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Special senses > Neurology > Flashcards

Neurology Flashcards

1
Q

two types of stroke

A

Ischaemia or infarction of the brain tissue secondary to a disrupted blood supply (ischaemic stroke)
Intracranial haemorrhage, with bleeding in or around the brain (haemorrhagic stroke)

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2
Q

blood supply disrupted by 4 possible things

A

thrombus/embolus
atherosclerosis
shock
vasculitis

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3
Q

TIA definition
why different from stroke

A

temporary neurological dysfunction (lasting less than 24 hours) caused by ischaemia but without infarction. Symptoms have a rapid onset and often resolve before the patient is seen. TIAs may precede a stroke.

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4
Q

crescendo TIA’s define

A

2 or more TIA’s within a week…high risk of stroke

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5
Q

clinical fx of stroke

A

sudden onset
asymmetrical
Limb weakness
Facial weakness
Dysphasia (speech disturbance)
Visual field defects
Sensory loss
Ataxia and vertigo (posterior circulation infarction)

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6
Q

risk factors for stroke

A

Previous stroke or TIA
Atrial fibrillation
Carotid artery stenosis
Hypertension
Diabetes
Raised cholesterol
Family history
Smoking
Obesity
Vasculitis
Thrombophilia
Combined contraceptive pill

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7
Q

increased risk of stroke with COCP

A

migraines with aura
smoker >34 yrs
hx of stroke/TIA

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8
Q

how assess possible stroke in community

A

FAST

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9
Q

what tool in secondary care risk of stroke

A

based on clinical fx and duration
ROSIER (recognition of stroke in the emergency room)

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10
Q

mx TIA

A

Aspirin 300mg daily (started immediately)
Referral for specialist assessment within 24 hours (within 7 days if more than 7 days since the episode)
Diffusion-weighted MRI scan

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11
Q

initial management of stroke

A

Exclude hypoglycaemia
Immediate CT brain to exclude haemorrhage
Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
Admission to a specialist stroke centre

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12
Q

what type of stoke must be excluded first

A

haemorrhagic

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13
Q

once haemorrhage excluded what next

A

thrombolysis with alteplase
thrombectomy is considered if confirmed blockage in proximal ant circ or proximal posterior circ…can be done alongside thrombolysis

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14
Q

blood pressure tx
haemorrhagic v ischaemic stroke

A

haemorrhagic - aggressively tx
ischaemic - lowering can worsen ischaemia, only tx in hypertensive emergency or to reduce risks in thrombolysis

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15
Q

possible underlying cause/risk fx of stroke

A

afib
cartoid artery stenosis

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16
Q

how assessed for underlying causes of stroke

A

carotid imaging
ECG

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17
Q

secondary prevention of stroke

A

clopidogrel
atorvastatin
BP and DM control
modifiable risk fx

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18
Q

4 types of IC haemorrhage

A

Extradural haemorrhage (bleeding between the skull and dura mater)
Subdural haemorrhage (bleeding between the dura mater and arachnoid mater)
Intracerebral haemorrhage (bleeding into brain tissue)
Subarachnoid haemorrhage (bleeding in the subarachnoid space)

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19
Q

risk factors for IC haemorrhage

A

Head injuries
Hypertension
Aneurysms
Ischaemic strokes (progressing to bleeding)
Brain tumours
Thrombocytopenia (low platelets)
Bleeding disorders (e.g., haemophilia)
Anticoagulant

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20
Q

clinical fx of IC haemorrhage

A

sudden onset headache
seizures
vomit
reduced GCS
focal neurological sx (weakness)

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21
Q

extradural haemorrhage
which artery
associations
on scan
sx

A

-middle meningeal in temporparietal region
- fracture of temporal bone
- CT - biconvex shape, do not cross cranial sutures
- period of improved neuro sx and consciousness follow by rapid decline over hrs

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22
Q

subdural haemorrhage
- vein
- imaging
- clinical fx

A
  • rupture of bridging vein
  • ct - crescent shape, cross sutures
  • elderly and alcoholics - more atrophy make vessels more prone to rupture
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23
Q

intracerebral haemorrhage
- clinical fx
- cause

A
  • sudden onset neuro sx - limb, facial weakness, dysphagia or vision loss
  • spontaenous, secondary to ischaemic stroke, tumour or aneurysm rupture
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24
Q

location of intracerebral haemorrhage

A

Lobar intracerebral haemorrhage
Deep intracerebral haemorrhage
Intraventricular haemorrhage
Basal ganglia haemorrhage
Cerebellar haemorrhage

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25
Q

subarachnoid
- cause
- hx

A

ruptures cerebral aneurysm
sudden onset occipital headache during strenuous activity, thunderclap

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26
Q

IC haemorrhage inv

A

CT head
blood - FBC and coag sceen

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27
Q

IC haemorrhage mx

A

Admission to a specialist stroke centre
Discuss with a specialist neurosurgical centre to consider surgical treatment
Consider intubation, ventilation and intensive care if they have reduced consciousness
Correct any clotting abnormality (e.g., platelet transfusions or vitamin K for warfarin)
Correct severe hypertension but avoid hypotension

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28
Q

surgical options indicated fo

A

extradural or subdural

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29
Q

what are surgical options

A

craniotomy
burr holes

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30
Q

more common in SAH

A

45-70
woman
black

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31
Q

risk factors SAH

A

HTN
smoking
excess alcohol

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32
Q

SAH associations

A

Family history
Cocaine use
Sickle cell anaemia
Connective tissue disorders (e.g., Marfan syndrome or Ehlers-Danlos syndrome)
Neurofibromatosis
Autosomal dominant polycystic kidney disease

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33
Q

clinical fx SAH

A

sudden onset occipital headache - thunderclap
Neck stiffness
Photophobia
Vomiting
Neurological symptoms (e.g., visual changes, dysphasia, focal weakness, seizures and reduced consciousness)

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34
Q

SAH investigations

A

CT head (if normal does not exclude SAH)
if normal - LP 12 hrs after sx to allow bilirubin to accumulate…raised RBC, xanthochromia (caused by billirubin)
CT angiography - locate source

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35
Q

CAH mx

A

Intubation and ventilation
surgery for aneurysms ….endovascular coiling or neurosurgical clipping

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36
Q

complication of SAH and how tx

A

Vasospasm…resulting in brain ischaemia…tx with nimodipine
hydrocephalus - LP, external ventricular drain, VP shunt
seizures - anti drugs

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37
Q

MS definition

A

autoimmune condition involving demyelination in the central nervous system. The immune system attacks the myelin sheath of the myelinated neurones.

