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Nervous System > Nervous System Diseases > Flashcards

Nervous System Diseases Flashcards

1
Q

how is hydrocephalus classified?

A
  • communicating hydrocephalus

- non-communicating hydrocephalus

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2
Q

what is the pathology behind hydrocephalus?

A

excess CSF in ventricles

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3
Q

what is the difference between communicating and non-communicating hydrocephalus?

A

communicating - CSF pathway not affected

non-communicating - obstruction of the CSF pathway

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4
Q

what are the physiological processes behind production and absorption of CSF in the brain?

A

production: Na-K ATP-ase activity
absorption: pressure gradient between CSF and venous pressure

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5
Q

where is CSF produced?

A

in choroid plexus of ventricles

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6
Q

where is CSF reabsorbed from subarachnoid space into the venous sinuses?

A

at arachnoid villi protruding into the sinuses

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7
Q

where is CSF drained from the ventricles to the subarachnoid space?

A

through foramina at 4th ventricle

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8
Q

what are the names of the foramina in the 4th ventricle through which CSF drains into the subarachnoid space?

A

Laterally: foramen Lushka (x2)
Medially: foramen Magendie (x1)

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9
Q

what is usually the pathology behind communicating hydrocephalus?

A

impairment of CSF resorption

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10
Q

what are the common causes of communicating hydrocephalus?

A
  • infection (eg meningitis)
  • subarachnoid haemorrhage
  • post-operative
  • post-trauma
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11
Q

what is a common sign of hydrocephalus in young children? what is the reason for this?

A

enlarged head and failure to thrive - cranial sutures haven’t fused yet, so enlarged ventricles expand the skull

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12
Q

what are common symptoms of hydrocephalus in older children and adults?

A

raised ICP symptoms:

  • nausea and vomiting
  • headache
  • papilloedema
  • visual disturbance/upgaze difficulty
  • balance problems
  • cranial nerve palsy
  • drowsiness
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13
Q

what is the pathology behind non-communicating hydrocephalus?

A

obstruction of CSF pathway

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14
Q

what are common causes of non-communicating hydrocephalus?

A
  • acqueductal stenosis (most common!)
  • tumours
  • cysts
  • infection
  • haemorrhage
  • congenital abnormalities
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15
Q

what is the imaging investigation and immediate treatment for acute hydrocephalus?

A

imaging: CT head

immediate intervention: external ventricular drain (EVD) - to drain excess CSF

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16
Q

what is the gold standard treatment for communicating hydrocephalus?

A

shunt - normally ventriculo-peritoneal

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17
Q

what disadvantages are associated with shunts used to treat hydrocephalus?

A
  • high failure rate after 1 year
  • disconnection/occlusion
  • under/overdrainage
  • migration
  • infection
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18
Q

what are treatment options in non-communicating hydrocephalus, other than shunting?

A
  • surgical removal of obstruction

- 3rd ventriculostomy

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19
Q

what is among the first symptoms a patient will experience if their hydrocephalus-treating shunt fails?

A

headache

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20
Q

what measures are used to diagnose hydrocephalus on radiological imaging?

A
  • ventricular index (>50%)

- Evans ratio (>30%)

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21
Q

how is normal pressure hydrocephalus treated?

A

by using a programmable ventriculo-peritoneal shunt to control the drainage of CSF

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22
Q

what is normal pressure hydrocephalus commonly misdiagnosed as?

A

dementia/Alzheimer’s

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23
Q

what is the symptom triad for normal pressure hydrocephalus?

A

Wet - urinary incontinence
Wobbly - gait and balance difficulty
Wacky - fast progressive dementia

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24
Q

which symptoms of normal pressure hydrocephalus are more or less likely to improve once the hydrocephalus is treated?

A

likely to improve: incontinence, memory and gait

less likely to improve: dementia

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25
Q

what is likely to happen to a patient’s symptoms if they have normal pressure hydrocephalus and they receive a lumbar puncture?

A

their symptoms improve

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26
Q

why is normal pressure hydrocephalus important?

A

because it may be the reason for a patient presenting with dementia - can be reversed if treated early

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27
Q

what are the indications for a lumbar puncture?

A

diagnostic: meningitis, meningoencephalitis, cancer, neurological disease, inflammation, subarachnoid haemorrhage, idiopathic ICP
- therapeutic: contrast, intrathecal chemotherapy

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28
Q

what are the contraindications for a lumbar puncture?

