?

A 
diabetes
chronic alcohol abuse
hypothyroidism
vasculitis
chemotherapy
337
Q

What is radiculopathy?

A

compression or irritation of the nerves as they exit the spine.
can be due to mechanical compression by a disc herniation, an osteophyte, from osteoarthritis, or from thickening of surrounding ligaments.

338
Q

What causes anterior horn cell damage?

A

motor neuron disease

poliomyelitis

339
Q

What are the signs of a LMN lesion?

A 
flaccid paralysis
muscle atrophy
hypotonia
hyporeflexia
fasciculations
340
Q

Why does flaccid paralysis occur in LMN lesions?

A

denervation of muscles due to damage to the lower motor neurones
the muscle cannot be stimulated to contract

341
Q

Why does atrophy occur in LMN lesions?

A

denervation

342
Q

Why does hypotonia occur in LMN lesions?

A

failure of communication between α-motor neurones and muscles of that limb.

343
Q

Why does hyporeflexia occur in LMN lesions?

A

loss of innervation to the muscles

loss of reflex arc

344
Q

Why do fasciculations occur in LMN lesions?

A

denervation

individual motor units fire spontaneously

345
Q

When can a lower motor neuron lesion not result in regeneration?

A

when the cell body of the neuron in damaged

axons cannot regenerate

346
Q

When can a lower motor neuron lesion result in regeneration?

A

cell body intact
axon damaged
wallerian degeneration can occur

347
Q

What is the pyramidal system responsible for?

A

fractionation of finger movements

348
Q

What does the extrapyramidal system provide to the LMNs?

A

constant descending inhibition

349
Q

what is the postural result of spastic paralysis?

A

in upper limbs, flexors are stronger than extensors
so overall flexion

in lower limbs, extensors are stronger than flexors
so overall extension

350
Q

Where are the most common sites of UMN damage?

A

internal capsule

cerebral cortex

351
Q

State the signs of UMN lesions

A 
hyperreflexia
hypertonia - rigidity or spasticity
spastic paralysis
muscle weakness
Babinski sign
clonus
choreas
hemiplegic gait
352
Q

Why does hypereflexia occur in UMN lesions?

A

loss of the descending inhibition
loss of the inhibition of the spinal reflexes;
excessive action of the muscle reflexes

353
Q

Why does hypertonia occur in UMN lesions?

A

loss of inhibition to lower motor neurones

reflex circuit no longer inhibited

354
Q

What is spasticity in UMN lesions?

A

velocity dependent resistance to passive movement.

Detected with quick movements

355
Q

What is rigidity in UMN lesions?

A

sustained resistance throughout the range of movement.

Detected with slow movements

356
Q

Why does spastic paralysis occur in UMN lesions?

A

muscle tone becomes very high
overall flexion of upper limb
overall extension of lower limb

357
Q

What is a positive Babinski sign?

A

blunted instrument run along the sole of the foot laterally from heel to toe,

abduction of the toes and excessive dorsiflexion of the big toe.

358
Q

What is a hemiplegic gait seen in UMN lesions?

A

extension at the hip, knee and ankle.

foot on the affected side will be plantar flexed and move in a semicircular fashion.

The upper limb will be flexed.

359
Q

what is cortical localisation?

A

different areas of the cortex have a different histological structure and therefore different function

360
Q

where is the somatosensory association area?

A

parietal lobe

posterior to central sulcus

361
Q

where is the gustatory area?

A

frontal lobe

inferior to primary motor area

362
Q

where is the olfactory cortex?

A

temporal lobe

superior

363
Q

where is the primary visual cortex?

A

posterior occipital

364
Q

where is the primary auditory cortex?

A

temproral lobe middle superior

365
Q

where is the auditory association area?

A

superior temporal lobe

366
Q

Where is Broca’s area?

A

posterior frontal

anterior to primary motor cortex

367
Q

Where is Wernicke’s area?

A

superior temporal lobe

368
Q

What are the functions of the frontal lobe?

A 
motor
expression of speech (left)
behavioural regulation
eye movements
continence
personality, mood
369
Q

What are the functions of the parietal lobe?

A

sensory!
body image = right
awareness of external environment = right
calculation and writing = left

370
Q

What are the functions of the temporal lobe?

A 
hearing
comprehension of speech = left
olfaction
memory
emotion
371
Q

What are the functions of the occipital lobe?

A

vision

372
Q

What symptoms would be seen in a frontal lobe lesion?

