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Y6 Senior Med COPY LaLz > Laz neuro > Flashcards

Laz neuro Flashcards

1
Q

What four lobes is the brain composed of? Draw diagram and label

A

Frontal lobe (anteriorly)
Parietal lobe (between frontal and occip)
Occipital lobe (posteriorly)
Temporal lobe ( lateral)

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2
Q

Where is the primary motor cortex?

A

in the posterior aspect of the frontal lobe

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3
Q

Where is the primary somatosensory cortex=

A

In the anterior aspect of the parietal lobe (so right behind the primary motor cortex)

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4
Q

Where is the primary visual cortex?

A

right at the BACK = posterior aspect of occipital lobe

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5
Q

How are visual signals transmitted to the primary visual cortex

A

from retinal to LGN
LGN to primary visual cortex

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6
Q

where is the LGN located

A

in the temporal lobe

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7
Q

Where is Broca’s area located and what is it responsible for?

A

Located in Frontal lobe (anterior to 1’ motor cortex)
PRODUCTION of speech (b-b-broca)

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8
Q

Where is Wernicke’s area located and what is it responsible for?

A

Located in Temporal Lobe
responsible for understanding of speech

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9
Q

What are the three key arteries to the brain

A

anterior cerebral
middle cerebral
posterior cerebraL

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10
Q

What artery supplies the anterior and miiddle cerebral arteries?

A

the internal carotid

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11
Q

what artery supplies the posterior cerebral?

A

the vertebral artery

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12
Q

What area does the anterior cerebral artery vascularise in the brain?

A

Frontal lobe (medially region)
Parietal lobe (anterior)

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13
Q

What sx does a ischaemia in anterior cerebral artery territory cause?

A

change in behaviour
weakness in LEGS > ARMS (remember homunculus is upside down)
mild sensory defect

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14
Q

What region does the Middle CA supply

A

some frontal, parietal and temporal lobe

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15
Q

What sx does ischaemia in middle cerebral artery territory cause?

A

Weakness in FACE > ARMS > LEGS
Hemisensory defect
Homonymous hemianopia (as it includes LGN / some of the optic tract in the temporal lobe

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16
Q

What sx does ischaemia in posterior cerebral artery territory cause?

A

VISUAL (as it affects the visual cortex)
- homonymous hemianopiaa
- visual agnosia
- prosopagnosia

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17
Q

what is the difference between ascending and descendiing pathways in the spinal cord?

A

ascending pathways: carry SENSORY inputs from skin etc to brain
descending pathway: carry MOTOR inputs from brain to muscle

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18
Q

How is white and grey matter distributed in SC, and how does this compare to the brain?

A

grey matter = centre of SC = bodies of neurons
white matter = periphery of SC = neuronal tracts

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19
Q

what are the sensory pathways in the SC

A

dorsal column (posterior)
spinocerebellar tract (lateral)
spinothalamic tract (anterior)

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20
Q

what sensory function does the dorsal column carry?

A

FINE TOUCH, PROPRIOCEPTION, VIBRATION (ascending, aka transmits to the brain)

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21
Q

what is the pathway of the dorsal column?

A

first order neuron: sensory receptor to medulla
second order: medulla to thalamus
third order: thalamus to priumary somatosensory cortex

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22
Q

where does the dorsal column decussate?=

A

at the level of the MEDULLA

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23
Q

what sensory function does the SPINOTHALAMIC TRACT carry?

A

pain and temperature

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24
Q

what s the pathway of the spinothalamic tract=

A

first order neuron: nociceptor to substantia gelatiinosa (in SC grey matter)
second order: substantia gelatinosa to thalamus)
third order: thalamus to primary somatosensory cortex

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25
Q

where does the spinothalamic tract decussate

A

at the substantia gelatinosa, at the LEVEL OF ENTRY INTO SC

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26
Q

what does the corticospinal tract carry?

A

MOTOR info from brain to muscle

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27
Q

outline the corticospinal tract pathway

A

primary motor cortex > (UMN) > anterior horn > (LMN) >muscle

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28
Q

where does UMN and LMN cross ovr

A

at the anterior horn

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29
Q

what else must you do for ischaemiic stroke management once pt has recieved CT head, aspirin +/- thrombolysis?

A

Investigate for CAUSE of STROKE
- AF: ECG
- structural heart disease: echo
- carotid atherosclerosis: carotid doppler

30
Q

why must you always suspend anticoagulants once you start stroke pt on aspirin?

A

because of high risk of haemorrhagic transformation (i.e. bleeding into the space where ischaemia had occurred)

risk is highest in the first 2 weeks after stroke
after which you may consider restarting or starting the anticoags

31
Q

What are the three meningeal layers in the brain?

