Neuro Flashcards
1
Q
State the function of astrocytes
A
regulate the chemical content of the extracellular space
Envelope synaptic junctions in the brain.
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
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
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.
5
Q
Describe the structure of afferent neurones
A
from PNS to CNS
cell body in dorsal root ganglia
6
Q
Describe the structure of efferent neurones
A
from CNS to PNS
cell bodies within the CNS derived from the ventral spinal cord
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.
8
Q
Which lobes of the brain does the central sulcus separate?
A
frontal
parietal
9
Q
Which lobes of the brain does the lateral fissure separate?
A
frontal and parietal
temporal
10
Q
Which lobes of the brain does the transverse fissure separate?
A
occipital
cerebellum
11
Q
Which lobes of the brain does the longitudinal fissure separate?
A
right and left frontal and parietal
12
Q
Where is the precentral gyrus found?
A
anterior to the central sulcus
13
Q
Where is the postcentral gyrus found?
A
posterior to the central sulcus
14
Q
Where is the parahippocampal gyrus found?
A
inferior to the hippocampus
15
Q
where is the anterior commissure found?
A
inferior to the septum pellucidum
Superior to the hypothalamus
16
Q
describe the location of the septum pellucidum
A
inferior to the corpus callosum
anterior and superior to the fornix
17
Q
describe the location of the cingulate gyrus
A
superior to the corpus callosum
18
Q
describe the location of the corpus callosum
A
inferior to cingulate gyrus
superior to fornix
19
Q
describe the location of the fornix
A
surrounds thalamus
inferior to corpus callosum
20
Q
describe the location of the hippocampus
A
inferior to fornix and thalamus
superior to parahippocampal gyrus and brain stem
Posterior to amygdala
21
Q
describe the location of the thalamus
A
surrounded by fornix
superior to hippocampus
22
Q
describe the location of the hypothalamus
A
anterior to fornix and thalamus
superior to pituitary gland
23
Q
describe the location of the pituitary gland
A
inferior to hypothalamus
24
Q
state the layers of the meninges
A
periosteal dura meningeal dura arachnoid mater (subarachnoid space) pia mater
25
describe the location of the uncus
superior anterior to parahippocampal gyrus
26
describe the location of the calcarine sulcus
medial surface of the occipital lobe
| divides the visual cortex (aka calcarine cortex) into two.
27
describe the location of the parieto-occipital sulcus
between parietal and occipital lobes of cortex
28
describe the location of the pineal gland
inferior to thalamus
| superior to cerebellum and cerebral aqueduct
29
describe the location of the optic chiasm
superior to pituitary gland
30
where is the vermis found in the cerebellum?
centrally
31
where are the tonsils found in the cerebellum?
lateral to the inferior vermis
32
State where the spinal cord enlarges
cervical
| lumbar
33
What is the conus medullaris?
lower end of the spinal cord
34
State the location of the conus medullaris?
L1/2
35
What is the cauda equina?
spinal nerves and nerve roots
| L2-S5
36
What is the filum terminale?
connective tissue
| stretches from apex of conus medullaris to the coccyx
37
What is the lumbar cistern?
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;
38
What is the clinical significance of the lumbar cistern?
site for lumbar puncture and spinal anaesthesia
39
What is the notochord?
| How is it formed?
solid rod of cells running down the midline
| formed from prenotochordal cells migrating through primitive pit
40
How is neurulation initiated?
ectodermal cells above the notochord differentiate to become the neural plate
41
How is the neural tube formed?
neural plate thickens
lateral edges rise up
midline depresses (forms neural groove)
lateral edges fuse in midline
42
Where does fusion of the neural folds begin?
| How does it spread?
cervical region
| cephalo-caudally
43
Why are neuropores formed?
last parts of neural tube to fuse anteriorly and posteriorly
44
Which neuropore closes first?
anterior (day 25)
| posterior (day 28)
45
What fails to develop in anencephaly?
| What is the result?
failure of anterior neuropore closure
| absence of cranial structures, including brain
46
What fails to develop in spina bifida?
failure of posterior neuropore to close
can occur anywhere from base of skull to sacrum
vertebral arch incompletely formed or absent
47
Where along the spine is spina bifida most common?
lumbosacral region
48
Describe spina bifida occulta
overlying skin intact
bony vertebral arch defect
no visible external overlying sac
no protusion of spinal cord or membranes
49
Describe spina bifida cystica
both vertebral defect and visible cystic mass
50
Describe a meningocoele
cystic swellng of dura and arachnoid mater
protrudes through vertebral arch defect
no spinal neural tissue present within sac
51
Describe myelomeningocoele
cystic swellng of dura and arachnoid mater
protrudes through vertebral arch defect
spinal neural tissue forms part of the sac
52
Describe rachischisis
cystic swellng of dura and arachnoid mater
spine lies widely open
neural plate has spread out on to the surface
53
Which form of spina bifida is most common?
spina bifida occulta
| then myelomeningocoele
54
How can a neural tube defect be detected in a fetus?
raised maternal serum α-fetoprotein
| USS
55
How can neural tube defects be prevented?
Increased folic acid intake pre-conceptually (3 months) and in first trimester
56
State in general terms how the neuroectoderm tube forms the developed neural tissues
lumen = ventricular system
cranial dilations = brain
caudal tail = spinal cord
57
Why does the cauda equina form?
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
58
What are the three primary brain regions?
* forebrain (prosencephalon),
* midbrain (mesencephalon)
* hindbrain (rhombencephalom)
59
In what week do the three primary brain regions form?
week 4
60
In what week do the five secondary brain regions form?
week 5
61
State which primary brain region each of the secondary brain regions developed from
prosencephalon -> telencephalon and diencephalon
mesencephalon -> mesencephalon
rhombencephalon -> metencephalon and myelencephalon
62
What does the telencephalon develop into?
cerebral hemispheres
63
What does the diencephalon develop into?
thalamus
64
What does the mesencephalon develop into?
midbrain
65
What does the metencephalon develop into?
pons
| cerebellum
66
What does the myelencephalon develop into?
medulla oblongata
67
Why do flexures form in the neural tube?
cranial end of the neural tube develops rapidly
exceeds available space
folds up
68
Where is the cervical flexure found?
spinal cord hindbrain junction
69
Where is the cephalic flexure found?
in the midbrain region
70
Which secondary brain region lumen does the lateral ventricle develop from?
telencephalon
71
Which secondary brain region lumen does the third ventricle develop from?
diencephalon
72
Which secondary brain region lumen does the cerebral aqueduct develop from?
mesencephalon
73
Which secondary brain region lumen does the fourth ventricle develop from?
metencephlon and myelencephalon
74
How does hydrocephalus develop in newborns?
blockage of ventriular system
| impaired absorption of CSF
75
What are the symptoms of hydrocephalus?
What are the signs?
irritability
vomiting
impaired conscious level
dis-junction of sutures
dilated veins
rapid increase in head circumference
76
How is hydrocephalus treated?
shunt
77
Describe the organisation of the neural tube from inside to out
neuroepithelial layer
intermediate layer = neuroblasts
marginal layer = processes
78
How is dorsal and ventral patterning of the neural tube achieved?
roof and floor plates
79
State the dorsal and ventral patterns of the neural tube
roof = alar plate = sensory
floor = basal plate = motor
80
Where do the neural crest cells originate from?
lateral border of the neuroectoderm tube
81
What transition do the neural crest cells undergo?
displaced and enter mesoderm
| epithelial to mesenchymal transisition
82
Give examples of where the neural crest cells are used in development
adrenal medulla
schwann cells
c cells
thyroid gland
83
Why are the neural crest cells vulnerable to environmental insults such as alcohol?
complex migratory pattern
84
What is Hirschprung's Disease?
failure of neural crest cells to migrate to intestine
affected segment of colon fails to relax
obstruction occurs
85
State the functions of an anstrovyte
```
structural support
provide nutrition for neurones
remove neurotransmitters
maintain ionic environment
help form BBB
```
86
Why do neurones require a constant source of glucose?
cannot store or produce glycogen
87
Describe how astrocytes provide a direct source of glucose or lactate to neurones
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
88
Why do astrocytes have transporters specific for neurotransmitters?
remove neurotransmitter after an action potential
extracellular conc remain low
prevents toxicity of neurotransmitter
prevents spread of neurotransmitter to other receptors
89
Why do astrocytes have a very negative resting membrane potential?
high intracellular K+ conc
| due to removal of K+ after an action potential
90
What is the function of oligodendrocytes?
myelination in CNS
91
What is the function of microglia?
immune system
APC
phagocytosis
92
Where to microglial cells originate from?
| Why is this important?
mesoderm
other glial cell are ectodermal
93
why is the CNS described as immune privileged?
