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Phase 3A > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the 3 types of primary headaches?

A
  • Migraine
  • Cluster
  • Tension-type
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2
Q

What are some causes of secondary headaches? x5

A

Meningitis
Subarachnoid haemorrhage
GCA
Idiopathic intracranial hypertension
Medication overuse

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3
Q

What are some red flags for headaches?

A
  • thunderclap headache (SAH)
  • seizure + new headache
  • suspected meningitis/encephalitis
  • red eye (acute glaucoma)
  • headache + new focal neurology
  • significantly altered consciousness
  • memory
  • confusion
  • coordination
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4
Q

What is a migraine?

A

An episode of recurrent throbbing headache +/- aura, often with visual changes

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5
Q

What are the main triggers for migraines? (acronym)

A

Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult (↑noise)
Exercise

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6
Q

What are the 3 main stages of migraines?

A

Prodrome (days before attack) - mood changes, cravings, excessive yawning

Aura (part of attack, minutes before headache onset) - visual phenomena e.g. zigzag lines

Throbbing headache (lasting 4-72hrs)

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7
Q

What is the management for migraines?

A

Acute = oral triptan (sumatriptan) or aspirin 900mg
Prophylaxis - Bb (propranolol) or Topiramate (anti-convulsant which should be avoided in women of child-bearing age) if asthmatic or TCA e.g. amitriptyline (2nd line)

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8
Q

What is the effect of lesions in the dorsal column pathway?

A

ipsilateral loss of/impaired fine touch and proprioception

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9
Q

What is the effect of lesions in the spinothalamic tract?

A

contralateral loss of/impaired pain and temperature sensation

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10
Q

What is a dermatome?

A

area of skin supplied by a single spinal nerve

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11
Q

What is a myotome?

A

muscles supplied by a single spinal nerve

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12
Q

What are the tests for CN II?

A

visual acuity - snellen chart, read through a pinhole
visual fields
fundoscopy
pupillary light reflex
colour vision (Ishihara plates)

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13
Q

What are the investigations for CN III damage?

A

look for ptosis (drooping eyelid)
eye movements (MR, SR, IR, IO)
pupillary light reflex (parasympathetic)

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14
Q

What is the test for CN IV function?

A

ask patient to look medially and down

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15
Q

What is the test for the abducens nerve (CN VI)?

A

ask patient to abduct their eye
(if affected there will be medial deviation due to LR paralysis)

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16
Q

What are the tests for the trigeminal nerve (CN V)?

A

facial sensation
corneal reflex (touching the cornea–> blinking)
facial muscles - check for wasting,

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17
Q

What are the tests for the facial nerve (CN VII)?

A

taste anterior 2/3
muscles of facial expression

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18
Q

What are the tests for the vestibulocochlear nerve (CN VIII)?

A

hearing (Gross hearing test, Rinne’s test, Weber’s test)
balance, gait (Vestibular testing)
caloric test

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19
Q

What are the tests for the glossopharyngeal nerve (CN IX)?

A

taste posterior 1/3 of tongue
gag reflex

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20
Q

What are the test for the vagus nerve (CN X)?

A

hoarseness of the voice? Unilateral vocal cord paralysis.
Difficulty swallowing?
Gag reflex: Light touch to the back of the pharynx (afferents = CN IX; efferents = CN X). Look for reflex contraction / elevation of the palate.
Unilateral lesion of X = palate and uvula deviate away from the side of the lesion (towards the normal side).

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21
Q

What are the tests for acessory nerve function? (CN XI)

A

test sternocleidomastoid (patient turns their head against resistance)
test trapezius (look for symmtery - atrophy?) - shrug shoulders

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22
Q

What is the test for the hypoglossal nerve? (CN XII)

A

tongue deviation (patient sticks out tongue - look for atrophy)

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23
Q

What are the 3 symptoms of meningism?

A

neck stiffness
photophobia
severe headache

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24
Q

What are the common bacterial causes of meningism in neonates?

A

E. coli
Group B streptococcus
Listeria monocytogenes

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25
Q

What are the common causes of bacterial meningitis in infants?

A

Neisseria meningitidis
Haemophilus influenzae
Streptococcus pneumoniae

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26
Q

What are the common causes of bacterial meningitis in young adults?

A

Neisseria meningitidis
Streptococcus pneumoniae

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27
Q

What are the common causes of bacterial meningitis in the elderly?

A

Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes

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28
Q

Which viruses can cause meningitis? x3

A

enteroviruses (e.g. coxsackievirus)
herpes zoster virus
varicella zoster virus

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29
Q

What is meningitis?

A

inflammation of the meninges

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30
Q

What are the fungal causes of meningitis?

A

cryptococcus, histoplasma, blastomyces

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31
Q

What are the risk factors for meningitis? x5+

A

extremes of age
immunnocompromised
non-vaccination
crowding
exposure to pathogens
cranial anatomical defects
cochlear implants
sickle cell disease (due to impaired splenic function)

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32
Q

What are the key presentations of meningitis? x4

A

meningism (photophobia, neck stiffness, severe headache)
fever
altered consciousness
seizures

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33
Q

What are 3 key signs of meningitis?

A

non-blanching rash in children (meningococcal septicaemia)
Kernig sign (can’t extend knee when hip is flexed without pain)
Brudzinski sign (when neck is flexed, knees + hips automatically flexed)

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34
Q

What non-specific signs of meningitis can neonates present with? x5

A

hypotonia
poor feeding
lethargy
hypothermia
bulging fontanelle

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35
Q

What are the gold standard investigations for meningitis?

A

lumbar puncture + CSF analysis (sample taken from L3/4)

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36
Q

What is the management for bacterial meningitis?

A

ceftriaxone/cefotaxime (3rd gen. cephalosporin)
+ steroids (dexamethasone)

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37
Q

What is the management for viral meningitis?

A

none if enteroviral cause
Aciclovir if cause is HSV or VZV

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38
Q

What is the management for fungal meningitis?

A

long course, high dose antifungals (e.g. fluconazole)

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39
Q

What CSF changes are seen in bacterial meningitis?

A

Increased opening pressure
Cloudy yellow appearance
Increased WCC (neutrophilia)
Increased protein (>1g/L)
Decreased glucose (<50% serum level)

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40
Q

What are the CSF changes seen in fungal meningitis?

A

Increased opening pressure
Cloudy + fibrinous appearance
Increased WCC (lymphocytosis)
Increased protein (>1g/L)
Decreased glucose (<50% serum level)

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41
Q

What CSF changes are seen in viral meningitis?

A

Normal opening pressure
Clear, normal colour CSF
Increased WCC (lymphocytosis)
Normal protein levels
Increased glucose (>60% serum level)

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42
Q

What is encephalitis?

A

inflammation of the cerebral cortex

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43
Q

What is it called when a patient has symptoms of encephalitis + meningism?

A

meningo-encephalitis

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44
Q

Which viruses can cause encephalitis? x6

A

Herpes simplex
varicella zoster
parvoviruses
HIV
mumps
measles

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45
Q

What virus causes 95% of cases of encephalitis?

A

herpes simplex virus 1

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46
Q

What are the risk factors for encephalitis? x7

A

immunocompromised
extremes of age
vaccination
post-infection
organ transplantation
animal or insect bites
location (e.g. increased risk of exposure to malaria, ebola, trypanosomiasis)

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47
Q

Which part of the brain is most commonly affected by encephalitis? How does it present?

A

temporal lobe, presents with aphasia

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48
Q

What are the key presentations of encephalitis?

A

fever
headache
focal neurology
altered cognition/consciousness
focal seizures
rash
lethargy and fatigue

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49
Q

What are the investigations for encephalitis?

A

lumbar puncture + CSF analysis (viral PCR testing)
MRI head (GS)
EEG recording
swabs
HIV testing

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50
Q

What is the management for encephalitis?

A

IV aciclovir if HSV encephalitis suspected

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51
Q

What are the complications of encephalitis?

A

lasting fatigue and prolonged recovery
change in mood/personality
changes to memory and cognition
chronic pain

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52
Q

What is a brain abscess?

A

a pus-filled pocket of infected material in the brain

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53
Q

What are the key presentations of brain abscesses? x8

A

fever
headache
changes to mental state
focal neurological deficits
grand mal seizures
nausea
vomiting
neck stiffness

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54
Q

What symptoms are associated with rupture of a brain abscess?

A

suddenly worsening headache, followed by emerging signs of meningism

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55
Q

What is the definition of a stroke?

A

acute neurological deficit lasting more than 24hrs of cerebrovascular cause

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56
Q

What is the gold standard investigation for a brain abscess and what does it show?

A

CT scan - abscess appears as a radiolucent space-occupying lesion

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57
Q

What is the management for brain abscesses?

A

drain intracranial collection
administer effective antibiotic therapy (early treatment is essential)
eliminate primary source of infection

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58
Q

What are the most common bacterial causes of brain abscesses? x4

A

staph. aureus
streptococus
bacteriodes
listeria spp.

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59
Q

What are some non-bacterial causes of brain abscesses?

A

fungi e.g. aspergillus, candida, cryptococcus
protozoa e.g. toxoplasma gondii, entamoeba histolytica
helminths e.g. taenia solium

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60
Q

What is the definition of stroke? (as a clinical syndrome)

A

Acute neurological deficit lasting more than 24hrs of cerebrovascular cause

Divided into ischaemic (caused by vascular occlusion or stenosis) and haemorrhagic (caused by vascular rupture)

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61
Q

What are the causes of ischaemic stroke? x4

A

thrombus formation or embolus
atherosclerosis
shock
vasculitis

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62
Q

What are the causes of haemorrhagic stroke? x3

A

trauma
hypertension
berry aneurysm rupture

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63
Q

What are the risk factors for stroke? x8(+)

A

CVD
previous stroke or TIA
atrial fibrillation
carotid artery disease
hypertension
diabetes
smoking
vasculitis
thrombophilia
combined contraceptive pill
over 55 years
FHx

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64
Q

What are the key presentations for stroke?

A

unilateral sudden onset of:
weakness of limbs
facial weakness
onset dysphagia
visual or sensory loss
headache

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65
Q

What is the FAST acronym for stroke recognition?

A

F-face
A - arm
S - speech
T - time (act fast and call 999)

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66
Q

What is the ROSIER tool?

A

Recognition Of Stroke In the Emergency Room

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67
Q

What are the factors assessed when using the ROSIER tool for stroke recognition?

A

Loss of consciousness or syncope
Seizure activity
Asymmetric facial weakness
Asymmetric arm weakness
Asymmetric leg weakness
Speech disturbance
Visual field defect

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68
Q

What is the immediate investigative step needed to diagnose stroke in an acute setting?

A

Non-contrast CT head

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69
Q

What are the differential diagnoses for stroke? x3

A

hypoglycaemia
hypertensive encephalopathy
TIA

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70
Q

What is the management for ischaemic stroke?

A

Aspirin 300mg STAT asap within 24hrs after ischaemic confirmed
Thombolysis with alteplase (started asap within 4.5hrs of stroke symptom onset)
Thrombectomy (offer asap and within 6 hrs of symptom onset)

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71
Q

What is the management for haemorrhagic stroke?