A 
loss of fine movements
loss of complex chains of movement
Broca's aphasia
personality change
apathy
lack of ability to plan and sequence tasks
disinhibition
emotional lability
373
Q

What are the functions of the dominant hemisphere?

A

comprehension and expression of speech
calculation and writing

NB dominant = left

374
Q

What are the functions of the non-dominant hemisphere?

A

body awareness
visuospatial awareness
emotion
music

375
Q

how are the two hemispheres able to pass information between them?

A

connections via corpus callosum and anterior and midbrain comissure

376
Q

What are the symptoms of a parietal lobe lesion?

A

impairment of postural and tactile sensation
inability to write = agraphism
astereognosis = inability to identify an object by active touch of the hands
sensory and visual inattention
lower homonomous quadrantanopia

377
Q

What are the symptoms of a dominant parietal lobe lesion?

A

Wernicke’s aphasia
• Gerstmann’s syndrome - characterized by:
o Dysgraphia/agraphia: deficiency in the ability to write.
o Dyscalculia/acalculia: difficulty in learning or comprehending mathematics.
o Finger agnosia: inability to distinguish the fingers on the hand.
o Left-right disorientation

378
Q

What are the symptoms of a non-dominant parietal lobe lesion?

A

neglect of contralateral limb
spatial neglect
loss of three dimensional sense
geographical agnosia

379
Q

What are the symptoms of a temporal lobe lesion?

A 
disturbance of hearing and vision
disturbance of language comprehension
impaired long term memory
altered personality
upper homonomous quadrantanopia
380
Q

What is the function of Wernicke’s area?

A

interpretation of written and spoken words

381
Q

What is the function of Broca’s area?

A

formulation of laguage

382
Q

describe the pathway for speaking a heard word

A

primary auditory area
wernicke’s area
broca’s area
motor cortex

383
Q

describe the pathway for speaking a written word

A

primary visual area
wernicke’s area
broca’s area
motor cortex

384
Q

Describe Wernicke’s aphasia

A

disorder of comprehension
fluent but unintelligible speech

NB: occurs when lesion affects dominant hemisphere

385
Q

Describe Broca’s aphasia

A 
poorly constructed sentences
disjointed speech
good comprehension (can carry out three stage command)

NB:occurs when lesion affects dominant side

386
Q

Describe the symptoms of an extradural haematoma

A 
Trauma to head
Loss of consciousness
Lucid interval recovery 
Progressive hemiparesis 
Rapid herniation 
Ipsilateral pupil dilation
387
Q

What are the signs and symptoms of a subdural haematoma

A 
Trauma
Slow deterioration 
Headache
Drowsiness
Confusion
Focal deficits
388
Q

How can you tell on CT when the onset of a subdural haematoma was?

A

Acute - White

Chronic - denser and darker on CT - blood has clotted

389
Q

Describe the signs and symptoms of a subarachnoid haemorrhage

A

Rapid onset severe headache - thunderclap
Vomiting
Coma
Neck stiffness

390
Q

What causes subarachnoid haemorrhage?

A

Berry aneurysms
Malformations
Marfan’s
Ehlers danlos

391
Q

What are the symptoms of a basal skull fracture?

A

Periorbital ecchymosis
Mastoid ecchymosis
CSF leakage

392
Q

What is a coup and contracoup injury?

A

Brain bruising ( contusion) due to force

Coup - contusion at site of impact
Contracoup - contusion on opposite side of skull

393
Q

What is diffuse axonal injury?

A

Acceleration and deceleration
Causes shearing, stretching and tearing at grey-White matter junction
Cell oedema

394
Q

What are the signs and symptoms of diffuse axonal injury?

A

Instant loss of consciousness

Persistent vegetative state

395
Q

What is coning?

A

Cerebellar tonsillar herniation through foramen magnum
Due to RICP
Increased P on brainstem
Brain stem death

396
Q

Define stroke

A

Abrupt loss of cerebral function
Lasting >24hrs
Due to spontaneous haemorrhage or inadequate blood supply

397
Q

Define a TIA

A

Focal deficit
Sudden onset
Resolves completely within 24hrs

398
Q

What signs will a dominant cortical stroke cause?

A

Dysphasia
Dysgraphia
Dyslexia

399
Q

What signs will a non dominant cortical stroke cause?

A

Visuospatial disorders

Neglect

400
Q

What vessel is affected in a TACS?