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)
94
What forms the BBB?
tight junctions between endothelial cells
basement membrane surrounding capillaries
end feet of astrocyte processes
95
Describe the structure and action of the tight junction of the BBB
bound by clodin and occluding proteins
| prevent hydrophilic molecules from entering the CSF
96
State the main categories of neurotransmitter, giving examples
amino acids - glutamate, GABA
biogenic amines - NA, ACh
peptides - somatostatin, neuropeptide P
97
What is the main excitatory amino acid?
glutamate
98
State the three main types of ionotropic glutamate receptors
AMPA
NMDA
kainate
99
What change does glutamate binding to AMPA receptors cause?
increases Na+ and K+ permeability
| initial fast DEPOLARISATION
100
What change does glutamate binding to NMDA receptors cause?
increases Na+, K+ and Ca2+ permeability
| DEPOLARISATION
101
How do ionotropic glutamate receptors allow more APs to fire?
depolarisation
| EPSP
102
Why does the cell membrane need to be depolarised in order for the NMDA receptor to open?
at resting potential the channel is blocked by an Mg2+ ion
103
What needs to occur for the NMDA channel to open?
glutamate binds
depolarisation of membrane
glycine binds as co-agonist
104
What is Long Term Potentiation?
increased synaptic strength in the long term
105
What causes long term potentiation?
activation of NMDA receptors
Ca2+ entry
phosphorylation and insertion of additional AMPA receptors in postsynaptic membrane
106
What is the main inhibitory neurotransmitter in the brain?
GABA
107
What is the main inhibitory neurotransmitter in the brainstem and spinal cord?
glycine
108
How do GABA(A) and glycine receptors cause inhibition?
integral Cl- ion channels
HYPERPOLARISATION
IPSP
decreased AP firing
109
What is the mechanism of action of barbiturates and benzodiazepines?
bind to GABA(A) receptors
enhance inhibitory response
leads to sedation and anti-anxiety actions
110
What is the role of GABA(B) receptors?
modulation
111
State the major biogenic amines
ACh
dopamine
NA
serotonin (5-HT)
112
State the main action of ACh in the CNS
excitatory neurotransmitter at nicotinic and muscarinic receptors
present on presynaptic terminals to enhance the release of other neurotransmitters
113
Where do ACh neurones originate?
basal forebrain
| pontomesencephalotegmental cholinergic complex
114
Which areas of the brain do ACh neurones originating in the basal forebrain innervate?
hippocampus
| neocortex
115
Which areas of the brain do ACh neurones originating in the pontomesencephalotegmental cholinergic complex innervate?
dorsal thalamus
| parts of forebrain
116
What actions are ACh receptors involved in?
arousal
memory
learning
motor control
117
Describe the link between cholinergic neurons and Alzheimer's disease
degeneration of cholinergic neurones in the nucleus basalis is associated with Alzheimer’s disease.
118
Which areas of the brain have a high concentration of dopamine receptors?
substantia nigra in midbrain
| ventral tegmental area of midbrain
119
Where do the dopaminergic neurons of the substantia nigra project axons into?
What is their function?
striatum
initiating voluntary movement
120
What causes Parkinson's disease?
degeneration of dopaminergic neurons that being in the substantia nigra
121
What disorder can too much dopamine in the CNS lead to?
schizophrenia
122
Which neurotransmitters does amphetamine cause the release of?
dopamine
| noradrenaline
123
How is Parkinson's treated?
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
124
Where are noradrenaline containing neurones found in the brain?
locus coeruleus in brainstem
125
Where in the brain do noradrenaline containing neurones innervate?
```
cerebral cortex,
thalamus
hypothalamus,
olfactory bulb,
cerebellum,
midbrain
spinal cord
```
126
What is the function of noradrenaline containing neurones?
behavioural arousal
| mood
127
Where are serotonin containing neurones found in the brain?
raphe nuclei in the midline of the brainstem
128
What is are dopamine containing neurones involved in the control of?
sleep/wakefulness
| mood
129
How is knowledge of serotonin used in treatment of depression and anxiety disorders?
SSRIs (Serotonin Selective Reuptake Inhibitors)
| increases serotonin at synapse
130
Which paired arteries supply the brain?
vertebral arteries
| internal carotids
131
Where do the internal carotid arteries arise?
bifurcation of common carotid
| C4
132
Describe the course of the carotid arteries
carotid sheath
enter brain via carotid canal of temporal bone
pass anteriorly through cavernous sinus
133
State the branches that the internal carotid arteries give rise to distal to the cavernous sinus
What does the ICA then continue as?
ophthalmic artery
posterior communicating artery
anterior cerebral
middle cerebral artery
134
What structures does the anterior cerebral artery supply?
medial surfaces of frontal and parietal lobes
135
What structures does the middle cerebral artery supply?
lateral portions of cerebrum
136
Describe the course of the vertebral arteries
arise from subclavian arteries medial to anterior scalene
ascends through transverse foramen of cervical vertebrae
enter cranium via foramen magnum
137
State the branches of the vertebral artery within the cranial vault
meningeal branch
anterior spinal arteries
posterior spinal arteries
posterior inferior cerebellar
138
How do the vertebral arteries terminate?
converge
| form basilar artery
139
How does the basilar artery terminate?
bifurcates
| forms posterior cerebral arteries
140
What structures does the posterior cerebral artery supply?
inferior surface of brain
| occipital lobes
141
State the components of the circle of willis
```
anterior cerebral arteries
anterior communicating artery
internal carotid arteries
posterior communicating arteries
posterior cerebral arteries
```
142
In disease states, what is the benefit of the circle of willis?
anastomoses can provide collateral circulation
if arteries have become progressively blocked
however, if the block happens suddenly, collateral supply would be inadequate
143
Describe the blood supply of the spinal cord
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
144
What is a stroke?
acute development of a neurological deficit,
| due to a disturbance in the blood supply of the brain.
145
What are the main causes of cerebrovascular accident?
thrombosis
embolism
hypoperfusion (due to systemically low BP)
haemorrhage - accumulation of blood within cranial cavity
146
What is an aneurysm?
dilation of an artery, which is greater than 50% of the normal diameter
147
What is spinal cord infarction?
the death of nervous tissue in the spinal cord
| resulting from an interruption of the arterial supply.
148
What are the causes of spinal cord infarction?
```
vertebral fractures
vertebral dislocations
vascular disease
atheroma
external compression (eg. abdominal tumour)
```
149
What are the signs and symptoms of spinal cord infarction?
muscle weakness
paralysis
loss of relfeces
150
Where are the dural venous sinuses found?
between the periosteal and meningeal layers of the dura mater
151
Where do the dural venous sinuses drain into?
internal jugular vein
152
Which dural sinuses are found in the flax cerebri?
Where do they meet?
straight
superior
inferior
confluence of sinuses (posterior)
153
Describe the course of the venous blood from the confluence of sinuses
transverse sinuses continue bilaterally
curves into sigmoid sinus
joins to internal jugular vein
154
how does blood enter the cavernous sinus?
How does blood drain from the cavernous sinus?
from ophthalmic veins
via the superior or inferior petrosal sinuses to the internal jugular vein
155
What is Cerebral venous sinus thrombosis?