A

IV mannitol for ↑ICP

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72
Q

What is the secondary prevention for stroke? x4

A

clopidogrel 75mg OS
atorvastatin 80mg
carotid endarterectomy or stenting in patients with carotid artery disease

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73
Q

What is the action of alteplase?

A

A tissue plasminogen activator which rapidly breaks down clots and can reserve stroke effects if given in time

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74
Q

What is the definition of TIA?

A

Transient ischaemic stroke - an episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction where symptoms resolve within 24hrs.

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75
Q

What is a crescendo TIA?

A

2 or more strokes in one week, carries very high risk of developing into a stroke

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76
Q

What are the causes of TIAs? x3

A

carotid thrombo-emboli (29%)
small-vessel occlusion (16%)
in situ thrombosis of intracranial artery-to-artery embolism of thrombus as a result of stenosis or unstable atherosclerotic plaque (16%)

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77
Q

What are the risk factors for TIA? x9

A

AF
valvular disease
carotid stenosis
congestive heart failure
hypertension
diabetes mellitus
smoking
alcohol abuse
advanced age

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78
Q

What are the key presentations of TIAs? x7

A

sudden onset and brief duration of symptoms (<24hrs)
unilateral weakness of paralysis
dysphagia
ataxia, vertigo or loss of balance
amaurosis fugax
homonymous hemianopia
diplopia

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79
Q

What are the investigations for TIAs

A

Often clinical diagnosis
blood glucose, FBC, platelets, PT, INR, lipids, electrolytes, ECG

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80
Q

What are the differential diagnoses for TIA? x4

A

stroke
hypoglycaemia
seizure
complex migraine

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81
Q

What is the management for TIA

A

aspirin 300mg daily for 2 weeks
then dual platelet therapy (aspirin and clopidogrel) for 3 weeks
then clopidogrel lifelong as secondary prevention for CVD/stroke

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82
Q

What are the secondary prevention measures for stroke/CVD? x9

A
  • BP control
  • Antiplatelet agents (clopidogrel/aspirin)
  • Anticoagulants
  • stop smoking
  • statin for high cholesterol
  • reduce alcohol intake
  • lose weight
  • increase physical activity
  • healthy diet
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83
Q

What is a subarachnoid haemorrhage?

A

rapidly developing signs of neurological dysfunction and/or headaches due to bleeding into the subarachnoid space

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84
Q

What are the causes of subarachnoid haemorrhage

A

MC: berry aneurysm rupture in the circle of willis
trauma

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85
Q

What are the risk factors for subarachnoid haemorrhage? x8

A

hypertension
smoking
family history
Autosomal dominant polycystic kidney disease (ADPKD)
alcohol /drug use
Marfan
Ehlers-danlos syndrome
Pseudoxanthoma elasticum (connective tissue disorder)
Neurofibromatosis type I

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86
Q

What are the key presentations for subarachnoid haemorrhage? x7

A

severe sudden onset headache
Kernig sign (cant extend leg when knee is flexed)
Brudzinski sign (knees automatically flex when neck is elevated)
Depressed consciousness/loss of consciousness
Nerve palsies CN III/VI (III - fixed dilated pupil, VI - non-specific signs of ↑ICP)
neck stiffness and muscle aches
eyelid, drooping, diplopia with mydriasis, orbital pain

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87
Q

What are the investigations for subarachnoid haemorrhage?

A

CT head (star shape bleed)
If CT head is indicative –> CT angiogram
If CT head is unclear –> lumbar puncture (xanthochromia)

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88
Q

What is the management for subarachnoid haemorrhage?

A

1st line = neurosurgery (endovascular coiling)
+ Nimodipine (CCB, ↓vasospasm + ↓BP)

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89
Q

What are the causes of subdural haemorrhage?

A

caused by rupture of a bridging vein
often due to deceleration injuries
also seen in abused children (e.g. shaken baby syndrome)

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90
Q

What are the risk factors for subdural haemorrhage? x6

A

trauma
child abuse
cortical atrophy (e.g. dementia)
coagulopathy
anticoagulant use
advanced age (65+)

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91
Q

What is the pathophysiology of subdural haemorrhage?

A

typically result from torsional or shear forces causing disruption of bridging cortical veins emptying into dural venous sinuses

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92
Q

What are the key presentations of subdural haemorrhage?

A

gradual onset with latent period –> small amount of bleeding which accumulates over time + autolysis of blood –> symptoms after days/weeks/months

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93
Q

What are the symptoms of subdural haemorrhage?

A

nausea/vomiting
headache
diminished eye/verbal/motor responses
confusion

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94
Q

What is the investigation for subdural haemorrhage?

A

NCCT head (sickle-shaped haematuria)

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95
Q

What is the management for subdural haemorrhage?

A

sugery: burr hole + craniotomy
IV mannitol to ↓ICP

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96
Q

What is an extradural haemorrhage?

A

an acute haemorrhage between the dura mater and inner surface of the skull

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97
Q

What is the aetiology of extradural haemorrhage?

A

most commonly caused by skull trauma in the temporoparietal region, typically following a fall, assault or sporting injury
can also occur secondary to vein rupture, arteriovenous abnormalities or bleeding disorders

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98
Q

What are the risk factors for extradural haemorrhage?

A

head trauma
age 20-30yrs

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99
Q

What are the key presentations of extradural haemorrhage? x6

A

reduced GCS (with lucid interval intially)
headaches
vomiting
confusion
seizures
pupil dilation

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100
Q

What is the gold standard investigation for extradural haemorrhage? What indicates EDH diagnosis?

A

NCCT (egg shaped haematoma - due to blood being contained by dura and skull)

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101
Q

What is the management for extradural haemorrhage?

A

Urgent surgery (craniotomy + vessel ligation)
IV mannitol to ↓ICP

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102
Q

What are the differentials for extradural haemorrhage? x5

A

epilepsy
carotid dissection
carbon monoxide poisoning
subdural haematoma
subarachnoid haemorrhage

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103
Q

What is amaurosis fugax?

A

also known as retinal transient ischaemic attack
= a sudden, short-term, painless loss of vision in one eye

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104
Q

What are the causes of amaurosis fugax? x4

A

stenosis or occlusion of internal carotid artery or central retinal artery
inflammation of optic nerve or nervous system
giant cell arteritis in individuals >60yrs old

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105
Q

What is multiple sclerosis?

A

chronic and progressive neurological disorder caused by demyelination of the myelinated neurons in the CNS

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106
Q

What are the types of MS?

A

Relapsing-remitting = symptoms then incomplete recovery then symptoms return
Primary progressive = gradual deterioration without recovery
Secondary progressive = relapsing remitting –> primary progressive (around 75% of RR cases evolve to this)

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107
Q

What are the risk factors for MS? x6

A

female
20-40yrs
autoimmune disease
FHx
EBV
vitamin D deficiency

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108
Q

What is the pathophysiology of MS?

A

Inflammation around the myelin covering nerves in the CNS and infiltration of immune cells causes damage to the myelin and affects the way the electrical signals travel along the nerves

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109
Q

What are the key presentations of MS?

A

optic neuritis (mc)
eye movement abnormalities (double vision, internuclear ophthalmoplegia, conjugate lateral gaze disorder)
focal weakness (Bell’s palsy, Horner’s syndrome, limb paralysis, incontinence)
focal sensory symptoms (trigeminal neuralgia, numbness, paraesthesia, Lhermitte’s sign)
ataxia (sensory or cerebellar)

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110
Q

What are the investigations for MS?

A

McDonald criteria (2 attacks disseminated in time (separate events) + space (different parts of CNS affected)
MRI scan (GS)

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111
Q

What is the management for MS?

A

acutely (during symptomatic episodes) –> IV methylprednisolone
patient education
prophylaxis –> B interferon (DMARDs, biologic therapies)

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112
Q

What are the most common differentials for MS?

A

migraine with aura
hypoglycaemia
hypothyroidism
electrolyte abnormalities

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113
Q

What is the epidemiology of MS?

A

More common in women
20-40 most common age for diagnosis
More common in white
More common in northern latitudes
Symptoms will improve in pregnancy and post-partum period

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114
Q

What is Uhthoff’s phenomenon?

A

worsening of MS symptoms following a rise in temperature, such as a hot bath

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115
Q

What is optic neuritis?

A

demyelination of the optic nerve which presents with:
- unilateral reduced vision
- central scotoma
- pain on eye movement
- impaired colour vision (red)

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116
Q

What is the McDonald criteria based on ?

A

2 or more relapses and either:
- objective evidence of two or more lesions
- objective evidence of one and a reasonable history of a previous relapse

‘objective evidence’ = abnormality on neurological exam, MRI or visual evoked potentials

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117
Q

What is used to treat a MS relapse?

A

oral or IV prednisolone
plasma exchange: to remove disease-causing antibodies

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118
Q

What is used for maintenance of MS?

A

flare ups - IV methylprednisolone
DMARDs - ocrelizumab
Beta-interferon - decreases the level of inflammatory cytokines
Monoclonal antibodies
Glatiramer acetate (immunomodulator)
Fingolimod

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119
Q

What are the stroke symptoms from anterior circulation strokes?

A

either hemisphere:
hemiparesis
hemisensory loss
visual field defect

dominant hemisphere (usually left)
language dysfunction
- expressive dysphasia
- receptive dysphasia
- dyslexia
- dysgraphia (inability to write)

non-dominant hemisphere
anosognosia (impaired ability to comprehend illness)
- neglect of paralysed limb
- denial of weakness
visuospatial dysfunction
- geographical agnosia
- dressing apraxia
- contructional apraxia

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120
Q

What are the posterior circulation symptoms of stroke?

A
  • unsteadiness
  • visual disturbance
  • slurred speech
  • headache
  • vomiting
  • others e.g. memory loss, confusion
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121
Q

What percentage of strokes are ischaemic/haemorrhagic?

A

Ischaemic - 80%
Haemorrhagic - 20%

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122
Q

What are the pathological subtypes of ischaemic strokes?

A

large vessel disease (50%)
small vessel disease (25%)
cardioembolic (20%)
cryptogenic/rarities (5%)

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123
Q

What are the pathological subtypes of haemorrhagic stroke?

A

primary intracerebral haemorrhage
subarachnoid haemorrhage

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124
Q

What are some examples of stroke mimics?

A

epileptic seizure
space occupying lesion (subdural, tumour, arteriovenous malformation)
infection
metabolic (e.g. hyponatraemia/hypoglycaemia/alcohol/drugs)
multiple sclerosis
functional neurological disorder (FND)
migraine

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125
Q

What is the TOAST classification for types of ischaemic stroke?

A

1) large-artery atherosclerosis
2) cardioembolism
3) small-vessel occlusion
4) stroke of other determined etiology
5) stroke of undetermined etiology

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126
Q

What is the most common cause of ischaemic strokes in under 45 yr olds?

A

carotid or vertebral dissection

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127
Q

What is a primary intracerebral haemorrhage (PICH)?

A

leakage of blood directly into brain tissue due to :
- hypertension (weakens deep perforating blood vessels)
- amyloidosis
- arteriovenous malformation
- aneurysm rupture

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128
Q

What are the causes of secondary intracerebral haemorrhages? Are they classed as strokes?