A

dura
arachnoid
pia

32
Q

where does an extradural haemorrhage occur

A

between the skull and the dura

33
Q

what is the most common cause of an extradural haemorrhage

A

rupture of the Middle meningeal artery (which is superficial)
usually due to trauma > skull fracture

34
Q

what are sx of an extradural haemorrhage

A

transient LOC > lucid interval> gradual headache, eventual reduction in consciousness

35
Q

how does an extradural haemorrhage appear on CT

A

pear shaped (biconvex, lens shaped), does NOT cross suture lines (which connect dura to skull)

36
Q

where does a subdural haemorrhage occur

A

between dura and arachnoid

37
Q

what is cause of subdural haemorrhage

A

tearing of the bridging VEINS
(occasionally precipitated by mild trauma)

most common in elderly and alcoholics, who have brain atrophy > greater tension on the bridging veins

38
Q

what are the two different types of subdural haemorrhage, what are the differences in their causes and what do they look like on CT

A

acute vs chronic
acute: often precipitated by mild trauma, white crescent (banana) shaped blood
chronic: black bleed on CT very extensive

CROSS SUTURE LINES

39
Q

What are the two key causes of a subarachnoid haemorrhage

A

aneurysm rupture
severe trauma

40
Q

symptoms of subaarachnoid

A

sudden onset worse headache ever
may have meningeal irritation (photophobia, neck stiffness)

41
Q

how does a subarachnoid appear on CT

A

white blood along sulci and fissures

42
Q

what is parkinson’s disease

A

neurodegenerative disease of dopaminergic neurons in the substantia nigra

43
Q

What are the two tract categories in the motor system (from thhe primary motor cortex) and what are their function

A

PYRAMIDS > corticobulbar / corticospinal (VOLUNTARY MOVEMENT)

EXTRAPYRAMIDAL > basal ganglia, cereellum, vestibulart nucleus and substantia nigrqa (INVOLUNTARY; regulates movement and SMOOTHNESS)

44
Q

what are the four core symptoms of PD

A

Bradykinesia
Rigidity
Resting tremor (4-6hz, usually asymmetrical)
Postural instability

45
Q

what are the core symptoms of PD due to

A

malfunction of the extrapyramidal tract

46
Q

what is the aim of PD medication

A

to increase dopamine within the substantia nigra

47
Q

what is the mainstay of PD treatment and why is it DUAL

A

L-DOPA + peripheral DOPA-decarboxylase inhibitor

e.g. co-careldopa, co-demeldopa

needed because L-DOPA alone is converted by peripheral dopa-decarboxylase into dopamine, which cannot cross the BBB and instead triggers the CTZ to cause N&V

by giving an inhibitor you stop this enzyme’s function
so L-DOPA crosses into the brain
And in the brain is coverted to dopamine by dopa-decarboxylase

48
Q

what is another type of treatment for PD and how does it work

A

Dopamine agonist e.g. ropinirole, pramipexole
stimulates dopamine receptors and can cross the BBB

49
Q

what characterises progression of alzheimers

A

PROGRESSIVE decline in cognitive function

50
Q

give all the types of dementia

A

alzheimers (most common)
vascular
lewy body
frontotemporal
depressive pseudodementia

51
Q

explain key fts of vascular dementia

A

STEPWISE DECLINE in cognitive function
background of vascular disease

52
Q

explain key fts of lewy body dementia

A

TRIAD of
- dementia
- hallucinations
- parkinsonism

53
Q

explain key fts of frontotemporal dementia

A

personality change, early onset

54
Q

what is epilepsy

A

recurrent unprovoked seizures (2 or more, or 1 + epileptogenic markers)

55
Q

what management is used for epliepsy

A

valproate for all types
except:
- absence seizures = valproate or ethosuximide
- focal seizures: lamotrigine

DO NOT give valproate in women of childbearing age. Give:
- lamotrigine (tonic clonic/absence)
- levetiracetam (tonic, atonic, myoclonic)

56
Q

UMN signs

A

spasticity
hyperreflexia
upgoing plantars

57
Q

LMN signs

A

hypotonia
hyporeflexia
fasciculations
muscle wasting

58
Q

What does a brainstem lesion present as in terms of MOTOR deficit?

A

Weakness in limbs CONTRALATERALLY
Weakness in face IPSILATERAL

59
Q

How do you differentiate between motor lesion in brain vs spinal cord?

A

SC: likely bilateral
Brain: likely unilat

60
Q

which types of dementia have parkinsonism

A

Lewy body
Frontotemporal

61
Q

explain frontotemporal dementia

A

Parkinsonism
Behavioural change s
Self neglect and abandonment of habits

62
Q

what is hydrocephalus

A

accumulation of CSF within ventricular system

63
Q

types of hydrocephalys

A

OBSTRUCTIVE (non communicating)
COmmunicating (normal pressure hydrocheph)

64
Q

causes of obstructive hydroceph

A

tumour
aqueduct stenosis

65
Q

causes of non-obstructive hydroceph / Normal presssure hydrocephalus

A

impaired CSF reabsorption in subarachnoid villi
e.g. meningitis

66
Q

triad NPH

A

DUG

dementia
urinary incontinence
gait disturbance

67
Q

ix hydroceph

A

CT head
LP (also curative in NPH)

68
Q

what are bulbar signs

A

LMN signs of CN 9-12
impaired speech and swlalowing!!

69
Q

what is the progression of ALS

A

bulba rsigns > spastic weakness, paralysis > resp failure

70
Q

which functions are spared in ALS

A

oculomotor, sensory, autonomic functions! think hawking

71
Q

whhat is the mode of inheritance of neurofibromatosis

A

AUTOSSOMAL DOMINANT

Y6 Senior Med COPY LaLz (29 decks)

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