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
156
What are the symptoms of Cerebral venous sinus thrombosis?
headache
nausea
vomiting
neurological defects
157
How is a Cerebral venous sinus thrombosis treated?
anticoagulation
158
What is the role of the veins of the cerebrum?
carrying blood from the brain tissue
| depositing it in the dural venous sinuses
159
How are cerebral veins divided into superficial and deep groups?
```
deep = emerge from transverse fissure
superficial = in subarachnoid space. pierce meninges to drain blood into venous sinuses
```
160
state the three layers of the meninges
dura mater
arachnoid mater
pia mater
161
Describe the dura mater
lies directly beneath the skull
thick, tough, inextensible
periosteal layer
meningeal layer
162
What is a dural reflection?
meningeal layer of the dura mater folds inwards
partitions the brain, and divide the cranial cavity into several compartments
163
Describe the blood supply and innervation of the dura mater
middle meningeal artery and vein
trigeminal nerve
164
What is an extradural haematoma?
What is the common cause?
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
165
What is a subdural haematoma?
What is the common cause?
Venous blood collects between the dura and the arachnoid mater.
damage to cerebral veins as they empty into the dural venous sinuses.
166
Describe the arachnoid mater
middle layer of the meninges,
lies directly underneath the dura mate
consists of layers of connective tissue
avascular.
167
What does the subarachnoid space contain?
CSF
168
How does CSF re-enter the circulation from the subarachnoid space?
arachnoid granulations = projections of arachnoid mater into the dura
enters dural venous sinuses
169
Meningitis causes cerebral oedema, raising ICP.
| What are the life-threatening effects of this?
cranial herniation = parts of the brain forced out of the cranial cavity
reduced cerebral perfusion
170
How does a fracture of the skull vault lead to a haematoma formation?
disruption of dura and blood vessels
171
Why does CSF rhioorrhoea occur?
What is a complication of this?
fracture of frontal sinus or cribriform plate
dura (normally adheres to periosteum) tears
CSF leaks out
infections
172
What are the functions of CSF?
protection - cushions the brain
bouyancy
chemical stability
173
Where is CSF produced?
ependymal cells of choroid plexus in ventricles
174
What is the embryological derivative of the ventricles?
neural tube
175
Name the paired ventricles
left ad right lateral ventricles
176
How are the lateral ventricles connected to the third ventricle?
foramen Monro
177
Describe the location and anterior projections of the third ventricle
between the left and right thalamus
supra-optic recess - above optic chiasm
infundibular recess - above optic stalk
178
How is the third ventricle connected to the fourth ventricle?
cerebral aqueduct
179
Describe the location of the fourth ventricle
within the brainstem
| a the junction between the pons and medulla
180
Where does the fluid drain into from the fourth ventricle?
central spinal canal - bathes the spinal cord
subarachnoid cisterns - bathes the brain. between arachnoid mater and pia mater.
181
How is the chemical composition of the CSF controlled?
plasma is filtered by the epithelial cells of the choroid plexus
182
What is hydrocephalus?
abnormal collection of CSF within the vetricles
183
Describe communicating non-obstructive hydrocephalus and what causes it
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
184
Describe non-communicating obstructive hydrocephalus and what causes it
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.
185
Describe hydrocephalus ex vacuo and what causes it
ventricular expansion, secondary to brain atrophy.
neurodegenerative conditions, such as Alzheimer’s disease.
186
How is hydrocephalus treated?
reversal of cause
| shunt, draining fluid into right atrium or peritoneum
187
Describe the features of first order sensory neurons
sensory receptors in dermis
188
How many neurones make up the somatosensory ascending tracts?
three:
primary - sensory receptors
secondary
tertiary
189
What modality do Merkel discs detect?
vibration
pressure
texture
190
What modality do Mesissner's Corpuscles detect?
light touch
| vibration
191
What modality do Riffini Corpuscles detect?
temperature
192
What modality do Pacinian Corpuscles detect?
vibration
| pressure
193
How is information about the intensity and duration of a stimulus encoded by the primary afferent?
frequency - faster rate of action potential = stronger stimulus
activation of neighbouring cells - activation of neighbouring cells = stronger stimulus
194
Describe the difference between tonic and phasic receptors
tonic = respond continuously in presence of adequate stimulus
phasic = adapt to stimulus, so action potential frequency decreases during a maintained stimulus
195
What is acuity?1
the precision by which a stimulus can be located
196
What determines acuity?
size of the receptive field
lateral inhibition
convergence and divergence
197
What is a receptive field?
area of receptors innervated by the same sensory neuron.
small receptive field = greater acuity
198
Describe lateral inhibition
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
199
What is two point discrimination?
minimal distance required to perceive two simultaneously applied skin indentations
200
What is two point discrimination determined by?
density of receptors
| size of neuronal receptive field
201
What is convergence between primary and secondary neurons?
How does this affect acuity?
when multiple primary afferents synapse onto one secondary neuron
decreases acuity
202
What is divergence between primary and secondary neurons?
How does this affect acuity?
one primary neuron splits to synapse with multiple secondary neurons
causes amplification
203
What modalities does the DCML ascending tract carry?
fine touch
| conscious proprioception
204
In the DCML ascending tract, where are the cell bodies of primary neurons found?
dorsal root ganglion
205
In the DCML ascending tract, where are the cell bodies of tertiary neurons found?
thalamus
206
In the DCML ascending tract, where does decussation occur?
medulla
207
Where does the DCML ascending tract terminate?
sensory cortex
208
In the DCML ascending tract, describe the route of the first order neurones
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)
209
In the DCML ascending tract, describe the route of the secondary neurones
travel from medulla oblongata in contralateral medial lemniscus to the thalamus
210
In the DCML ascending tract, describe the route of the tertiary neurones
from the ventral posterolateral nucleus of the thalamus
through the internal capsule
to the sensory cortex
211
What can cause a spinal cord lesion affecting the DCML?
```
vitamin 12 deficiency
tabes dorsalis (syphilis)
```
212
What modalities does the lateral spinothalamic tract carry?
pain
| temperature
213
What modalities does the anterior spinothalamic tract carry?
crude touch
| pressure
214
In the spinothalamic tracts, where are the cell bodies of primary neurons found?
dorsal root ganglion
215
In the spinothalamic tracts, where are the cell bodies of secondary neurons found?
dorsal horn - substantia gelatinosa
216
In the spinothalamic tracts, where are the cell bodies of tertiary neurons found?
thalamus
217
In the spinothalamic tracts, where does decussation occur?
spinal cord - via the vental white commissure
218
In the spinothalamic tracts, where does the tertiary neuron terminate?
sensory cortex
219
In the spinothalamic tracts, describe the route of the secondary neurones
```
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
```
220
In the spinothalamic tracts, describe the route of the tertiary neurones
from the ventral posterolateral nucleus of the thalamus,
through the internal capsule,
terminating at the sensory cortex.
221
What will damage to the lateral spinothalamic tract in the spinal cord cause?
complete loss of pain and temperature sensation on opposite side
222
How does sacral sparing of sensation occur?
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,
223
What is Brown-Séquard syndrome?
(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.
224
Where are the cell bodies of primary neurons of the pathways of unconscious sensation found?
dorsal root ganglion
225
Where are the cell bodies of secondary neurons of the pathways of unconscious sensation found?
```
spinocerebellar = spinal grey matter
cuneocerebellar = accessory cuneate nucleus in brainstem
```
226
Describe the tertiary neuron of the pathways of unconscious sensation
there are none!!!
227
Describe the decussation of the pathways of unconscious sensation
anterior spinocerebellar decussates once in cord and again in pons
posterior spinocerebellar and cuneocerebellar DO NOT
228
Describe the course of the second order neurons of the spinocerebellar tracts
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
229
If the anterior spinocerebellar tract is damaged in the spinal cord, what will happen?
loss of proprioception and co-ordination in the contralateral side
230
If the posterior spinocerebellar tract is damaged in the spinal cord, what will happen?
in loss of proprioception and co-ordinated movement on the ipsilateral side.