A

trauma
warfarin
bleeding into a tumour
Not classed as strokes but can cause similar symptoms

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129
Q

What is the most common type of brain cancer/

A

High grade glioma (85% of all new cases of malignant primary brain tumour)

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130
Q

What are the red flags for brain tumour?

A

headache + features of raised ICP and/or focal neurology
new onset focal seizure
rapidly progressive focal neurology
past history of other cancer

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131
Q

What is a glioblastoma multiforme?

A

a grade IV glioma, which is a fast-growing and aggressive brain tumour

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132
Q

What are the types of glioblastoma

A

multifocal - can be seen to have multiple areas of high grade cancerous formations joined together by other abnormal brain tissue (2-20% of all glioblastomas)
multicentric - more than one GBM tumour that has arisen in the brain at the same time, or within a very short timeframe which have normal brain tissue between them

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133
Q

What is a primary brain tumour?

A

abnormal growth originating from cells within the brain (gliomas, germ cell tumours, meninigiomas)

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134
Q

Where do brain tumours commonly metastasise from?

A

lungs
breast
colorectal
testicular
renal cell
malignant melanoma

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135
Q

What is the aetiology of brain tumours? x4

A

majority no cause found
ionising radiation
5% family history (associated genetic syndromes (neurofibromatosis, tuberose sclerosis, Von Hippel-Lindau disease)
immunosuppression

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136
Q

What are the key presentations of brain tumours? x5(+)

A

Wide variation depending on tumour type, grade and site

Headache (woken by headache, worse in the morning, associated with N/V, exacerbated by coughing, sneezing, drowsiness)
Seizures
Focal neurological symptoms (symptoms specific to site in the brain e.g. loss of right arm motor function due to damage to left side motor cortex) - hemiparesis, hemisensory loss, visual field defect, dysphasia
Other non-focal symptoms (personality change/behaviour, memory disturbance, confusion)
Signs of ↑ICP - altered mental state, visual field defects, seizures, unilateral ptosis, 3rd and 6th nerve palsies, papilloedema (on fundoscopy)

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137
Q

How can low grade and high grade brain tumours be differentiated clinically?

A

low grade - typically present with seizures (can be incidental finding)
high grade - rapidly progressive neurological deficit + symptoms of raised intracranial pressure

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138
Q

What are the investigations for brain tumours?

A

1st line - contrast CT
GS - MRI
other - functional MRI (shows which areas of the brain are most active)

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139
Q

What is the management for high grade brain tumours? x5

A

Steroids - reduce oedema
Palliative care
Chemotherapy - temozolamide, PCV (procarbazine, lomustine + vincristine)
Radiotherapy - mainstay, radical vs palliative
Surgery - biopsy or resection

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140
Q

What is the management for low grade brain tumour?

A

Surgery - early resection
Radiotherapy and early chemotherapy

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141
Q

What is the grading for brain tumours?

A

1 - slow growing, non-malignant, and associated with long-term survival
2 - have cytological atypia. These tumours are slow growing but recur as higher-grade tumours
3 - have anaplasia and mitotic activity. These tumours are malignant
4 - anaplasia, mitotic activity with microvascular proliferation, and/or necrosis. These tumours reproduce rapidly and are very aggressive malignant tumours.

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142
Q

What is the action of sodium valproate in epilepsy treatment?

A

increases the activity of GABA which has a relaxant affect on the brain by stopping the release of excitatory neurotransmitters

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143
Q

What is status epilepticus?

A

medical emergency defined as seizures lasting more than 5 minute
or
>= 2 seizures within a 5-minute period without the person returning to normal between them

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144
Q

What is the management for status epilepticus?

A

ABCDE approach:
- securing the airway
- giving high concentration O2
- checking blood glucose levels
- gaining IV access

Medical treatment:
- benzodiazepine 1st line, repeated after 5-10 mins if the seizure continues
- 2nd line options (following 2x benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate
- 3rd line options are phenobarbital or general anaesthesia

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145
Q

What is epilepsy?

A

an umbrella term for chronic conditions where patients have a tendency to have recurrent, unprovoked epileptic seizures

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146
Q

What are seizures?

A

Transient episodes of abnormal electrical in the brain which cause changes in behaviour, sensation or cognitive processes

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147
Q

What are 3 types of generalised seizure?

A

Myoclonic jerks
Absence
Primary generalised tonic clonic

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148
Q

What is a focal seizure?

A

also known as a partial seizure, these occur in an isolated brain area and affect hearing, speech, memory and emotions
- patients remain awake during simple focal seizures (focal aware seizure) but lose awareness during complex focal seizures (focal impaired awareness seizure)

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149
Q

What are the symptoms associated with focal/partial seizures? x4

A

these depend on the location of the abnormal activity:
- deja vu
- strange smells, tastes, sight or sound sensations
- unusual emotions
- abnormal behaviours

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150
Q

In focal seizures what lobe of the brain would be affected if a patient had limb jerking?

A

the frontal lobe

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151
Q

In focal seizures what lobe of the brain would be affected if a patient had paraesthesia?

A

the parietal lobe

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152
Q

What are examples of generalised seizures? x5

A

tonic-clonic, absence, myoclonic, tonic, atonic

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153
Q

What are the risk factors for epilepsy? x7

A

FHx
CNS infection history
Head trauma
Prior seizure events/suspected seizure events
Hx of substance use
Premature birth
Multiple or complicated febrile seizures

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154
Q

What are the stages of an epileptic seizure? x4

A

prodrome = mood changes, days before
aura = minutes before, deja vu + automatisms (lip smacking, rapid blinking) - not always present (most commonly seen in temporal lobe epilepsy)
ictal event = seizure
post-ictal period = symptoms such as headache, confusion, ↓GCS, Todd’s paralysis, dysphasia, amnesia, sore tongue (pts bite tongue during ictal phase)

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155
Q

What are the positive ictal symptoms? x7

A

loss of awareness
memory lapse
feeling confused
difficulty hearing
odd smells, sounds or tastes
loss of muscle control
changes in speech/ability to speak

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156
Q

What are examples of post-ictal symptoms? x6

A

confusion
amnesia
drowsiness
hypertension
headache
nausea

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157
Q

What are some other common features of epileptic seizures? x5

A

can occur from sleep
can be associated with other brain dysfunction
lateral tongue bite
deja vu
incontinence

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158
Q

What are the investigations for epilepsy?

A

EEG, ECG, CT head + MRI

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159
Q

What are the criteria for epilepsy diagnosis?

A

1 of:
- 2+ unprovoked seizures occurring more than 24hrs apart
- 1 unprovoked seizure and a probability of future seizures (considered >60% risk in 10yrs)
- Diagnosis of an epileptic syndrome

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160
Q

What is the management for epilepsy?

A

aim is to be seizure free on the minimum anti-epileptic medications
1st line = sodium valproate
also lamotrigine (sv is teratogenic)

ideally pts should be on monotherapy with a single anti-epileptic drug

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161
Q

What are the features of generalised tonic-clonic seizures? x8

A

no aura
loss of consciousness
tonic (muscle tensing, fall to floor) and clonic (muscle jerking) episodes
typically tonic before clonic
eyes open and upward gazing
incontinence
tongue biting
post-ictal period

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162
Q

What is the 1st and 2nd line treatment for generalised seizures?

A

1st line: sodium valproate
2nd line: lamotrigine or carbamazepine

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163
Q

What are the characteristics of absence seizures?

A

typically occur in children
patient becomes blank, stares into space and then abruptly returns to normal
last 10-20 seconds

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164
Q

What are the characteristic features of myoclonic seizures?

A

sudden brief muscle contractions like a sudden jump
patient normally remains awake during the episode
occur in various forms of epilepsy but typically happen in children as part of juvenile myoclonic epilepsy

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165
Q

What are the features of a frontal focal seizure?

A

Jacksonian march + Todd’s palsy

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166
Q

What are the features of a temporal focal seizure?

A

aura, dysphagia, post-ictal period

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167
Q

what are the features of an occipital focal seizure?

A

vision changes

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168
Q

What are the 1st and 2nd line treatments for focal seizures?

A

1st: carbamazepine or lamotrigine
2nd: sodium valproate or levetiracetam

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169
Q

What is the difference between simple and complex focal seizures?

A

simple: no LOC, patient awake + aware, uncontrollable muscle jerking confined to one part of body
complex: LOC, patient unaware, post-ictal period

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170
Q

What are the causes of seizures? (VITAMINDE)

A

Vascular
Infection
Trauma
Autoimmune e.g. SLE
Metabolic e,g. Hypocalcaemia
Idiopathic e.g. epilepsy
Neoplasms
Dementia + Drugs (cocaine)
Eclampsia

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171
Q

What are functional/dissociative seizures?

A

non-epileptic seizures which present with ictal symptoms as a result of mental processes triggered by internal or external aversive stimuli

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172
Q

What are the characteristics of functional/dissociative seizures? x7

A

situational
duration 1-20 mins
dramatic motor phenomena/prolonged atonia
eyes closed
ictal crying and speaking
suprisingly rapid or slow post-ictal recovery
history of psychiatric illlness, other somatoform disorders

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173
Q

What is syncope?

A

transient loss of consciousness due to cerebral hypoperfusion, characterised by a rapid onset, short duration, and spontaneous compete recovery

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174
Q

What are some potential pre-syncopal changes? x6

A

sweating,
nausea,
pallor,
prolonged standing position,
hyperventilation,
increased heart rate

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175
Q

What are the causes of syncope? x7

A

neurally mediated/reflex syncope
orthostatic hypotension
cardiac arrhythmias
structural cardiac or cardiopulmonary disease
cerebrovascular
substance abuse, alcohol intoxication
psychogenic

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176
Q

What is the treatment for syncope?

A

most patients with neurally mediated syncope (NMS) just need reassurance and education about how to avoid recurrence

if syncope is very frequent, unpredictable or could occur during high risk activities like driving treatments like tilt-training, isometric counterpressure manoeuvres can help

for syncope with a clear cause this should be treated

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177
Q

What is essential tremor?

A

a rhythmic oscillatory movement of a body part, resulting from the contraction of opposing muscle groups

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178
Q

What are the characteristics of essential tremor? x6

A

fine tremor (low amplitude)
symmetrical
more prominent with voluntary movement
worse when tired, stressed or after caffeine
improved by alcohol
absent during sleep

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179
Q

What are the differentials for essential tremor?

A

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

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180
Q

What is the management for essential tremor?

A

There is no definitive treatment
If not causing functional or psychological problems it does not require treatment
Medications which may improve symptoms are:
- Propanol (non-selective beta-blocker)
- Primidone (barbiturate anti-epileptic)

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181
Q

What is Parkinson’s disease?

A

progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movement

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182
Q

What are the risk factors for Parkinson’s? x3

A

FHx
increased age
male

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183
Q

What is the classic triad of features of Parkinson’s?

A

resting tremor, rigidity, bradykinesia

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184
Q

What are the features of the Parkinson’s tremor?

A

“pill rolling tremor”, asymmetrical, 4-6hz, worse at rest, improves with intentional movement

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185
Q

What are the features of rigidity with Parkinson’s?