A

ACA or MCA

401
Q

What vessel is affected in PACS?

A

ACA

MCA

402
Q

What vessel is affected in POCS?

A

PCA

403
Q

What vessels are affected in LACS?

A

Small sub cortical vessels

404
Q

What are the symptoms of a TACS and PACS?

A

Hemiparesis contra lateral to lesion
Hemianopia contra lateral to lesion
Disturbance of higher cortical function

TACS - all
PACS - 2/3

405
Q

What are the signs of a POCS?

A

Cerebellar syndromes
loss of consciousness
Cranial nerve deficits - ipsilateral

406
Q

What is the treatment for an ischaemic stroke?

A

Thrombolysis
Alteplase

Given within 3 hours any age
4.5 hours under 80

24 hrs later aspirin

Long term anti platelet, statins

407
Q

What are the signs and symptoms of anterior spinal infarction?

A

Spinal shock - flaccid weakness, areflexia, loss of pain and temperature

Fine touch and proprioception and vibration sense remain

408
Q

What can cause Parkinsonism?

A 
Multiple system atrophy
Wilson's disease
Corticobasal degeneration 
Drug induced 
Encephalitis
409
Q

What are the classical symptoms of Parkinson’s disease?

A

Tremor at rest
Bradykinesia
Rigidity

410
Q

What signs show that Parkinson’s is the most likely cause?

A 
Unilateral onset
Rest tremor
Progressive 
Persistent Asymmetry 
Good response to L-DOPA
L- DOPA induced chorea
Clinical course of 10 years or more
Hallucinations 
Hyposmia
411
Q

Describe the pathogenesis of PD

A

Destruction dopaminergic neurons in substantial Nigra pars compact
Reduction in dopamine action at striatum

More inhibition at thalamus
Slow movement

412
Q

Describe the synthesis of dopamine

A

In cytosol

L-tyrosine -> l-dopa -> dopamine

Tyrosine hydroxylase
Dopa decarboxylase

413
Q

Describe the degradation of dopamine

A

Monoamine oxidase in CNS
OR
COMT - catechol-o-methyl transferase in peripheries

414
Q

Why can dopamine not be used as a treatment of PD?

A

It cannot cross BBB

415
Q

Describe the mechanism of action of l-dopa

A

Crosses BBB
Taken up by dopaminergic cells in substantial Nigra
Converted to dopamine by dopamine decarboxylase

416
Q

Why does l-dopa stop having an effect in the late stages of PD?

A

Needs dopaminergic neurones to remain

417
Q

What is administered with L-DOPA?

Why?

A

Carbidopa - peripheral dopa decarboxylase inhibitor

More crosses BBB
Less peripheral effect

418
Q

What are the disadvantages of L- dopa?

A

Loses efficacy
Causes involuntary movements
Motor complications - on/off, wearing off, dyskinesia, dystopia, freezing

419
Q

What are the ADRs of l-dopa?

A

Nausea
Vomiting
Arrhythmias
Hypotension

420
Q

What drugs can interact with l-dopa?

A

Vitamin b6 increases peripheral breakdown l-dopa

MAOIs plus l-dopa enhances catecholamine production and causes hypertensive crisis

421
Q

Name some dopamine receptor agonists

A

Apomorphine
Bromocriptine
Ropinirole

422
Q

Describe the mechanism of action of dopamine receptor agonists

A

Bind to dopamine receptors

Produce response in neurons

423
Q

What are the advantages of dopamine receptor agonists?

A

Direct acting
Cause less dyskinesia
Neuroprotective (?)

424
Q

What are the disadvantages of dopamine receptor agonists?

A

Less efficacy than l-dopa
Produce impulse control disorders
Psychiatric side effects

425
Q

What are the symptoms of impulse control disorders?

A 
Pathological gambling
Hypersexuality 
Compulsive shopping 
Desire to increase dosage 
Punding- compulsive collecting, sorting or continually handling of objects
426
Q

What are the ADRs of dopamine receptor agonists?

A 
Sedation
Hallucinations
Confusion
Nausea
Vomiting
Constipation
427
Q

Name a monoamine oxidase B inhibitor

A

Selegiline

428
Q

Describe the mechanism of action of monoamine oxidase B inhibitors

A

Inhibits breakdown dopamine

Enhances dopamine levels in brain

429
Q

What happens if monoamine oxidase B inhibitors are used above recommended dose?

