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(SG) Phase 2A lectures > neuro > Flashcards

neuro Flashcards

1
Q

what is superiorly at the brainstem

A

thalamus n internal capsule

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2
Q

what is inferiorly at the brainstem

A

spinal cord

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3
Q

what are descending motor tracts

A

pyramidal tracts

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4
Q

what are ascending sensory tracts

A

lemnisci

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5
Q

what are some tumours affecting brainstem?

A

meningioma
schwannoma
astrocytoma
metastasis

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6
Q

what is an inflammatory disorder affecting brainstem

A

MS

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7
Q

what is criteria for brainstem death?

A 
pupils
corneal reflex
cough reflex
gag reflex
respirations
response to pain
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8
Q

what does peripheral neuropathy refer to?

A

any disorder of the PNS

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9
Q

what is diff btwn acute and chronic neuropathies?

A

acute - evolve rapidly, severe enough to make pt seek A&E help

chronic - outpatient setting, can be further classified based on pathology and neurophysiological findings

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10
Q

which are the large myelinated fibres?

A

a alpha (proprioception)

a beta (light touch, pressure and vibration)

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11
Q

which re the small fibres?

A 
a alpha (myelinated)
c (unmyelinated)

both transmit signals regarding pain

also a alpha - cold sensation
c - warm sensation

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12
Q

what is mononeuropathy

A

problem w/ 1 nerve

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13
Q

what is polyneuropathy

A

problem w/ many nerves

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14
Q

name some common mononeuropathies

A

carpal tunnel syndrome (median nerve)

ulnar neuropathy (entrapment at cubital tunnel)

peroneal neuropathy (entrapment at fibular head)

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15
Q

what is ataxia?

A

poor balance
sensory (loss of proprioception) or cerebellar

when sensory, ataxia gets worse w/ eyes closed or when dark

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16
Q

how do peripheral neuropathies present differently?

A

symmetrical (sensorimotor)
asymmetrical (sensory)
asymmetrical (sensorimotor)

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17
Q

how do symmetrical peripheral neuropathies present?

A

initially sensory, but eventually sensorimotor

commonest type

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18
Q

how does asymmetrical peripheral neuropathies present?

A

patchy distribution of symptoms

dorsal root ganglia affected

uncommon - paraneoplastic, sjogre, gluten sensitivity

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19
Q

how do asymmetrical sensorimotor peripheral neuropathies present?

A

mononeuritis multiplex
very uncommon
painful

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20
Q

how do u clinically examine peripheral neuropathies?

A

reduced/absent tendon reflexes
sensory deficit
weakness - muscle trophies

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21
Q

what is axonal peripheral neuropathy associated with?

A

systemic disease

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22
Q

what does chronic mean?

A

develops over at least 6m

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23
Q

what does idiopathic mean?

A

no aetiology can be identified despite extensive investigations

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24
Q

how do u treat chronic neuropathies?

A

symptomatic treatment

aim to stop disease progression

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25
Q

what are the 3 main branches of the aortic arch?

A

brachiocephalic (R CC & R sub)
L common carotid
L subclavian

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26
Q

where does the R CCA arise from?

A

brachiocephalic artery

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27
Q

where does the L CCA arise from??

A

aortic arch

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28
Q

does the CCA have any branches? where do they bifurcate?

A

no - C3-4

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29
Q

what do the CCA split into?

A

internal and external carotid arteries (At upper border of thyroid cartilage)

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30
Q

where is a typical area to see carotid artery dissection?

A

carotid canal - vulnerability of anatomical dissection bc of

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31
Q

what are the 4 “parts” of the internal carotid artery?

A

cervical
petrous
cavernous
supraclinoid (intradural)

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32
Q

what do the sup hypophyseal arteries supply?

A

pit gland/stalk
hypothalamus
optic chiasm

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33
Q

what does the anterior choroidal artery supply?

A 
choroid plexus
optic tract
cerebral peduncle
internal capsule
medial temporal lobe
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34
Q

look at territories supplied by MCA/ACA/PCA

A

!

middle - outer bits on both sides
anterior - where 2 hemispheres connect
posterior - back of head, post lobe

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35
Q

what are the 2 types of head injury?

A

non-missile - BLUNT (most common)

missile - PENETRATING (penetration of skull/brain)

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36
Q

how can lesions be distributed?

A

focal

diffuse brain lesions

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37
Q

what is primary vs secondary time course of trauma?

A

primary - immediate biophysical forces of trauma

secondary - presenting some time after traumatic event

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38
Q

what is some focal damage in diff areas after non-missile (blunt) trauma

(scalp, skull, meninges, brain)

A

scalp - lacerations
skull - fracture
meninges - haemorrhage, infections
brain - confusions, infection etc

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39
Q

what is some diffuse brain lesion damage ???? after non missile/blunt trauma

A

diffuse axonal/vascular injury
hypoxia-ischaemia
swelling

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40
Q

what does skull fracture imply? (4)

A

considerable force

incr risk of haematoma/infection/aerocele

angled/pointed objects - localised fractures, open/depressed

flat surfaces - linear fractures, can extend to skull base

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41
Q

what is sig abt fracture lines?

A

1 fracture line will not cross any other fracture lines … can deduce order from this

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42
Q

what are extradural haematomas like ? (3)

cause? time frame? how can they cause death?