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38
Q

MS age and sex

A

<50
women

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39
Q

oligodendrocytes

A

CNS

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40
Q

scHwann cells

A

PNS

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41
Q

MS affect what

A

CNS

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42
Q

patho MS attack

A

there are often other demyelinating lesions throughout the central nervous system, most of which are not causing symptoms

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43
Q

early disease v later patho MS

A

re-myelination can occur, and the symptoms can resolve. In the later stages of the disease, re-myelination is incomplete, and the symptoms gradually become more permanent.

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44
Q

characteristic fx of MS

A

sx vary as lesions vary in location

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45
Q

causes of MS

A

Multiple genes
Epstein–Barr virus (EBV)
Low vitamin D
Smoking
Obesity

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46
Q

onset MS

A

progress over more than 24 hrs
sx last days to week at first presentation and then improve

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47
Q

most common presentation of MS

A

optic neuritis - demyelination of optic nerve
unilateral reduced vision over hrs to days
Central scotoma (an enlarged central blind spot)
Pain with eye movement
Impaired colour vision
Relative afferent pupillary defect (pupil constricts more in contralateral eye than in affected eye)
direct reflex redcued response and normal consensual

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48
Q

other causes of optic neuritis

A

Sarcoidosis
Systemic lupus erythematosus
Syphilis
Measles or mumps
Neuromyelitis optica
Lyme disease

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49
Q

optic neuritis mx

A

urgent opthal input
high dose steroids

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50
Q

possible eye movement abnormalities MS

A

diplopia
nystagmus
oscillopsia (environment moving)
internuclear opthalmoplegia
conjugate lateral gaze disorder

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51
Q

internuclear opthalmoplegia

A

caused by a lesion in the medial longitudinal fasciculus. The nerve fibres of the medial longitudinal fasciculus connect the cranial nerve nuclei (“internuclear”) that control eye movements (the 3rd, 4th and 6th cranial nerve nuclei). These fibres are responsible for coordinating the eye movements to ensure the eyes move together. It causes impaired adduction on the same side as the lesion (the ipsilateral eye) and nystagmus in the contralateral abducting eye.

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52
Q

conjugate lateral gaze disorder

A

lesion in abducens
Conjugate means connected. Lateral gaze is where both eyes move to look laterally to the left or right. When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct. For example, in a lesion involving the left eye, when looking to the left, the right eye will adduct (move towards the nose), and the left eye will remain in the middle

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53
Q

MS focal neurological signs

A

Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis
Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign

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54
Q

Lhermitte’s sign

A

an electric shock sensation that travels down the spine and into the limbs when flexing the neck. It indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column.

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55
Q

ataxia MS
types

A

sensory or cerebellar

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56
Q

sensory ataxia

A

loss of proprioception
positive romberg’s test
caused by lesion in dorsal column

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57
Q

cerebellar ataxia cause

A

cerebellar lesion

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58
Q

disease patterns of MS

A

clinically isolated syndrome - the first episode of demyelination and neurological signs and symptoms. Patients with clinically isolated syndrome may never have another episode or may go on to develop MS. Lesions on an MRI scan suggest they are more likely to progress to MS.
relapsing-remitting - most common, episodes followed by recovery. different areas. further classified (active, not active, worsening, not worsening)
secondary progressive - was relapsing remitting but not progressive
primary progressive - worsening disease from point of disease without remissions

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59
Q

diagnosis MS

A

neurologist
clinical fx
MRI - lesions
LP - oligoclonal bands in CSF

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60
Q

mx of MS

A

MDT
disease modifying therapies
relapses with steroids
exercise
fatigue tx xwith amantadine, modafinil
neuropathic pain tx
depression tx
urge incontinence tx
spasitisity tx with baclofen
oscillopsia tx with gabapentin

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61
Q

MND definition

A

encompasses variety of specific diseases affecting motor nerves
no sensory sx

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62
Q

types of MND

A

Amyotrophic lateral sclerosis
progressive bulbar palsy
progressive muscular atrophy
primary lateral sclerosis

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63
Q

MND patho

A

Motor neurone disease involves a progressive degeneration of both the upper and lower motor neurones. The sensory neurones are spared.

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64
Q

increased risk MND

A

many genes - family hx
smoking
exposure to heavy metals and pesticides
generally 60 yr old man

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65
Q

clinical fx MND

A

There is an insidious, progressive weakness of the muscles throughout the body, affecting the limbs, trunk, face and speech
increased fatigue
clumsiness
slurred speech (dysarthria)

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66
Q

signs of LMND

A

Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes

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67
Q

signs of UMND

A

Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex

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68
Q

mx of MND

A

riluzole can slow progression
NIV
mdt
Baclofen for spasticity
antimuscarinic for saliva
benzo to help anxiety
advanced directive and end of life care

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69
Q

cause of death MND

A

resp failure or pneumonia

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70
Q

parkinsons classical triad

A

Resting tremor (a tremor that is worse at rest)
Rigidity (resisting passive movement)
Bradykinesia (slowness of movement)

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71
Q

parkinsons patho

A

progressive reduction in dopamine in basal ganglia…disorders of movement

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72
Q

clinical fx parkinsons

A

tremor worse on one side, 4-6 Hz frequency, pill rolling, resting, worse when distracted, performing task with other hand exaggerates tremor
rigidity - when passive flex and extend arms…results in jerks called cogwheel rigidity
bradykinesia - micrographia, shuffling gait, festinating gait, difficulty initiating movement and turning around, hypomimia
depression
insomnia
anosmia
postural instability
cognitive impairment