A

Lose selectivity

Inhibits MAO type A which metabolises noradrenaline too

430
Q

Name a COMT inhibitor

A

Entacapone

431
Q

Describe the mechanism of action of COMT inhibitors

A

Reduce peripheral breakdown of dopamine

No therapeutic effect alone

432
Q

Describe the ADRs of COMT inhibitors

A 
Diarrhoea
Postural hypotension
Nausea
Anorexia
Dyskinesia
Hallucinations 
Sleep disorders
433
Q

Name an anticholinergic used in PD

A

Procyclidine

434
Q

Describe the mechanism of action of anticholinergics used in PD

A

ACh may have antagonistic effect to dopamine

Anticholinergics may be able to treat tremor in some
No effect on bradykinesia

435
Q

Describe the ADRs of anticholinergics in PD

A

Mood changes
Xerostomia
Visual probs
Interfere with peristalsis

436
Q

Describe the mechanism of action of amantadine

A

Increases release dopamine in CNS
Blocks cholinergic receptors
Inhibits NMDA receptors

437
Q

What are the disadvantages of amantadine in PD?

A

Poorly effective

Little effect on tremor

438
Q

Define consciousness

A

Awake state in which one is fully aware of oneself and the environment
Ability to perceive and interpret stimuli
Ability to interact and communicate with others

439
Q

What does consciousness require?

A

Function of:
Reticular system
Cerebral cortex

440
Q

What part of the brain stimulated wakefulness in consciousness?

A

Reticular formation

441
Q

What part of the brain stimulates awareness in consciousness?

A

Cerebral cortex

442
Q

Where is the reticular formation located?

A

Centre of brainstem

443
Q

What structures input into the reticular formation?

A

Cortex

Sensory system from body

444
Q

Where does the reticular formation send outputs to?

A

Thalamus
Hypothalamus
Basal forebrain nuclei
Spinal cord

445
Q

What neurotransmitter do the inter neurons projecting from the reticular formation use?

A

ACh

446
Q

What neurotransmitter do neurones projecting from the basal forebrain nuclei going to the cortex use?

A

ACh

447
Q

What neurotransmitter do neurones going from the hypothalamus to the cortex use?

A

Histamine

448
Q

What neurotransmitter do neurones going from the thalamus to the cortex use?

A

Glutamate

449
Q

Why do antihistamines cause drowsiness?

A

Less histamine transmitted from hypothalamus to cortex

Decreased wakefulness from reticular activating system

450
Q

What causes impaired wakefulness?

A

Problems with reticular activating system

451
Q

What causes impaired awareness?

A

Problems with cortex

452
Q

What is the name for impaired wakefulness and awareness?

A

Coma

453
Q

What conditions is impaired wakefulness, but normal awareness, seen in?

A

REM sleep

Lucid dreaming

454
Q

What conditions is impaired awareness but normal wakefulness seen in?

A

Vegetative state

Acute confusional state

455
Q

What can cause a diffuse decrease in cortical function?

A

Metabolic disturbance

456
Q

What can damage the RAS?

A

RICP - compress brainstem

Lesion in brainstem

457
Q

What are intracranial causes of reduced consciousness?

A 
Haemorrhage
Stoke
Neoplasm
RICP
Infection
Trauma 
Epilepsy
458
Q

What are some extra cranial causes of reduced consciousness?

A 
Hypoxia 
Electrolyte disturbances 
Metabolic disorder
Sepsis 
Toxins
Endocrine disorders
459
Q

What are the signs of coma?

A

Absence of consciousness
No purposeful movement
No response to stimuli
GCS <8/15

460
Q

Describe the signs of acute confusional state/delirium

A

Fluctuating arousal
Impaired awareness
Disorientation
Hallucinations

461
Q

What are the first signs of impaired consciousness?

A

Change in behaviour or mood
Unsteady
Difficulty finding words
Slurred speech

462
Q

Describe the AVPU scale

A

Alert
Voice - response to verbal stimulus
Pain - response to pain stimulus
Unresponsive

463
Q

What is the AVPU score used for?

A

Emergency settings

Scoring less than A requires further investigation

464
Q

Describe the GCS scale

A 
Eye response 
1 none
2 to pain 
3 to speech
4 spontaneous
Verbal response
1 none
2 incomprehensible 
3 inappropriate words
4 confused
5 orientated 
Motor response 
1 none
2 extensor response - decerebrate 
3 flexor response - decorticate 
4 flexion to pain 
5 localises pain
6 obeys command
465
Q

When is GCS used?

