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Year 2 - Semester 1 > Neuro- week 2 > Flashcards

Neuro- week 2 Flashcards

1
Q

what is used for imaging muscle?

A

MRI

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2
Q

what is used for imaging peripheral nerves?

A

ultrasound - useful in assessing nerve entrapment syndromes

MRI - rarely used

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3
Q

what is used for imaging plexii?

A

MRI

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4
Q

what is used for imaging the spinal cord?

A

MRI

CT can be used when MRI is contraindicated

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5
Q

what is used for imaging the brain?

A

MRI - most detailed for seeing brain structures and pathology

CT - fast, can be used when MRI contraindicated and is good for detecting haemorrhage

nuclear medicine - for parkinsons and dementias

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6
Q

what is used for imaging blood vessels?

A

Doppler ultrasound - for carotid assessment

CT and MRI angiography - used extensively

angiography - not used much except for intracranial assessment

CT and MRI venography - used extensively

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7
Q

describe the uses of CT scans

A

fast, well tolerated
good for detecting blood
good for patients with metal parts or who need ventilation

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8
Q

describe the types of MRI

A

T1 - CSF in black, good for anatomy

T2 - CSF white, good for pathology as most has a lot of water in it

Flair - T2 with supressed CSF (does not show up as white) - good for lesions around the ventricles and for MS

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9
Q

describe metabotropic receptors

A

• Induction of second messenger system
o Receptor coupled to G-protein
o Activated intracellular enzyme systems to
produce and intracellular signal, the second
messenger
• Slow neurotransmission
• Neuromodulation

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10
Q

describe ionotropic receptors

A

• Ligand gated ion channels
• Fast neurotransmission
• Inhibitory
o Chloride influx causes hyperpolarization
• Excitatory
o Sodium influx causes depolarization

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11
Q

what are the classes of neurotransmitter and some examples

A

• Amino acid
o Glutamate
o GABA

•	Biogenic amines
       o	Acetylcholine
       o 	Monoamines
               	Serotonin
               	Catecholamines
  • Dopamine
  • Noradrenaline
  • Norepinephrine

• Peptides
o Substance P

• Others
o ATP
o Nitric oxide

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12
Q

which pathways is glutamate involved in

A
  • Cortical association
  • Cortico-thalamic
  • Cortico-spinal
  • Basal ganglia
  • Hippocampal
  • Cerebellar
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13
Q

describe glutamates role

A

Glutamate is important in learning and memory

  • High densities of NMDA and AMPA receptors in the hippocampus
  • Role for glutamate receptors in long term potentiation
  • Glutamate receptor antagonists inhibit LTP and learning and memory
  • AMPA receptor potentiators enhance LTP and learning and memory
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14
Q

why does glutamate level need to be controlled

A

Glutamate is an excitotoxin

  • High levels of glutamate, NMDA or AMPA can kill neurons
  • Glutamate levels rise following stroke
  • Glutamate receptor antagonists reduce brain damage following experimental stroke
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15
Q

describe glutamates cycle

A

Synthesised from glutamine taken up into the neurone from astrocytes
Removed from the synapse by glutamate transporters

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16
Q

what type of neurotransmitter is glutamate and what are its receptors

A

Glutamate is the major excitatory neurotransmitter

The ionotropic receptors for glutamate are AMPA and NMDA and glutamate also has metabotropic receptors

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17
Q

describe GABA

A
  • GABA is the main inhibitory neurotransmitter of the CNS (although in some settings it can be excitatory).
  • GABA acts via ionotropic (GABAA) and metabotropic (GABAB) receptors, and modulates flow of Cl- ions across the membrane.
  • Some anti-epileptic drugs mimic the effects of GABA or increase bioavailability of GABA (eg gabapentin, vigabatrin)
  • Benzodiazepines enhance the effects of GABA – sedative, anxiolytic and anti-convulsant.
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18
Q

how is serotonin synthesised

A

Tryptophan -> 5-Hydroxytryptophan -> Serotonin (5-hydroxytryptamine; 5-HT)