A

skull fracture

occurs slowly over hrs

can cause death by: brain displacement, herniation, raised ICP

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43
Q

what are extradural haematomas?

what are they usually associated with?

A

collection of blood that forms between the inner surface of the skull and outer layer of the dura (endosteal layer).

usually associated with a history of head trauma and frequently associated skull fracture.

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44
Q

what are subdural haematomas like ? (4)

why do they happen?
what is the onset?
what are they usually surrounded by?
what can they cause?

A

(underneath dura mater)

usually due to tears in bridging veins

can occur slowly (‘chronic’) in shrunken (old, alcoholic?) brains as well as acutely

usually surrounded by membrane of granulation tissue

cause of cog decline in elderly ! treatable

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45
Q

what are some causes of a traumatic subarachnoid haematoma?

A

punch in the neck - rupture of vertebral artery

laceration

base of skull fracture

IV haemorrhage

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46
Q

what is diff btwn superficial and deep cerebral/bellar haemorrhage

A

superficial: due tos evere contusion (bruise)
deep: related to diffuse axonal injury

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47
Q

what is a contusion?

A

bruise

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48
Q

what is a risk for any head injuries in A&E?

A

meningitis

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49
Q

what is a neuro laceration?

A

when contusion sufficient enough to tear in layer of brain (pia mater)

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50
Q

what is diff btwn coup contusion and contre coup?

A

coup = at site of impact

contre coup = away from site of impact

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51
Q

what is mild traumatic axonal injury?

A

hurt ur head, have recovery of consciousness ± LT, variable severity deficit

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52
Q

what is severe traumatic axonal injury?

A

hurt ur head, become unconscious from impact & remain so or severe disability

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53
Q

what does brain swelling lead to?

A

increased ICP

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54
Q

name 2 causes of brain herniation

A

bleeding

brain swelling

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55
Q

hypoxia-ischaemia is likely in which patients who’ve had? (3)

A
  • clinically evident hypoxia
  • hypotension w systolic BP <80mmHg for ≥15mins
  • raised ICP
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56
Q

what is 1 of the LT consequences of head injuries?

A

chronic traumatic encephalopathy eg Muhammad Ali

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57
Q

what happens in chronic traumatic encephalopathy?

A

repetitive mild traumatic brain injury

initially irritability, aggression, depression, memory loss

then dementia, gait/speech issues, parkinsonism

some have MND-like symptoms

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58
Q

what are some infective causes of meningitis?

A

bacterial
viral
fungal parasitic

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59
Q

what is the first line of treatment usually before diagnosis of meningitis?

A

antimicrobials

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60
Q

the syndrome of meningitis must be administered from what?

A

brain abscesses and encephalitis, other major CNS syndromes

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61
Q

what is meningitis?

A

inflammation of meninges (Pia mater, arachnoid, dura)

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62
Q

what are some non-infective causes of meningitis?

A

paraneoplastic
drug side effects
auto immune eg vasculitis/SLE

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63
Q

how does brain infection get in?

A

neurosurgical complications eg post op, trauma

extracranial infection eg nasopharynx, ear, sinuses

via bloodstream ie bacteraemic

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64
Q

what is the pathophysiology of meningitis?

A

bacteria enters CSF

can be isolated from immune cells due to BBB

replicates

BVs become leaky - WBCs enter CSF/meninges/brain

results in meningeal inflammation ± brain swelling

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65
Q

what are 3 classic symptoms of meningitis?

A

fever
headache
neck stiffness - “meningism”

(can’t tolerate bright light)

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66
Q

20% of bacterial meningitis patients can have permanent effects. list some

A 
skin scars
amputation
hearing loss
seizures
brain damage
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67
Q

what does GCS (Glasgow coma score) help us determine

A

how sick pt - lower score = sicker
if they can maintain own airway
if there’s any raised ICP

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68
Q

what are 4 immediate management steps for someone who has bacterial meningitis?

A
  1. assess GCS
  2. blood cultures
  3. broad spectrum ABs (ceftriaxone, cefotaxime - both cross BBB)
  4. steroids (IV dexamethasone)
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69
Q

what is a definitive investigation to diagnose meningitis?

A

lumbar puncture

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70
Q

what are some contraindications to lumbar puncture?

A 
abnormal clotting (platelets/coagulation)
petechial rash
raised ICP
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71
Q

what are some risk factors for bacterial meningitis

A

students
travel
(immunosuppressed)

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72
Q

what are some risk factors for viral meningitis

A

small children

immunosuppressed

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73
Q

if meningitis is in bloodstream, what do u get?

A

meningococcal septicaemia

non-blanching purpuric rash, necrosis, high mortality !

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74
Q

differential diagnosis for meningitis :

A

!subarachnoid haemorrhage! - trauma - “thunderclap” onset

also migraines, flu, brain abscess, malaria

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75
Q

what is encephalitis?

A

inflammation of the brain

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76
Q

what are causes of encephalitis?

A

p much always viral - herpes simplex (coldsore)

varicella zoster virus (chickenpox/shingles)

ask abt TRAVEL! eg rabies etc

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77
Q

what is the clinical present of encephalitis:

A

hrs to days: preceding ‘flu-like’ illness

then: altered GCS (confusion, drowsiness), fever, seizures, memory loss, ± meningism)

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78
Q

how do u manage encephalitis

A

MRI head ± EEG
lumbar puncture
DO A HIV TEST

treat: mostly supportive
recovery can be v long process

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79
Q

how does tetanus happen?