A

Used to see change in consciousness over time

Viewed as a pattern of change

466
Q

What is declarative memory?

A

Naming objects, recognising places, remembering events

Stored in cortex

Assessed consciously

Rapidly learned and rapidly forgotten

467
Q

What is nondeclarative memory?

A

Performance of motor skills

Difficult to form

Long lasting and performed without conscious recollection

Stored in cerebellum and basal ganglia

468
Q

What neural changes are seen when memories are formed?

A

Synaptic changes

Neuroplasticity

469
Q

What is memory consolidation?

What makes this more likely?

A

Memories committed from short term to long term

Emotion
Rehearsal and repetition
Association

470
Q

What is the role of the hippocampus in memory?

A

Consolidation declarative memory

Integrates visual, auditory and somatosensory

Gives context and association to memories

471
Q

What is long term potentiation?

A

Long lasting enhancement in signal transmission between two neurones
Due to synchronous stimulation

472
Q

What is long term depression?

A

Weakening of synaptic strength
In infrequently used synapses

Causes gradual loss of memory

473
Q

What is anterograde amnesia?

A

Cannot form new memories

474
Q

What is retrograde amnesia?

A

Cannot remember previous memories

475
Q

Describe dementia

A

Progressive decline of cognitive function
Memory declines
Intellect falls

476
Q

What are the signs and symptoms of AD?

A 
Progressive memory loss
Aphasia 
Apraxia
Agnosia
Behavioural changes
Depression
477
Q

What is seen on MRI in AD?

A

Generalised atrophy - disproportionate in hippocampus

478
Q

What are the histological markers of AD?

A

Neurofibrillatory tangles

Plaques

479
Q

What are the neurofibrillatory tangles and plaques in AD made from?

A

NT - intracellular twisted hyperphosphorylated tau proteins

Plaques - amyloid deposition extracellular

480
Q

What stimuli activate the reticular formation?

A

Sensory inputs from body
Visual inputs
Stimulation from cortex

481
Q

How does visual stimulation reach the reticular formation?

A

Eye stimulates hypothalamus

Hypothalamus stimulates reticular formation - uses orexin as neurotransmitter

482
Q

Describe non-REM sleep

A

Slow wave
Active body and inactive brain
Made of 4 stages

483
Q

Describe REM sleep compared to non-REM sleep

A

active brain and inactive body
Will appear awake on EEG
Difficult to disturb from sleep
Muscle tone lost due to descending inhibition from glycinergic fibres from reticular formation
Eye movements and cranial nerve function preserved

484
Q

Describe what is seen on EEG when awake

A

Beta waves - >14 Hz

485
Q

What is seen on EEG when someone closed their eyes

A

Alpha waves - 8-13 Hz

Synchronous

486
Q

Describe an EEG during stage 1 of sleep

A

Theta waves 4-7 Hz

Lower amplitude than alpha waves

487
Q

What is seen on EEG in stage 2 and 3 of sleep?

A

Sleep spindles - almost fibrillation like. Due to thalamic activity
K complexes - tall

488
Q

What is seen on EEG in stage 4 of sleep?

A

Delta waves - oscillations. <3.5 Hz

489
Q

What is seen on EEG in REM sleep?

A

Beta waves!!!

490
Q

What is narcolepsy?

What is thought to cause it?

A

Spontaneously falling asleep
Sleep paralysis - remain awake but unable to move

Loss of orexinergic neurones stimulating reticular formation leading to abnormal function cholinergic neurones

491
Q

What is sleep apnoea?

A

Interruption of breathing during REM sleep, leading to aeousal from sleep
Caused by airway narrowing

492
Q

Describe how an EEG is taken

A

Place 16-25 electrodes on head

Measure electrical activity

493
Q

State the frequency of the waves seen during sleep on EEG

A

Alpha 8-13 Hz
Beta >14
Theta 4-7
Delta <3.5

494
Q

What is cerebral perfusion pressure?

A

Difference between mean arterial pressure and intracranial pressure
Represents the pressure gradient driving cerebral blood flow

495
Q

What is a normal ICP?

A

Between 5 and 15 mmHg

496
Q

What causes venous pressure to change and increase ICP?

A

Raises in intrathoracic pressure

Due to breathing out, coughing, laughing, sneezing of straining

497
Q

What are the components of the volume of the brain?