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73
Q

parkinsons v essential tremor

A

Parkinson’s Tremor

Benign Essential Tremor

Asymmetrical

Symmetrical

4-6 hertz

6-12 hertz

Worse at rest

Improves at rest

Improves with intentional movement

Worse with intentional movement

Other Parkinson’s features

No other Parkinson’s features

No change with alcohol

Improves with alcohol

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74
Q

parkinson’s-plus syndromes

A

multiple system atrophy - neurones of various systems in brain degenerate…including basal ganglia = parkinsons
dementia with lewy bodies
progressive supranuclear palsy
corticobasal degeneration

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75
Q

parkinson’s diagnosis

A

diagnostic criteria
specialist

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76
Q

parkinson’s mx

A

levodopa (combined with peripheral decarboxylase inhibitors)
COMT inhibitors
dopamine agonist
MAO B inhibitors
or combination drugs such as co-careldopa

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77
Q

main s/e of levodopa and how tx

A

dyskinesia - dystonia, chorea, athetosis
tx with amantadine

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78
Q

dopamine agonists
examples
s/e

A

bromocriptine
pergolide
cabergoline
pulmonary fibrosis

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79
Q

benign essential tremor define

A

a relatively common condition associated with older age. It is characterised by a fine tremor affecting all the voluntary muscles. It is most notable in the hands but can affect other areas, for example, causing a head tremor, jaw tremor and vocal tremor.

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80
Q

clinical fx of benign essential tremor

A

Fine tremor (6-12 Hz)
Symmetrical
More prominent with voluntary movement
Worse when tired, stressed or after caffeine
Improved by alcohol
Absent during sleep

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81
Q

ddx of tremor

A

Parkinson’s disease
Multiple sclerosis
Huntington’s chorea
Hyperthyroidism
Fever
Dopamine antagonists (e.g., antipsychotics)

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82
Q

mx of benign tremor

A

not treated, harmless
sx management - propranolol, primidone

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83
Q

more common types of seizures in adult

A

Generalised tonic-clonic seizures
Partial seizures (or focal seizures)
Myoclonic seizures
Tonic seizures
Atonic seizures

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84
Q

more common types of seizures in children

A

Absence seizures
Infantile spasms
Febrile convulsions

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85
Q

generalised tonic clonic seizures fx

A

tonic (tense) and clonic (jerk)
complete loss of consciousness
AKA grand mal
before might experience aura
tongue biting, incontinence, groaning and irregular breathing
post-ictal period

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86
Q

partial/focal seizures fx

A

isolated brain area -> temporal lobe usually
affect hearing, speech, memory and emotions. Patients remain awake during partial seizures. They remain aware during simple partial seizures but lose awareness during complex partial seizures
Déjà vu
Strange smells, tastes, sight or sound sensations
Unusual emotions
Abnormal behaviours

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87
Q

myoclonic seizures fx

A

sudden, brief muscle contractions
remain awake
can occur as part of juvenile myoclonic epilepsy

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88
Q

tonic seizures fx

A

a sudden onset of increased muscle tone, where the entire body stiffens. This results in a fall if the patient is standing, usually backwards. They last only a few seconds, or at most a few minutes.

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89
Q

atonic seizures fx

A

sudden loss of muscle tone…fall
only brief and pt aware
often begin in childhood
associated with lennox-gastaut syndrome

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90
Q

absence seizures fx

A

usually children
blank, stare into space, abruptly returns to normal, unaware, last 10-20 secs

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91
Q

infantile spasms fx

A

AKA west syndrome
rare
6mths of age
cluster of full body spasms
hypsarrhythmia on EEG
developmental regression and poor prognosis
tx with ACTH and vigabatrin

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92
Q

febrile convulsions fx

A

tonic clonic
during high feve
6 mths to 5 yrs
not usually any damage
increase risk of developing epilepsy

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93
Q

ddx seizures

A

Vasovagal syncope (fainting)
Pseudoseizures (non-epileptic attacks)
Cardiac syncope (e.g., arrhythmias or structural heart disease)
Hypoglycaemia
Hemiplegic migraine
Transient ischaemic attack

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94
Q

investigations seizure

A

EEG
MRI brain
ECG, serum electrolytes, blood glucose, blood culture/urine/LP

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95
Q

seizures mx

A

inform DVLA
taking showers than baths
caution with heights, swimming and dangeous equiptment

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96
Q

generalised tonic clonic medical mx

A

men/no children - sodium valp
women who can have children - lamotrigine or levetiracetam

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97
Q

partial medical mx

A

lamotrigine or levetiracetam

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98
Q

myoclonic medical mx

A

men - sod valporate
women - levetiracetam

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99
Q

tonic and atonic medical mx

A

men - sod valporate
women - lamotrigene

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100
Q

absence medical mx

A

ethosuximide

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101
Q

sodium valp
- mechanism
- s/e
- risk

A

increasing the activity of gamma-aminobutyric acid (GABA), which has a calming effect on the brain.

Teratogenic (harmful in pregnancy)
Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility

neural tube defects/developmental delay…Valproate Pregnancy Prevention Programme

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102
Q

status epilepticus definition

A

A seizure lasting more than 5 minutes
Multiple seizures without regaining consciousness in the interim

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103
Q

initial mx of status epilepticus

A

A-E
secure airway
high flow o2
check blood glucose
IV access
benzo repeat after 5-10 mins, then try IV levetiracetam/phenytoin/sod valporate, then general anaesthesia

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104
Q

benzo doses and route

A

Buccal midazolam (10mg)
Rectal diazepam (10mg)
Intravenous lorazepam (4mg)

105
Q

define pain

A

“An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage”

106
Q

acute v chronic pain

A

chronic = >3 or more months

107
Q

basic physiology of pain

A

sensory - from pain receptor
affective - unpleasant emotional reaction to pain
pain is subjective
pain threshold - the point at which sensory input is reported as painful
allodynia - when pain is experienced with sensory inputs that do not normally cause pain (e.g., light touch).
Pain tolerance is different to pain threshold. It is more difficult to define and generally refers to a person’s response to pain. One person may experience pain but think little of it and carry on with their activities as usual.