A

inoculation through skin w/ clostridium tetani spores found globally in soil

eg stepping on nail, dirty wounds

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80
Q

what happens in tetanus?

A

tetanospasmin (toxin that bacteria prod) - travels retrogradely along axons

interferes w neurotransmitter release - incr neutron firing - unopposed muscle contraction/spasm

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81
Q

how can tetanus be managed?

A

if at risk injury - vaccinate!

if symptomatic - support (muscle relaxants), IG, AB (metronidazole to clear any residual bacteria that may prod toxins)

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82
Q

how does rabies happen?

A

viral infection

inoculation through skin with saliva of rabid animal eg dogs/cats/foxes eg lick, bite, splash

travels retrogradely along nerves

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83
Q

how is rabies managed?

A

most ppl die
managed with sedatives
prophylaxis is key

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84
Q

what is dementia?

A

a set of symptoms - inc memory loss, problem solving language

gradual onset and progressive

Alzheimer’s is the commonest cause of dementia

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85
Q

what is Alzheimer’s disease a problem w?

A

storing of memories

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86
Q

what makes up the exclusion criteria for Alzheimer’s?

A

sudden onset

early occurrence of: gait, seizures, major behavioural changes

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87
Q

which med cond are severe enough that u can’t diagnose Alzheimers?

A

major depression

cerebrovascular disease

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88
Q

what is pseudodementia?

A

depressie dementia

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89
Q

what is the diff in depression/dementia on onset?

A

depression - trigger, onset/decline rapid

dementia - vague, insidious onset

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90
Q

what is the diff in depression/dementia on memory loss?

A

depression - aware, complaints of memory loss

dementia - unaware/attempt to hide problems

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91
Q

what is mood diff in depression vs dementia

A

depression - patient unhappy. “don’t know” answers

dementia - mood labile. attempts all questions

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92
Q

why Is temp lobe important?

A 
hearing
language comprehention
semantics
memory
emotional/affecting behaviour
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93
Q

what happens in dementia with levy bodies (3)

A

fluctuation cognition
visual hallucinations
spontaneous Parkinsonism

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94
Q

why do u do a structural MRI in dementia patients?

A

to rule out other causes

see atrophy as a biomarker

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95
Q

what are the 2 main medications for dementia?

A

acetylcholine esterase inhibitors

memantine (anti-glutamate)

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96
Q

which diagnostic tests can be used for Alzheimer’s pathology

A

non-invasive (amyloid and tau PET ? imaging)

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97
Q

what are some key features of MS?

A

inflammatory, demyelinating tissue

specific to CNS

usually begins 20-40 yrs

progressive disability over time

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98
Q

which pops is MS more common in?

A

caucasian

prevalence can be altered by env change - age of migration is critical

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99
Q

what are the 2 types of lesions in MS?

A

active and inactive

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100
Q

what are common sites for plaque distribution in MS?

A

cerebral hemispheres
spinal cord
optic nerves
medulla/pons

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101
Q

what are some typical symptom in MS?

A

optic neuritis
spasticity
sensory symptoms/signs
bladder/sexual dysfunction

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102
Q

what are some atypical symptoms in MS?

A

aphasia
hemianopia
severe muscle wasting

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103
Q

what is the majority of MS patient’s course of illness?

A

in a relapsing/remitting fashion … full recovery from disease, stable until next attack etc etc cycles !

don’t need to recover fully each time

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104
Q

what are the 2 essential diagnostic criteria for MS?

A

2+ CNS lesions disseminated in time/space

exclusion of cond giving a similar clinical picture

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105
Q

what are some conditions misdiagnosed as MS?

A

SLE
lyme disease
syphilis
AIDS

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106
Q

what is the gold standard investigation for MS?

A

imaging !!!!!!!! MRI

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107
Q

blackouts can be bc of what?

A

problem w/ blood circulation (heart/BP)

disturbance of brain function (epilepsy)

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108
Q

what are the 2 types of seizures?

A

epileptic seizures and stress-related (non-epileptic) seizures

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109
Q

what are the 3 types of epilepsy - following epileptic seizures

A

idiopathic generalised epilepsy
unclassifiable epilepsy
focal epilsepsy

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110
Q

what is an epileptic seizure?

A

paroxysmal event in which changes of behaviour/sensation/cog processes are caused by excessive, hypersynchrous neuronal discharges in the brain

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111
Q

what is the usual duration of epileptic seizures

A

30-120s

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112
Q

what happens in an epileptic seizure?

A

“positive” ictal symptoms (seeing/hearing/feeling stuff that aren’t there)

may occur from sleep

may be associated with other brain dysfunction

typical seizure phenomena: lateral tongue bite, deja vu etc

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113
Q

what is syncope?

A

paroxysmal event in which changes in behaviour/sensation/cog processes are caused by an INSUFFICIENT BLOOD/OXYGEN SUPPLY to the brain

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114
Q

list some syncope characteristics

A

situational

sitting/standing

rarely from sleep

presyncopal symptoms (seeing stars, distorted noises, dizzy/light headed, blacked out vision)

duration 5-30 seconds

recovery within 30 seconds

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115
Q

what is cariogenic syncope like ?