A

Brain
Arterial blood
Venous blood
CSF

498
Q

What is meant by the brain being in a compensated state?

A

The CSF and venous volumes have decreased

ICP remains within normal limits

499
Q

What is meant by the brain being in a decompensated state?

A 
Brain has reached critical volume
RICP 
ICP > CCP 
Cerebral perfusion is prevented 
Brain becomes ischaemic
500
Q

How does the body attempt to compensate for brain ischaemia in RICP?

A

Cerebral vessels vasodilator
BP increase
Attempts to increase cerebral perfusion

But only raises ICP more!

501
Q

How can blood cause RICP?

A 
Venous sinus thrombosis - increased intravascular volume
Extradural haematoma
Subdural haematoma
Subarachnoid haemorrhage 
Intracerebral haemorrhage
502
Q

How does the brain cause RICP?

A

Tumour

Oedema- trauma, infarct, malignancy, infection, water intoxication

503
Q

How does the CSF cause RICP?

A

Hydrocephalus

504
Q

What causes hydrocephalus?

A

Increased production - choroid plexus papilloma
Disruption of flow - spina bifida, aqueduct stenosis, clot, space occupying lesion
Disruption of absorption by arachnoid granules

505
Q

What are the signs and symptoms of RICP?

A 
Headache
Nausea and vomiting
Uni ocular loss of vision
CNIII nerve palsy 
CN vi nerve palsy 
Papilloedema 
Reduced GCS 
Loss of vestibule-ocular reflex
Cushing's triad
506
Q

Describe the headache seen in RICP

A 
Generalised 
Bilateral
Worse first thing in morning, on lying down, coughing, sneezing, bending forwards
Wakes them up at night
Relieved by sitting or standing
507
Q

Why does CN III palsy occur in RICP?

A

Uncal herniation compresses

508
Q

Why does CN vi palsy occur in RICP?

A

Long course through cranium

509
Q

What is the vestibulo-ocular reflex?

Why is it lost in RICP?

A

Eyes normally look towards cold water placed next to ear and away from warm water placed next to ear

Brainstem death

510
Q

What is cushing’s triad?

A

Irregular respiration
Bradycardia
Systolic hypertension

511
Q

Why does Cushing’s reflex happen?

A 
Brain ischaemia 
Increase in symp tone to vessels
Increases BP
Carotid detectors sense rise in BP
Increase parasympathetic tone 
Bradycardia
512
Q

What is decorticate posturing?

A

Lower limbs extended

Upper limbs flexed

513
Q

Why does the decorticate response occur?

A

Destruction connection between cortex and thalamus

Isolates cortex from lower brain and spinal cord

514
Q

What is decerebrate posturing?

A

Extension lower limb
Extension upper limbs
Extension head

515
Q

Why does the decerebrate response occur?

A

Lower parts of brain and brainstem damaged

All descending inhibition lost

516
Q

What is a hernia?

A

Protrusion of an organ or part of an organ into a region that does not normally contain it

517
Q

Describe subfalcine herniation

A

Herniation occurs on same side as mass

Cingulate gyrus pushed under free edge falx cerebri

518
Q

What are the consequences of subfalcine herniation?

A

Compresses anterior cerebral artery

Causes ischaemia medial parts frontal and parietal lobe

519
Q

Describe uncal herniation

A

Uncus herniates through tentorial notch (edge of tentorium cerebelli)

520
Q

What are the consequences of uncal herniation?

A

Compression CN III
Compresses cerebellar peduncles
Occludes cerebellar arteries

521
Q

Describe tonsillar herniation

A

Cerebellar tonsils pushed through foramen magnum

522
Q

What are the consequences of tonsillar herniation?

A

Brainstem compression - affects cardiac and resp control centres
Coma

523
Q

Describe the phases of migraine

A

Well being
Prodromal symptoms - visual or sensory
Pain! Begins locally then becomes generalised
Feeling drained

524
Q

What causes tension headaches?

A

Neurovascular irritation

Due to excessive tension on scalp muscles

525
Q

What causes migraines?

A

Vasodilation and oedema in blood vessels

Stimulates nerve endings

526
Q

What is temporal arteritis?

A

Also known as giant cell arteritis
Systemic immune mediated vasculitis
Chronic inflammation large arteries

527
Q

What are the signs and symptoms of temporal arteritis?