A
  • raised ICP
  • suspicion of intracranial mass
  • patient cardiovascular/respiratory unstable
  • skin infection over area to puncture
  • clotting abnormality
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29
Q

why should a lumbar puncture not be carried out on a patient with raised ICP because of a lesion?

A

because the change in pressure from the puncture could cause coning of the cerebellar tonsils

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30
Q

what are the two positions a patient can be in for a lumbar puncture to be carried out? in which cases is each position used?

A
  • decubitus position (most patients)

- sitting position (obese and infants)

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31
Q

which position used for a lumbar puncture also allows to measure the ICP of the CSF? what is the tool used to do this?

A

decubitus position (by using manometer)

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32
Q

at which level should a lumbar puncture be carried out and why?

A

between L3/4 or L4/5 - because that sits sufficiently below the conus medullaris

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33
Q

what layers does a lumbar puncture needle pierce before entering the dural space?

A
  • skin
  • subcutaneous tissue
  • supraspinous ligament
  • interspinous ligament
  • ligamentum flavum
  • dura mater
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34
Q

what piece of equipment should always be attached to the needle when piercing the interspace and coming out of it again during a lumbar puncture?

A

the stylet

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35
Q

why should the bevel of the needle be parallel to the fibres in the cauda equina?

A

so that the fibers are separated rather than cut through

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36
Q

after a lumbar puncture, three samples are sent to labs to test what?

A
  • culture/gram stain
  • glucose/proteins
  • cell count
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37
Q

what are possible complications of a lumbar puncture?

A
  • headache
  • back pain
  • bleeding from site or into dural space
  • nerve damage/irritation
  • transient abducens palsy
  • coning
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38
Q

what are the indications for a paramedian approach in a lumbar puncture?

A

if there is fibrosis in interspace due to previous LP’s, or to avoid site of previous lumbar surgery

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39
Q

why is there less incidence of spinal headache with a paramedian approach to a lumbar puncture?

A

because the needle goes through the erector spinae muscles - CSF can’t leak through the muscle, and the holes made by the needle don’t overlap because of the angle of insertion

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40
Q

what position should patients adopt during a lumbar puncture and why?

A

ideally decubitus position with back flexed - maximise space between spinous processes of vertebrae

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41
Q

what is the purpose of a blood patch in lumbar punctures?

A

it stops leakage of CSF into the epidural space following a lumbar puncture

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42
Q

what are solutions to spinal headaches after lumbar punctures?

A
  • lying flat
  • consuming caffeine/IV caffeine
  • hydration
  • blood patch
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43
Q

what immediate steps should be taken if a patient experiences coning following a lumbar puncture?

A 
remove needle immediately
raise backrest to 45 degrees
give mannitol/3% saline
intubate/hyperventilate
get urgent neurosurgery consultation
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44
Q

what is a common cause of an epidermal inclusion cyst after a lumbar puncture?

A

the use of a needle without a stylet

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45
Q

what steps should be taken if a lumbar puncture fails?

A

ask someone else to try

guided LP with use of USS, CT or fluoroscopy

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46
Q

how can a spinal headache from a lumbar puncture be avoided?

A
  • using smaller diameter needles
  • always using the stylet
  • ensuring bevel of needle is parallel to nerve roots
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47
Q

What are the three main causes of localised cerebrovascular disease?

A
  1. Atheroma/thrombosis
  2. Thromboembolism
  3. Haemorrhage
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48
Q

What are the three factors contributing to cerebrovascular disease? What are they called collectively?

A

Virchow’s Triad:

  • changes in blood vessel wall
  • changes in blood flow/pressure
  • changes in blood components
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49
Q

What is the pathological presentation of an ischaemic stroke on a brain specimen?

A

Wedge shaped lesion in area supplied by blocked artery

Tissue loss, yellow discolouration, cyst formation

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50
Q

How does a haemorrhagic stroke cause ischaemia?

A

Distal ischaemia - causes by spasm of ruptured artery in attempt to stop bleeding. Protective mechanism

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51
Q

What are the most common regions in the brain for haemorrhagic strokes to occur?

A
  • basal ganglia, around internal capsule

- circle of Willis, berry aneurysms

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52
Q

what are three common presentations of syncope?

A
  • cardiogenic (MI, arrhythmia)
  • reflex (vasovagal reaction)
  • orthostatic (hypotension, endocrine)
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53
Q

with which type of seizure are tongue biting at tip or lateral side of tongue associated respectively?

A

tip - syncopal seizure

lateral side - epileptic seizure

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54
Q

what are the two main criteria for diagnosing epilepsy?