A

less warning

history of heart disease

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116
Q

define non-epileptic seizure

A

paroxysmal event in which changes in behaviour/sensation/cog function caused by MENTAL PROCESSES ASSOCIATED W/ PSYCHOSOCIAL DISTRESS

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117
Q

what are some characteristics of non-epileptic seizures

A

situational

duration 1-20 mins

eyes closed

ictal crying/speaking

instead of panic attack ?

surprisingly rapid/slow postictal recovery

history of psych illness esp PTSD

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118
Q

what are some factors suggestive of epilepsy

A

tongue biting
head turning
muscle pain

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119
Q

what are some factors suggestive of syncope

A

prolonged upright position
sweating prior
nausea
presyncopal symptoms

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120
Q

what is focal epilepsy?

A

associated w/ focal brain abnormality, starts at any age

partial seizures w or w/o impairment of consciousness

1st line treatment: carbamazepine

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121
Q

what is idiopathic (primary) generalised epilepsy?

A

no associated brain abnormality, manifestation usually <30 years

absence seizures, myoclonic seizures or primary generalised tonic clonic seizures

1st line treatment:
valproate

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122
Q

how do anti-epileptics work?

A

taget GABA receptor/transporter or GABA transaminase

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123
Q

what do u do if anti-epileptics don’t work?

A

alternative mono therapy, combo therapy

consider epilepsy surgery - vagal nerve stimulator

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124
Q

what is essential in epilepsy diagnosis?

A

patient and witness history !

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125
Q

what’s the diff btwn new and conventional anti-eleptics

A

not much in terms of effectiveness but fewer side effects

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126
Q

define stroke

A

a clinical syndrome, caused by cerebral infarction/haemorrhage, typified by rapidly developing signs of focal/global disturbance of cerebral functions lasting more than 24h or leading to death

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127
Q

define TIA (transient ischaemic attack)

A

acute loss of cerebral/ocular function with symptoms lasting less than 24h caused by an inadequate cerebral or ocular blood supply as a result of low blood flow, ischaemia, or embolism associated with disease of the BV, heart or blood

128
Q

what are the majority of strokes?

A

ischaemic (85%)

129
Q

what happens in ischaemic strokes

A

BV in brain blocked

usually atherosclerotic plaque/clot in larger artery ruptures, travels downstream, gets trapped in narrower artery in brain

embolic strokes are common complications of atrial fib and atherosclerosis of carotid arteries

130
Q

what are the minority of strokes caused by (15%)?

A

haemorrhage

bleeding from BV in the brain

high BP is main cause of intracerebral haemorrhagic stroke

131
Q

someone presenting w/ an acute onset, ongoing focal near deficit that cannot be explained by hypoglycaemia or other stroke mimics .. suspect what?

A

stroke

132
Q

obstruction ot MCA can cause what

A

facial weakness
unilateral weakness of upper/lower limb
unilateral sensory loss of upper/lower limb
speech problems

133
Q

obstruction of PCA can cause what

A

visual defects
disorders of perception
disorders of balance
co-ordination disorders

134
Q

obstruction of ACA can cause what

A

unilateral weakness + sensory loss of upper/lower limb

135
Q

what cond does stroke mimic?

A

migrainous aura
hypoglycaemia
mass lesions eg subdural haematoma, tumour

136
Q

how do u manage a suspected stroke

A

arrange emergency admission to specialist stroke unit

999 or 1 hr admission

137
Q

what do u do in a TIA?

A

assess risk of stroke in next 7d using ABCD^2 score

138
Q

how do u assess risk of stroke in next 7d - and how is this scored

A

ABCD^2 score

A - age (60+) = 1pt
B - BP at pres (140/90+) = 1 pt
C - clinical features (unilateral weakness = 2pt, speech disturbance w/o weakness = 1pt)
D - duration (60min+ = 2pts, 10-59mins = 1pt)
D - diabetes presence = 1pt

139
Q

what is high risk ABCD^2 score

A

4+

atrial fib
more than 1 TIA in a week
TIA whilst on anticoagulant

140
Q

what do u do for a low risk stroke patient

how does this differ to a high risk?

A

refer for specialist assessment within 7d of symptom onset

start statin - simvastatin 40mg

antiplatelets - aspirin/clopidogrel 300mg

treat BP if raised

no driving until seen by specialist

HIGH RISK - same as above but within 24H

141
Q

what is primary health care

A

1st point of contact for healthcare - for new issues inc urgent/emergency and for ongoing issues

eg GP, walk-in, minor injuries, dentist, ?999

142
Q

what is MND aka?

A

ALS (amyotrophic lateral sclerosis)

143
Q

what does ALS stand for

A

amyotrophic lateral sclerosis aka MND

144
Q

why are brain tumours sig?

A

20% of childhood cases !

145
Q

where do the majority of brain tumours occur in adults?

A

supratentorial

146
Q

where do the majority of brain tumours in children occur?

A

posterior fossa

147
Q

list some neuroepithelial tumours

A 
astrocytic
oligodendroglial
neuronal and neuro-glial
choroid plexus
embryonal etc
148
Q

how do brain tumours clinically manifest?

A

loss function
seizures
raised ICP!

149
Q

what is the most frequent primary brain tumour and who does it occur in?

A

astrocytic tumours

150
Q

how can astrocytic tumours be classified

A

diffuse astrocytomas

other types eg pilocytic

151
Q

what are diffuse astrocytomas like ?