231
Describe the course of the first order neurons of the cuneocerebellar tract
cell body in dorsal root ganglion
ascend on ipsilateral side in the fasciculus cuneatus
synapse in brain stem in accessory cuneate nucleus
232
Describe the course of the second order neurons of the cuneocerebellar tract
begin in accessory cuneate nucleus
travel in the cuneocerebellar tract
terminate in the cerebellum.
233
Describe the ascending tract from the trigeminal nerve of the face
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.
234
What is a nociceptor?
free dendritic nerve endings that respond to noxious stimuli which would cause injury if they persisted
235
Describe nociceptive afferent C-fibres
Small in diameter
Unmyelinated with slow conduction
Associated with dull, aching pain
Activated by all three noxious stimuli, so are polymodal
236
Describe nociceptive afferent Aδ-fibres
```
Myelinated so faster conduction velocity
Larger diameter
Associated with sharp pain
Mechano-heat fibres
activated by chemical stimuli
```
237
What are the three noxious modalities?
chemical
mechanical
temperature
238
Where do first order nociceptive afferent fibres terminate?
dorsal horn of spinal cord
A delta fibres in lamina I and V
C fibres in lamina II
239
Where do first order nociceptive afferent fibres synapse with second order nociceptive afferent fibres?
laminae I and V of the dorsal horn
240
If nociceptive afferents synapse in lamina II of the dorsal horn (substantia gelatinosa), what occurs?
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
How is output from the substantia gelatinosa regulated?
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
Describe the course of the nociceptive second order afferents
ascend the spinal cord in the anterior and lateral spinothalamic tracts
terminate in the thalamus, brain stem, limbic system and frontal cortex.
243
Describe the course of the nociceptive third order afferents
from the thalamus, brain stem, limbic system and frontal cortex
to the cerebral cortex
244
Describe descending inhibitory control of pain
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
Describe chronic pain
lasts for more than three months
persists after all possible healing has occurred
cause often unknown
246
How does tissue damage lead to pain?
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
What is peripheral sensitisation?
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
What is hyperalgesia?
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
What is allodynia?
pain is felt from stimuli which are not normally painful.
| Pain which occurs at an area other than in the area stimulated.
250
What is central sensitisation?
Repeated stimulation increases spinal processing
| of the same stimulus intensity, there is a greater pain intensity
251
What is neuropathic pain?
pain of neural origin
| burning, tingling or shooting sensation
252
What are the symptoms of a peripheral nociceptive nerve injury?
Decreased threshold of Nociceptor activation
Increased receptive field
allodynia
hyperalgesia
prolonged post-stimulus sensations = hyperpathia
emergence of spontaneous activity
253
What is Complex Regional Pain Syndrome?
What is it caused by?
neuropathic disease of the extremities. diagnosis of exclusion
can be triggered by minor trauma, bone trauma, surgery, stroke or MI
254
What are the symptoms of Complex Regional Pain Syndrome?
* Continuous burning pain, hyperalgesia, allodynia
* Temperature and skin colour asymmetry
* Oedema, sweating changes
* Decreased range of motion, motor dysfunction, trophic changes
255
Describe the mechanism of action of opioids
```
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
What are some of the effects of opioids?
```
respiratory depression
nausea and vomiting
antitussive (preventing cough)
constipation,
itching,
euphoria
```
257
State the names of some weak opioids
codeine
tramadol
dihydrocodeine
258
State the names of some strong opioids
morphine,
diamorphine
fentanyl,
oxycodone,
hydromorphone
259
Describe the steps of the WHO analgesics ladder
step one = non-opioids
step two = incorporate weak opioids
step three = adding strong opioids
260
What kind of pain are opioids poor at controlling?
neuropathic pain
261
What are adjuvant analgesics?
drugs that increase or aid the effect of the analgesia already being used
262
What is a lower motor neurone?
cell bodies in spinal cord or cranial nerve motor nuclei
| act directly on muscle
263
What is a motor unit?
group of muscle fibres innervated by one motor neuron.
| The muscle fibres are not a discrete group, but are distributed at random.
264
Describe S motor units
```
o Slow contracting
o Very resistant to fatigue
o Very small force
o Oxidative metabolism
o Well vascularised (so red)
```
265
Describe FR motor units
o Faster contracting
o Fatigue resistant
o Low force
o Oxidative and glycolytic
266
Describe FF motor units
```
o Fast contracting
o Fast fatigue
o High force
o Glycolytic
o Low vascularisation (so pale)
```
267
What are S fibres used for?
maintaining posture
268
What are FF fibres used for?
rapid motor movements
269
What is the force of muscle contraction affected by?
frequency of activation of motor units
| number and type of motor units activated
270
What is a spinal reflex?
involuntary, unlearned, automatic reaction to a specific stimulus that does not require the brain,
271
What are the components of a reflex arc?
```
receptor
afferent fibre
integration centre (in spinal cord)
efferent fibre
effector
```
272
Describe the structure of muscle spindle
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
Describe intrafusal fibres of muscle spindle
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
How is an action potential triggered in the muscle spindle afferent?
muscle lengthens and the muscle spindle is stretched
opens mechanically-gated ion channels in the sensory dendrites,
receptor potential that triggers action potentials
275
State the function of the two types of afferent fibre in the muscle spindle
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
Describe the efferent innervation of the intrafusal fibres
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
What is the role of the efferent innervation of intrafusal fibres
to maintain muscle spindle sensitivity, regardless of muscle length.
278
What are Golgi tendon organs?
high-threshold receptors located at the junction of muscle and tendon
provide nformation about muscle tension.
279
Describe the structure of Golgi tendon organs
bare nerve endings of group 1b axons that invest a collagen matrix
sit at the junction between a muscle fibre and the tendon
280
How is an action potential triggered in the golgi tendon organ afferent?
When tension is created in the muscle, the collagen fibres distort and squeeze the mechanosensetive nerve endings, triggering an action potential.
281
Describe the stretch reflex
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
Describe the inhibitory pathway in the stretch reflex
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
Describe the flexion reflex
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
Describe an alpha motor neuron
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
Describe a gamma motor neuron
* 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
What is an upper motor neuron?
* Cell body in cerebral cortex or brain stem
| * Remain within CNS
287
State the names of the pyramidal descending tracts
corticospinal
| corticobulbar
288
State the names of the extrapyramidal descending tracts
* Vestibulospinal
* Tectospinal
* Reticulospial
* Rubrospinal
* Olivospinal
289
State difference between the pyramidal and extrapyramidal descending tracts
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
What is the function of the corticospinal tract?
control of voluntary movements
291
Where are the cell bodies of the upper motor neurons of the corticospinal motor tract found?
cerebral cortex
30% motor cortex,
30% premotor cortex and supplementary motor areas,
40% somatosensory cortex
292
Describe the course of the upper motor neurons of the corticospinal tract
pass through internal capsule
descend through midbrain, pons and medulla
descend in spinal cord to ventral horn of spinal level
293
State how fibres form either the lateral or anterior corticospinal tract and state their level of decussation
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
What is the function of the corticobulbar tract?
controlling muscles of facial expression, extra-oculuar muscles etc
mainly BILATERAL innervation
295
Where are the cell bodies of the upper motor neurons of the corticobulbar motor tract found?
cerebral cortex
30% motor cortex,
30% premotor cortex and supplementary motor areas,
40% somatosensory cortex
296
Describe the course of the upper motor neurons of the corticobulbar tract
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
What is the function of the vestibulospinal tract?
balance and posture
298
State the source, decussation and termination of the vestibulospinal tract
arises from the vestibular nucleus
the fibres DO NOT decussate.
termination in the spinal cord
299
What is the function of the reticulospinal tract?
control of posture and rhythmic movements.
| facilitate flexor and extensor spinal reflexes.
300
State the source and decussation of the reticulospinal tract
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
What is the function of the tectospinal tract?
aids the directing of head movements in response to visual and auditory stimuli.
302
State the source, decussation and termination of the tectospinal tract
arise from the tectum (superior and inferior colliculi) of the brainstem
DECUSSATE within the brainstem
terminate in neck and upper thoracic spinal cord
303
What is the function of the rubrospinal and rubrobulbar tracts?
control flexor tone in distal muscles and also the tone of facial muscles.