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19
Q

what is 5-HT broken down by

A

5-HT is broken down by monoamine oxidase into 5-Hydroxy indole acetic acid

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20
Q

what are 5-HT’s recepor families

A 
•	5-HT1 receptor family
      o	Metabotropic
•	5-HT2 receptor family
      o	Metabotropic
•	5-HT3 receptor family
      o	Ionotropic
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21
Q

describe serotonin projections

A

o Originate in raphe nuclei
o Project throughout cerebral cortex
o Sleep-wake cycles
o Mood and emotional behaviour

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22
Q

describe some drugs which work on the serotonin pathway

A

o Tricyclic Compounds
 Imipramine
 Block uptake of serotonin

o Selective Uptake Inhibitors
 Fluoxetine (prozac)

o Monoamine Oxidase Inhibitors
 Phenelzine
 Reduce enzymatic degradation of serotonin

o Along with anti-depressants, other drugs that use the 5-HT pathways include anti-emetics and drugs used to treat migraine (triptans).

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23
Q

which nuclei contain cholinergic neurons and where do they project

A

nucleus basalis, the amygdala and brainstem nuclei.

Project through the thalamus and neocortex

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24
Q

what is loss of cholinergic pathways postulated to be involved with?

A

alzheimer’s

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25
Q

describe acetylcholinesterase inhibitors

A

developed to try to increases cholinergic function

o Gradual loss of efficacy
o Narrow therapeutic index
o Limited range of effects on cognition and behaviour
o Only effective in mild-moderate Alzheimer’s and certainly not curative

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26
Q

describe amyloid

A

• Component of amyloid precursor protein (APP)

APP is
• an integral transmembrane protein
• axonally transported
• synaptic transmission, neuroprotectant

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27
Q

describe the cleavage of APP

A

alpha secretase cleaves APP into two fragments which are not amyloidogenic

beta secretase cleaves APP into two fragments and then another called gamma secretase cleaves one of the fragments into an amyloidogenic fragment. This fragment is called beta amyloid and accumulates in brain parenchyma in Alzheimer’s.

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28
Q

how many cases of alzheimer’s are attributed to APP mutations

A

1%

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29
Q

describe Bapineuzumab

A

antibody targeted against amyloid β, is a passive immunotherapy that might bind to amyloid β and facilitate its clearance.

Beta amyloid immunisation reduces amyloid load but does not improve CNS activity. In the future hope to immunise earlier like with most injections, not when you already have Alzheimer’s.

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30
Q

describe the synthesis of dopamine

A

tyrosine -> DOPA - by tyrosine hydroxylase

DOPA -> Dopamine - dopa decarboxylase

dopamine -> either DOPAC - monoamine oxidase

dopamine -> or noradrenaline - dopamine beta hydroxyalse

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31
Q

what are the main pathways for dopamine

A

nigrostriatal projections from the substantia nigra to basal ganglia.

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32
Q

what does degeneration of dopaminergic neurones in the basal ganglia lead to?

A

parkinson’s

Diminished substantia nigra shows up less dark on a section.

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33
Q

what is the treatment for parkinson’s

A

increasing dopamine levels with L-DOPA which can lead to psychosis.

L-Dopa (precursor) will cross BBB but dopamine wont
o Via protein transport carrier (large neutral amino acid carrier)

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34
Q

what is increased dopamine function in the frontal cortex is associated with

A

schizophrenia

35
Q

what are neuroleptics

A

to treat schizophrenia

include Chlorpromazine and related antipsychotics

They are dopamine receptor antagonists / blockers.

can cause parkinsonian syndrome from blocking dopamine.

36
Q

describe the BBB

A

dynamic interface between the endothelium of capillaries and astrocyte processes.