A

infiltrate diffusely

propensity to undergo progressive anaplasia

152
Q

what is anaplasia?

A

condition of cells with poor cellular differentiation, losing the morphological characteristics of mature cells and their orientation with respect to each other and to endothelial cells.

153
Q

how does a pilocytic astrocytoma grade into a glioblastoma? (more severe, worse prognosis)

A

pilocytic astrocytoma - diffuse astrocytoma - anaplastic astrocytoma - glioblastoma

154
Q

discuss oligodendroglioma

A

most common 4/5th decades
may have seizures
WHO grade 2
calcification recognised on scan

155
Q

what are the aims with gliomas? to identify?

A

tumour type
tumour grade
additional prognostic markers
predictive markers

156
Q

discuss pilocytic astrocytomas (WHO grade 1)

A 
children!
posterior fossa - cerebellum
also at optic nerves, hypothalamus
often cystic
good prognosis
157
Q

what is medulloblastoma like ? (who grade 4)

A

primitive “small blue cell” tumour of cerebellum
childhood
highly malignant
may respond to exicison/radio/chemo

158
Q

what is a meningioma?

A

dural based

push into brain

most grade 1, more aggressive variants (2/3) exist

159
Q

what are the most common sites for metastases to the brain?

A

lung (45%)
breast (25%)
melanoma (12%)

160
Q

discuss 4 point about brain tumours !

A

unique features associated with CNS env

mass effects are important

graded by WHO scheme, but conventional pathological staging not used

moving towards integrated histo/molec diagnosis for better treatment stratification

161
Q

what are some anatomical effects of a mass lesion? (3)

A
  1. local deformity and shift of structures
  2. decreased CSF volume
  3. pressure gradients - internal herniation
162
Q

list some examples of inter-cranial haemorrhages

A

extradural haemorrhage
subdural “ “
subarachnoid “ “
intracerebral “ “

163
Q

what are the 3 layers of meninges, n give. adescription of each

A

Pia - on surface, cannot be separated from brain

Arachnoid - more adherent to brain

Dura - usually firmly adherent to inside of skull

164
Q

where are meningeal vessels?

A

in the extradural space

165
Q

where do bridging veins cross

A

subdural space

166
Q

which space does the circle of willis lie in?

A

subarachnoid pace

167
Q

are there any vessels deep to the Pia?

A

no - Pia forms part of BBB

168
Q

list 6 points about extradural haemorrhages

A
  1. traumatic
  2. fractured skull
  3. bleeding from middle meningeal artery
  4. lucid period
  5. rapid rise in ICP
  6. coning and death if not treated
169
Q

bleeding from MMA can result in which haemorrhage?

A

extradural

170
Q

list 5 points about subdural haemorrhages

A
  1. bleeding from bridging veins
  2. these bridging veins bleed, low pressure so soon stops
  3. days/weeks later, haematoma starts to autolyse
  4. massive increase in oncotic/osmotic pressure - sucks water into haematoma
  5. gradual rise in ICP over many weeks
171
Q

which type of haemorrhage is commonest where the patient has a small brain? and list why someone might have a small brain

A

subdural haemorrhage

alcoholics, dementia

172
Q

list 5 points about subarachnoid haemorrhages

A
  1. rupture of arteries forming circle of willis
  2. often bc of berry aneurysms
  3. sudden onset severe headache, photophobia and reduced conciousness
  4. ‘thunderclap headache’
  5. rapidly fatal - commonest source of organs for transplant since seat belts made compulsory
173
Q

bleeding from bridging veins can result in which type of haemorrhage?

A

subdural

174
Q

berry aneurysms can result in which haemorrhage?

A

subarachnoid

175
Q

trauma can result in which haemorrhage and why?

A

extradural - bleeding from MMA

176
Q

is there recovery with embolic strokes?

A

no

177
Q

is there recovery from haemorrhage strokes?

A

possibly

178
Q

what happens in an embolic stroke?

A

death of cell bodies in cortex

‘small’ well defined territory of loss of motor/sensory function

179
Q

what happens in a haemorrhage stroke?

A

compression of internal capsule - no death of cells

large territory of loss of motor/sensory function

180
Q

which type of stroke is where cell death occurs?

A

embolic

181
Q

what is the function of CN I?

A

olfactory - smell

182
Q

what is the function of CN II?

A

optic - light pathway, neuronal pathway

183
Q

what is the function of CN III?

A

oculomotor - bilateral cortical

innervation of nuclei, eye movements

184
Q

what is the function of CN IV?

A

trochlear - bilateral cortical

innervation of nuclei, eye movements

185
Q

what is the function of CN V

A

trigeminal - motor, bilateral;
sensory, contralateral.

sensation face, muscles of mastication

186
Q

what is the function of CN VI

A

abducens - bilateral cortical

innervation of nuclei, eye movements

187
Q

what is the function of CN VII

A

motor, bilateral to forehead

motor, contralateral to the rest of the face

sensory, contralateral (taste)

188
Q

what is the function of CN VIII

A

vestibular, ipsilateral; cochlear, bilateral

hearing, balance

189
Q

what is the function of CN IX

A

glossopharyngeal

motor, bilateral; sensory, contralateral

sensation back of throat

190
Q

what is the function of CN X

A

vagus

motor, bilateral; sensory, contralateral

motor pharynx; autonomics complex

191
Q

what is the function of CN XI

A

spinal accessory

motor, bilateral

shrugging shoulders, turning head

192
Q

what is the function of CN XII

A

hypoglossal

motor, bilateral

sticking tongue out

193
Q

what proportion of brain tumours are malignant?

