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Phase 2A > Neuroscience > Flashcards

Neuroscience Flashcards

1
Q

What types of fibres are carried by the spinal nerves?

A

somatic motor and somatic sensory fibres
sympathetic fibres

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2
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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3
Q

What is the effect of lesions in the spinothalamic tract?

A

contralateral loss of/impaired pain and temperature sensation

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4
Q

What is a dermatome?

A

area of skin supplied by a single spinal nerve

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5
Q

What is a myotome?

A

muscles supplied by a single spinal nerve

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6
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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7
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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8
Q

WHat is the test for CN IV function?

A

ask patient to look medially and down

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9
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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10
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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11
Q

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

A

taste anterior 2/3
muscles of facial expression

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12
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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13
Q

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

A

taste posterior 1/3 of tongue
gag reflex

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14
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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15
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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16
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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17
Q

What are the 3 symptoms of meningism?

A

neck stiffness
photophobia
severe headache

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18
Q

What are the common bacterial causes of meningism in neonates?

A

E. coli
Group B streptococcus
Listeria monocytogenes

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19
Q

What are the common causes of bacterial meningitis in infants?

A

Neisseria meningitidis
Haemophilus influenzae
Streptococcus pneumoniae

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20
Q

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

A

Neisseria meningitidis
Streptococcus pneumoniae

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21
Q

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

A

Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes

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22
Q

What % of meningitis cases are caused by viruses?

A

80%

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23
Q

Which viruses can cause meningitis?

A

enteroviruses (echo virus, coxsackie virus)
herpes simplex virus
mumps virus
lymphocytic chorio meningitis virus
historically poliovirus

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24
Q

What is meningitis?

A

inflammation of the meninges

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25
Q

What are the fungal causes of meningitis?

A

cryptococcus, histoplasma, blastomyces

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26
Q

What are the risk factors for meningitis?

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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27
Q

What is the pathophysiology of bacterial meningitis?

A
  1. bacteria reach the CNS by haematogenous or contiguous spread and colonise the arachnoid space
  2. bacterial components in the CSF induce the production of various inflammatory mediators
  3. this leads to an influx of leukocytes into the CSF
  4. the inflammatory cascade leads to cerebral oedema and increased ICP
  5. result is neurological damage and even death
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28
Q

What are the key presentations of meningitis?

A

meningism
fever
altered consciousness
seizures

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29
Q

What are the 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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30
Q

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

A

hypotonia
poor feeding
lethargy
hypothermia
bulging fontanelle

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31
Q

What are the investigations for meningitis?

A

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

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32
Q

What is the mortality rate of treated bacterial meningitis?

A

5%

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33
Q

What are the bacterial causes of acute meningitis\?

A

Neisseria meningitidis (gram negative diplococci)
Strep. pneumoniae (gram positive diplococci)
Listeria spp. (gram positive rod)
Group B Strep (gram positive cocci)
Haemophilus influenzae B (gram negative rod)
E.coli (gram negative rod)

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34
Q

What are the bacterial causes of chronic meningitis

A

Mycobacterium tuberculosis (TB) (Phenol-auramine)
Syphilis §

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35
Q

What is the management for bacterial meningitis?

A

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

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36
Q

What is the management for viral meningitis?

A

none if enteroviral cause
Aciclovir if cause is HSV or VZV

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37
Q

What is the management for fungal meningitis?

A

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

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38
Q

What is encephalitis?

A

inflammation of the cerebral cortex

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39
Q

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

A

meningo-encephalitis

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40
Q

Which viruses can cause encephalitis?

A

Herpes simplex
varicella zoster
parvoviruses
HIV
mumps
measles

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41
Q

What are the risk factors for encephalitis?

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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42
Q

What is the pathophysiology of encephalitis?

A

in viral encephalitis the virus gains entry and replicates in local or regional tissue, such as the GI tract to skin and then disseminates to the CNS via haematogenous routes (enterovirus, HSV, HIV, mumps) or retrograde axonal transport (herpes virus, rabies)

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43
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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44
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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45
Q

What are the investigations for encephalitis?