– separates the brain from the circulatory system
– protects the central nervous system from potentially harmful chemicals
– regulates transport of essential molecules and maintains a stable environment

37
Q

what can cross the BBB

A

• Lipid soluble agents

• Transport carriers
o Glucose
o Amino acids

• Receptor mediated endocytosis and transcytosis
o Insulin

• <400g per mol of molecular weight

38
Q

describe intrathecal drug administration

A

– Ie. Baclofen for spasticity in multiple sclerosis
• Only a small proportion of oral baclofen
penetrates brain/spinal cord
– Intrathecal pump administers drug
directly into CSF (sub-arachnoid space)
– Experimental BBB opening

– Opening of the BBB using intracarotid infusion of
hyperosmolar solutions
• Effective delivery of chemotherapy drugs for
brain tumours

39
Q

describe the locations of the three nerve cell bodies which make up sensory systems

A

first order in the dorsal root ganglion
second order in the spinal cord grey matter
third order in contralateral thalamus

40
Q

what kind of fibres does the dorsal column medial lemniscus have

A

tends to have larger myelinated fibres

41
Q

what kind of fibres does the spinothalamic tract have

A

tends to have smaller myelinated and unmyelinated fibres

42
Q

what is proprioception mediated by

A

mechanoreceptors in the muscle spindles, golgi tendon organs, joint capsule receptors

43
Q

where do the fibres associated with proprioception run

A

in dorsal columns (position sense and kinaesthesia) ventral and dorsal spinocerebellar tracts (co-ordination of movements)

Fibres pass into ipsilateral cerebellum.

44
Q

what does the dorsal column medial lemniscus pathway sense

A

proprioception and fine touch

45
Q

what does the spinothalamic pathway sense

A

pain and temperature

46
Q

how do nerves differ in different parts of the body

A

In areas with no fine touch such as the skin on our back, many neurons will be activated by a pin prick so pressure is applied over a wide area. On the fingertips, nearby neurons are activated but there are interneuronal cells which switch off adjacent fibres so there is very precise localisation.

47
Q

where are the second order neurons for the dorsal column system

A

nucleus cuneatus or nucleus gracilis

48
Q

how does the first order neurone synapse with the second order in the spinothalamic pathway

A

very soon after it enters the grey matter. they then cross over and travel to the thalamic nuclei

49
Q

where is the dorsal column situated

A

between the two dorsal roots. the fasciculus cuneatus is more lateral than the fasciculus gracilis

50
Q

where is the spinothalamic tract situated

A

in between the ventral horn and the ventral aspect of the spinal cord

51
Q

what are the thalamic nuclei

A

– Ventral posterior- general sensory afferents. these travel to the primary sensory cortex

– Ventral anterior and lateral- efferents to motor cortices

– Medial geniculate- auditory afferents relayed to primary auditory cortex

– Lateral geniculate- visual afferents relayed to primary visual cortex

52
Q

what body part is at the level of T4?

A

nipples

53
Q

what body part is at the level of T10?

A

umbilicus

54
Q

what is general somatic pain from the head conveyed by

A

the trigeminal nerve

55
Q

describe the path of general somatic head pain

A

afferent fibres pass to the first order neurones in the trigeminal ganglion. then pass into the pons and terminate in the trigeminal sensory nuclei (second order). the trigeminothalamic pathway ascends mostly in the medial lemniscal pathway. then cross over to the thalamic nuclei

56
Q

causes of headache

A
  • Direct stimulation of nociceptors via trigeminal nerve- sinuses, toothache, ocular, skin
  • Stimulation of; periostium, arteries, venous sinuses, areas of the dura, muscle
  • Unknown causes- migraine
57
Q

describe subacute combined degeneration

A
  • Vit D deficiency
  • Chronic alcoholics are prone to this
  • Degeneration of the dorsal columns
  • Reduced proprioception
  • Wide gait
  • They increase the pressure of their feet on the ground when they walk to increase information to the brain
58
Q

describe tabes dorsalis

A
  • Now very rare
  • Chronic syphilitic infection
  • Degeneration of dorsal columns
59
Q

describe syringomyelia

A
  • Fluid build up in the spinal cord

* Shown as the large black space in the spinal cord

60
Q

what are layers 2 and 3 of the grey matter in the spinal cord called

A

substantia gelatinosa

61
Q

what can pain be modulated by

A

at the point of synapse with second order neurones by descending pathways from the periaqueductal grey matter.