A

over 50%

194
Q

what is the commonest brain tumour?

A

secondary/metastatic tumour with another primary source eg lung, breast

195
Q

do you use the TNM staging system for brain tumours

A

no

use WHO classification - histology

196
Q

for brain malignancy what does grade I mean? what does grade IV mean?

A

grade I - most benign

grade IV - most malignant

197
Q

what is the most common primary brain tumour

A

glioma

198
Q

what is a glioma a tumour of?

A

glial cells: astrocytes, oligodendrocytes, ependymal cells

199
Q

85% of all new cases of malignant primary brain tumour are what?

A

high grade glioma

200
Q

what are symptoms of brain tumour

A

variable
headaches
seizures
focal neuro symptoms

201
Q

what is the classic brain tumour symptom?

A

raised ICP headache

worse in morning/lying down
associated with N&V
exacerbated by cough/sneezing
drowsiness

202
Q

what are signs of a brain tumour?

A

papilloedema (swelling of optic disc)

focal neuro deficit eg visual field defect, dysphasia

203
Q

what are red flags with headaches?

A

features of raised ICP
papilloedema
focal neuro
check for field defect

204
Q

if there’s a long history of isolated headaches, what is unlikely?

A

a brain tumour

205
Q

how do low grade brain tumours typically present

A

w/ seizures

can be incidental

206
Q

how do high grade brain tumours typically present

A

rapidly progressive neuro deficit

symptoms of raised ICP

207
Q

what are investigations for brain tumours

A

CT w/ contrast
MRI
brain biopsy

208
Q

what is treatment for brain tumours like

A

non-curative, except for grade I

only 19% survive 5+ years

209
Q

what are some treatments for a high grade glioma?

A

steroids - reduce oedema
surgery - biopsy/resection
radiotherapy
chemotherapy

210
Q

what are some “hardware” diseases of basal ganglia

A

parkinson’s

huntington’s

211
Q

what are some “software” diseases of the basal ganglia

A

essential tremor
dystonia
tourette

212
Q

what are the 3 main symptoms in Parkinson’s?

A

brady/akinesia

tremor

rigidity

213
Q

what is brady/akinesia like in Parkinson’s?

A

problems w doing up buttons, keyboards etc

writing smaller

walking deteriorated: small stepped, dragging 1 foot etc

214
Q

what is tremor like in Parkinson’s?

A

at rest

may be unilateral

215
Q

what is rigidity like in Parkinson’s?

A

pain

problems w turning in bed

216
Q

what can u see in the midbrain in Parkinson’s disease?

A

diminished/paler substantial nigra

presence of Lewy bodies?

217
Q

what is the main drug for Parkinson’s?

A

L-Dopa

218
Q

what is L-dopa changed into in the body?

A

dopamine

219
Q

how can l-dopa action be supported?

A

dopamine agonists

or monoamine-oxidases (enzyme inhibitors) - red breakdown of naturally occurring dopamine

220
Q

what is the issue with anticholinergics?

A

many side effects:

  • cognition
  • confusion
  • systemic
221
Q

what are some motor complications of late-stage PD?

A

med doesn’t work as long as before

freezing - unpredictable loss of motility

on and off dyskinesias

222
Q

what else is common in Parkinson’s?

A

depression

other psych problems

dementia

autonomic problems eg constipation, incr urine frequency

223
Q

which symptoms shouldn’t be present in Parkinson’s?

A

incontinence

dementia

symmetry

early falls

224
Q

what are the 3 cardinal features of Huntington’s disease?

A

chorea (jerky involuntary movements affecting esp shoulders, hips, n face.

dementia

psychiatric problems

225
Q

what do u find o/e of a Huntington’s patient?

A

abnormal eye movements

chorea

ataxia

often additional “touch of Parkinsonism”

226
Q

define weakness/paresis

A

impaired ability to move a body part in response to will

227
Q

define paralysis

A

ability to move a body part in response to will is completely lost

228
Q

define ataxia/incoordinationz

A

willed movements are clumsy, ill-directioner or uncontrolled

229
Q

what are involuntary movements?

A

spontaneous movement of a body part, independently of will

230
Q

what is apraxia?

A

disorder of consciously organised patterns of movement or impaired ability to recall acquired motor skills

231
Q

what are the 5 steps to movement organisation

A
  1. idea - association areas of cortex
  2. activation of UMN in precentral gyrus
  3. impulses travel to lMN and their motor units via corticospinal (pyramidal) tracts
  4. modulating activity of cerebellum n basal ganglia
  5. further modification of movement depending on sensory feedback
232
Q

where are LMNs located

A

anterior horns of SC and in CN nuclei in the brainstem

233
Q

what is the final common pathway by which the CNS controls voluntary movement

A

LMN –> axon (nerve root and peripheral nerve) –> NMJ –> muscle fibres

234
Q

what is a motor unit?

A

basic functional unit of muscle activity

LMN + axon + several supplied muscle fibres

235
Q

what are stretch receptors in muscle called

A

muscle spindles

236
Q

what are stretch receptors in muscle (muscle spindles) innervated by?