A
  • at least 2 seizures more than 24hrs apart

- one seizure with high risk of recurrence

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55
Q

what are the two main classifications of seizures?

A

generalised and partial seizures

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56
Q

what do absent seizures, myoclonic seizures and tonic/clonic seizures have in common?

A

they are all generalised seizures

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57
Q

in which age group are absent seizures common?

A

in children

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58
Q

list some of the signs of a tonic/clonic seizure

A 
groaning sounds
stiff limbs followed by jerking
foaming at mouth
eyes open/rolling back
drowsy/no recollection afterwards
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59
Q

list some risk factors for seizures

A 
sleep deprivation/fatigue
drug and alcohol use
stress/anxiety
hormone changes
missed medications
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60
Q

what is status epilepticus?

A

one continuous seizure or multiple seizures with no recovery time, lasting >30mins

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61
Q

how is status epilepticus treated?

A

benzodiazepines + phenytoin/sodium valproate

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62
Q

what is the mortality of status epilepticus due to?

A

normally due to underlying condition (eg stroke, tumour, trauma)

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63
Q

what is the first line treatment for partial seizures, generalised seizures and status epilepticus respectively?

A

partial seizures - carbamazepine
generalised seizures - sodium valproate
status epilepticus - benzodiazepines

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64
Q

what are DVLA regulations for epilepsy in case of one-off seizures and diagnosed epilepsy?

A

one-off seizure - no driving for 6 months

epileptic patients - after seizure no driving for 1 year, HGV drivers no driving for 10 years

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65
Q

what are some of the reversible causes for dementia-like symptoms?

A

b12 deficiency
thyrotoxicosis
HIV
tertiary syphilis

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66
Q

is frontotemporal dementia normally early or late onset?

A

early onset

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67
Q

list some common forms of dementia

A

Alzheimer’s
vascular dementia
Lewy body dementia
frontotemporal dementia

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68
Q

what is the pathogenesis behind vascular dementia?

A

multiple very small strokes

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69
Q

what are common features of Alzheimer’s?

A

loss of skills, speech, memory, executive decision making, visuo-temporal impairment

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70
Q

what drugs can help to relieve Alzheimer’s symptoms?

A 
acetylcholinesterase inhibitors (rivastigmine)
glutamate inhibitors (memantine)
antipsychotics
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71
Q

list some of the differences between frontotemporal and temporoparietal dementia

A
  • frontotemporal dementia has earlier loss of personality compared to temporoparietal
  • frontotemporal retains visuo-spatial awareness until late disease, temporoparietal loses it sooner
  • frontotemporal has earlier speech/auditory impairment compared to temporoparietal
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72
Q

what is the pathology behind alzheimer’s disease?

A 
beta amyloid build up
tau protein build up
neurofibrillary tangles
brain tissue shrinkage
enlarged ventricles
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73
Q

what is the pathology behind parkinson’s disease?

A

dopaminergic cell loss in substantia nigra

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74
Q

what are the common symptoms of parkinson’s disease?

A

TRAP - tremor, rigidity, akinesia/bradykinesia, postural instability
urinary frequency/retention

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75
Q

list some complications of parkinson’s disease

A

depression
dementia
bowel/bladder problems
speech impediments

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76
Q

name some features of parkinsonian gait

A

shuffling
hunched over
arm swing absent
head down

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77
Q

list some of the drug treatments used in parkinson’s

A

levodopa (+ COMT/MAO-B inhibitors)
carboxylase inhibitors - carbidopa, madopar
dopamine agonists

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78
Q

if a dementia has fast progression, what underlying cause should be considered?

A

Creutzfeld-Jakob Disease

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79
Q

what is the characteristic of vascular parkinsonianism?

A

only lower half of body affected

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80
Q

name some of the possible aetiologies and risk factors of multiple sclerosis

A 
EBV
vitamin D deficiency/temperate climate
genetics (HLA)
autoimmune (MBP)
female
early 20's
caucasian
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81
Q

name some investigations carried out to diagnose MS

A

MRI scan
lumbar puncture - oligoclonal IgG bands
bloods - look for infection or other inflammatory cause
visual evoked potentials

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82
Q

what are the three management principles for MS

A
  • treat symptoms
  • manage relapses
  • disease modifying treatments
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83
Q

name some common presentations of MS

A

optic neuritis
limb weakness
sensory disturbance
ataxia/diplopia/vertigo

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84
Q

how is neuromyelitis optica treated?

A

with immunosuppression

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85
Q

what is the variant of MS which immunosuppressed patients are more at risk of developing?