62
Q

what is the analgesic ladder

A
  • Paracetamol +/- NSAID eg aspirin, ibuprofen
  • Codeine containing drugs +/- NSAID eg aspirin, ibuprofen
  • Morphine +/- NSAID eg aspirin, ibuprofen
63
Q

how many neurons does the cerebellum have

A

100 billion, 50% of all neurones in the brain

64
Q

what is the function of the cerebellum

A

motor control and increasingly known to be involved in cognitive processes

65
Q

where does the cerebellum sit

A

in the posterior fossa, effectively forming the roof of the fourth ventricle, more or less oppsite to the pons

66
Q

what separates the cerebellum from the rest of the brain

A

tentorium cerebelli

67
Q

what separates the two hemispheres of the cerebellum

A

the vermis

68
Q

what is the small inferior part of the cerebellum?

A

flocculonodular lobe

69
Q

other than the vermis, how is the cerebellum separated

A

by the primary fissure into the anterior and posterior lobes

70
Q

what are the grooves in the cerebellum called

A

folia, much more detailed than sulci in the brain

71
Q

what are the three parts of the cerebellum

A

vestibulocerebellum - most medial part, associated with balance, its associated nucleus is the fastigial nucleus

spinocerebellum - in between vestibulocerebellum and pontocerebellum, associated with the spinal cord, its associated nucleus is the interposed which is made up of the Eboliform and Globose

pontocerebellum - most lateral part and communicates with the brainstem. associated nucleus is the dentate nucleus which is a wavy horse shoe shape.
the pontocerebellum is uniquely large in humans for fine motor control of the hands

72
Q

what do the cerebellar peduncles contain

A

the input and output tracts of the cerebellum

73
Q

which cerebellar peduncle is which

A

the middle is the largest and the superior and inferior are at the side of the middle and superior/inferior respectively

74
Q

what do the cerebellar peduncles communicate with

A

the superior with the midbrain, the middle with the poins and the inferior with the medulla

75
Q

what are the layers of the cerebellum

A

the molecular layer (made up of stellate and basket cells) on the outside,

then the piriform layer (purkinje cells)

and finally the granule layer (granule and golgi cells)

beneath this is the white matter

76
Q

describe purkinke cells

A

have large dendritic trees which are the largest in the nervous system
these reach up into the molecular layer

granule cells also send axons up into the molecular layer

77
Q

where does input into the cerebellum come in

A

in the granule layer in “mossy” fibres and into the molecular layer in “climbing” fibres

78
Q

what forms loops in the cerebellum and why

A

information coming into central nuclei from mossy/climbing fibres and axons from purkinje cells. loops are vital for control mechanisms, a main function of the cerebellum

79
Q

what is the output of the cerebellum

A

control, modification or coordination of motor function

80
Q

what are the cerebellar afferents

A 
•	Spinal cord
      o	Posterior spinocerebellar
      o	Cuneocerebellar
      o	Anterior spinocerebellar
      o	Rostral spinocerebellar
•	Head, neck and brainstem
      o	Olivocerebellar 
      o	Tectocerebellar
      o	Pontocerebellar
      o	Reticulocerebellar	
      o 	Trigeminal nerve
81
Q

what are th cerebellar efferents

A
  • Vestibular nuclei
  • Reticular formation
  • Red nucleus
  • Ventrolateral thalamus
82
Q

what can cerebellar dysfunction lead to?

A

ataxia of upper limbs (clumsiness of movement)

ataxia of lower limbs

tuncal ataxia – postural (incoordination of postural sense – unsteady)

Gait ataxia – uncoordinated gain

Dysarthria - speech

Nystagmus – jerky movement of eyes

incoodination can be related to input, processing or output

83
Q

if the right cerebellum was damaged, what side would be affected

A

right
In cerebellar ataxia, it affects the limbs unilaterally and ipsilaterally. If it is in the midline then gait, posture and the trunk are affected.
Disease of the cerebellum could also be disease of the input or output tracts i.e. the brain stem

84
Q

what can cause cerebellar input/output disease

A
  • Neoplasia
  • MS
  • Trauma
  • Drugs and toxins (alcohol, phenytoin, carbamazepine)
  • Hereditary and degenerative ataxias (ADCAs, SCAs, others)
  • neurodegeneration

Year 2 - Semester 1 (13 decks)

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