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year 2 sem 1 > wk 1 neorology > Flashcards

wk 1 neorology Flashcards

1
Q

regional neuroanatomy

A

The name and location of structures at macro- and microscopic resolution

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2
Q

cellular neuroanatomy

A

The types and microstructure of the cells that make up the nervous system

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3
Q

functional neuroanatomy

A

The pathways that deliver coherent functions of the nervous system

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4
Q

dorsal column pathway

A

Proprioception
Vibration
Fine touch

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5
Q

spinothalamic pathway

A

Pain

Temperature

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6
Q

types of glia

A

Astrocytes, oligodendrocytes / Schwann cells, microglia

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7
Q

key concepts of neurones

A

chemical synapse for cell-signalling
slow (diffusion) can induce ‘GAIN’
‘drugable’

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8
Q

gain

A

measured as the slope of the current-frequency (input-output) relationship over any given range of inputs

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9
Q

sensory receptors can be…

A

‘Free’ nerve endings (NEs)
Specialised NEs
Specialised nerve cells

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10
Q

schwann cells

A

insulation - myelin sheath
1:1 ratio with axon
PNS

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11
Q

oligodendrocytes

A

insulation - myelin sheath
1:n ratio with axon
CNS

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12
Q

astrocytes

A

Central to BBB integrity - vascular foot process that wraps round capillaries
maintain chemical concentrations
remove waste
repair

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13
Q

microglia

A

Resident macrophage of the CNS

Complex roles in development, immune surveillance, disease response & tissue repair

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14
Q

action potential summary

A

Stimulus depolarises the membrane

Triggers opening of voltage-gated Na channels – depolarisation

Then voltage-gated Na channels close and K channels open – repolarisation

This leads to brief ‘hyper-polarisation’

A further AP cannot be induced until the end of the refractory period

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15
Q

triggers of AP

A

1) Localised ion channel state-change (open/closed)

Ligand gated ion channels (open when appropriate ligand bind)
Voltage gated ion channels (open in response to voltage change)

2) Propagation of charge from adjacent region

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16
Q

saltatory conduction/propagation

A

Increases conduction velocity

Lowers energy expenditure (Na/K-ATPase)

along myelinated axons from one node of Ranvier to the next node

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17
Q

Glutamate

A

AMPA – fast acting
NMDA – have Mg2+ block
Metabotropic – G-protein coupled
ex

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18
Q

Acetylcholine

A

Nicotinic – fast acting

Muscarinic – slower acting

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19
Q

Noradrenaline

A

Flight or fight
α and β receptors
ex

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20
Q

serotonin

A

Multiple roles

ex

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21
Q

dopamine

A

Basal ganglia functions & reward

ex

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22
Q

GABA

A

Linked to a Cl- channel
Cl- hyperpolarises the cell making it more difficult for the cell to fire
Alcohol is a GABA-like molecule
Act through benzodiazepine receptors – utilised in clinical medicine with benzodiazepines e.g. Diazepam
inh

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23
Q

chemical transmission

A

ACh release into synaptic cleft
Rapidly degraded by Acetylcholinesterase
AChR binding at motor end plate opens ion-channel
Na+ influx / K+ efflux causes depolarisation of muscle
Depolarisation triggers propagation of AP in muscle fibre

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24
Q

anatomy of muscle

A

Repeating unit is the sarcomere
Sarcomere comprises: Z-disc, thick (actin) and thin (myosin) filaments
Actin is blocked from interacting with myosin by tropomyosin, in turn controlled by troponin.

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25
Q

muscle contraction

A

Ca+ influx binds to troponin and unblocks the action of tropomysosin exposing actin activity sites
Myosin heads alternatively attach and detach, pulling the actin filaments towards the centre of the sarcomere
Ca+ actively removed by uptake into the SR
Tropomyosin block restored

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26
Q

bilaminar disc

A

epiblast and the hypoblast, evolved from the embryoblast.

These two layers are sandwiched between two balloons: the primitive yolk sac and the amniotic cavity.