A

progressive multifocal leukencelopathy

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86
Q

what are the three main causes of ischaemia in the brain?

A
  • atheroma/thrombosis
  • thromboembolus
  • ruptured aneurysm
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87
Q

in a brain specimen, what would an ischemic stroke caused by thrombosis look like?

A

wedge shaped area, soft and later cystic

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88
Q

name the common point of origin of an thromboembolus causing an ischemic stroke, and where in the brain it’s most likely to end up

A

origin: left atrium

often gets stuck in middle cerebral artery

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89
Q

a wedge shaped area of soft and cystic brain tissue is indicative of what?

A

ischaemic stroke

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90
Q

which two types of ischaemic stroke are likely to cause a wedge shaped area of neuronal damage?

A

thromboembolic

thrombotic

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91
Q

what is the most common cause of a haemorrhagic stroke?

A

rupture of aneurysm

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92
Q

what causes the hypoxia in haemorrhagic strokes?

A

distal vasospasm of ruptured artery in attempt to stem bleeding

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93
Q

name two common areas in the brain where aneurysms are found, and what kind of aneurysms are likely to form there

A

circle of willis - berry aneurysms

basal ganglia - microaneurysms

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94
Q

through which three mechanisms could generalised ischaemia in the brain occur?

A
  • reduced oxygen in blood
  • reduced blood flow
  • reduced ability to use O2 in cells
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95
Q

name a few common causes of generalised ischaemia in the brain

A

cardiac arrest
respiratory arrest
hypotension
haemorrhage

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96
Q

what are watershed zones in the brain, and what causes ischaemia in those areas?

A

junctions between areas of brain tissue supplied by different arteries
ischaemia at these junctions is caused by generalised hypotension, causing adequate perfusion in main arteries but less in peripheral arteries

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97
Q

what type of ischaemia pattern is visible in the brain, when the cause of ischaemia is a generalised lack of perfusion?

A

cortical necrosis

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98
Q

what is cortical necrosis in the brain often due to?

A

generalised hypoxia/lack of perfusion

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99
Q

an epidural haematoma is most likely caused by rupture of what?

A

middle meningeal artery

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100
Q

a subdural haematoma is most likely caused by rupture of what?

A

bridging veins

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101
Q

a subarachnoid haemorrhage is most likely caused by rupture of what?

A

aneurysm (berry or microaneurysm)

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102
Q

haemorrhagic and ischaemic strokes are better visualised which which imaging techniques respectively?

A

haemorrhagic - CT scan

ischaemic - MRI scan

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4
5
Perfectly
103
Q

during a stroke, the area of brain affected by ischaemia is divided in two zones. what are they called?

A

ischaemic core

ischaemic penumbra

104
Q

what is the radiological appearance of an epidural haematoma?

A

lens shaped

105
Q

what is the radiological appearance of a subdural haematoma?

A

crescent shaped

106
Q

what is small vessel lipohyalinosis, what causes it and what can it lead to?

A

it’s thickening and narrowing of small arteries in the brain

it’s often caused by hypertension, and can lead to lacunar strokes

107
Q

what is a stroke of the anterior cerebral artery likely to affect?

A

lower limbs - motor and sensory input

gait

108
Q

what is a stroke of the middle cerebral artery likely to affect?

A

face, arm and leg paralysis/sensation
speech affected - aphasia
vision affected - homonymous hemianopia, gaze paralysis to opposite side
sensation affected - one-sided neglect

109
Q

what is a stroke in the posterior cerebral artery likely to affect?

A

vision
balance
breathing/HR control

110
Q

name the arteries that supply the basal ganglia, and what artery they are branches of

A

lenticulostriate arteries, branches of MCA

111
Q

name some contraindications to using thrombolysis for stroke treatment

A

> 3hrs since onset
any cause of potential bleeding
high blood pressure
glucose too low or too high

112
Q

what are the two main treatments for acute ischaemic stroke?

A
  • tPa (thrombolysis)

- thrombectomy

113
Q

what percentage of TIA patients go on to have a larger stroke within 2 weeks?

A

10%

114
Q

name the common investigations carried out to confirm stroke diagnosis

A

bloods
ECG
CT scan
carotid doppler ultrasound

115
Q

name two common causes for young onset ischaemic stroke

A

arterial dissection
cardioembolic
arteriovenous malformation

116
Q

what are the signs of an upper motor neuron lesion?

A 
muscle weakness
increased reflexes
increased tone
muscle wasting (only if lack of use)
positive Babinski sign
117
Q

what are the signs of a lower motor neuron lesion?