108
Q

how feel pain?

A

Nociceptors at ends of nerves detect damage or potential damage to tissues -> nerve signals transmitted along afferent nerves->spinal cord
Afferent sensory nerves that transmit pain signals are part of the peripheral nervous system and are called primary afferent nociceptors
Nerve fibres transmit pain to CNS , up CNS (mainly spinothalamic tract and spinoreticular tract) to brain where it is interpreted as pain, mainly in thalamus and cortex

109
Q

which fibres transmit pain
- speed and type of pain

A

C fibres (unmyelinated and small diameter) – transmit signals slowly and produce dull and diffuse pain sensations
A-delta fibres (myelinated and larger diameter) – transmit signals fast and produce sharp and localised pain sensations

110
Q

types of pain sensory inputs

A

Mechanical (e.g., pressure)
Heat
Chemical (e.g., prostaglandins)

111
Q

why feel referred pain

A

Nerves may share the innervation of multiple parts of the body (e.g., the heart and left arm)
Pain in one area amplifies the sensitivity in the spinal cord to signals coming from other areas
Activation of the sympathetic nervous system in response to pain results in pain in other areas

112
Q

neuropathic pain cause

A

caused by abnormal functioning or damage of the sensory nerves, resulting in pain signals being transmitted to the brain.

113
Q

ways to rate pain

A

Visual analogue scale
numerical rating scale
graphical rating scale

114
Q

analgesic ladder

A

Step 1: Non-opioid medications such as paracetamol and NSAIDs
Step 2: Weak opioids such as codeine and tramadol
Step 3: Strong opioids such as morphine, oxycodone, fentanyl and buprenorphine

115
Q

opioids in palliative care

A

Background opioids (e.g., 12-hourly modified-release oral morphine)
Rescue doses for breakthrough pain (e.g., immediate-release oral morphine solution)
The rescue dose is usually 1/6 of the background 24-hour dose

116
Q

oral morphine to IV/SC mophine

A

/2

117
Q

oral morphine to oral codeine

A

x10

118
Q

chronic pain two types

A

Chronic primary pain – where no underlying condition can adequately explain the pain
Chronic secondary pain – where an underlying condition can explain the pain (e.g., arthritis)

119
Q

options for mx of chronic pain

A

Supervised group exercise programs
Acceptance and commitment therapy (ACT)
Cognitive behavioural therapy (CBT)
Acupuncture
Antidepressants (e.g., amitriptyline, duloxetine or an SSRI)
avoid all form sof analegesia

120
Q

common causes of neuropathic pain

A

Post-herpetic neuralgia from shingles is in the distribution of a dermatome and usually on the trunk
Nerve damage from surgery
Multiple sclerosis
Diabetic neuralgia (typically affecting the feet)
Trigeminal neuralgia
Complex regional pain syndrome

121
Q

four first line tx for neuropathic pain

A

Amitriptyline – a tricyclic antidepressant
Duloxetine – an SNRI antidepressant
Gabapentin – an anticonvulsant
Pregabalin – an anticonvulsant

122
Q

1st line for trigeminal neuralgia

A

carbamezapine

123
Q

CRPS definition and clinical fx

A

areas of abnormal nerve functioning, causing neuropathic pain, abnormal sensations and skin changes. It is often triggered by an injury and isolated to one limb.

The area can become hypersensitive, with pain associated with normal sensations (allodynia). There may be intermittent swelling, colour changes, temperature changes, skin flushing and abnormal sweating.

124
Q

facial nerve palsy definition

A

isolated dysfunction of facial nerve…unilateral facial weakness

125
Q

facial nerve pathway

A

facial nerve exits the brainstem at the cerebellopontine angle. On its journey to the face, it passes through the temporal bone and parotid gland.

It then divides into five branches:

Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical

126
Q

functions of facial nerve
- motor
-sensory
- parasympathetic

A

Motor function for:

Facial expression
Stapedius in the inner ear
Posterior digastric, stylohyoid and platysma muscles

Sensory function for taste from the anterior 2/3 of the tongue.

Parasympathetic supply to the:

Submandibular and sublingual salivary glands
Lacrimal gland (stimulating tear production)

127
Q

2 types of facial nerve palsy

A

UMN and LMN facial nerve palsy

128
Q

difference between UMN and LMN facial nerve palsy

A

UMN - immediate mx as possible stroke, foreheard spared (innervation from both sides of brain)
LMN - less urgently mx, forehead not spared (innervation from one side of brain)

129
Q

upper motor neurone lesions types

A

unilateral
bilateral

130
Q

unilateral UMN lesions causes

A

stroke
tumour

131
Q

b/l UMN lesions causes

A

pseudobulbar palsies
MND

132
Q

bell’s palsy presentation

A

unilateral LMN facial nerve palsy

133
Q

bells palsy prognosis

A

fully recover mostly over several week…can take 12 mths
may have residual weakness

134
Q

bell’s palsy tx

A

prednisolone within 72 hrs of sx onset for 10 days
lubricating eye drops, taped at nite (risk of exposure keratopathy)

135
Q

ramsay hunt syndrome cause

A

varicella zoster virus

136
Q

ramsay hunt syndrome clinical fx

A

unilateral LMN facial nerve palsy
painful tender vesicular rash in ear canal, pinna and can extend to tongue and hard palate

137
Q

ramsay hunt syndrome tx

A

aciclovir and prednisolone
lubricating eye drops

138
Q

other causes of LMN facial nerve palsy

A

Infections:

Otitis media
Otitis externa
HIV
Lyme disease
Systemic diseases:

Diabetes
Sarcoidosis
Leukaemia
Multiple sclerosis
Guillain–Barré

Tumours:

Acoustic neuroma
Parotid tumour
Cholesteatoma

Trauma:

Direct nerve trauma
Surgery
Base of skull fractures

139
Q

presentation of brain tumours

A

can be asx
progressive focal neuro sx
raised ICP (intracranial HTN)…eg: change in personality frontal lobe tumour

140
Q

causes of ICP

A

Brain tumours
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscesses or infection