A

“cogwheel”, when limb is passively flexed and extended tension in the arm will be felt which gives way to movement in small increments

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186
Q

What are some other symptoms of Parkinson’s? x5

A

Depression
Sleep disturbance and insomnia
Loss of the sense of smell (anosmia)
Postural instability
Cognitive impairment and memory problems

187
Q

How is Parkinson’s diagnosed?

A

clinical diagnosis based on symptoms and examination
DaTSCAN (shows whether there is a loss of dopaminergic neurons in the striatum)

188
Q

What is the management for Parkinson’s?

A

Individual specific depending on symptoms, response to medications
No cure

Levodopa (synthetic dopamine) combined with peripheral decarboxylase inhibitors (stop levodopa being broken down before it reaches the brain) => co-benyldopa (levodopa + benserazide), co-careldopa (levodopa + carbidopa)

COMT inhibitors - entacapone (metabolises levodopa in the body and brain, taken with levodopa + decarboxylase inhibitor)

Dopamine agonists - mimic dopamine in the basal ganglia and stimulate dopamine receptors - bromocriptine, pergolide, cabergoline

Monoamine oxidase-B inhibitors

189
Q

What are is the main potential side effect of levodopa?

A

dyskinesia (abnormal movements associated with excessive motor activity) e.g.
- dystonia (excessive muscle contraction leading to abnormal postures or exaggerated movements)
- chorea (abnormal jerking/random movements)
- athetosis (involuntary twisting or writhing movements, usually in the fingers, hands or feet)

190
Q

What is Motor Neuron Disease?

A

Neurodegenerative disease which causes upper and lower motor neuron signs

191
Q

What are the 4 diagnoses encompassed in MND?

A

amyotrophic lateral sclerosis - most common
progressive bulbar palsy
progressive muscular atrophy
primary lateral sclerosis

192
Q

What are the risk factors for MND? x4

A

FHx
Smoking
Exposure to heavy metals and certain pesticides
Age

193
Q

What are the key presentations of MND? x7

A

gradual progressive weakness of the muscles throughout the body (particularly affecting the limbs, trunk, face and speech)
Fatigue when exercising
Clumsiness
Dropping things more often
Dysarthria (slurred speech)
Signs of LMN disease - muscle wasting, hypotonia, fasciculations, hyporeflexia
Signs of UMN: hypertonia, spasticity, hyperreflexia, plantar responses

194
Q

What are the signs of LMN disease? x4

A

muscle wasting
hypotonia
fasciculations
hyporeflexia

195
Q

What are the signs of UMN disease? x4

A

hypertonia
spasticity
hyperreflexia
plantar responses

196
Q

What are the investigations for MND?

A

mainly clinical
EMG (shows fibrillation potentials due to degeneration of muscle with LMN dysfunction)

197
Q

What is the management for MND?

A

No cure

Riluzole (antiglutaminergic) - slows progression of disease and can extend survival by a few months in ALS

Non-invasive ventilation (breathing support at night)

Supportive - physiotherapy, breathing support if necessary

198
Q

What are some potential complications of MND? x3

A

respiratory failure, aspiration pneumonia, swallowing failure

199
Q

What is Guillain-barre syndrome?

A

acute paralytic polyneuropathy affecting the peripheral nervous system

200
Q

What is the cause of Guillain-Barre syndrome?

A

campylobacter jejuni + viruses; CMV, EBV, HSV

201
Q

What are the risk factors for Guillain-Barre Syndrome? x6

A

undercooked poultry (risk of C. jejuni)
influenza, CMV , EBV, Zika, Hep A,B,C,E
surgery
trauma
hodgkin’s lymphoma
mycoplasma pneumonia

202
Q

What is the pathophysiology of G-B syndrome?

A

molecular mimicry - organisms produce antigens very similar to those on schwann cells
results in antibody production against schwann cell –> demyelination + acute polyneuropathy

203
Q

What are the key presentations of G-B syndrome? x5

A

Ascending symmetrical muscle weakness (+paralysis)
Loss of deep tendon reflexes
Loss of sensation in the peripheries or neuropathic pain
Autonomic involvement in around 50%
Respiratory failure in 35% → must always monitor GB patients breathing

204
Q

What are the Brighton criteria for GBS diagnosis? x7

A

Bilateral and flaccid limb weakness
Decreased or absent deep tendon reflexes in weak limbs
Monophasic course and time between onset-nadir 12-28 days
CSF cell count <50/ul
CSF protein concentration > normal
NCS findings consistent with one of the subtypes of GBS
Absence of alternative diagnosis for weakness

The criteria are marked from 1-4 levels of diagnostic certainty

205
Q

What are the investigations for G-B syndrome?

A

Diagnosis is made using the Brighton criteria supported by investigations:
- nerve conduction studies (showing reduced signal through the nerves)
- lumbar puncture at L3/4 –> raised protein + normal WCC (=inflammation but no infection)

206
Q

What is the management for G-B syndrome?

A

IV Ig for 5 days (1st line)
Plasmapheresis
Supportive care
Venous thromboembolism prophylaxis
Severe case + resp failure –> need intubation, ventilation and ITU admission

207
Q

What is Wernicke’s encephalopathy?

A

neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations typically involving mental status changes and gait and oculomotor dysfunction

208
Q

What are the risk factors for Wernicke’s encephalopathy? x5

A

alcohol dependence
AIDS
cancer and treatment with chemotherapeutic agents
malnutrition
Hx of GI surgery

209
Q

What is the pathophysiology of Wernicke’s encephalopathy?

A

Acute or subacute thiamine deficiency in a susceptible person.

Thiamine deficiency leads to decreased activity of thiamine-dependent enzymes which triggers a sequence of metabolic events resulting in energy compromise and ultimately neuronal death. The areas commonly affected include the medial dorsal thalamic nucleus, mammillary bodies, the periaqueductal grey matter, and the floor of the fourth ventricle.

210
Q

What are the presentations of Wernicke’s encephalopathy? x6

A

Ataxia
Confusion
Mental slowing, impaired concentration, and apathy
Classic triad: ophthalmoplegia, mental status changes, gait dysfunction (present in only 10% patients)

211
Q

What are the investigations for Wernicke’s encephalopathy?

A

FBC (macrocytic anaemia), LFTS (deranged)
Clinically diagnosed

212
Q

What is the management for Wernicke’s encephalopathy?

A

high dose parenteral thiamine for 5 days acutely
+ magnesium sulphate
+ multivitamins
oral thiamine prophylactically

213
Q

What is Korsakoff syndrome?

A

when Wernicke’s left too long without treatment –> severe thiamine deficiency

214
Q

What is Wernicke-Korsakoff syndrome?

A

describes the spectrum of disease resulting from thiamine deficiency

215
Q

What is Duchenne Muscular Dystrophy?

A

most common and rapidly progressive type of muscular dystrophy (progressive generalised muscle disease) caused by the absence of dystrophin on the X-chromosome

216
Q

What is the cause of DMD?

A

X-linked recessive mutated dystrophin gene

217
Q

What is the pathophysiology of DMD?

A

Dystrophin is a cytoskeletal protein providing structural stability to the dystroglycan complex in cell membranes, most significantly in skeletal muscle.
The absence of dystrophin results in ongoing cell membrane depolarisation due to calcium entering the cell which causes ongoing degeneration and regeneration of muscle fibres.
Degeneration is faster than regeneration, and muscle fibres undergo necrosis.
Muscle proteins are replaced by adipose and connective tissue, causing progressive muscle weakening.

218
Q

What are the key presentations of DMD? x7

A

Imbalance of lower limb strength
Lower extremity musculotendinous contractures
Delayed motor milestones
Calf hypertrophy
Ambulation difficulty and falls
Diminished muscle tone and deep tendon reflexes
Normal sensation

219
Q

What is Gower’s sign for DMD?

A

Specific technique to stand up from a lying position where the person uses their hands and arms to ‘walk’ up their own body from a squatting position due to lack of thigh and hip muscle strength.

220
Q

What are the investigations for DMD? x5

A

serum creatine kinase
genetic testing
clinical presentation
electromyogram
muscle biopsy

221
Q

What are the differential diagnoses for DMD? x4

A

Becker muscular dystrophy
Limb-gordle muscular dystrophies
Emery-dreifuss muscular dystrophies
Polymyositis

222
Q

What is the management for DMD?

A

No curative treatment
Oral steroids to slow muscle weakness progression
Creatine supplements
occupational therapy, physio, medical appliances
surgical and medical management of complications (e.g. spinal scoliosis, heart failure)

223
Q

What is the life expectancy of DMD patients?

A

25-35 yrs

224
Q

What is Brown-Sequard syndrome?

A

rare neurological condition characterised by a lesion in the spinal cord which results in weakness or paralysis on one side of the body and a loss of sensation on the opposite side

225
Q

What are the causes/risk factors for Brown-Sequard syndrome? x5

A

traumatic injury to spine or neck
other spinal disorders (cervical spondylosis, arachnoid cyst, epidural haematoma)
bacterial/viral infection (meningitis, myelitis, herpes, tuberculosis)
radiation exposure
MS

226
Q

What is the pathophysiology of B-S syndrome?

A

caused by lateral hemi-section of the spinal cord severing the pyramidal tract (already crossed in the medulla), the uncrossed dorsal columns and the crossed spinothalamic tract

227
Q

What is the classic presentation of B-S syndrome?

A

Ipsilateral loss of all sensory modalities at level of lesion
Ipsilateral flaccid paralysis at the level of the lesion
Ipsilateral loss of position sense and vibration below the lesion
Contralateral loss of pain/temperature sensation below the lesion
Ipsilateral motor loss below the level of the lesion

228
Q

What are the investigations for B-S syndrome?

A

MRI (GS)
Myelogram + CT, blood tests, lumbar puncture

229
Q

What are the differential diagnoses for B-S syndrome? x4

A

MND
Progressive spinal muscular atrophy
Primary lateral sclerosis
Stroke

230
Q

What is the management for B-S syndrome?

A

Most individuals with this syndrome will recover majority of function
No specific treatment, will usually focus on underlying cause
Occupational therapy, physiotherapy, medical appliances
High dose steroids (methylprednisolone)
Surgery
Analgesia

231
Q

What are the complications of B-S syndrome? x7

A

low bp
spinal shock
depression
abdominal enlargement
lung/UT infections
PE
paralysis

232
Q

What is Charcot-Marie-Tooth syndrome?

A

inherited disease affecting the peripheral motor and sensory neurones
- also known as hereditary motor and sensory neuropathy
- there are various types with different genetic mutations and pathophysiology

233
Q

What is the mutation which causes CMT syndrome?

A

autodominant mutation on chromosome 17;PUP 22 gene

234
Q

What are the risk factors for CMT syndrome?

A

A- alcohol
B- B12 deficiency
C- cancer and CKD
D- diabetes + drugs
E - every vasculitis

235
Q

What are the key presentations of CMT syndrome? x8

A

Foot drop (common peroneal palsy)
Stork legs (very thin calves)
Hammer toes (curled up toes)
Pes cavus → high arched feet
↓Deep tendon reflexes
Awkward or unusually high gait
Frequent tripping or falling
Decreased sensation or a loss of feeling in legs and feet

236
Q

What are the investigations for CMT syndrome?