A

decreased reflexes
decreased tone
muscle weakness
fasciculations

118
Q

name some common surgical causes of myelopathy

A

tumour
vascular abnormalities
trauma
degenerative spine disorders

119
Q

name some common medical causes of myelopathy

A

spinal cord stroke
demyelination
inflammation
B12 deficiency

120
Q

what is the area of the spinal cord most vulnerable to spinal cord strokes, and why?

A

thoracic spinal cord

because it’s in a watershed zone between two joining blood supply regions

121
Q

which spinal artery is most commonly affected in a spinal cord stroke?

A

anterior spinal artery

122
Q

name some symptoms of a spinal cord stroke

A 
onset over hours
back pain
increasing limb weakness
increasing sensory loss
urinary retention/incontinence
123
Q

name some of the causes of a spinal cord stroke

A 
atherosclerosis
thromboembolism
vasculitis/inflammation
hypotension
venous occlusion
hypercoagulability
124
Q

how is a spinal cord stroke treated?

A

same as a normal stroke: address risk factors, anticoagulate, thrombolysis

125
Q

define Brown-Sequard syndrome

A

myelopathy that only affects one half of the spinal cord

126
Q

which imaging technique is normally used to diagnose a spinal cord lesion?

A

MRI scan

127
Q

what kind of lesion does MS related spinal cord myelopathy often present as?

A

transverse myelitis

128
Q

what is the treatment for myelopathy caused by B12 deficiency?

A

intramuscular B12 injection

129
Q

where is the junction between the UMN and LMN?

A

when the fibres from the descending tract synapse with a second neuron

130
Q

define myelopathy

A

injury to spinal cord due to compression causing UMN deficits

131
Q

define radiculopathy

A

injury to spinal nerve root causing dermatome and myotome LMN deficits

132
Q

what is the management of a disc prolapse?

A

discectomy

rehabilitation

133
Q

what are is the classic symptom triad of Cauda Equina Syndrome?

A
  • saddle anesthesia
  • bilateral sciatica
  • urinary problems
134
Q

how is Cauda Equina Syndrome diagnosed?

A 
clinical diagnosis
radiological diagnosis (MRI)
135
Q

what is the management of Cauda Equina Syndrome?

A

emergency discectomy

136
Q

where are the majority of cord-compressing tumours located?

A

intradural/extramedullary

extradural

137
Q

what is the triad of symptoms to help diagnose a spinal abscess?

A
  • pyrexia
  • focal symptoms
  • back pain
138
Q

name two types of degenerative conditions which may require surgery for myelopathy or radiculopathy

A

cervical spondylosis

spinal stenosis

139
Q

what characterises lumbar spinal stenosis?

A

bilateral claudication

140
Q

how is a spinal abscess managed?

A
  • decompression

- antibiotics

141
Q

how is a spinal abscess diagnosed?

A

urgent MRI

142
Q

list some risk factors which may contribute to spinal infections

A
  • immunocompromised
  • diabetes
  • CKD
  • alcoholism
143
Q

name three common causes of myelopathy that require surgery, with examples of each type

A

infection - osteomyelitis, spinal abscess
degenerative - disc prolapse, spondylosis, stenosis
tumour - intra/extradural, intramedullary

144
Q

how is lumbar spinal stenosis treated if it’s causing neurological symptoms?

A

surgical laminectomy

145
Q

how is cervical spondylosis treated if it’s causing neurological symptoms?

A

conservative if mild, decompression surgery if severe

146
Q

how are spinal tumours investigated and treated if causing neurological symptoms?

A

urgent MRI

surgical decompression and radiotherapy

147
Q

name three common organisms to cause epidural spinal abscesses

A

E coli
staph aureus
streptococci

148
Q

what is a common cause of oculomotor (CNIII) palsy and why?

A

diabetes, microvascular changes affect nerve function

149
Q

how is trigeminal neuralgia treated?

A

with carbamazepine or surgery

150
Q

how is Bell’s palsy treated? what is an important consideration in terms of the eyes?

A

with steroids

give eye drops as palsy causes inability to close eye, drying it out and risking damage

151
Q

what causes Horner’s syndrome?

A

damage to sympathetic nerves to the face

152
Q

list the three main symptoms of Horner’s syndrome

A

ptosis
constricted pupil (miosis)
lack of sweating (anhydrosis)

153
Q

describe the main presentation of CNIII (oculomotor) palsy

A

unilateral dilated pupil
impaired adduction of affected eye - “down and out” gaze
ptosis

154
Q

describe the main presentation of CNVI (abducens) palsy

A

impaired abduction of affected eye

155
Q

what is a common disorder affecting CNV (trigeminal), what can cause it and how is it treated?