141
Q

concerning fx of headache indicate IC HTN

A

Constant headache
Nocturnal (occurring at night)
Worse on waking
Worse on coughing, straining or bending forward
Vomiting
Papilloedema on fundoscopy
Altered mental state - personality, mental state and memory
Visual field defects
Seizures (particularly partial seizures) - may have aura
Unilateral ptosis (drooping upper eyelid)
Third and sixth nerve palsies

142
Q

investigations raised ICP

A

non contrast CT usually (contrast if suspect tumour or haemorrhage, if renal function ok)
MRI with contrast
diffusion weighted MRI - different tumour

143
Q

how to describe space occupying lesion on MRI/CT

A

Particularly Interesting Surgeons Love Carefully Drilling Massive Burr Holes
Patient
Intra or extra axial - in brain parenchyma? Pituitary lesions are extra axial
location - supra or infratentorial, lobes
Density - hypo/hyper (how white)
Border - defined?, oedema
Contrast enhancement - homogenous/heterogenous
mass effect - effacement of sulci, midline shift, ventricle compression
hydrocephalus

144
Q

ddx for raised ICP/space occupying lesion

A

haemorrhage, infarct, vascular malformation, aneurysm
abscess
mets, primary brain tumour
cyst
MS, granulomatous disease

145
Q

why raised icp causes papilloedema

A

Papilloedema describes swelling of the optic disc secondary to raised intracranial pressure. Papill- refers to a small, rounded, raised area (the optic disc) and -oedema refers to the swelling.

The sheath around the optic nerve is connected with the subarachnoid space. The raised cerebrospinal fluid (CSF) pressure flows into the optic nerve sheath, increasing the pressure around the optic nerve behind the optic disc causing the optic disc to bulge forward.

146
Q

how papilloedema seen on fundoscopy

A

Blurring of the optic disc margin
Elevated optic disc (look for the way the retinal vessels flow across the disc to see the elevation)
Loss of venous pulsation
Engorged retinal veins
Haemorrhages around the optic disc
Paton’s lines, which are creases or folds in the retina around the optic disc

147
Q

gliomas definition

A

tumours of the glial cells in the brain or spinal cord. Glial cells surround and support the neurones. Glial cells include astrocytes, oligodendrocytes and ependymal cells.

148
Q

gliomas grade

A

1-4

149
Q

types of gliomas

A

Astrocytoma (the most common and aggressive form is glioblastoma)
Oligodendroglioma
Ependymoma

150
Q

meingiomas definition and how serious

A

tumours growing from the cells of the meninges. They are usually benign. However, they take up space, and this “mass effect” can lead to raised intracranial pressure and neurological symptoms

151
Q

cancers most often spreading to brain

A

Lung
Breast
Renal cell carcinoma
Melanoma

152
Q

pituitary tumours clinical fx

A

press on optic chiasm - bitemporal hemianopia
Acromegaly (excessive growth hormone)
Hyperprolactinaemia (excessive prolactin)
Cushing’s disease (excessive ACTH and cortisol)
Thyrotoxicosis (excessive TSH and thyroid hormone)

153
Q

management of pituiray tumours

A

Trans-sphenoidal surgery (through the nose and sphenoid bone)
Radiotherapy
Bromocriptine to block excess prolactin
Somatostatin analogues (e.g., octreotide) to block excess growth hormone

154
Q

acoustic neuroma definition

A

benign tumours of the Schwann cells that surround the auditory nerve (vestibulocochlear nerve) that innervates the inner ear. Schwann cells provide the myelin sheath around neurones of the peripheral nervous system.
AKA vestibular schwannomas
AKA cerebellopontine angle tumours

155
Q

bilateral acoustic neuromas associated

A

neurofibromatosis type 2

156
Q

acoustic neuromas clinical fx

A

40-60 year old presenting with a gradual onset of:

Unilateral sensorineural hearing loss (often the first symptom)
Unilateral tinnitus
Dizziness or imbalance
Sensation of fullness in the ear
Facial nerve palsy (if the tumour grows large enough to compress the facial nerve)

157
Q

acoustic neuroma mx

A

monitor
surgery to remove
radiotherapy

158
Q

1st line investigation for suspected brain tumour

A

MRI Brain
biopsy for histological diagnosis

159
Q

brain atumours mx options

A

surgery
chemo
radio
palliative

160
Q

huntington’s chorea inheriteance

A

aut dom

161
Q

huntington’s genetics

A

trinucleotide repeat disorder involving a genetic mutation in the HTT gene on chromosome 4, which codes for the huntingtin (HTT) protein.

162
Q

huntingtons age

A

30-50

163
Q

genetic anticipation

A

Anticipation is a feature of trinucleotide repeat disorders, where successive generations have more repeats in the gene, resulting in:

Earlier age of onset
Increased severity of disease

164
Q

presentation huntington’s

A

Chorea (involuntary, random, irregular and abnormal body movements)
Dystonia (abnormal muscle tone, leading to abnormal postures)
Rigidity (increased resistance to the passive movement of a joint)
Eye movement disorders
Dysarthria (speech difficulties)
Dysphagia (swallowing difficulties)

165
Q

huntington’s inv

A

genetic testing

166
Q

huntingtons mx

A

genetic counselling
MDT
physio to improve mobility, maintain joint function
SALT
Tetrabenazine - chorea sx
antidepressants
advanced directives

167
Q

prognosis huntington’s

A

progressive
life expectancy 10-20yrs after sx onset
death due to aspiration penumonia most commonly
suicide also

168
Q

myasthenia gravis definition

A

an autoimmune condition affecting the neuromuscular junction. It causes muscle weakness that progressively worsens with activity and improves with rest.