304
State the source, decussation and termination of the rubrospinal and rubrobulbar tracts
arise from neurones of the red nucleus, DECUSSATE in the midbrain
descend contralaterally in the spinal cord
terminate in contralateral spinal cord.
305
What is Amyotrophic Lateral Sclerosis?
progressive degenerative disease
the corticospinal tracts and ventral horn cells degenerate
often beginning with the lower limbs
306
What is Brown-Sequard Syndrome?
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
What is Anterior Spinal Artery Syndrome ?
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
What is Syringomyelia?
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
What are the functions of the cerebellum?
coordination
precision and timing of movement
motor learning
310
Name the anatomical lobes of the cerebellum
anterior lobe
posterior lobe
flocculonodular lobe
311
State how the anatomical lobes of the cerebellum are divided
primary fissure divides anterior and posterior
posterolateral fissure divides posterior and flocculonodular loves
312
Name the zones of the cerebellum
vermis
intermediate zone
lateral hemispheres
313
Name the functional divisions of the cerebellum
what parts of the cerebellum are these formed from?
cerebrocerebellum - lateral hemispheres
spinocerebellum - vermis and intermediate zone
vestibulocerebellum - flocculonodular lobe
314
What is the function of the cerebrocerebellum?
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
What is the function of the spinocerebellum?
regulating body movements by allowing for error correction.
receives proprioceptive information
316
What is the function of the vestibulocerebellum?
controlling balance and ocular reflexes eg. fixation on a target.
receives inputs from vestibular system
sends outputs to the vestibular nuclei
317
What are the causes of cerebellar dysfunction?
stroke
trauma
tumours
ageing
318
What are the signs of cerebellar dysfunction
```
ataxia
dysarthria
scanning speech
dysmetria (past-pointing)
dysdiadochokinesia
inability to learn new movements
nystagmus
abnormal gait
wide stance
loss of balance
```
319
Describe the function of the basal ganglia
regulate the amplitude and velocity of planned movement,
320
Name the basal ganglia
```
caudate nucleus
putamen
globus pallidus interna and externa
substantia nigra
subthalamic nucleus
```
321
Which structures together form the striatum?
caudate nucleus
| putamen
322
Which structures together form the lenticular nucleus
putamen
| globus pallidus
323
What is the effect on movement of the direct pathway through the basal ganglia?
acts to increase movement
324
Describe the direct pathway
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
How does the substantia nigra impact the direct pathway?
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
What is the effect on movement of the indirect pathway through the basal ganglia?
acts to inhibit movement
327
Describe the indirect pathway
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
How does the substantia nigra impact the indirect pathway?
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
Describe the pathogenesis of Parkinson's disease?
degeneration of dopaminergic neurons of the substantia nigra, affecting the nigro-striatal pathway
330
How does Parkinson's disease affect the direct pathway?
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
How does Parkinson's disease affect the indirect pathway?
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
Describe the signs seen in Parkinson's disease?
```
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
What is muscle tone?
The minimal muscle power that allows us to maintain our posture and minimal stiffness in our muscles
334
What creates muscle tone?
stretch reflex
when a muscle is stretched, muscle spindle afferent detect it
reflex contraction of muscles
335
What are some causes of LMN lesions?
peripheral neuropathy
radiculopathy
anterior horn cell damage
336
What causes peripheral neuropathy?
```
diabetes
chronic alcohol abuse
hypothyroidism
vasculitis
chemotherapy
```
337
What is radiculopathy?
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
What causes anterior horn cell damage?
motor neuron disease
| poliomyelitis
339
What are the signs of a LMN lesion?
```
flaccid paralysis
muscle atrophy
hypotonia
hyporeflexia
fasciculations
```
340
Why does flaccid paralysis occur in LMN lesions?
denervation of muscles due to damage to the lower motor neurones
the muscle cannot be stimulated to contract
341
Why does atrophy occur in LMN lesions?
denervation
342
Why does hypotonia occur in LMN lesions?
failure of communication between α-motor neurones and muscles of that limb.
343
Why does hyporeflexia occur in LMN lesions?
loss of innervation to the muscles
| loss of reflex arc
344
Why do fasciculations occur in LMN lesions?
denervation
| individual motor units fire spontaneously
345
When can a lower motor neuron lesion not result in regeneration?
when the cell body of the neuron in damaged
| axons cannot regenerate
346
When can a lower motor neuron lesion result in regeneration?
cell body intact
axon damaged
wallerian degeneration can occur
347
What is the pyramidal system responsible for?
fractionation of finger movements
348
What does the extrapyramidal system provide to the LMNs?
constant descending inhibition
349
what is the postural result of spastic paralysis?
in upper limbs, flexors are stronger than extensors
so overall flexion
in lower limbs, extensors are stronger than flexors
so overall extension
350
Where are the most common sites of UMN damage?
internal capsule
| cerebral cortex
351
State the signs of UMN lesions
```
hyperreflexia
hypertonia - rigidity or spasticity
spastic paralysis
muscle weakness
Babinski sign
clonus
choreas
hemiplegic gait
```
352
Why does hypereflexia occur in UMN lesions?
loss of the descending inhibition
loss of the inhibition of the spinal reflexes;
excessive action of the muscle reflexes
353
Why does hypertonia occur in UMN lesions?
loss of inhibition to lower motor neurones
| reflex circuit no longer inhibited
354
What is spasticity in UMN lesions?
velocity dependent resistance to passive movement.
| Detected with quick movements
355
What is rigidity in UMN lesions?
sustained resistance throughout the range of movement.
| Detected with slow movements
356
Why does spastic paralysis occur in UMN lesions?
muscle tone becomes very high
overall flexion of upper limb
overall extension of lower limb
357
What is a positive Babinski sign?
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
What is a hemiplegic gait seen in UMN lesions?
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
what is cortical localisation?
different areas of the cortex have a different histological structure and therefore different function
360
where is the somatosensory association area?
parietal lobe
| posterior to central sulcus
361
where is the gustatory area?
frontal lobe
| inferior to primary motor area
362
where is the olfactory cortex?
temporal lobe
| superior
363
where is the primary visual cortex?
posterior occipital
364
where is the primary auditory cortex?
temproral lobe middle superior
365
where is the auditory association area?
superior temporal lobe
366
Where is Broca's area?
posterior frontal
| anterior to primary motor cortex
367
Where is Wernicke's area?
superior temporal lobe
368
What are the functions of the frontal lobe?
```
motor
expression of speech (left)
behavioural regulation
eye movements
continence
personality, mood
```
369
What are the functions of the parietal lobe?
sensory!
body image = right
awareness of external environment = right
calculation and writing = left
370
What are the functions of the temporal lobe?
```
hearing
comprehension of speech = left
olfaction
memory
emotion
```
371
What are the functions of the occipital lobe?
vision
372
What symptoms would be seen in a frontal lobe lesion?
```
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
What are the functions of the dominant hemisphere?
comprehension and expression of speech
calculation and writing
NB dominant = left
374
What are the functions of the non-dominant hemisphere?
body awareness
visuospatial awareness
emotion
music
375
how are the two hemispheres able to pass information between them?
connections via corpus callosum and anterior and midbrain comissure
376
What are the symptoms of a parietal lobe lesion?
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
What are the symptoms of a dominant parietal lobe lesion?
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
What are the symptoms of a non-dominant parietal lobe lesion?
neglect of contralateral limb
spatial neglect
loss of three dimensional sense
geographical agnosia
379
What are the symptoms of a temporal lobe lesion?