A

gamma motor neurones

237
Q

what are some potential sites of damage along the final common pathway

A 
motor nuclei of CN
motor neurones in SC
spinal ventral roots
peripheral nerves
NMJ
muscle
238
Q

list 4 clinical features of LMN lesions

A

muscle tone normal/reduced (flaccid)

muscle wasting

fasciculation - visible

spontaneous contraction of motor units

reflexes depressed/absent

239
Q

what do LMN lesions usually result in?

A

everything going DOWN

240
Q

how do u investigate LMNs

A

neurophysiology nerve conduction studies

neuro-imaging - MRI scan head/spine

blood tests eg muscle enzymes, auto-antibodies

lumbar puncture

241
Q

what is the corticospinal tract?

A

a major descending pathway connecting UMN & LMNs, important in control of voluntary movements

242
Q

what is the corticospinal tract aka

A

pyramidal tract

243
Q

list some clinical features of UMN pathology

A

muscle tone increased (spasticity)

tendon reflexes/jaw jerk are brisk

plantar responses extensor (+ Babinski sign)

characteristic pattern of limb muscle weakness, pyramidal pattern

emotional lability may be present

244
Q

what do UMN lesions usually result in?

A

everything goes UP

245
Q

what are some common causes of UMN pathology

A

vascular disease

inflammatory eg MS

compression of brain/spine

neurodegenerative disease of UMN ± LMN eg MND

246
Q

how do u investigate UMN issues

A

neuroimaging - MRI brain/spine

blood tests for metabolic disorders

CSF exam

247
Q

what are the likely levels of UMN

A

cortex

internal capsule

brainstem

SC

248
Q

what are the likely levels of LMN

A

LMN

spinal root

peripheral nerve

NMJ

muscle

249
Q

what is prophylaxis?

A

treatment given or action taken to prevent disease

250
Q

what does the cerebellum do?

A

contains complete motor/sensory rep of whole body

contains timing/pattern of motor activating during movement

251
Q

what does cerebellar dysfunction cause?

A

ataxia

252
Q

what are the only output element of cerebellum?

A

purkinje cells

253
Q

list symptoms of cerebellar dysfunction

A

slurring of speech (Staccato speech)

swallowing dificulties

clumsiness (arms/legs)

tremor

unsteadiness when walking

stumbles n falls

254
Q

what do u examine for cerebellar dysfunction

A 
gait
limb ataxia
eye movements
speech
sensory ataxia
255
Q

list some signs of cerebellar dysfunction

A

nystagmus (other abnormalities of eye movements)

dysarthria

action tremor

truncal ataxia

limb ataxia

256
Q

what is mild ataxia?

A

mobilising independently or walking with 1 walking aid

257
Q

what is severe ataxia?

A

predominantly wheelchair dependent

258
Q

what is moderate ataxia?

A

mobilising with 2 walking aids/walking frame

259
Q

how can ataxias be classified?

A

congenital

diseases where ataxia is 1 of many features

familial ataxias (presumed genetic) - AD & AR

sproadic (acquired) ataxias

260
Q

what are some history clues to classify ataxia

A

congenital vs early onset s late

rate of progression

episodic

pure ataxia or ataxia + sensory symptoms/leg stiffness/deafness etc

speech affected early

urinary, postural, nocturnal symptoms

261
Q

what are some investigations for ataxia

A

MRI will exclude:

  • post circ stroke
  • tumours
  • MS

etc

262
Q

what is the commonest genetic ataxia?

A

Friedrichs ataxia (FA)

can cause CV issues

263
Q

name some vaccine preventable neurological cond

A

polio
tetanus
measles
tuberculosis

264
Q

define epidemiology

A

study of the distribution/determinants of health-related states/events in specified pops; and the application of this study to control health problems

265
Q

define migraine (3)

A

unilateral pain distribution

premonitory visual disturbance

presence of nausea or vomiting

266
Q

what is MS

A

multiple areas of demyelination in brain/SC

267
Q

what does myasthenia mean?

A

muscle weakness

268
Q

what do myasthenia gravis patients have?

A

antibodies against nicotinic acetyl choline receptors

269
Q

what is the history of myasthenia gravis like?

A

fluctuating ocular weakness

bulbar (speech n swallow)

limb smyptoms

fatigability

SOB

270
Q

what do u see in a myasthenia gravis exam?

A

complex ophthalmoplegia: ask look to RHS - left eye should adduct

ptosis (drooping of the upper eyelid)

head drop

limb fatiguability

271
Q

if a patient has complex ophthalmoplegia … what 3 cones do u think?

A

myasthenia gravis

thyroid eye disease - graves’ disease

mitochondrial disorders

272
Q

what is opthalmoplegia

A

paralysis of the muscles within or surrounding the eye

273
Q

what is the ice pack test?

A

if pt has drooping of upper eyelid (ptosis)

put ice pack for 2ish mins

if the eyelid improves - + test

probs myasthenia gravis !

274
Q

what is complete ptosis?

A

when eyelid covers pupil

275
Q

what imaging do u do on a newly diagnosed MG patient

A

CT thorax

276
Q

what investigations do u do for myasthenia gravis?

A

antibodies - AchR

EMG - repetitive stimulation

277
Q

myasthenia gravis patients can also have issues w what?