169
Q

myasthenia gravis sex and age

A

women <40
men >60

170
Q

myasthenia gravis link

A

thymomas

171
Q

myasthenia gravis patho

A

The axons release acetylcholine from the presynaptic membrane. Acetylcholine travels across the synapse and attaches to receptors on the postsynaptic membrane, simulating muscle contraction.
Acetylcholine receptor (AChR) antibodies are found in most patients with myasthenia gravis. These antibodies bind to the postsynaptic acetylcholine receptors, blocking them and preventing stimulation by acetylcholine. The more the receptors are used during muscle activity, the more they become blocked.
Antibodies also activate complement system within neuromuscular junction…cell damage at postsynaptic membrane

172
Q

other antibodies causing myasthenia gravis

A

Muscle-specific kinase (MuSK) antibodies
Low-density lipoprotein receptor-related protein 4 (LRP4) antibodies

173
Q

clinical fx of myasthenia gravis

A

vary
weakness worse with muscle use and improves with rest, sx best in morning…affect proximal limbs and small muscles of head and neck
Difficulty climbing stairs, standing from a seat or raising their hands above their head
Extraocular muscle weakness, causing double vision (diplopia)
Eyelid weakness, causing drooping of the eyelids (ptosis)
Weakness in facial movements
Difficulty with swallowing
Fatigue in the jaw when chewing
Slurred speech

174
Q

examinations myasthenia gravis

A

elicit fatigue - Repeated blinking will exacerbate ptosis
Prolonged upward gazing will exacerbate diplopia on further testing
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
- check for thymectomy scar
- test FVC

175
Q

investigations myasthenia gravis

A

antibody tests - AChR antibodies (around 85%)
MuSK antibodies (less than 10%)
LRP4 antibodies (less than 5%)
CT/MRI of thymus
edrophonium test (reduce breakdown of Ach…temporarily relieves weakness)

176
Q

tx myasthenia gravis

A

Pyridostigmine is a cholinesterase inhibitor that prolongs the action of acetylcholine and improves symptoms
Immunosuppression (e.g., prednisolone or azathioprine) suppresses the production of antibodies
Thymectomy
rituximab

177
Q

myasthenic crisis
- what
- triggers
-clinical fx
- tx

A

potentially life-threatening complication of myasthenia gravis. It causes an acute worsening of symptoms, often triggered by another illness, such as a respiratory tract infection. Respiratory muscle weakness can lead to respiratory failure. Patients may require non-invasive ventilation or mechanical ventilation.

Treatment is with IV immunoglobulins and plasmapheresis.

178
Q

lambert eaton myasthenic syndrome definition

A

an autoimmune condition affecting the neuromuscular junction, similar to myasthenia gravis. The symptoms tend to be more insidious and less pronounced than myasthenia gravis

179
Q

lambert eaten myasthenic syndrome associations

A

paraneoplastic syndrome - SCLC

180
Q

LEMS patho

A

results from antibodies against voltage-gated calcium channels. These antibodies may be produced in response to small-cell lung cancer (SCLC) cells that express voltage-gated calcium channels. They target and damage voltage-gated calcium channels in the presynaptic membrane of the neuromuscular junction. responsible for release of ach into synapse…attaches to post synpatic membrane..less ach release so weaker muscle contraction

181
Q

presenting fx LEMS

A

proximal muscle wekaness
dry mouth
blurred vision
impotence
dizziness
reduced or absent tendon reflexes

182
Q

how presenting fx different to myasthenia gravis

A

improves after periods of muscle contraction

183
Q

LEMS mx

A

exclude underlying malignancy
Amifampridine - block VG K channels in pre synaptic membrnae…prolongs depolarisation of cell membrane and assists calcium to carry out their action
other options - pyridostigmine, immunosuppressants, IV IG, plasmapheresis

184
Q

charcot marie tooth disease definition

A

an inherited disease that affects the peripheral motor and sensory neurones. It is also known as hereditary motor and sensory neuropathy. There are various types, with different genetic mutations and pathophysiology, causing myelin or axon dysfunction

185
Q

CMT disease inheritance

A

aut dom

186
Q

CMT age

A

before age of 10 but can be until 40 or later

187
Q

classical fx CMT disease

A

High foot arches (pes cavus)
Distal muscle wasting causing “inverted champagne bottle legs”
Lower leg weakness, particularly loss of ankle dorsiflexion (with a high stepping gait due to foot drop)
Weakness in the hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

188
Q

other causes of peripheral neuropathy

A

A – Alcohol
B – B12 deficiency
C – Cancer (e.g., myeloma) and Chronic kidney disease
D – Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
E – Every vasculitis

189
Q

mx of CMT disease

A

progressive
Neurologists and geneticists to make the diagnosis
Physiotherapists to maintain muscle strength and joint range of motion
Occupational therapists to assist with activities of living
Podiatrists to help with foot symptoms and suggest insoles and other orthoses to improve symptoms
Analgesia for neuropathic pain (e.g., amitriptyline)
Orthopaedic surgeons for severe joint deformities

190
Q

definition GB syndrome

A

an acute paralytic polyneuropathy that affects the peripheral nervous system. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms.

191
Q

GB syndrome triggered

A

Campylobacter jejuni, cytomegalovirus (CMV) and Epstein-Barr virus (EBV).

192
Q

GB syndrome patho

A

caused by molecular mimicry. B cells create antibodies against antigens on pathogen. these antibodies can also target proteins on the myelin sheath or the nerve axon itself

193
Q

presentation of GB syndrome

A

sx begin within 4 weeks of triggering infection…begin in feet and progress upwards
peak within 2-4 wks
recovery period lasts mths to yrs
- symmetrical ascending weakness
- reduced reflexes
- peripheral loss of sensation or neuropathic pain
- may cause facial weakness
- can lead to urinary retention, ileus or heart arrythmias

194
Q

diagnosis GB syndrome

A

brighton criteria supported by investigations - nerve conduction studies, LP (raised protein)

195
Q

mx GB syndrome

A

Supportive care
VTE prophylaxis (pulmonary embolism is a leading cause of death)
IV immunoglobulins (IVIG) first-line
Plasmapheresis is an alternative to IVIG
intubation and ventilation

196
Q

prognosis GB syndrome

A

mths to yrs
can continue regaining function up to 5 yrs…usually full recovery, some have signifcant disability
mortality low but due to resp or CVS complications

197
Q

neurofibromatosis definition

A

a genetic condition that causes nerve tumours (neuromas) to develop throughout the nervous system. These tumours are benign but can cause neurological and structural problems.
2 types but 1 is most common

198
Q

neurofibromatosis type 1 gene

A

found on chromosome 17
codes for a protein called neurofibromin, which is a tumour suppressor protein.