A 
Temporal headache - acute severe 
Myalgia
Malaise 
Fever 
Visual disturbances on same side 
Jaw or tongue claudication 
Scalp tenderness 
Older than 50
Temporal artery abnormality - prominent, beaded, tender, pulse less
528
Q

What is the main causative organism of meningitis?

A

Under 2 - E. Coli
2-5 - H. influenzae type B
5-30 - N. meningitidis
Over 30 - S. Pneumoniae

529
Q

What is encephalitis?

A

Infection of neural parenchyma

530
Q

What causes encephalitis?

What regions are affected?

A 
Viral!
Herpes - temporal lobe
Polio - spinal cord
Rabies - brain stem
Cytomegalovirus
531
Q

What are the symptoms of encephalitis?

A 
Headache
Confusion
Fever
Drowsiness
Fatigue
Seizures
Tremors
532
Q

Describe the function of the cones in the retina

A

Provide high acuity vision
Day vision
Colour vision

533
Q

Describe the location of the cones in the retina

A

Concentrated at fovea

534
Q

Describe the function of the rods of the retina

A

Specialised for night vision

Highly light sensitive

535
Q

What three functional classes of cells are present in the retina?

A

Photoreceptors - rods and cones

Inter neurons - combine signals from the photoreceptors

Ganglion cells - output cells

536
Q

What is a visual field?

A

Region of space that the eye can see whilst looking straight ahead

537
Q

What part of the retina are images present in the left visual fields recognised by?

A

Nasal hemiretina of left eye

Temporal hemiretina of right eye

538
Q

State the order of neurones after leaving the retina

A 
Optic nerve
Optic chiasm 
Optic tract
Lateral geniculate ganglion
Optic radiations
539
Q

What fibres does the right optic tract contain?

A

Nasal fibres from left eye

Temporal fibres from right eye

540
Q

Where is the lateral geniculate nucleus found?

A

In the thalamus

541
Q

What fibres does the upper optic radiation carry?

A

Fibres from superior retinal quadrants

So vision from inferior visual quadrants

542
Q

Describe the course of the superior optic radiations

A

Through parietal lobe

To visual cortex in occipital lobe

543
Q

What fibres does the lower optic radiation carry?

A

Fibres from the inferior retinal fibres

So vision from the superior visual field quadrants

544
Q

Describe the course of the lower optic radiation

A

Through temporal lobe
Pathway is called Meyer’s loop
To reach visual cortex in occipital lobe

545
Q

Where is the primary visual cortex found?

A

Medial aspect of occipital lobe

546
Q

Describe the steps in the light reflex

A

Light stimulates optic nerve
Synapses with interneurones in midbrain
Interneurones project bilaterally to edinger-westphal nucleus
Preganglionic parasympathetic neurones then travel to ciliary ganglion
Postganglionic fibres then innervate sphincter papillae

547
Q

What is seen in accommodation of the eye?

A

Convergence of eye
Constriction of pupil
Lens becomes convex to increase refractive power

548
Q

When is the accommodation reflex used?

A

When the eyes changes focus from distant to near

549
Q

Why must the accommodation reflex involve the cortex?

A

Relates to analysis

550
Q

Where in the visual pathway is the damage in complete loss of vision in one eye?

A

The optic nerve

551
Q

What causes an optic nerve lesion?

A

Optic nerve glioma
Retinoblastoma in children
Optic sheath meningioma in middle aged

552
Q

What part of the visual pathway is damaged in a bitemporal hemianopia?

A

Optic chiasm

553
Q

What causes an optic chiasm lesion?

A

Pituitary adenoma

Anterior communicating artery aneurysm

554
Q

Where in the visual pathway is damaged in a patient with left homonymous hemianopia

A

Loss of left field of vision

Right optic tract

555
Q

What can cause damage to the optic tracts?

A

Stroke
Neoplasm
Trauma

556
Q

Where in the visual pathway is the lesion in superior left homonymous hemianopia?

A

Right lower optic radiations

557
Q

What causes damage to the lower optic radiations?

A

Damage to the temporal lobe

vascular occlusion In middle cerebral artery

558
Q

Why does macular sparing occur in a posterior cerebral artery stroke?

A

Dual blood supply to occipital lobe

  • posterior cerebral artery
  • middle cerebral artery (normally supplies occipital pole representing macula)
559
Q

What is an otic placode?