A

Clinical evaluation

EEGs, motor conduction velocities, DNA bloods

237
Q

What is the management for CMT syndrome?

A

No cure
Supportive treatment e.g. analgesia for neuropathic pain
Orthotics
Physiotherapy
Surgical treatment (for severe joint deformities)

238
Q

What are the types of peripheral neuropathy? x4

A

motor neuropathy
sensory neuropathy
autonomic nerve neuropathy
combination neuropathies

239
Q

What are the causes of peripheral neuropathy? x4

A

demyelination (Guillain-Barre, B-12 deficiency)
T2DM
surgery
pathology e.g. infection, endocrine, RA

240
Q

What are the mechanisms of peripheral neuropathy? x5

A

demyelination
axonal damage
nerve compression
vasanervosum infarction
wallerian degeneration - nerve cut and distally die

241
Q

What are the key presentations of peripheral neuropathy? x10

A

Muscle weakness
Cramps
Muscle twitching
Loss of muscle and bone
Changes in skin, hair or nails
Numbness
Loss of sensation or feeling in body parts
Loss of balance or other functions as a side effect of the loss of feeling in the legs, arms or other body parts
Emotional/sleep disturbances
Loss of bladder control

242
Q

What are the investigations for peripheral neuropathy?

A

bloods, spinal fluid tests, muscle strength tests, vibration detection tests
GS: CT/MRI
electromyography and nerve conduction studies
nerve and skin biopsy

243
Q

What is the management for peripheral neuropathies?

A

treat underlying condition (e.g. diabetes)
analgesia

244
Q

What is mononeuritis multiplex?

A

describes a clinical presentation of progressive motor and sensory deficits in the distribution of specific peripheral nerves

245
Q

What are the causes of mononeuritis multiplex? x8 (acronym)

A

Wegeners
AIDS/amyloidosis
RA
DMT2
Sarcoidosis
Polyarteritis nodosa
Leprosy
Carcinomas

246
Q

What are the symptoms of mononeuritis multiplex? x6

A

numbness
tingling
abnormal sensation
burning pain
paralysis
lack of controlled movement of a body part

247
Q

What is carpal tunnel syndrome?

A

symptoms caused by pressure on median nerve as it passes through the carpal tunnel

248
Q

What are the risk factors for carpal tunnel syndrome? x9

A

Female
Hypothyroidism
Acromegaly
Pregnancy
RA
Obesity
Diabetes
Perimenopause
Repetitive strain

249
Q

What is the pathophysiology of carpal tunnel syndrome?

A

Compression is the result of either swelling of the tunnel contents (e.g. tendon sheath inflammation due to repetitive strain) or narrowing of the tunnel
The median nerve provides sensation to the palm and motor function to the thenar muscle responsible for thumb movements.

250
Q

What are the key presentations of carpal tunnel syndrome? x5

A

gradual onset
- weakness of grip + aching hand/forearm (worse at night and relieved by hanging hand over side of bed, wake + shake)
- paraesthesia of hand
- burning sensation
- wasting of thenar eminence

251
Q

What is the phalen test for CTS?

A

flex fist at wrist for 1 minute –> positive = paraesthesia + pain

252
Q

What is the tinel test for CTS?

A

tapping wrist causes tingling

253
Q

What is the gold standard test for CTS?

A

EMG (electromyography)

254
Q

What is the management for CTS

A

Wrist splint at night + steroid injection (acutely very painful)
Last resort = surgical decompression

255
Q

What nerve palsy causes wrist drop?

A

nerve (roots C5-T1)
Radial nerve mostly innervates extensor arm muscle so lesion causes weakness of extensor muscle –> wrist drop

256
Q

What are the functions of the cerebellum? x5(+)

A

accuracy and coordination
motor control and learning
helps with timing and sensory acquisition
helps prediction of the sensory consequences of action
eye movements, speech, limb movements, fine motor skills, gait, posture, balance, cognition

257
Q

What is ataxia?

A

‘lack of order’
describes heterogenous group of disorders affecting balance, coordination and speech

258
Q

What are the types of ataxia?

A

inherited: autosomal dominant (SCA6, EA2) and recessive (Friedrich’s ataxia, SPG7)
acquired: toxic/metabolic (alcohol, vitamin defs, drugs), immune mediated (paraneoplastic cerebellar degeneration, gluten related), infective (post-infectious), degenerative (multi-system atrophy cerebellar variant), structural (trauma, neoplastic)

259
Q

What is Friedrich’s ataxia?

A

Genetic, progressive, neurodegenerative movement disorder which typically presents at age 10-15 years old

260
Q

What are the symptoms of cerebellar dysfunction? x7

A

dizzy - unsteady/wobbly/clumsy
falls, stumbles
difficulty focusing/double vision/ ‘oscillopsia’ (blurred, jumpy vision)
slurred speech
problems with swallowing
tremor
problems with dexterity /fine motor skills

261
Q

What are the clinical signs of ataxia? x6

A
  • nystagmus/jerky (saccadic) pursuit/hypo or hypermetropic saccades/optic atrophy/ptosis
    dysarthria
  • intention tremor/myoclonus
  • dysmetria/past pointing/dysdiadochokinaesia (difficulty performing quick/alternating movements)
  • heel - shin ataxia
  • gait/limb/truncal ataxia
  • decreased tone/reflexes
262
Q

What are the levels of clinical severity of ataxia? x3

A

mild - mobilising independently or with one walking aid

moderate - mobilising with 2 walking aids or walking frame

severe - predominantly wheelchair dependent

263
Q

Which blood tests are used in ataxia diagnosis? x4

A
  • FBC, U&E, extended LFT’s
  • HbA1c, B12, folate, TSH
  • ESR, CRP
  • gluten related serology* (can only be requested in sheffield)
264
Q

What is MRI used for in ataxia? x2

A

to demonstrate cerebellar atrophy and/or dysfunction
to exclude cerebrovascular damage, primary tumours, hydrocephalus, demyelinating disorders, white matter disease, cerebellar dysgenesis/malformations

265
Q

What is the bamford classification?

A

Criteria which differentiate the types of ischaemic stroke according to the circulation affected

266
Q

What are the 4 types of stroke according to the Bamford classification?

A

TACS, PACS, POCS, Lacunar stroke

267
Q

What are the 3 features are needed for TACS diagnosis?

A
  • Unilateral weakness and/or sensory deficit of the face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial disorder)
268
Q

What is a TACS?

A

total anterior circulation stroke, which affects the areas of the cortex supplied by both the middle and anterior cerebral arteries

269
Q

What is a PACS?

A

posterior anterior circulation stroke = less severe form of TACS where only part of the anterior circulation has been compromised

270
Q

What criteria need to be present for a diagnosis of PACS?

A

Two of the following:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)

271
Q

What is a POCS?

A

posterior circulation stroke = damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem)

272
Q

What criteria need to be present for a diagnosis of POCS?

A

One of the following:
- cranial nerve palsy and a contralateral motor/sensory deficit
- bilateral motor/sensory deficit
- conjugate eye movement disorder
cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
- isolated homonymous hemianopia

273
Q

What is a lacunar stroke?

A

subcortical stroke which occurs secondary to small vessel disease
no loss of higher cerebral functions

274
Q

What features need to be present for a lacunar stroke diagnosis? x4

A

pure sensory stroke
pure motor stroke
sensori-motor
ataxic hemiparesis

275
Q

What is the presentation of polyneuropathy?

A

glove and stocking loss of sensation

276
Q

What are the causes of neuropathy? x9

A

30% unknown
endocrine- DM, hypothyroidism
inflammatory - Guillain-Barre, CIDP, SLE
infective - lyme disease, HIV
nutritional - Vitamin B12 def, B6 toxicity
metabolic - porphyria, copper def
genetic - CMT disease, Friedrich’s ataxia
neoplastic and paraneoplastic - MGUS, SSCA
drugs - vincristine, phenytoin, amiodarone

277
Q

What nerve palsy causes claw hand? What is the treatment?

A

ulnar nerve
treatment = splint , simple analgesia

278
Q

What nerve palsy causes foot drop? + what is the treatment?

A

peroneal nerve palsy
treatment = physiotherapy, splint/brace + analgesia

279
Q

What is Lambert-Eaton Myasthenic syndrome?

A

progressive muscle weakness which is a result of autoimmune attack directed against the voltage-gated calcium channels on the presynaptic membrane

280
Q

What is the pathophysiology of LEMS?

A

typically occurs in patients with SCLC and is a result of antibodies produced by the immune system against voltage-gated calcium channels in SCLC cells
these antibodies also target and damage voltage-gated calcium channels on the presynaptic motor nerve terminal resulting in a loss of functional voltage gated calcium channels at the motor nerve terminals

281
Q

What are the key presentations of LEMS? x5

A
  • proximal leg muscle weakness
  • affects intraocular muscle causing diplopia, levator muscles causing ptosis, oropharyngeal muscle causing - slurred speech and dysphagia
  • dry mouth, blurred vision, impotence, dizziness due to autonomic dysfunction
  • reduced DTRs
282
Q

What is post-tetanic potentiation?

A

when reflexes can become temporarily normal following period of strong muscle contraction

283
Q

What are the investigations for LEMS?

A

FBC, serology, CT or MRI
Repetitive nerve stimulation studies
Electromyography

284
Q

What are the differential diagnoses for LEMS? x3

A

Acute/chronic inflammatory demyelinating polyradiculopathy
Dermatomyositis
Multiple sclerosis

285
Q

What is the management for LEMS? x4

A

Amifampridine (blocks voltage gated K+ channels in the presynaptic cells)
Immunosuppressants (prednisolone/azathioprine)
IV immunoglobulins
Plasmapheresis

286
Q

What is myasthenia gravis?

A

an autoimmune condition that causes muscle weakness which progressively worsens with exercise and improves on rest

287
Q

What is the pathophysiology of myasthenia gravis?

A

In around 85% of patients with MG, acetylcholine receptor antibodies are produced by the immune system which bind to postsynaptic neuromuscular junction receptors and prevents acetylcholine from stimulating the receptor and triggering muscle contraction.
As the receptors are used more during muscle activity, more of them become blocked up and so muscle weakness increases with use.
The antibodies also activate the complement system leading to damage to cells at the postsynaptic membrane which worsens symptoms.

288
Q

What are the key presentations of myasthenia gravis? x7

A

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
Progressive weakness with repetitive movements

289
Q

What are the investigations for myasthenia gravis?

A

FVC, muscle fatigability testing (repeated blinking → ptosis, prolonged upward gazing → diplopia)
Serology (ACH-R, MuSK, LRP4 antibodies)
CT/MRI, edrophonium test (blocks enzymes and stops breakdown of ACh → temporarily increased ACh and relieved muscle weakness)

290
Q

What is the management for myasthenia gravis? x4

A

Reversible ACh inhibitors (pyridostigmine or neostigmine)
Immunosuppression (prednisolone or azathioprine)
Thymectomy
Monoclonal antibodies (rituximab, ecluzimab)

291
Q

What is a myasthenic crisis?

A

acute worsening of symptoms which can lead to resp failure

292
Q

What is the treatment for a myasthenic crisis?

A

IV immunoglobulins and plasmapheresis

293
Q

What is huntington’s disease?