199
Q

neurofibromatosis inheritance

A

aut dom

200
Q

diagnostic criteria of neurofibromatosis type 1

A

CRABBING pneumonic:
C – Café-au-lait spots (more than 15mm diameter is significant in adults)
R – Relative with NF1
A – Axillary or inguinal freckling
BB – Bony dysplasia, such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules), which are yellow-brown spots on the iris
N – Neurofibromas
G – Glioma of the optic pathway

201
Q

skin neurofibromas

A

skin coloured raised nodules or papules with a smooth, regular surgace. two or more of these are significant
plexiform neurofibroma - a larger, irregular complex neurofibroma, a single one is significant

202
Q

neurofibromatosis mx

A

no tx
monitor and mx sx and complications

203
Q

complications of neurofibrotomasis

A

Migraines
Epilepsy
Renal artery stenosis, causing hypertension
Learning disability
Behavioural problems (e.g., ADHD)
Scoliosis of the spine
Vision loss (secondary to optic nerve gliomas)
Malignant peripheral nerve sheath tumours!!!!!
Gastrointestinal stromal tumour (a type of sarcoma)!!!!
Brain tumours
Spinal cord tumours with associated neurology (e.g., paraplegia)
Increased risk of cancer (e.g., breast cancer and leukaemia)

204
Q

neurofibromatosis type 2 genetics

A

gene is found on chromosome 22. It codes for a protein called merlin, a tumour suppressor protein important in Schwann cells. Schwann cells provide the myelin sheath that surrounds neurones of the peripheral nervous system. Mutations in this gene lead to schwannomas (benign tumours of the Schwann cells). Inheritance is also autosomal dominant.

205
Q

neurofibromatosis type 2 associations

A

bilateral acoustic neuromas

206
Q

tuberous sclerosis inheritance

A

aut dom

207
Q

characteristic fx of tuberous sclerosis

A

hamartomas - benign tissue growths, affecting
Skin
Brain
Lungs
Heart
Kidneys
Eyes

208
Q

tuberous sclerosis mutation in

A

TSC1 gene on chromosome 9, which codes for hamartin
TSC2 gene on chromosome 16, which codes for tuberin
…interact with each other to control size and growth of cells

209
Q

skin fx tuberous sclerosis

A

Ash leaf spots (depigmented areas of skin shaped like an ash leaf)
Shagreen patches (thickened, dimpled, pigmented patches of skin)
Angiofibromas (small skin-coloured or pigmented papules that occur over the nose and cheeks)
Ungual fibromas (circular painless lumps that slowly grow from the nail bed and displace the nail)
Cafe-au-lait spots (light brown “coffee and milk” coloured flat pigmented lesions on the skin)
Poliosis (an isolated patch of white hair on the head, eyebrows, eyelashes or beard)

210
Q

neurological fx of tuberous sclerosis

A

epilepsy
learning disabilities
brain tumours

211
Q

multi system fx of tuberous sclerosis

A

Rhabdomyomas in the heart
Angiomyolipoma in the kidneys
Lymphangioleiomyomatosis in the lungs
Subependymal giant cell astrocytoma in the brain
Retinal hamartomas in the eyes

212
Q

tuberous sclerosis mx

A

no tx
supportive
tx complications - epilepsy
mTOR inhibitors (everolmus or sirolimus) - suppress growth of brain, lung or kidney tumours

213
Q

causes of headaches

A

Tension headaches
Migraines
Cluster headaches
Secondary headaches
Sinusitis
Giant cell arteritis
Glaucoma
Intracranial haemorrhage
Venous sinus thrombosis
Subarachnoid haemorrhage
Medication overuse
Hormonal headache
Cervical spondylosis
Carbon monoxide poisoning
Trigeminal neuralgia
Raised intracranial pressure
Brain tumours
Meningitis
Encephalitis
Brain abscess
Pre-eclampsia

214
Q

red flag sx of headaches

A

Fever, photophobia or neck stiffness (meningitis, encephalitis or brain abscess)
New neurological symptoms (haemorrhage or tumours)
Visual disturbance (giant cell arteritis, glaucoma or tumours)
Sudden-onset occipital headache (subarachnoid haemorrhage)
Worse on coughing or straining (raised intracranial pressure)
Postural, worse on standing, lying or bending over (raised intracranial pressure)
Vomiting (raised intracranial pressure or carbon monoxide poisoning)
History of trauma (intracranial haemorrhage)
History of cancer (brain metastasis)
Pregnancy (pre-eclampsia)

215
Q

tension headaches
- sx
- cause
-mx

A

mild ache or band like restriction
resolve gradually
depression, stress, alcohol, skipping meals, dehydration
reassurance and analgesia
if frequent or recurrent = amitriptyline

216
Q

secondary headaches
- presentation
- cause

A

similar to tension
causes include Infections (e.g., viral upper respiratory tract infection)
Obstructive sleep apnoea
Pre-eclampsia
Head injury
Carbon monoxide poisoning

217
Q

sinusitis
- clinical fx
- cause
- tx

A

pain and pressure following recent URTI, tenderness on palpation
>10 days tx with steroid nasal spray or phenoxymethylpenicillin

218
Q

medication overuse headache

A

non specific fx
withdrawal of analgesia

219
Q

hormonal headaches
- cause
- clinical fx
- when
- tx

A

low oestrogen
unilateral, pulsatile, nausea
Two days before and the first three days of the menstrual period
In the perimenopausal period
Early pregnancy (headaches in the second half of pregnancy should prompt investigations for pre-eclampsia)
tx with triptans and nsaids

220
Q

cervical spondylosis
- cause
- clinical fx

A

degenerative changes in spine
neck pain, worse on movement, headache

221
Q

trigeminal neuralgia
- fx
- associations
- tx

A

intense facial pain in distribution of trigeminal nerve
unilateral usually
suddenly and lasts secs to hts, shooting/burning, triggered by touch or eating
MS
carbamazepine