A

Thickened ectodermal patch on back of head

Goes on to form ear

560
Q

How does the otic placode turn into the otic vesicle

A

Thicken
Invaginate
Sink below surface
Pinched off to form otic vesicle

561
Q

Describe how the otic vesicle transforms into the inner ear

A

Saccule - cochlea

Utricle - semicircular canals

562
Q

State the origins of the component of the middle ear

A

Tympanic cavity - first pharyngeal pouch
Malleus and incus - Meckel’s cartilage - 1st pharyngeal arch
Stapes - Reichert’s cartilage - 2nd pharyngeal arch

563
Q

What does the first pharyngeal pouch turn into?

A

Distal end - tympanic cavity

Proximal end - Eustachian tube

564
Q

State the innervation of the muscles of the middle ear. Why is this?

A

Tensor tympani - mandibular branch CN V - 1st pharyngeal arch
Stapedius - facial nerve - second pharyngeal arch

565
Q

What does the external auditory meatus develop from?

A

1st pharyngeal cleft

566
Q

What do the auricles develop from?

A

Auricular hillocks - proliferations within first and second pharyngeal arches

567
Q

How do the ears move from the back of the head to the side?

A

Mandible grows and pushes them into place

568
Q

What can be the cause of congenital deafness?

A

Middle ear deafness - 1st and second pharyngeal arch probs

Inner ear deafness - malformation organ of corti - commonly due to teratogenic agents

569
Q

When does development of the eye begin?

A

Week 4

570
Q

Describe formation of the eye from the forebrain

A 
Optic vesicles (part of forebrain) grow toward lens placode in ectoderm
Lens placode thickens, invaginates and pinches off. Sinks down into optic vesicle 
Optic vesicle stretches out to grasp lens placode
571
Q

What is the choroid fissure?

A

Long slit running down stalk of optic vesicle

572
Q

What does failure of closure of the choroid fissure result in?

A

Coloboma

573
Q

The optic vesicles closes around the hyoid artery

What is the fate of this artery?

A

Degenerated dismally

Becomes central retinal artery proximally

574
Q

What forms the ciliary body musculature and the extra ocular muscles?

A

Ciliary body - rim of optic vesicle

Extra ocular muscles - pre optic myotomes

575
Q

What does the optic vesicle develop into?

A

Optic cup

Retina, iris, ciliary body

576
Q

Why can retinal detachment occur?

A

Retina develops from two separate layers

Intraretinal space can open up again

577
Q

What are congenital cataracts?

A

Opacity of lenses

Due to genetic defect or teratogen

578
Q

What is congenital rubella syndrome?

A 
When pregnancy woman gets rubella during first trimester 
Triad of symptoms in fetus:
Sensorineural deafness
Cataracts or retinopathy 
Congenital heart disease (PDA)
579
Q

Define a partial seizure

A

Only affects one hemisphere of the brain

580
Q

What is the difference between a simple and complex partial seizure?

A

Simple - no loss of consciousness

Complex - loss of consciousness

581
Q

What are the symptoms of a partial seizure affecting the frontal lobe?

A

Abnormal head movements
Swearing/shouting out
Abnormal posturing
Repeated movements

582
Q

Describe the features of a partial seizure affecting the parietal lobe

A

Abnormal sensations
Hallucinations
Difficulty understanding speech and language

583
Q

Describe the features of a partial seizure affecting the temporal lobe

A

Deja vu
Strange taste/smell
Lip smacking
Swallowing or chewing

584
Q

Describe the features of a partial seizure affecting the occipital lobe

A

Hallucinations
Disturbed vision
Eye pain
Nystagmus

585
Q

What is a generalised seizure?

A

Affects both hemispheres

586
Q

Describe a tonic-clonic seizure

A 
Loss of consciousness 
Body stiffens 
Fall
Limb jerking
Loss of bladder control
Post ictal period
587
Q

Describe the difference between a clonic and myoclonic seizure

A

Clonic - jerking lasts two mins. Loss of consciousness

Myoclonic - jerking lasts fraction of second. No loss of consciousness. Happens early in morning

588
Q

What are the main causes of secondary epilepsy?

A 
Brain injury or hypoxia 
Pyrexia in children
Alcohol
Drugs
Encephalitis
Metabolic disturbances
589
Q

What can generate an epileptic fit?

A

Increased excitatory activity
Decreased inhibitory activity
Loss homeostatic control
Spread neuronal hyperactivity

590
Q

What is status epilepticus

A

Medical emergency
Continuous seizures without period of recovery
More than 30 mins
High risk mortality

ESA5 (2 decks)

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