A

trigeminal neuralgia
can be caused by nerve compression by an artery
treated with carbamazepine

156
Q

what disease presents when the facial nerve (CNVII) be affected? how is it treated?

A

Bell’s palsy

treated with steroids

157
Q

how can a patient’s ability to lift their eyebrows determine whether they have an UMN or LMN lesion?

A

UMN - forehead spared

LMN - unilateral forehead paralysis

158
Q

what happens as a result of inflammation to the vestibular nerve?

A

labyrinthitis/vestibular neuritis

159
Q

what does bulbar refer to?

A

anything related to the medulla

160
Q

what is bulbar palsy?

A

damage to LMN in medulla related to CNVIII, CNIX, CNX and CNXI

161
Q

what is pseudobulbar palsy?

A

bilateral damage to UMN coming from the cortex

162
Q

name some symptoms which can occur in bulbar and pseudobulbar palsy

A

dysarthria
dysphagia
dysphonia

163
Q

what signs are found in bulbar but not pseudobulbar palsy? why is that?

A

tongue fasciculations
tongue wasting
LMN lesion signs, fasciculations and wasting not present in UMN lesions

164
Q

which cranial nerves are affected in bulbar palsy?

A

CNIX (glossopharyngeal), CNX (vagus), CNXII (hypoglossal)

165
Q

in general terms, what does a cranial nerve palsy present with?

A

impaired function of that nerve

166
Q

name a common disorder affecting the optic nerve (CNII) and what disease it’s associated with

A

optic neuritis, commonly affects patients with multiple sclerosis

167
Q

name a few causes of dilated pupils

A 
young age
dark lighting
amphetamines
anxiety
CNIII palsy
coma
168
Q

name a few causes of narrowed pupils

A

old age
bright light
opiates
Horner’s syndrome

169
Q

where is the cause of the problem likely to be if CNIII, CNIV and CNVI are all affected?

A

superior orbital fissure

170
Q

how can a subarachnoid haemorrhage lead to communicating hydrocephalus?

A

breakdown blood products can block the arachnoid granulations into the venous sinuses

171
Q

what are two commonest organisms causing meningitis?

A 
strep pneumoniae (pneumococcus)
neisseria meningitidis (meningococcus)
172
Q

what is the first line treatment for meningitis?

A

ceftriaxone

173
Q

list some features of meningitis

A 
meningism (photophobia, stiff neck)
fever
headache
seizures
raised ICP
focal symptoms
cranial nerve palsy
174
Q

what investigations are done to diagnose meningitis?

A

bloods
blood cultures
lumbar puncture: CSF culture (bacterial) and PCR (viral)

175
Q

which viral organisms may be involved in meningitis?

A

enteroviruses

176
Q

what is the most common organism causing encephalitis?

A

HSV virus

177
Q

what is the treatment of viral encephalitis?

A

aciclovir

178
Q

name some organisms which may be involved in encephalitis

A

HSV
enteroviruses
arboviruses

179
Q

which receptors are affected in auto-immune encephalitis?

A

NMDA receptors

VGKC receptors

180
Q

list some common features of encephalitis

A 
preceding flu symptoms
headache
seizures
focal signs
raised ICP
181
Q

list the investigations done to diagnose encephalitis

A 
bloods
blood cultures
LP: CSF cultures (bacterial) and PCR (viral)
CT/MRI
EEG
182
Q

what investigations are done for brain abscesses?

A

bloods
LP
CT/MRI
aspirate biopsy

183
Q

how is a brain abscess/empyema treated?

A

drainage

antibiotics - penicillin/ceftriaxone/metronidazole

184
Q

what is the aetiology of Guillain-Barre syndrome?

A

post-infectious neuropathy - autoimmune reaction to neurons a few weeks after an infection

185
Q

does Guillain-Barre syndrome present with ascending or descending paralysis?

A

ascending paralysis

186
Q

does botulism present with ascending or descending paralysis?

A

descending paralysis

187
Q

when should botulism be suspected?

A

IVDA
dilated pupils
descending paralysis

188
Q

how are diseases like polio, rabies, tetanus and botulism treated?

A

vaccination
antibodies
antibiotics

189
Q

how does tetanus present, and why?

A

presents with rigidity and spasticity, due to blockage of NMJ

190
Q

how does botulism present, and why?