A

thyroid !!!!!!!!

278
Q

treatment of myasthenia gravis

A

AChE inhibitors

immunosuppressants - prednisolone (SE: Htn, weight gain, glucose intolerance)

steroids

279
Q

what is a positive safety culture

A

staff have constant n active awareness of potential for things to go wrong

  • open n fair culture - encourages ppl to speak up abt mistakes
  • shared values n resp
280
Q

how can a headache be classified?

A

primary

secondary

painful cranial neuropathies, other face pains and other headaches

281
Q

what comes under primary headaches?

A

migraine

cluster

tension type

282
Q

what comes under secondary headaches?

A

meningitis

subarachnoid haemorrhage

idiopathic

intracranial

Htn medication overuse

283
Q

what are some reasons for further referral/investigation?

A

thunderclap headache ?SAH

seizure n new headache

suspected meningitis

suspected encephalitis

red eye ?acute glaucma

284
Q

what do u look at in a headache history?

A

types/number

time - onset/duration/why not/freq n pattern

pain - severity/quality/site

triggers - aggravating factors/relieving/FHx

285
Q

what are red flags in a headache exam?

A

fever

altered consciousness

neck stiffness

focal neuro signs

BP

286
Q

what is migraine?

A

episodic migraine with or without an aura

287
Q

what is the criteria for a migraine disorder?

A

a) 5 attacks fulfilling B-D
b) attacks last 4-72h

c) 2 of:
- unilateral
- pulsing
- moderate/severe
- aggravation by routine physical activity

d) during headache at least 1 of:
1) nausea and/or vomiting
2) photophobia and phonotobia

3) not attributed to another disorder

288
Q

what are some principles of migraine treatment?

A

accurate diagnosis, manage expectations

lifestyle modification, trigger management

pharmacological treatments

psych/behavioural treatments

surgical treatments

289
Q

what medication can you use for migraine?

A

oral triptan and and NSAID/paracetamol

290
Q

headache with

  • pyraxial
  • photophobia
  • neck stiffness + pyrexia
  • rash

diagnosis??

A

treat for meningitis bc suspected

bloods
blood cultures
HIV test
CXR
CT head
CSF
291
Q

what is a subarachnoid haemorrhage like ?

A

thunderclap headache

  • max severity within seconds
  • “worse” ever
292
Q

what do u do if SA haemorrhage suspected

A

CT

angiography

293
Q

how do u manage a subarachnoid haemorrhage?

A

resuscitation

nimodipine (Ca channel blocker)

early intervention to prevent re-bleeding (radiologically/surgically)

monitor for complications

294
Q

what is a raised ICP headache like

A

worse on waking

worse when coughing, sneezing, straining

postural, worse when lying down

nausea, vomiting

295
Q

what are some risk factors for idiopathic intracranial Htn

A

obesity

drugs eg tetracycline

296
Q

how long does a chronic daily headache last?

A

≥ 15 days per month

297
Q

should the WHO analgesic ladder be applied to headache management?

A

NO

codeine is not a long term treatment option

298
Q

the cognitive, psych, and behavioural sequelae of CNS disorders depends upon: (4)

A
  1. tempo of underlying disorder
  2. brain region it affects
  3. neurotransmitter systems it involves
  4. individual characteristics, such as age/sex/psychosocial background
299
Q

what are acute pathologies caused by

A

trauma

metabolic issues

drugs/infections

300
Q

what is an example of a chronic pathology?

A

dementia

301
Q

RH stroke can give rise to what?

A

mania

302
Q

orbitofrontal cortex is associated with what?

A

disinhibited behaviour

303
Q

what is anterograde amnesia?

A

unable learn new info

304
Q

what is retrograde amnesia?

A

unable to recall events from recent past

305
Q

what does an ACA stroke result in?

A

leg weakness

sensory disturbance in legs

gait apraxia

incontinence

drowsiness

306
Q

what does a MCA stroke result in?

A

contralateral arm and leg weakness

contralateral sensory loss

hemianopia

aphasia

dysphasia

307
Q

what happens with a PCA stroke?

A

contralateral homonymous hemianopia

cortical blindness

visual agnosia

prosopagnosia

308
Q

how is stroke risk managed?

A

platelet treatments (aspirin/clopidogrel)

cholesterol treatments (statins)

AF treatments (warfarin)

antihypertensives

309
Q

list 5 things that happen with an ACA territory stroke

A

leg weakness

sensory disturbance in legs

gait apraxia

incontinence

drowsiness

310
Q

list 6 things that happen with a MCA stroke

A

contralateral arm/leg weakness

contralateral sensory loss

hemianopia

aphasia

dysphasia

facial droop

311
Q

list 5 things that happen with a PCA stroke

A

contralateral homonymous hemianopia

cortical blindness - bilateral involvement of occipital lobe branches

visual agnosia

prosopagnosia (can’t recognise familiar faces)

312
Q

what is agnosia?

A

inability to interpret sensations and hence to recognize things

313
Q

what happens in visual agnosia?

A

can see

but

can’t interpret visual info

314
Q

what is prosopagnosia

A

can’t recognise familiar faces

315
Q

what is thrombolysis

A

the dissolution of a blood clot

316
Q

what is a treatment for AF

A

warfarin

(SG) Phase 2A lectures (14 decks)

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