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27
Q

trilaminar disc

A

created through migration of epiblast cells through the primitive streak

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28
Q

what layer is the NS derived from

A

ectoderm layer

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29
Q

what are the 3 primary brain vessels

A

prosencephalon - forebrain
mesencephalon - midbrain
rhombencephalon - hindbrain

30
Q

more direct / linear motor system

A

‘DIRECT’ CEREBRAL CORTEX CONTROL OF LMNs

Often called the U(upper)MN system

31
Q

a less direct / less linear system

A

SYSTEM ‘ORGANIZING’ MOVEMENTS INTO ACTIONS

32
Q

what are the 2 upper motor neurone systems calles

A

CORTICO-SPINAL & CORTICO-BULBAR SYSTEM

33
Q

cortico-bulbar system

A
  • controls cranial motor LMNs
  • UMN CELL BODIES IN THE CEREBRAL CORTEX
  • AXONS PASS DOWN
    TO CONTROL LOWER MOTOR NEURONES
    IN THE BRAIN STEM NUCLEI
34
Q

cortico-spinal system

A
  • goes to trunk & limb musculature
  • controls the spinal LMNs
  • UMN cell bodies in cerebral cortex
  • Axons pass down to control the LMNs (AHCs) in the spinal cord
  • AHC – anterior horn cells (in grey matter of spinal cord)
35
Q

what are the descending cortico-spinal fibres called

A

they form prominences on medulla called pyramids

cortico-spinal system also called Pyramidal system

36
Q

where are the C-S & C-B systems located

A

cell bodies mainly in primary motor cortex (frontal lobe ; precentral gyrus)
some in the supplementary motor area

37
Q

primary motor area

A 
body represented upside down
unilateral(1 side of the brain controls 1 side of the body)
individual movements (cells control 1 motor neurone)
38
Q

supplementary motor area

A

body represented horizontally
head forwards
generally complicated
bilateral movement > actions eg walking

39
Q

CS cell bodies pathway

A
  • cell bodies in the cortex axons run through to the internal capsule
  • internal capsule travels down brainstem to medulla
  • 85% change side at the medulla
  • 15% remain ipsilateral at pyramid level most then cross over lower down
40
Q

what are the 2 spinal tracts for the CS and CB systems

A

lateral (bigger and further out) and ventral (smaller and in the middle more)

41
Q

what tract so most CSp axons run down?

A

contra-lateral cortico-spinal tracts

42
Q

ventral cortico-spinal tract fibres

A

terminate in ventral grey matter of the cervical & upper thoracic cord (control LMNs in upper part of spinal cord)

43
Q

lateral cortico-spinal tract fibres

A

run down the whole cord with fibres terminating in the ventral grey matter of all the cord

44
Q

how cortico-bulbar fibres cross over

A
  • cranio-spinal fibre don’t cross bc desire to have some neck and trunk bilateral movement
  • face and cranial movements have to be bilateral sometimes eg closing eyes
45
Q

cranial nerves

A
  • nuclei mostly in the brainstem (apart form I, II, XI)
  • mixed sensort-motor nerves mostly
  • motor fibres are the LMN supply to muscles around head and neck
46
Q

cortico-bulbar fibres and tract

A

originate from primary motor cortex
lower down than C-S fibre as body inverted (head at bottom of cortex)
fibres go through white matter of brain and collect together to form a tract down into the brain stem
runs alomngside CS tract

47
Q

trigeminal nerve

A

V (5)

  • UMN control of LMNs supplying jaw
  • ipsilateral & contralateral (50:50 basis)
  • jaw muscle innervation is bilateral
  • stroke rarely results in significant weakness of jaw muscles
48
Q

facial nerve upper

A

VII (7)

  • UMN fibres that control LMNs supplying forehead and eye closure (upper facial muscles)
  • terminate ipsilaterally & contralaterally on a 50:50 basis
  • forehead and eye closure is bilateral
49
Q

facial nerve lower

A

VII (7)

  • UMN fibres control LMNs supplying mouth muscles terminate on strongly contralateral basis
  • mouth muscles unilateral innervation
50
Q

unilateral hemisphere problem

A
  • contralateral side of the face

- effects lower face only (as lower face is one sided and contralateral)

51
Q

accesory nerve

A

XI (11)