A

presents with flaccid paralysis, stops ACh release at NMJ

191
Q

how is neurosyphilis treated?

A

with penicillin

192
Q

how is lyme disease treated?

A

with ceftriaxone and doxicycline

193
Q

what organism is responsible for syphilis?

A

treponema pallidum

194
Q

what organism is responsible for lyme disease?

A

borrelia burgdorferi

195
Q

what organism is responsible for leptospirosis?

A

leptospira interrogans

196
Q

what class of bacteria do the organisms causing lyme disease and syphilis belong to?

A

spirochaetes

197
Q

what is a common sign found on imaging in patients with variant CJD?

A

pulvinar sign

198
Q

what causes CJD?

A

prions (eg misfolded proteins) causing other proteins to misfold

199
Q

when should CJD be borne in mind as a differential?

A

when a patient presents with rapidly progressing dementia

200
Q

what investigations are done for CJD?

A

bloods
LP - CSF culture/PCR
MRI
EEG

201
Q

name a few possible types of CJD

A

sporadic CJD
familiar CJD
variant CJD

202
Q

neurotropic infections from which organisms are more likely to present in immunocompromised patients?

A 
toxoplasmosis gandii
cryptococcus neoformans
cytomegalovirus
aseptic meningitis/encephalitis
progressive multifocal leukoencelopathy (PML)
cerebral abscess
203
Q

list a few types of skull fracture

A 
linear fracture
depressed fracture
mosaic fracture
ring fracture
basal skull fracture
204
Q

which types of brain haemorrhage are not associated with skull fractures?

A

subdural hematoma

subarachnoid hematoma

205
Q

in subarachnoid, subdural and epidural haemorrhages, which vessels are most likely affected?

A

subarachnoid - circle of Willis (berry aneurysms)
subdural - bridging veins
epidural - middle meningeal artery

206
Q

why is it important to perform a head CT after an event which may have caused head trauma, even if the patient feels fine?

A

because the patient might be experiencing a lucid interval, before the haemorrage builds up and causes raised ICP

207
Q

how does a patient present who has diffuse axonal injury (DAI)?

A

usually comatose

208
Q

explain the term “one punch killer”

A

it’s the term for punches which cause the head to suddenly swing upwards, causing a laceration of the vertebral artery and resulting in a traumatic basal subarachnoid haemorrhage

209
Q

what is a contre-coup brain contusion?

A

damage to the brain surface caused by trauma to the opposite side of the brain

210
Q

what is normally responsible for scalp lacerations vs incise injuries?

A

laceration injury - often blunt force trauma

incise injury - normally sharp object eg knife

211
Q

what is the physiological activity in vegetative state?

A

brainstem recovery post injury, but no recovery from cortex

212
Q

what can cause “locked-in” syndrome, and what does it result in?

A

stroke in pons

causes all nerve activity below CNIII to cease, so no motor or sensory activity

213
Q

what GCS score counts as comatose?

A

GCS 8 or less

214
Q

what needs to be looked for specifically when someone presents with a coma, to work out a possible differential?

A
  • meningism

- focal symptoms/lateralising

215
Q

if a comatose patient presents with no meningism or focal symptoms/lateralising, what are some of the likely causes?

A

hypoxia/hypercapnia
metabolic causes
alcohol/drug intoxication
hypo/hyperthermia

216
Q

if a comatose patient presents with meningism but no focal symptoms/lateralising, what are the likely causes?

A

meningitis
encephalitis
subarachnoid haemorrhage

217
Q

if a comatose patient presents with focal symptoms and lateralising to one side (with or without meningism), what are the likely causes?

A

stroke (haemorrhage or infarct)
tumour
cerebral abscess

218
Q

how is brainstem function assessed in comatose patients?

A

cranial nerve reflexes

219
Q

name a few examples of metabolic causes which may result in a coma

A 
hypoglycaemia
diabetic ketoacidosis
hepatic failure
renal failure
sepsis
220
Q

what is the system called that determines being awake?

A

ascending reticular activating system

221
Q

name the three initial neurological assessments carried out if someone presents in a coma

A

GCS
brainstem function
motor function and reflexes

222
Q

which muscle disease can present with a rash, an what type of condition is it?

A

dermatomyositis - an inflammatory muscle condition

223
Q

how are inflammatory muscle conditions investigated?

A

bloods: CK, ESR, AST, LDH levels
electromyography
serology for autoantibodies
muscle biopsy

224
Q

how are inflammatory muscle conditions treated?