A

autosomal dominant genetic condition that causes a progressive deterioration in the nervous system

294
Q

What is the aetiology of huntington’s disease?

A

trinucleotide repeat disorder involving the HTT on chromosome 4
<35 repeats –> normal
35-55 –> huntington’s
60+ –> severe huntington’s

295
Q

What is a key feature of the Huntington’s disease affecting genetic inheritance?

A

genetic anticipation which is where successive generations have more repeats resulting in earlier age of onset and increased severity of disease

296
Q

What are the key presentations of Huntington’s? x7

A

Typically begins with cognitive, psychiatric or mood problems (e.g. depression)
Chorea (excessive limb jerking)
Eye movement disorders
Dysarthria
Dysphagia
Dementia
Motor impersistence (can sustain movement)

297
Q

What is the management for HD?

A

no treatment options to slow or stop the progression of the disease
aim of management is to support and maintain quality of life and relieve symptoms
medical: antipsychotics (olanzapine), benzodiazepines (diazepam), dopamine-depleting agents (tetrabenazine), antidepressants
speech and language therapy
genetic couselling
palliative care

298
Q

What is the prognosis of Huntington’s?

A

15-20 years after symptom onset

299
Q

What is Alzheimer’s?

A

the most common form of dementia which progressively destroys memory and cognitive ability

300
Q

What is vascular dementia?

A

dementia resulting from cerebrovascular damage and stroke

301
Q

What are the types of vascular dementia? x3

A

Multi-infarct dementia → series of small strokes which together cause symptoms
Subcortical dementia → small penetrating arteries affected (small vessel damage)
Stroke-related dementia → 3-% of ischaemic strokes lead to this

302
Q

What are the risk factors for dementia? x7

A

Vascular: smoking, diabetes, AF< dyslipidemia, hypertension, age
Age
Genetics
FHx (10-30% increased risk with affected 1st degree relative)
Trisomy 21 (early onset dementia)
Gender - more common in women
Cognitive reserve (social isolation, left education early

303
Q

What is the pathophysiology of alzheimer’s?

A

increased quantities of B-amyloid mostly in hippocampus, parietal and temporal lobes causes damage to brain tissue

304
Q

What is the pathophysiology of vascular dementia

A

reduced blood flow to neurons leading to ischemia and cell death

305
Q

What is the pathophysiology of lewy body dementia?

A

spherical intracellular deposits formed from a-synuclein + ubiquitin

306
Q

What is the pathophysiology of frontotemporal dementia?

A

caused by mutations in TDP43 (DNA binding protein) or TAU protein (microtubule protein)

307
Q

What are the key presentations of alzheimer’s? x4

A

short term memory loss,
difficulty finding words,
poor insight,
disorientation

308
Q

What are the key presentations of vascular dementia? x2

A

stepwise deterioration,
impaired planning, organising, and judgements which present early

309
Q

What are the key presentations of lewy body dementia? x3

A

fluctuating cognition,
visual hallucinations,
parkinsonian features (e.g. bradykinesia, cogwheel rigidity, falls risk, autonomic dysregulation)

310
Q

What are the key presentations of frontal temporal dementia? x3 main variants

A

Behavioural variant (most common) - personality/behaviour changes early on, disinhibition/social withdrawal, pick bodies in cytoplasm

Semantic variant - language difficulties - finding words, comprehension, fluent aphasia

Non-fluent variant - progressive non-fluent speech

311
Q

What are the investigations for dementia?

A

clinical history + physical exam, MMSE
brain biopsy (GS)
bloods, CT head, genetic testing

312
Q

What is the management for dementia?

A

Conservative, risk reduction, slow progression ; social stimulation, exercise
No cure
For Alzheimer’s = Acetylcholinesterase-inhibitors (Donepezil/Rivastigmine)
Vascular = hypertensives e.g. ramipril

313
Q

What are cluster headaches?

A

unilateral periorbital pain with autonomic features (15-180 mins duration)

314
Q

What are the risk factors for cluster headaches? x3

A

Male
Smoking
Genetics

315
Q

What are the key presentations of cluster headaches? x6

A

Crescendo unilateral periorbital excruciating pain, may affect temples too
Autonomic features of face flushing
Conjunctival infection + lacrimation
Ptosis
Miosis
Rhinorrhoea (running nose)

316
Q

What confirms diagnosis of cluster headache?

A

5 ≤ similar attack

317
Q

What is the management for cluster headaches?

A

Acute = triptans (sumatriptan)
Prophylaxis = verapamil (CCB)

318
Q

What are tension headaches?

A

bilateral generalised headaches which radiate to neck

319
Q

What are the risk factors for tension headaches? x8

A

Stress
Sleep deprivation
Bad posture
eyestrain
Depression
Alcohol
Skipping meals
dehydration

320
Q

What are the key presentations for tension headaches?.

A

Rubber band, tight around head, bilateral pain, also feel it in trapezius
mild -moderate severity
No motion sickness, photophobia, aura

321
Q

What is the treatment for tension headaches?

A

simple analgesia

322
Q

What is trigeminal neuralgia?

A

Unilateral pain in 1≤ trigeminal branches (90%)
10% are bilateral

323
Q

What are the triggers of trigeminal neuralgia? x8

A

eating,
shaving,
talking,
brushing teeth,
cold weather,
spicy food,
caffeine
and citrus fruits

324
Q

What are the risk factors for trigeminal neuralgia? x3

A

MS (20x more likely)
Increased age
Female

325
Q

What does trigeminal neuralgia feel like?

A

electric shock pain lasting up to 2 mins

326
Q

What is the management for trigeminal neuralgia?

A

Treatment = carbamazepine (anti-convulsant)
Consider surgery if no other treatment effective (decompression or intentional damage to trigeminal nerve e.g. stereotactic radiotherapy)

327
Q

What is cauda equina syndrome?

A

surgical emergency caused by compression of the nerve roots of the cauda equina

328
Q

What are the causes of cauda equina syndrome? x5

A

Compression can be caused by:
Herniated disc
Tumours
Spondylolisthesis
Abscess
Trauma

329
Q

What are the risk factors for cauda equina syndrome? x8

A

Lumbar disc herniation
Spinal trauma
Spinal surgery
spinal epidural abscess
Anticoagulation therapy
Spinal stenosis
Spinal tumour
Under 50yrs old

330
Q

What are the key presentations of cauda equina syndrome? x7

A

Bladder dysfunction
Lower limb weakness
Saddle paraesthesia/anaesthesia
Bowel dysfunction
Lower back pain
Sciatica
Sexual dysfunction

331
Q

What is the gold standard investigation for cauda equina syndrome?

A

Spinal MRI + testing nerve roots/reflexes

332
Q

What is the management for cauda equina syndrome?

A

Emergency decompression surgery to prevent permanent neurological dysfunction

333
Q

What are the red flags for cauda equina syndrome? x7

A

saddle anaesthesia,
loss of sensation in bladder or rectum,
urinary retention or incontinence, faecal incontinence,
bilateral sciatica,
bilateral or severe motor weakness in the legs ,
reduced anal tone on PR examination

334
Q

What is spinal cord compression?

A

compression of C1-L1/2

335
Q

What are the risk factors for spinal cord compression? x5

A

Cancer + metastases
≥40 years old
Immune system disorders
Radiation
Genotype features

336
Q

What are the key presentations of spinal cord compression? x4

A

progressive leg weakness with limbs signs (e.g. contralateral hyperreflexia, Babinski +ve, spasticity)
back pain
sensory loss below lesion
sphincter involvement uncommon (late = v bad sign)

337
Q

What is the gold standard investigation for spinal cord compression?

A

MRI, CXR if malignancy suspected

338
Q

What is the management for spinal cord compression?

A

neurosurgery - laminectomy, microdisectomy

339
Q

What is sciatica?

A

L5/S1 lesion due to spinal; IV disc herniation/prolapse
non-spinal; piriformis syndrome, tumours, pregnancy

340
Q

What is distinctive about the pain in sciatica?

A

the pain radiates through the buttock and back of one leg
it is often described as a shooting pain, although some patients report numbness or tingling/burning sensation along the nerve path in the leg

341
Q

What are the causes of sciatica? x3

A

herniated disc, sponylolisthesis, spinal stenosis

342
Q

What are the risk factors for sciatica? x5

A

Age
Obesity
Occupation
Prolonged sitting
Diabetes

343
Q

What are the investigations for sciatica?

A

Sciatic stretch test - can’t perform straight leg raise test without pain
Spinal MRI (GS)

344
Q

What is the management for sciatica?

A

Analgesia + physiotherapy
Neuropathic med if symptoms persisting/worsening - amitriptyline, duloxetine
Neurosurgery

345
Q

What is raised ICP?

A

Increased intracranial pressure which occurs when a brain injury or other problem causes the brain to press on the skull

346
Q

What are some potential causes of raised ICP? x8

A
  • hydrocephalus
  • traumatic haematomas
  • tumours (glioma, meningioma)
  • abscess
  • focal oedema secondary to trauma, infarction, tumour
  • obstruction to major venous sinuses
  • diffuse brain oedema or swelling e.g. encephalitis, meningitis, SAH, near drowning
  • idiopathic intracranial hypertension
347
Q

What are the symptoms of raised ICP? x9

A

Headache
Blurred vision, pupillary changes
Vomiting
Confusion
Hypertension
Shallow breathing
Changes in behaviour - slow decision making, abnormal social behaviour
Weakness or mobility problems (hemiparesis)
Fatigue, drowsiness

348
Q

What is a sign of sustained high ICP?

A

papilledema

349
Q

What is a late sign of raised ICP and what is the causative pathology?

A

fixed dilated pupil
result of unopposed pressure on parasympathetic fibres on the outside of the oculomotor nerve (CNIII) leading to there being only sympathetic innervation of the iris –> pupil is constantly dilated

350
Q

What are the investigations for raised ICP? x5

A

Nervous system examination
GCS assessment
Spinal tap (measure the pressure of cerebrospinal fluid)
CT scan
MRI

351
Q

What is the treatment for raised ICP? x6

A

Anticonvulsants to manage seizures
CSF drainage using an intraventricular catheter
Head of bed elevation
Analgesia and sedation (usually with propofol, etomidate or midazolam and morphine or alfentanil)
Neuromuscular blockade
Treat underlying cause

352
Q

What is a serious potential complication of raised ICP?

A

brain herniation - when the ICP is so great that is forces brain tissue through one of the rigid intracranial barriers (tentorial notch, falx cerebri, foramen magnum)

353
Q

What is Cushing’s reflex?

A

Systolic hypertension with a triad of increased pulse pressure, irregular respirations and bradycardia as a result of raised ICP

354
Q

What is a coma?

A

a state of profound unconsciousness caused by disease, injury or poison

355
Q

What are the signs of coma? x6

A

unresponsive and unrousable
closed eyes
depressed brainstem reflexes (e.g. unresponsive pupils)
no limb response except reflex movements
no response to painful stimuli except for reflexes
irregular breathing

356
Q

How is coma assessed?