```
disturbance of hearing and vision
disturbance of language comprehension
impaired long term memory
altered personality
upper homonomous quadrantanopia
```
380
What is the function of Wernicke's area?
interpretation of written and spoken words
381
What is the function of Broca's area?
formulation of laguage
382
describe the pathway for speaking a heard word
primary auditory area
wernicke's area
broca's area
motor cortex
383
describe the pathway for speaking a written word
primary visual area
wernicke's area
broca's area
motor cortex
384
Describe Wernicke's aphasia
disorder of comprehension
fluent but unintelligible speech
NB: occurs when lesion affects dominant hemisphere
385
Describe Broca's aphasia
```
poorly constructed sentences
disjointed speech
good comprehension (can carry out three stage command)
```
NB:occurs when lesion affects dominant side
386
Describe the symptoms of an extradural haematoma
```
Trauma to head
Loss of consciousness
Lucid interval recovery
Progressive hemiparesis
Rapid herniation
Ipsilateral pupil dilation
```
387
What are the signs and symptoms of a subdural haematoma
```
Trauma
Slow deterioration
Headache
Drowsiness
Confusion
Focal deficits
```
388
How can you tell on CT when the onset of a subdural haematoma was?
Acute - White
| Chronic - denser and darker on CT - blood has clotted
389
Describe the signs and symptoms of a subarachnoid haemorrhage
Rapid onset severe headache - thunderclap
Vomiting
Coma
Neck stiffness
390
What causes subarachnoid haemorrhage?
Berry aneurysms
Malformations
Marfan's
Ehlers danlos
391
What are the symptoms of a basal skull fracture?
Periorbital ecchymosis
Mastoid ecchymosis
CSF leakage
392
What is a coup and contracoup injury?
Brain bruising ( contusion) due to force
Coup - contusion at site of impact
Contracoup - contusion on opposite side of skull
393
What is diffuse axonal injury?
Acceleration and deceleration
Causes shearing, stretching and tearing at grey-White matter junction
Cell oedema
394
What are the signs and symptoms of diffuse axonal injury?
Instant loss of consciousness
| Persistent vegetative state
395
What is coning?
Cerebellar tonsillar herniation through foramen magnum
Due to RICP
Increased P on brainstem
Brain stem death
396
Define stroke
Abrupt loss of cerebral function
Lasting >24hrs
Due to spontaneous haemorrhage or inadequate blood supply
397
Define a TIA
Focal deficit
Sudden onset
Resolves completely within 24hrs
398
What signs will a dominant cortical stroke cause?
Dysphasia
Dysgraphia
Dyslexia
399
What signs will a non dominant cortical stroke cause?
Visuospatial disorders
| Neglect
400
What vessel is affected in a TACS?
ACA or MCA
401
What vessel is affected in PACS?
ACA
| MCA
402
What vessel is affected in POCS?
PCA
403
What vessels are affected in LACS?
Small sub cortical vessels
404
What are the symptoms of a TACS and PACS?
Hemiparesis contra lateral to lesion
Hemianopia contra lateral to lesion
Disturbance of higher cortical function
TACS - all
PACS - 2/3
405
What are the signs of a POCS?
Cerebellar syndromes
loss of consciousness
Cranial nerve deficits - ipsilateral
406
What is the treatment for an ischaemic stroke?
Thrombolysis
Alteplase
Given within 3 hours any age
4.5 hours under 80
24 hrs later aspirin
Long term anti platelet, statins
407
What are the signs and symptoms of anterior spinal infarction?
Spinal shock - flaccid weakness, areflexia, loss of pain and temperature
Fine touch and proprioception and vibration sense remain
408
What can cause Parkinsonism?
```
Multiple system atrophy
Wilson's disease
Corticobasal degeneration
Drug induced
Encephalitis
```
409
What are the classical symptoms of Parkinson's disease?
Tremor at rest
Bradykinesia
Rigidity
410
What signs show that Parkinson's is the most likely cause?
```
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
Describe the pathogenesis of PD
Destruction dopaminergic neurons in substantial Nigra pars compact
Reduction in dopamine action at striatum
More inhibition at thalamus
Slow movement
412
Describe the synthesis of dopamine
In cytosol
L-tyrosine -> l-dopa -> dopamine
Tyrosine hydroxylase
Dopa decarboxylase
413
Describe the degradation of dopamine
Monoamine oxidase in CNS
OR
COMT - catechol-o-methyl transferase in peripheries
414
Why can dopamine not be used as a treatment of PD?
It cannot cross BBB
415
Describe the mechanism of action of l-dopa
Crosses BBB
Taken up by dopaminergic cells in substantial Nigra
Converted to dopamine by dopamine decarboxylase
416
Why does l-dopa stop having an effect in the late stages of PD?
Needs dopaminergic neurones to remain
417
What is administered with L-DOPA?
Why?
Carbidopa - peripheral dopa decarboxylase inhibitor
More crosses BBB
Less peripheral effect
418
What are the disadvantages of L- dopa?
Loses efficacy
Causes involuntary movements
Motor complications - on/off, wearing off, dyskinesia, dystopia, freezing
419
What are the ADRs of l-dopa?
Nausea
Vomiting
Arrhythmias
Hypotension
420
What drugs can interact with l-dopa?
Vitamin b6 increases peripheral breakdown l-dopa
MAOIs plus l-dopa enhances catecholamine production and causes hypertensive crisis
421
Name some dopamine receptor agonists
Apomorphine
Bromocriptine
Ropinirole
422
Describe the mechanism of action of dopamine receptor agonists
Bind to dopamine receptors
| Produce response in neurons
423
What are the advantages of dopamine receptor agonists?
Direct acting
Cause less dyskinesia
Neuroprotective (?)
424
What are the disadvantages of dopamine receptor agonists?
Less efficacy than l-dopa
Produce impulse control disorders
Psychiatric side effects
425
What are the symptoms of impulse control disorders?
```
Pathological gambling
Hypersexuality
Compulsive shopping
Desire to increase dosage
Punding- compulsive collecting, sorting or continually handling of objects
```
426
What are the ADRs of dopamine receptor agonists?
```
Sedation
Hallucinations
Confusion
Nausea
Vomiting
Constipation
```
427
Name a monoamine oxidase B inhibitor
Selegiline
428
Describe the mechanism of action of monoamine oxidase B inhibitors
Inhibits breakdown dopamine
| Enhances dopamine levels in brain
429
What happens if monoamine oxidase B inhibitors are used above recommended dose?
Lose selectivity
| Inhibits MAO type A which metabolises noradrenaline too
430
Name a COMT inhibitor
Entacapone
431
Describe the mechanism of action of COMT inhibitors
Reduce peripheral breakdown of dopamine
No therapeutic effect alone
432
Describe the ADRs of COMT inhibitors
```
Diarrhoea
Postural hypotension
Nausea
Anorexia
Dyskinesia
Hallucinations
Sleep disorders
```
433
Name an anticholinergic used in PD
Procyclidine
434
Describe the mechanism of action of anticholinergics used in PD
ACh may have antagonistic effect to dopamine
Anticholinergics may be able to treat tremor in some
No effect on bradykinesia
435
Describe the ADRs of anticholinergics in PD
Mood changes
Xerostomia
Visual probs
Interfere with peristalsis
436
Describe the mechanism of action of amantadine
Increases release dopamine in CNS
Blocks cholinergic receptors
Inhibits NMDA receptors
437
What are the disadvantages of amantadine in PD?
Poorly effective
| Little effect on tremor
438
Define consciousness
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
What does consciousness require?
Function of:
Reticular system
Cerebral cortex
440
What part of the brain stimulated wakefulness in consciousness?
Reticular formation
441
What part of the brain stimulates awareness in consciousness?
Cerebral cortex
442
Where is the reticular formation located?
Centre of brainstem
443
What structures input into the reticular formation?
Cortex
| Sensory system from body
444
Where does the reticular formation send outputs to?
Thalamus
Hypothalamus
Basal forebrain nuclei
Spinal cord
445
What neurotransmitter do the inter neurons projecting from the reticular formation use?
ACh
446
What neurotransmitter do neurones projecting from the basal forebrain nuclei going to the cortex use?
ACh
447
What neurotransmitter do neurones going from the hypothalamus to the cortex use?
Histamine
448
What neurotransmitter do neurones going from the thalamus to the cortex use?
Glutamate
449
Why do antihistamines cause drowsiness?