222
Q

migraines more common in

A

women
teenagers/young adults

223
Q

4 types of migraine

A

Migraine without aura
Migraine with aura
Silent migraine (migraine with aura but without a headache)
Hemiplegic migraine

224
Q

5 stages of migraine

A

Premonitory or prodromal stage (can begin several days before the headache)
Aura (lasting up to 60 minutes)
Headache stage (lasts 4 to 72 hours)
Resolution stage (the headache may fade away or be relieved abruptly by vomiting or sleeping)
Postdromal or recovery phase

225
Q

typical fx of migraine

A

last 4-72 hrs
Usually unilateral but can be bilateral
Moderate-severe intensity
Pounding or throbbing in nature
Photophobia (discomfort with lights)
Phonophobia (discomfort with loud noises)
Osmophobia (discomfort with strong smells)
Aura (visual changes)
Nausea and vomiting

226
Q

what is aura

A

Sparks in the vision
Blurred vision
Lines across the vision
Loss of visual fields (e.g., scotoma)
Sensation changes may include tingling or numbness. Language symptoms include dysphasia (difficulty speaking).

227
Q

sx of hemiplegic migraine

A

hemiplegia
ataxia
impaired consciousness
…must exclude tia/stroke

228
Q

familial hemiplegic migraine

A

aut dom

229
Q

triggers of migraines

A

Stress
Bright lights
Strong smells
Certain foods (e.g., chocolate, cheese and caffeine)
Dehydration
Menstruation
Disrupted sleep
Trauma

230
Q

migraine tx

A

dark room, sleep
NSAIDS
paracetamol
triptans
antiemetics

231
Q

triptans mechanism

A

5-HT receptor agonists (they bind to and stimulate serotonin receptors), specifically 5-HT1B and 5-HT1D.
Cranial vasoconstriction
Inhibiting the transmission of pain signals
Inhibiting the release of inflammatory neuropeptides

232
Q

when take triptans

A

ASAP
if attack resolves and reoccurs second dose can be taken but not if in same attack

233
Q

c/i triptans

A

HTN
CAD
stroke
MI

234
Q

prophylaxis migraine

A

headachde diary
Propranolol (a non-selective beta blocker)
Amitriptyline (a tricyclic antidepressant)
Topiramate (teratogenic and very effective contraception is needed)
Pizotifen
Candesartan
Sodium valproate
Monoclonal antibodies (e.g., erenumab and fremanezumab)
CBT
mindfulness
acupuncture
vit b2

235
Q

menstrual migraines prophylactic

A

frovatriptan
zolmitriptan

236
Q

migraine with aura contraception

A

COCP C/I

237
Q

cluster headaches how often

A

clusters of attacks and then disappear
attack lasts 15 mins to 3 hrs

238
Q

cluster headache typical person

A

30-50 yr old male smoker

239
Q

cluster headache triggers

A

alcohol
strong smells
exercise

240
Q

sx cluster headache

A

SEVERE
unilateral
Red, swollen and watering eye
Pupil constriction (miosis)
Eyelid drooping (ptosis)
Nasal discharge
Facial sweating

241
Q

cluster headache mx

A

triptans
high flow o2

242
Q

cluster headaches prophylaxis

A

verapamil is 1st line
occipital nerve block
prednisolone
lithium

243
Q

causes of spinal cord compression

A

trauma
prolapsed intervertebral disc
atlantoaxial subluxation (RA)
infection (pott’s, discitis)
bony mets

244
Q

CES definition

A

compression of nerve roots caudal to termination of cord resulting in characteristic sx

245
Q

SCC sx

A

above level of T1 - tetraplegia
below T1 - paraplegia
minor - paraesis or parathesia
major - complete paralysis
L1 - CES

246
Q

SCC red flag sx

A

weakness
paraesthsia
ataxia
urinary retenion
UMN signs

247
Q

mets to bone

A

breast
kidney
thyroid
lung
prostate

248
Q

most common prolapse site

A

L4/5 or L5/S1

249
Q

clinical sx CES

A

sudden onset - hours
saddle paraesthesia
bowel etc dysfunction
CES-I (incomplete - reduced urinary function)
CES-R (retention)
loss of lower limb reflexes
reduced anal tone
lower limb weakness/sensory

250
Q

ix for CES

A

urgent MRI of lumbar spine

251
Q

mx of CES

A

surgical decompression within 48 hrs of sx onset
some causes can be tx without surgery - eg radiotherapy or if anklyosing sponydlitis - steroids

252
Q

giant cell arteries clinical fx

A

typically patient > 60 years old
usually rapid onset (e.g. < 1 month)
headache (found in 85%)
jaw claudication (65%)
vision testing is a key investigation in all patients
anterior ischemic optic neuropathy accounts for the majority of ocular complications. It results from occlusion of the posterior ciliary artery (a branch of the ophthalmic artery) → ischaemia of the optic nerve head. Fundoscopy typically shows a swollen pale disc and blurred margins
may result in temporary visual loss - amaurosis fugax
permanent visual loss is the most feared complication of temporal arteritis and may develop suddenly
diplopia may also result from the involvement of any part of the oculomotor system (e.g. cranial nerves)
tender, palpable temporal artery
around 50% have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)
also lethargy, depression, low-grade fever, anorexia, night sweats

253
Q

giant cell arteritis association

A

polymyalgia rheumaticag

254
Q

giant cell arteritis mx

A

urgent high-dose glucocorticoids should be given as soon as the diagnosis is suspected and before the temporal artery biopsy
if there is no visual loss then high-dose prednisolone is used
if there is evolving visual loss IV methylprednisolone is usually given prior to starting high-dose prednisolone
there should be a dramatic response, if not the diagnosis should be reconsidered
urgent ophthalmology review

255
Q

s/e of steroids

A

DM, osteoporosis, mood changes, weight gain

256
Q

dopamine agonists for parkinson’s examples

A

ropinirole, apomorphine

257
Q

s/e of MAO-B inhibitors

A

headache, wpost hypotension, abdo pain

258
Q
A

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