A

with steroids/immunosuppression

225
Q

name two examples of similar NMJ diseases and explain the difference between them

A

myasthenia gravis

lambert-eaton syndrome

226
Q

what is the pathophysiology behind myasthenia gravis and lambert-eaton syndrome?

A

myasthenia gravis - ACh antibodies blocking post-synaptic ACh receptors
lambert-eaton syndrome - Calcium channel antibodies blocking vesicle exocytosis from pre-synaptic terminal

227
Q

how does myasthenia gravis present?

A 
fatiguability - symptoms worse as day goes on
ptosis
lid lag
diplopia
slurred speech
swallowing problems
respiratory problems
muscle weakness
228
Q

how can lambert-eaton syndrome be differentiated from myasthenia gravis in terms of symptoms?

A

in lambert-eaton syndrome, symptoms improve after exercise

in myasthenia gravis, symptoms get worse throughout the day

229
Q

how are NMJ disorders investigated?

A

serology - autoantibodies
bloods - CK, AST, LDH
muscle biopsy
EMG

230
Q

what imaging test is always done in myasthenia gravis, and why?

A

CT chest to look for thymus abnormalities - can cause myasthenia gravis-like symptoms

231
Q

what structural abnormality is associated with myasthenia gravis?

A

thymus hyperplasia or thymoma

232
Q

how is myasthenia gravis treated?

A 
acetylcholinesterase inhibitors (pyridostigmine)
immunosuppression
immunoglobulins
plasmapheresis
thymectomy
233
Q

name the types of nerve fibres found in a peripheral nerve

A 
motor fibres
sensory fibres (pain/temp and touch/pressure./vibration)
autonomic fibres (symp and parasymp)
234
Q

list a few common causes of peripheral neuropathy

A

diabetes
alcohol
drugs
inflammatory (guillain-barre syndrome)

235
Q

what are the two most common pathophysiological processes behind peripheral neuropathy?

A

axonal damage

demyelination

236
Q

list some investigations that are done for nerve diseases

A 
bloods
genetic testing
nerve conduction tests
nerve biopsy
lumbar puncture
237
Q

what characterises motor neuron disease symptoms?

A

they have both UMN and LMN features

238
Q

list some features of motor neuron disease

A 
weakness
increased reflexes
increased tone
fasciculations
muscle wasting
239
Q

in which order are motor neurons often affected in motor neurone disease?

A

limbs first
bulbar next
respiratory last

240
Q

how is MND investigated?

A

examination - UMN and LMN signs
nerve conduction studies
genetic testing

241
Q

how is MND treated?

A

supportive and palliative care

242
Q

list some of the types of brain herniation which can occur

A 
cingulate
central
uncal
transcalvarial
cerebellotonsillar
243
Q

name two common symptoms/signs found in raised intracranial pressure due to a tumour

A

morning headache + vomiting

papilloedema

244
Q

name a common malignant brain tumour in children

A

medulloblastoma

245
Q

why are all glial brain tumours classed as malignant?

A

because they can cause significant damage even if slow growing

246
Q

what is an unusual characteristic of malignant gliomas?

A

they can’t metastasise outside CNS despite aggressiveness, because they can’t cross BBB

247
Q

where are the majority of brain tumours found in adults and children?

A

adults - cerebrum

children - cerebellum and brainstem

248
Q

are meningiomas slow or fast growing?

A

slow growing

249
Q

name a few common tumours which metastasise in the brain

A 
breast
lung
melanoma
renal
colorectal
250
Q

what is an acoustic neuroma?

A

shwannoma of CNVIII (vestibulocochlear)

251
Q

why are CNS lymphomas difficult to biopsy?

A

because they often sit in a deep central area of the brain

252
Q

list some presenting symptoms of brain tumours

A 
morning headache
nausea and vomiting
vision problems
drowsiness
reduced conscious level
seizures
focal symptoms
253
Q

list some presenting signs of brain tumours

A 
papilloedema
CNIII and CNVI palsy
reduced GCS
altered consciousness
focal signs
254
Q

what investigations should be done if a brain tumour is suspected

A

identify lesion: CT/MRI scan
find out if primary or met: chest/abdo or pelvic XR
characterise lesion: biopsy

255
Q

what are the management options for brain tumours?

A

treat symptoms: mannitol, steroids, antiemetics, anticonvulsants

surgery: remove tumour or debulk
medical: radiotherapy/chemotherapy

256
Q

what drugs are sometimes used to alleviate cluster headaches?

A

with the use of triptans

257
Q

how is paroxysmal hemicrania treated?

A

with indomethacin

Nervous System (3 decks)

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