Less histamine transmitted from hypothalamus to cortex
| Decreased wakefulness from reticular activating system
450
What causes impaired wakefulness?
Problems with reticular activating system
451
What causes impaired awareness?
Problems with cortex
452
What is the name for impaired wakefulness and awareness?
Coma
453
What conditions is impaired wakefulness, but normal awareness, seen in?
REM sleep
| Lucid dreaming
454
What conditions is impaired awareness but normal wakefulness seen in?
Vegetative state
| Acute confusional state
455
What can cause a diffuse decrease in cortical function?
Metabolic disturbance
456
What can damage the RAS?
RICP - compress brainstem
| Lesion in brainstem
457
What are intracranial causes of reduced consciousness?
```
Haemorrhage
Stoke
Neoplasm
RICP
Infection
Trauma
Epilepsy
```
458
What are some extra cranial causes of reduced consciousness?
```
Hypoxia
Electrolyte disturbances
Metabolic disorder
Sepsis
Toxins
Endocrine disorders
```
459
What are the signs of coma?
Absence of consciousness
No purposeful movement
No response to stimuli
GCS <8/15
460
Describe the signs of acute confusional state/delirium
Fluctuating arousal
Impaired awareness
Disorientation
Hallucinations
461
What are the first signs of impaired consciousness?
Change in behaviour or mood
Unsteady
Difficulty finding words
Slurred speech
462
Describe the AVPU scale
Alert
Voice - response to verbal stimulus
Pain - response to pain stimulus
Unresponsive
463
What is the AVPU score used for?
Emergency settings
| Scoring less than A requires further investigation
464
Describe the GCS scale
```
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
When is GCS used?
Used to see change in consciousness over time
| Viewed as a pattern of change
466
What is declarative memory?
Naming objects, recognising places, remembering events
Stored in cortex
Assessed consciously
Rapidly learned and rapidly forgotten
467
What is nondeclarative memory?
Performance of motor skills
Difficult to form
Long lasting and performed without conscious recollection
Stored in cerebellum and basal ganglia
468
What neural changes are seen when memories are formed?
Synaptic changes
| Neuroplasticity
469
What is memory consolidation?
What makes this more likely?
Memories committed from short term to long term
Emotion
Rehearsal and repetition
Association
470
What is the role of the hippocampus in memory?
Consolidation declarative memory
Integrates visual, auditory and somatosensory
Gives context and association to memories
471
What is long term potentiation?
Long lasting enhancement in signal transmission between two neurones
Due to synchronous stimulation
472
What is long term depression?
Weakening of synaptic strength
In infrequently used synapses
Causes gradual loss of memory
473
What is anterograde amnesia?
Cannot form new memories
474
What is retrograde amnesia?
Cannot remember previous memories
475
Describe dementia
Progressive decline of cognitive function
Memory declines
Intellect falls
476
What are the signs and symptoms of AD?
```
Progressive memory loss
Aphasia
Apraxia
Agnosia
Behavioural changes
Depression
```
477
What is seen on MRI in AD?
Generalised atrophy - disproportionate in hippocampus
478
What are the histological markers of AD?
Neurofibrillatory tangles
| Plaques
479
What are the neurofibrillatory tangles and plaques in AD made from?
NT - intracellular twisted hyperphosphorylated tau proteins
Plaques - amyloid deposition extracellular
480
What stimuli activate the reticular formation?
Sensory inputs from body
Visual inputs
Stimulation from cortex
481
How does visual stimulation reach the reticular formation?
Eye stimulates hypothalamus
| Hypothalamus stimulates reticular formation - uses orexin as neurotransmitter
482
Describe non-REM sleep
Slow wave
Active body and inactive brain
Made of 4 stages
483
Describe REM sleep compared to non-REM sleep
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
Describe what is seen on EEG when awake
Beta waves - >14 Hz
485
What is seen on EEG when someone closed their eyes
Alpha waves - 8-13 Hz
| Synchronous
486
Describe an EEG during stage 1 of sleep
Theta waves 4-7 Hz
| Lower amplitude than alpha waves
487
What is seen on EEG in stage 2 and 3 of sleep?
Sleep spindles - almost fibrillation like. Due to thalamic activity
K complexes - tall
488
What is seen on EEG in stage 4 of sleep?
Delta waves - oscillations. <3.5 Hz
489
What is seen on EEG in REM sleep?
Beta waves!!!
490
What is narcolepsy?
What is thought to cause it?
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
What is sleep apnoea?
Interruption of breathing during REM sleep, leading to aeousal from sleep
Caused by airway narrowing
492
Describe how an EEG is taken
Place 16-25 electrodes on head
| Measure electrical activity
493
State the frequency of the waves seen during sleep on EEG
Alpha 8-13 Hz
Beta >14
Theta 4-7
Delta <3.5
494
What is cerebral perfusion pressure?
Difference between mean arterial pressure and intracranial pressure
Represents the pressure gradient driving cerebral blood flow
495
What is a normal ICP?
Between 5 and 15 mmHg
496
What causes venous pressure to change and increase ICP?
Raises in intrathoracic pressure
| Due to breathing out, coughing, laughing, sneezing of straining
497
What are the components of the volume of the brain?
Brain
Arterial blood
Venous blood
CSF
498
What is meant by the brain being in a compensated state?
The CSF and venous volumes have decreased
| ICP remains within normal limits
499
What is meant by the brain being in a decompensated state?
```
Brain has reached critical volume
RICP
ICP > CCP
Cerebral perfusion is prevented
Brain becomes ischaemic
```
500
How does the body attempt to compensate for brain ischaemia in RICP?
Cerebral vessels vasodilator
BP increase
Attempts to increase cerebral perfusion
But only raises ICP more!
501
How can blood cause RICP?
```
Venous sinus thrombosis - increased intravascular volume
Extradural haematoma
Subdural haematoma
Subarachnoid haemorrhage
Intracerebral haemorrhage
```
502
How does the brain cause RICP?
Tumour
| Oedema- trauma, infarct, malignancy, infection, water intoxication
503
How does the CSF cause RICP?
Hydrocephalus
504
What causes hydrocephalus?
Increased production - choroid plexus papilloma
Disruption of flow - spina bifida, aqueduct stenosis, clot, space occupying lesion
Disruption of absorption by arachnoid granules
505
What are the signs and symptoms of RICP?
```
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
Describe the headache seen in RICP
```
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
Why does CN III palsy occur in RICP?
Uncal herniation compresses
508
Why does CN vi palsy occur in RICP?
Long course through cranium
509
What is the vestibulo-ocular reflex?
Why is it lost in RICP?
Eyes normally look towards cold water placed next to ear and away from warm water placed next to ear
Brainstem death
510
What is cushing's triad?
Irregular respiration
Bradycardia
Systolic hypertension
511
Why does Cushing's reflex happen?
```
Brain ischaemia
Increase in symp tone to vessels
Increases BP
Carotid detectors sense rise in BP
Increase parasympathetic tone
Bradycardia
```
512
What is decorticate posturing?
Lower limbs extended
| Upper limbs flexed
513
Why does the decorticate response occur?
Destruction connection between cortex and thalamus
| Isolates cortex from lower brain and spinal cord
514
What is decerebrate posturing?
Extension lower limb
Extension upper limbs
Extension head
515
Why does the decerebrate response occur?
Lower parts of brain and brainstem damaged
| All descending inhibition lost
516
What is a hernia?
Protrusion of an organ or part of an organ into a region that does not normally contain it
517
Describe subfalcine herniation
Herniation occurs on same side as mass
| Cingulate gyrus pushed under free edge falx cerebri
518
What are the consequences of subfalcine herniation?
Compresses anterior cerebral artery
| Causes ischaemia medial parts frontal and parietal lobe
519
Describe uncal herniation
Uncus herniates through tentorial notch (edge of tentorium cerebelli)
520
What are the consequences of uncal herniation?
Compression CN III
Compresses cerebellar peduncles
Occludes cerebellar arteries
521
Describe tonsillar herniation
Cerebellar tonsils pushed through foramen magnum
522
What are the consequences of tonsillar herniation?