A

Using the Glasgow coma scale:
3 - indicates deep coma or death
<8 - severe reduction in consciousness and patient unlikely to be able to maintain their airway spontaneously - require intubation and ventilation

Using the AVCPU scale - unresponsive

357
Q

What is the management for coma? x5

A

resuscitation with intubation and ventilation + rehydration (if needed)
intravenous thiamine and glucose (for patients without clear diagnosis)
trial naloxone or flumazenil
treat underlying cause
raised ICP may require mannitol infusion

358
Q

What is a persistent vegetative state?

A

where patients have lost cognition and external awareness, but retain non-cognitive brain function and normal or near-normal sleep-wake cycle

359
Q

What is spinal stenosis?

A

narrowing of the spinal canal or neural foramina producing root ischaemia and neurogenic claudication (muscle pain due to lack of oxygen which is triggered by activity and relieved by rest)

360
Q

What are the risk factors for spinal stenosis?

A

Congenital narrowing of the spinal cord
Hyperparathyroidism
Paget’s disease of bone
Ankylosing spondylitis
Cushing’s syndrome
Acromegaly

361
Q

What is the most common cause of spinal stenosis?

A

degenerative arthritis of the spine

362
Q

What are the key presentations of spinal stenosis? x5

A

neck pain with restricted ROM of the neck (cervical spine stenosis)
gait instability
loss of fine motor control of the upper limbs
weakness and sensory disturbance in the upper and lower limbs
urinary urge incontinence

363
Q

What are the investigations for spinal stenosis?

A

lumbar spine XR
lumbar spine MRI
CT myelography if MRI unavailable

364
Q

What are the differentials for spinal stenosis? x6

A

Cauda equina syndrome
Peripheral arterial disease
Spinal tumours
Large central disc herniation
Spondylolisthesis
Lumbar spine trauma

365
Q

What is the management for spinal stenosis?

A

NSAIDs, physiotherapy and epidural steroid injections
Surgery - occasionally indicated for patients not responding to conservative measures however there is currently little evidence on the efficacy of surgery in treating lumbar spinal stenosis

366
Q

What is narcolepsy?

A

a chronic neurological disorder in which the brain loses its normal ability to regulate the sleep-wake cycle

367
Q

What are the 2 types of narcolepsy?

A

Type 1 narcolepsy involves cataplexy and patients have low levels of orexin in their CSF

Type 2 does not involve cataplexy (more common, 80%)

368
Q

What is cataplexy?

A

a sudden loss of voluntary muscle tone with preserved consciousness, triggered by emotion

369
Q

What are the features of a cataplexy attack? x5

A
  • severity can vary e.g. from barely susceptible slackening of the facial muscles, dropping of the jaw or the entire head, to weakness at the knees or collapse onto the floor
  • slurred speech and visual symptoms
  • intact hearing, awareness and consciousness
  • variable frequency
  • usually bilateral weakness
370
Q

What are the risk factors for narcolepsy?

A

aged 10-30
family history
traumatic brain injury
certain HLA subtypes

371
Q

What are the key presentations of narcolepsy? x5

A

excessive daytime sleepiness (EDS)
disrupted nighttime sleep and/or vivid dreams
cataplexy caused by muscle atonia
hypnagogic/hypnopompic hallucinations
sleep paralysis

372
Q

What are the investigations for narcolepsy?

A

polysomnography
multiple sleep latency testing
CSF orexin levels

373
Q

What are the differentials in narcolepsy diagnosis?

A

obstructive sleep apnoea
sleep deprivation
automatism
sleep paralysis

374
Q

w

A
  • good sleep hygiene
  • scheduled naps
  • central nervous system stimulants (1st line: modafinil)
  • antidepressants (for cataplexy) e.g. clomipramine, SSRIs, venlafaxine
  • sodium oxybate (potent sedative which improves nocturnal sleep quality)
  • support and modifications (with school/work)
375
Q

What is shingles?

A

also known as herpes zoster virus, shingles is a disease which triggers a painful skin rash in a dermatomal distribution

376
Q

What causes shingles?

A

human herpesvirus-3

primary infection usually occurs in childhood, producing chickenpox (varicella)

after this the virus lies dormant in the sensory nervous system but is susceptible to reactivation in patients over 50 years old and is associate with immunosuppressive illness, or psychological/physical trauma

377
Q

What are the risk factors for shingles? x3

A

increased age (50+)
immunocompromise
HIV, Hodgkin’s lymphoma and bone marrow transplants

378
Q

What are the 3 phases of shingles infection?

A

Pre-eruptive phase
- itching, burning and paresthesia of single dermatome with flu-like symptoms but no visible rash
Eruptive phase
- appearance of skin lesions which form crusts over 7-10 days, accompanied by acute neuritic pain
Chronic phase
- postherpetic neuralgia - persistent or recurring pain lasting 30+ days after acute infection

379
Q

What are the investigations for shingles?

A

usually clinical diagnosis based on typical lesions in a single dermatome
PCR test, Tzanck smear

380
Q

What are the differentials for shingles? x5

A

atopic eczema, eczema herpeticum, contact dermatitis, herpes simplex or impetigo

381
Q

What is the management for shingles? x3

A

rash care
oral acyclovir
analgesia

382
Q

What is cerebral palsy?

A

An umbrella term which encompasses a group of permanent movement and posture disorders which limit activity

383
Q

What are the 4 types of cerebral palsy?

A

Spastic type - intermittently increased tone and pathological reflexes

Athetoid - characterised by increased activity (hyperkinesia)

Ataxic type - loss of orderly muscular coordination so that movements are performed with abnormal force, rhythm or accuracy

Mixed - there may be a combination of several forms

384
Q

What causes cerebral palsy?

A
  • acquired pathology within the developing brain during the prenatal or early infant period
  • the impaired movement associated with CP results from centrally-mediated abnormal muscle tone which leads (most commonly) to spasticity
  • the main causes are prematurity, multiple gestation, and maternal infection
385
Q

What are the antenatal risk factors for cerebral palsy? x6

A

preterm birth
congenital malformations
multiple births
intrauterine infections
chorioamnionitis
toxic or teratogenic agents

386
Q

What are the perinatal risk factors for cerebral palsy? x4

A

low birth weight
neonatal encephalopathy
neonatal sepsis
intraventricular haemorrhage

387
Q
A
388
Q

What are the postnatal risk factors for cerebral palsy? x7

A

meningitis
intracranial haemorrhage
trauma
infection
hyperbilirubinaemia
hypoxia
seizures

389
Q

What are the key presentations of cerebral palsy? x7

A
  • low Apgar score 5 mins post birth
  • delayed developmental milestones
  • abnormalities of posture and movement are common throughout the different types of cerebral palsy
  • unusual fidgety movements or other abnormalities of movement, including asymmetry or paucity of movement
  • abnormalities of tone, including hypotonia, spasticity or dystonia
    abnormal motor development, including late head control, rolling and crawling
  • feeding difficulties
  • non motor problems such as learning disabilities, difficulties with communication, emotion and behaviour, visual impairment, pain
390
Q

What are the investigations for cerebral palsy?

A

diagnosis is based on clinical examination and parental observations

also:
- thyroid studies
- chromosomal analysis
- MRI/CT

391
Q

What are the differentials for cerebral palsy? x6

A

Acute poliomyelitis
Becker’s muscular dystrophy
Charcot-Marie-Tooth disease
Kugelberg-Welander spinal muscular atrophy
Neonatal brachial plexus palsies
Stroke motor impairment

392
Q

What is the management for cerebral palsy?

A

Different for every individual
Significant involvement of physios, OTs, speech therapists and recreational therapists
Mobility aids, splinting
Oral diazepam or baclofen in children and young people if spasticity is contributing to discomfort or pain, muscle spasms or functional disability

393
Q

What is type 1 neurofibromatosis (NF1)?

A

also known as von Recklinghausen’s disease
genetic disorder causing lesions in the skin, nervous system and skeleton

394
Q

What is the cause of NF1?

A

a defect in the gene NF1
- neurofibromin, the gene product, is a ubiquitous nervous system protein and is believed to act as a tumour suppressor
- loss of neurofibromin leads to an increased risk of developing benign and malignant tumours but the effects of a mutation are very variable and can appear at any age due to a variety of mutations, differing penetration and mosaicism

395
Q

What are the symptoms of/criteria for NF1 diagnosis?

A
  • Cafe au lait spots
  • Neurofibromas
  • Freckling
  • Optic glioma
  • ≥2 Lisch nodules
  • Bone lesions
  • [1st degree relative with NF1] not a symptoms but a diagnostic criterion
396
Q

What are the investigations for NF1?

A

Usually clinically diagnosed
MRI
CT/XR

397
Q

What is the management for NF1?

A

no curative treatment
symptomatic neurofibromas are often removed, or in some cases treated neurologically
many patients have hundreds of cutaneous lesions so it is not possible or practical to removed them all
genetic counselling should be given to all patients

398
Q

What is type 2 Neurofibromatosis?

A

a much rarer, central form of neurofibromatosis with CNS tumours rather than skin lesions

399
Q

What is schwannomatosis?

A

a recently recognised form of neurofibromatosis, characterised by multiple non-cutaneous schwannomas

400
Q

What is Horner’s syndrome?

A

a rare condition which results from disruption to the sympathetic nerves supplying the eye

401
Q

What is the characteristic triad seen in Horner’s syndrome?

A

partial ptosis (upper eyelid drooping)
miosis (pupillary constriction)
hemifacial anhidrosis

402
Q

What are the central lesion causes of Horner’s syndrome? (4S’s)

A

Stroke
Multiple Sclerosis
Swelling
Syringomyelia (cyst in the spinal cord)

403
Q

What are the preganglionic lesion causes of Horner’s syndrome? (4T’s)

A

Tumour (Pancoast tumour)
Trauma
Thyroidectomy
Top rib

404
Q

What are the postganglionic lesion causes of Horner’s syndrome?

A

Carotid aneurysm
Carotid artery dissection
Cavernous sinus thrombosis
Cluster headache

405
Q

What are the investigations for Horner’s syndrome?

A

guided by suspected cause
CXR
CT/MRI
CT angiography/carotid USS
Pharmacological testing

406
Q

What is the management for Horner’s syndrome?

A

Horner’s syndrome is a physical sign so management involves diagnosis of the underlying condition and treatment specific to diagnosis

407
Q

What is Bell’s palsy?

A

a condition causing sudden weakness in the muscle on one side of the face

408
Q

What are some of the viruses which have been linked to Bell’s palsy? x9

A

herpes simplex
herpes zoster
EBV
cytomegalovirus infections
adenoviruses
rubella
mumps
influenza B
coxsackievirus

409
Q

What are the risk factors for Bell’s palsy?

A

20-50 yr olds
pregnancy
diabetes mellitus
hypertension
obesity

410
Q

What is the pathophysiology of Bell’s palsy?

A

the nerve that controls facial muscles passes through a narrow corridor of bone on its way to the face
in Bell’s palsy that nerve becomes inflamed and swollen - usually related to a viral infection

411
Q

What are the key presentations of Bell’s palsy?

A

rapid onset unilateral facial nerve weakness
generalised weakness of affected side
severe cases may also present with notable loss of taste sensation (classically anterior 2/3 of tongue), intolerance of high-pitched noises, mild dysarthria
lower motor neuron signs (forehead affected, unlike in UMN lesions where there is forehead sparing)

412
Q

What are the investigations for Bell’s palsy ?