  • motor control around the neck
  • junction of head (brain stem/cranial nerves) & trunk (spinal cord/spinal roots/peripheral nerve)
  • motor fibres originate in the NUCLEUS AMBIGUOUS in medulla
  • motor fibres also originate in the cervical cord grey matter
  • exit the cord as rootlets forming the spinal root of the accessory nerve - ascends up the spinal cord, through the FORAMEN MAGNUM to unite w the cranial root of the accessory nerve
52
Q

sternocleidomastoid

A
  • supplied by accessory nerve
  • goes to mastoid process in the head & the sternocleido region on the trunk
  • involved in movements of the head - right turns head left a=vv
  • brain controls this ipsilateral way as L side controls L muscle and vv
53
Q

clinical implications - accessory nerve and sternocleidomastoid

A
  • in focal epileptic seizures in L frontal region
    • R limbs stimulated but L SCM stimulated
  • in L hemisphere stroke
  • loss of control of R limbs and L SCM
54
Q

distribution of the pyramidal system

A

cervical spinal cord - LMN supply for upper limb
thoracic - trunk muscles
lumbar - leg

55
Q

2 common strokes

A

middle cerebral artery occlusion
- bc mid cerebral artery supplies mid of brain whole primary motor cortex may be wiped out = contralateral hemiplegia

internal capsule lesion

  • tiny arteries supplying centre of brain
  • affect central capsule
  • small event but pos same effect ^
56
Q

contralateral hemiplegia

A

This refers to paralysis on the opposite side of the body that brain damage occurs in

57
Q

extrapyramidal system

A
  • all motor centres and tracts that have significant influence on LMN
  • consist of UMN
  • cell bodies in central brain nuclei (deep grey matter not cortical grey matter)
  • axons from cell bodies have more complex networks
  • aim is to control, order and organise function of LMN
  • connections aren’t as direct or simple as CS?CB UMNS
58
Q

why is extrapyramidal system necessary

A

controls groups of muscles acting together in choreographed sequences eg walking

59
Q

Basal ganglia made up of…

A

corpus striatum
substantia nigra
subthalamic nucleus

60
Q

corpus striatum

A
  • Complex of nuclei in the brain
  • 2 main components
    • Caudate nucleus
    • Lenticular nucleus (globus pallidus + plutamen)
61
Q

neostriatum

A
  • caudat nucleus + plutamen = input area

- also called STRIATUM

62
Q

input areas of the basal ganglia

A

striatum, cerebral cortes, thalamus, substantia nigra

63
Q

output areas of basal ganglia

A 
globus pallidus
substantia nigra (input + output so forms a loop)
64
Q

substantia nigra

A
  • black substance
  • distinct pigmented nucleus in midbrain
  • affected in idiopathic parkinsons disease
65
Q

subthalamic nucleus

A

nucleus underneath the thalamus

66
Q

brainstem nuclei

A 
vestibular nuclei
olive 
red nucleus
reticular formation
superior colliculus
67
Q

functions of the EPS

A
  • organisation of indiv. movements to from actions
  • modifies & organises the movements controlled by the CS & CB systems
  • inhibits unwanted movements
  • emotional expression movement
  • bilateral control of vol. movement
  • postural adjustments
  • control of muscle tone
68
Q

pyramidal disease

A
  • muscle weakness due to lack of strength
  • CS UMN pyrmaidal disease = weakness due to loss of excitatory function from UMNs - LMNs not instructed so neither is muscle
  • spasticity due to loss of inhibition of UMNs on LMNs
  • increased muscle tone in lower extremities
  • hyperreflexia
  • pos. babinski
69
Q

extrapyramidal disease

A
  • disruption of coordination of the act as a whole
  • abnormal motor control (bradykinesia, akinesia)
  • slowness or poverty of movement
  • impairment of initiation, sequencing and cessation of movement
  • impairment of whole actions
  • impairment of ‘automatic’ emotionally related movement
70
Q

alteration of muscle tone is EP disease

A
  • rigidity
  • ‘lead-pipe’ smooth constant resistance to movement
  • ‘cog-wheel’ cogging effect on top of background hypertonia
71
Q

abnormal involuntary movements

A
  • flexed posture (arms, turn and neck flexed)
  • postural instability (trip, fall, instability)
  • tremor
  • ballismus
  • chorea
  • athetosis
  • myoclonus
    tucs
72
Q

parkinsonism

A
  • bradykinesia
  • rigidity
  • tremor
  • postural instability

year 2 sem 1 (13 decks)

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