Brainstem compression - affects cardiac and resp control centres
Coma
523
Describe the phases of migraine
Well being
Prodromal symptoms - visual or sensory
Pain! Begins locally then becomes generalised
Feeling drained
524
What causes tension headaches?
Neurovascular irritation
| Due to excessive tension on scalp muscles
525
What causes migraines?
Vasodilation and oedema in blood vessels
| Stimulates nerve endings
526
What is temporal arteritis?
Also known as giant cell arteritis
Systemic immune mediated vasculitis
Chronic inflammation large arteries
527
What are the signs and symptoms of temporal arteritis?
```
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
What is the main causative organism of meningitis?
Under 2 - E. Coli
2-5 - H. influenzae type B
5-30 - N. meningitidis
Over 30 - S. Pneumoniae
529
What is encephalitis?
Infection of neural parenchyma
530
What causes encephalitis?
What regions are affected?
```
Viral!
Herpes - temporal lobe
Polio - spinal cord
Rabies - brain stem
Cytomegalovirus
```
531
What are the symptoms of encephalitis?
```
Headache
Confusion
Fever
Drowsiness
Fatigue
Seizures
Tremors
```
532
Describe the function of the cones in the retina
Provide high acuity vision
Day vision
Colour vision
533
Describe the location of the cones in the retina
Concentrated at fovea
534
Describe the function of the rods of the retina
Specialised for night vision
| Highly light sensitive
535
What three functional classes of cells are present in the retina?
Photoreceptors - rods and cones
Inter neurons - combine signals from the photoreceptors
Ganglion cells - output cells
536
What is a visual field?
Region of space that the eye can see whilst looking straight ahead
537
What part of the retina are images present in the left visual fields recognised by?
Nasal hemiretina of left eye
| Temporal hemiretina of right eye
538
State the order of neurones after leaving the retina
```
Optic nerve
Optic chiasm
Optic tract
Lateral geniculate ganglion
Optic radiations
```
539
What fibres does the right optic tract contain?
Nasal fibres from left eye
| Temporal fibres from right eye
540
Where is the lateral geniculate nucleus found?
In the thalamus
541
What fibres does the upper optic radiation carry?
Fibres from superior retinal quadrants
| So vision from inferior visual quadrants
542
Describe the course of the superior optic radiations
Through parietal lobe
| To visual cortex in occipital lobe
543
What fibres does the lower optic radiation carry?
Fibres from the inferior retinal fibres
| So vision from the superior visual field quadrants
544
Describe the course of the lower optic radiation
Through temporal lobe
Pathway is called Meyer's loop
To reach visual cortex in occipital lobe
545
Where is the primary visual cortex found?
Medial aspect of occipital lobe
546
Describe the steps in the light reflex
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
What is seen in accommodation of the eye?
Convergence of eye
Constriction of pupil
Lens becomes convex to increase refractive power
548
When is the accommodation reflex used?
When the eyes changes focus from distant to near
549
Why must the accommodation reflex involve the cortex?
Relates to analysis
550
Where in the visual pathway is the damage in complete loss of vision in one eye?
The optic nerve
551
What causes an optic nerve lesion?
Optic nerve glioma
Retinoblastoma in children
Optic sheath meningioma in middle aged
552
What part of the visual pathway is damaged in a bitemporal hemianopia?
Optic chiasm
553
What causes an optic chiasm lesion?
Pituitary adenoma
| Anterior communicating artery aneurysm
554
Where in the visual pathway is damaged in a patient with left homonymous hemianopia
Loss of left field of vision
| Right optic tract
555
What can cause damage to the optic tracts?
Stroke
Neoplasm
Trauma
556
Where in the visual pathway is the lesion in superior left homonymous hemianopia?
Right lower optic radiations
557
What causes damage to the lower optic radiations?
Damage to the temporal lobe
| vascular occlusion In middle cerebral artery
558
Why does macular sparing occur in a posterior cerebral artery stroke?
Dual blood supply to occipital lobe
- posterior cerebral artery
- middle cerebral artery (normally supplies occipital pole representing macula)
559
What is an otic placode?
Thickened ectodermal patch on back of head
| Goes on to form ear
560
How does the otic placode turn into the otic vesicle
Thicken
Invaginate
Sink below surface
Pinched off to form otic vesicle
561
Describe how the otic vesicle transforms into the inner ear
Saccule - cochlea
| Utricle - semicircular canals
562
State the origins of the component of the middle ear
Tympanic cavity - first pharyngeal pouch
Malleus and incus - Meckel's cartilage - 1st pharyngeal arch
Stapes - Reichert's cartilage - 2nd pharyngeal arch
563
What does the first pharyngeal pouch turn into?
Distal end - tympanic cavity
| Proximal end - Eustachian tube
564
State the innervation of the muscles of the middle ear. Why is this?
Tensor tympani - mandibular branch CN V - 1st pharyngeal arch
Stapedius - facial nerve - second pharyngeal arch
565
What does the external auditory meatus develop from?
1st pharyngeal cleft
566
What do the auricles develop from?
Auricular hillocks - proliferations within first and second pharyngeal arches
567
How do the ears move from the back of the head to the side?
Mandible grows and pushes them into place
568
What can be the cause of congenital deafness?
Middle ear deafness - 1st and second pharyngeal arch probs
Inner ear deafness - malformation organ of corti - commonly due to teratogenic agents
569
When does development of the eye begin?
Week 4
570
Describe formation of the eye from the forebrain
```
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
What is the choroid fissure?
Long slit running down stalk of optic vesicle
572
What does failure of closure of the choroid fissure result in?
Coloboma
573
The optic vesicles closes around the hyoid artery
| What is the fate of this artery?
Degenerated dismally
| Becomes central retinal artery proximally
574
What forms the ciliary body musculature and the extra ocular muscles?
Ciliary body - rim of optic vesicle
| Extra ocular muscles - pre optic myotomes
575
What does the optic vesicle develop into?
Optic cup
| Retina, iris, ciliary body
576
Why can retinal detachment occur?
Retina develops from two separate layers
| Intraretinal space can open up again
577
What are congenital cataracts?
Opacity of lenses
| Due to genetic defect or teratogen
578
What is congenital rubella syndrome?
```
When pregnancy woman gets rubella during first trimester
Triad of symptoms in fetus:
Sensorineural deafness
Cataracts or retinopathy
Congenital heart disease (PDA)
```
579
Define a partial seizure
Only affects one hemisphere of the brain
580
What is the difference between a simple and complex partial seizure?
Simple - no loss of consciousness
| Complex - loss of consciousness
581
What are the symptoms of a partial seizure affecting the frontal lobe?
Abnormal head movements
Swearing/shouting out
Abnormal posturing
Repeated movements
582
Describe the features of a partial seizure affecting the parietal lobe
Abnormal sensations
Hallucinations
Difficulty understanding speech and language
583
Describe the features of a partial seizure affecting the temporal lobe
Deja vu
Strange taste/smell
Lip smacking
Swallowing or chewing
584
Describe the features of a partial seizure affecting the occipital lobe
Hallucinations
Disturbed vision
Eye pain
Nystagmus
585
What is a generalised seizure?
Affects both hemispheres
586
Describe a tonic-clonic seizure
```
Loss of consciousness
Body stiffens
Fall
Limb jerking
Loss of bladder control
Post ictal period
```
587
Describe the difference between a clonic and myoclonic seizure
Clonic - jerking lasts two mins. Loss of consciousness
Myoclonic - jerking lasts fraction of second. No loss of consciousness. Happens early in morning
588
What are the main causes of secondary epilepsy?
```
Brain injury or hypoxia
Pyrexia in children
Alcohol
Drugs
Encephalitis
Metabolic disturbances
```
589
What can generate an epileptic fit?
Increased excitatory activity
Decreased inhibitory activity
Loss homeostatic control
Spread neuronal hyperactivity
590
What is status epilepticus
Medical emergency
Continuous seizures without period of recovery
More than 30 mins
High risk mortality