A

usually clinically diagnosed, based on the clinical signs
House-Brackmann scale is occasionally used to describe the degree of paralysis (scale 1-6, 1 is normal, 6 is total paralysis)

413
Q

What are the differentials for Bell’s palsy?

A

Ramsay-Hunt syndrome
Guillain-barre syndrome
Lyme disease

414
Q

What is the management for Bell’s palsy?

A

steroids - prednisolone
antivirals - acyclovir
eye-care - reduced eye closing can lead to dry eye and corneal damage

415
Q

What is Bulbar palsy?

A

a condition caused by lesions in the motor nuclei of the medulla, so called bulbar palsy because this region of the brain is sometimes called the ‘bulb’ of the brainstem

416
Q

What are the causes of Bulbar palsy? x7

A

MND
Guillain-Barre Syndrome
Polio
Syringobulbia
Brainstem tumours
Myasthenia gravis
Myotonic dystrophy

417
Q

What are the key presentations of bulbar palsy? x8

A

Tremulous lips
Weak and wasted tongue which fasciculates in the mouth (‘bag of worms’)
Drooling
Absent palatal movements
Dysphonia
Articulation - difficulty pronouncing r; unable to pronounce consonants as dysarthria progresses
If the pathology progresses then speech becomes slurred and eventually becomes indistinct
There may also be neurological deficits in the limbs - e.g. flaccid tone, weakness with fasciculations

418
Q

What are the investigations for bulbar palsy? x5

A

electromagnetic articulography (EMA)
electropalatography (EPG)
pressure sensing EPG
routine bloods, brain/brainstem imaging, electromyography

419
Q

What is the management for Bulbar palsy?

A

treatment is directed to underlying cause
postural changes can help with drooling of saliva and may prevent aspiration
supportive measures
support from SALT and dieticians

420
Q

What is radiculopathy?

A

a clinical condition involving one or more nerves resulting in impaired function (neuropathy)

421
Q

What are the causes of radiculopathies? x6

A

degenerative disc disease
osteoarthritis
facet joint degeneration/hypertrophy
ligamentous hypertrophy
certain injuries e.g. car accident trauma
less common causes include injury by tumours and diabetes

422
Q

What are the risk factors for radiculopathy? x3

A

female
caucasian
smoking

423
Q

What are the key presentations of radiculopathy? x3

A

depends on nerves affected
most common symptoms;
- pain
- numbness
- tingling

424
Q

What is the management for radiculopathy? x5

A

ice or heat
adjusting posture or physiotherapy
OTC NSAIDs
corticosteroids
surgery

425
Q

What is meniere’s disease?

A

a disorder of the inner ear caused by a change in the fluid volume in the labyrinth

426
Q

What are the causes of meniere’s disease?

A

exact cause in unknown but thought to be a multifactorial and linked to:
- Allergy
- Autoimmunity
- Genetic susceptibility
- Metabolic disturbances involving the balance of sodium and potassium in the fluid of the inner ear
- Vascular factors
- Viral infection, otosyphilis, Cogan’s syndrome (non-syphilitic interstitial keratitis and bilateral audiovestibular deficits

427
Q

What are the 3 core symptoms of Meniere’s disease?

A
  • vertigo
  • tinnitus
  • fluctuating hearing loss with a sensation of aural pressure
428
Q

What is the pattern of symptoms in Meniere’s disease? x4

A
  • acute attacks typically last mins-hrs
  • acute episodes may occur in clusters of around 6-11 per year
  • remission of symptoms may last several months
  • most patients develop unilateral symptoms initially with bilateral symptoms sometimes developing later
429
Q

What are some investigations for Meniere’s disease? x4

A

bloods
audiometry
visual nystagmography
MRI

430
Q

What are some differentials for Meniere’s disease? x6

A

Acoustic neuroma
Otitis media
Earwax
Ototoxic drugs
Intracranial pathology e.g. tumours, migraine
Systemic illness e.g. anaemia, hypothyroidism

431
Q

What are the aims of therapy in Meniere’s disease? x4

A

alleviate acute attacks,
reduce severity and frequency of attacks,
improve hearing
reduce the impact of tinnitus

432
Q

What is are the medical managements for Meniere’s disease? x4

A

motion sickness medications (meclizine, diazepam)
antinausea medications (promethazine)
diuretics (furosemide, chlorthalidone)
middle ear injections (gentamicin)

433
Q

What procedures can be used treat Menieres disease?

A

endolymphatic sac procedure (help with decompression)
vestibular nerve section (helps to correct vertigo and maintain hearing)
labyrinthectomy (removal of labyrinth)

434
Q

What lifestyle changes/therapy input are indicated in Meniere’s disease?

A

hearing aids
vestibular rehab therapy
low sodium diet
avoid caffeine, alcohol

435
Q

What is giant cell arteritis?

A

also known as temporal arteritis

A type of systemic vasculitis affecting the medium and large arteries, there is a strong link with polymyalgia rheumatica

436
Q

What are the key presentations of GCA?

A

Unilateral headache typically severe and around the temple and forehead

Can be associated with:
Scalp tenderness
Jaw claudication
Blurred or double vision
Loss of vision if untreated

437
Q

What are some other features associated with GCA? x5

A

Symptoms of polymyalgia rheumatica
Systemic symptoms (e.g. weight loss, fatigue and low-grade fever)
Muscle tenderness
Carpal tunnel syndrome
Peripheral oedema

438
Q

What are the investigations for GCA?

A

usually clinically diagnosed

Inflammatory markers
Temporal artery biopsy (showing multinucleated giant cells)
Duplex USS (showing the hypoechoic “halo” sign and stenosis of the temporal artery

439
Q

What is the management for GCA?

A

Steroids are the main treatment and started immediately even before diagnosis is confirmed to reduce the risk of vision loss

  • 40-60mg prednisolone with no visual symptoms or jaw claudication
  • 500-1000mg methylprednisolone with visual symptoms/jaw claudication

Once diagnosis is confirmed and the condition is controlled, the steroid dose is slowly weaned over 1-2 years

Other medications include:
- Aspirin
- PPI for gastric protection on steroids
- Bisphosphonates and calcium and vitamin D for bone protection on steroids

440
Q

What are the potential complications of GCA?

A

Visual loss
Steroid -related complications e.g. cushingoid symptoms
Cerebrovascular accident e.g. stroke

441
Q

What is myalgic encephalomyelitis?

A

also known as chronic fatigue syndrome

A complex, chronic medical condition affecting multiple body systems and of unknown cause which has many different presentations

442
Q

What is the aetiology of myalgic encephalomyelitis?

A

Underlying cause is not well understood
Approximately 50-80% of people with ME start suddenly with a flu-like illness
Often found after infection suggesting an immunological dysfunction
Strong genetic predisposition
Life stressors

443
Q

What are the key presentations of myalgic encephalitis? x5

A

Debilitating fatigue
Post-exertional malaise
Unrefreshing sleep or sleep disturbance
‘Brain fog’
Significantly reduced ability to engage in occupational, educational, social or personal activities

444
Q

What are some other potential symptoms of myalgic encephalitis?x7

A

Orthostatic intolerance and autonomic dysfunction (e.g. dizziness, palpitations, fainting…)
Temperature hypersensitivity
Neuromuscular symptoms
Flu-like symptoms
Intolerance to alcohol
Heightened sensory sensitivities
Pain

445
Q

What are some differentials for myalgic encephalitis? x4

A

Postural tachycardia syndrome
Hypothyroidism, diabetes, anaemia
Metabolic muscle disorders
Psychiatric illness

446
Q

What is the management for myalgic encephalitis?

A

Lifestyle advice - pace yourself, rest as needed, maintain health diet, work adjustments
CBT

447
Q

What is acoustic neuroma?

A

a rare non-cancerous tumour which grows slowly from overproduction of schwann cells. It presses on the hearing and balance nerves in the inner ear and causes hearing loss and other auditory symptoms

448
Q

What is a febrile seizure?

A

a seizure accompanied by fever (temperature >38 degrees) without CNS infection, which occurs in infants and children aged 6mo-6yrs

449
Q

What is the difference between simple and complex febrile seizures?

A

simple = isolated, generalised, tonic-clonic seizures lasting <15 mins and don’t recur within 24 hrs of with same febrile illness, complete recovery in 1 hr
complex= 1 or more of a partial seizure, duration of 15+ mins, recurrence within 24 hrs or within same febrile illness and in complete recovery within 1 hr

450
Q

What is diabetic neuropathy?

A

peripheral nerve damage as a result of diabetes mellitus most commonly resulting in pain, burning, tingling or numbness in the toes or feet and extreme sensitivity to light touch

451
Q

What are the 4 main components of diabetic neuropathy treatment?

A

control of blood sugar levels
lifestyle interventions, specifically diet and exercise
care for the feet to prevent complications
control of pain caused by neuropathy

452
Q

What is anterior cord syndrome?

A

an incomplete spinal cord injury which is often related to flexion injuries of the cervical region which result in infarction of the anterior 2/3s of the cord and/or its vascular supply from the anterior spinal artery

453
Q

What are the key presentations of anterior cord syndrome?

A

impairments in the pain and temperature sensations bilaterally while vibratory and proprioceptive sensations are preserved
the corticospinal tracts are also likely to have been affected resulting in bilateral spastic paralysis and UMN signs

454
Q

What is syringomyelia?

A

also called central cord syndrome occurs due to the development of a fluid filled cyst (a syrinx) around the spinal canal

455
Q

What are the key presentations of syringomyelia?

A
  • the pattern of deficit seen in patients with syringomyelia initially seems confusing as it is different from other syndromes
  • the upper limbs are affected first whilst the lower limbs are spared until much later
  • as the cervical cord is the most likely location of the lesion, there is classically said to be a “cape-like” loss of pain and temperature sensation
456
Q

What is hydrocephalus?

A

abnormal build up of CSF within the brain and spinal cord, this is a result of either over-production of CSF or a problem with draining or absorbing CSF

457
Q

Where is CSF created and absorbed?

A

CSF is created in the four choroid plexuses (one in each ventricle) and by the walls of the ventricles
CSF is absorbed in to the venous system b the arachnoid granulations

458
Q

How is hydrocephalus classified?

A

Non-communicating/obstructive - the flow of CSF is obstructed within the ventricles or between the ventricles and the subarachnoid space
Communicating - there is communication between the ventricles and the subarachnoid space and the problem lies outside of the ventricular system (e.g. due to reduced absorption or blockage of the venous drainage system), may also be due to increased CSF production

459
Q

What is normal pressure hydrocephalus (NPH)?

A

ventricular dilatation in the absence of raised CSF pressure

460
Q

What is the classic triad of symptoms in NPH?

A

gait abnormality
urinary incontinence
dementia

461
Q

What are the investigations for NPH?

A

neuroimaging
large-volume lumbar puncture
intraventricular pressure monitoring
lumbar infusion test (intrathecal test)

462
Q

What are the treatments for NPH?

A

Medical = Carbonic anhydrase inhibitors (acetazolamide) and repeated lumbar puncture

Surgical = ventriculo-peritoneal shunt insertion (1st line), ventriculo-atrial shunt is an alternative

463
Q
A

Phase 3A (10 decks)

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