A

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

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46
Q

What is the management for encephalitis?

A

aciclovir

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47
Q

What are the complications of encephalitis?

A

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

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48
Q

What is the definition of a stroke?

A

acute neurological deficit lasting more than 24hrs of cerebrovascular cause

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49
Q

What percentage of strokes are ischaemic/haemorrhagic?

A

Ischaemic - 80%
Haemorrhagic - 20%

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50
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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51
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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52
Q

What are the pathological subtypes of haemorrhagic stroke?

A

primary intracerebral haemorrhage
subarachnoid haemorrhage

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53
Q

What are the causes of ischaemic stroke?

A

thrombus formation or embolus
atherosclerosis
shock
vasculitis

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54
Q

What are the causes of haemorrhagic stroke?

A

trauma
hypertension
berry aneurysm rupture

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55
Q

What are the risk factors for stroke?

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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56
Q

What is the pathophysiology of ischaemic stroke?

A

blood supply in a cerebral vascular territory is critically reduced due to occlusion or critical stenosis of a cerebral artery

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57
Q

What is the pathophysiology of haemorrhagic stroke?

A

cerebral vascular rupture causes bleeding into the brain parenchyma resulting in a primary mechanical injury to the brain tissue

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58
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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59
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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60
Q

What are the investigations for stroke?

A

Non-contrast CT head
Bloods - serum glucose, electrolytes, U+Es, cardiac enymes, FBC
ECG
PT and aPTT
carotid doppler
ECHO
CT or MR angiogram

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61
Q

What is the ROSIER tool?

A

Recognition Of Stroke In the Emergency Room

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62
Q

What are the differential diagnoses for stroke?

A

hypoglycaemia
hypertensive encephalopathy
TIA

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63
Q

What is the management for ischaemic stroke?

A

Thombolysis with alteplase
Thrombectomy (mechanical removal of clot)

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64
Q

What is the management for haemorrhagic stroke?

A

IV mannitol for ↑ICP

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65
Q

What is the secondary prevention for stroke?

A

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

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66
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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67
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

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68
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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69
Q

What are the causes of TIAs?

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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70
Q

What are the risk factors for TIA?

A

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

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71
Q

What are the key presentations of TIAs?

A

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

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72
Q

What are the investigations for TIAs

A

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

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73
Q

What are the differential diagnoses for TIA?

A

stroke
hypoglycaemia
seizure
complex migraine

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74
Q

What is the management for TIA

A

aspirin 300mg daily
secondary prevention for CVD/stroke

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75
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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76
Q

What are the causes of subarachnoid haemorrhage

A

MC: berry aneurysm rupture in the circle of willis
trauma

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77
Q

What are the risk factors for subarachnoid haemorrhage?

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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78
Q

What are the key presentations for subarachnoid haemorrhage?

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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79
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 uncelar –> lumbar puncture (xanthochromia)

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80
Q

What is the management for subarachnoid haemorrhage?

A

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

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81
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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82
Q

What are the risk factors for subdural haemorrhage

A

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

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83
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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84
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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85
Q

What are the signs of ↑ICP?

A

Cushing’s triad: bradycardia, increased pulse pressure, irregular breathing + fluctuating GCS + papilloderma

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86
Q

What are the symptoms of subdural haemorrhage?

A

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

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87
Q

What is the investigation for subdural haemorrhage/

A

NCCT head (banana, crescent-shaped haematuria)

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88
Q

What is the management for subdural haemorrhage?

A

sugery: burr hole + craniotomy
IV mannitol to ↓ICP

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89
Q

What is an extradural haemorrhage?

A

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

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90
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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91
Q

What are the risk factors for extradural haemorrhage?

A

head trauma
age 20-30yrs

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92
Q

What are the key presentations of extradural haemorrhage?

A

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

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93
Q

What is the gold standard investigation for extradural haemorrhage?

A

NCCT (lemon/lens shaped haematoma)

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94
Q

What is the management for extradural haemrorrhage?

A

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

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95
Q

What are the differentials for extradural haemorrhage?

A

epilepsy
carotid dissection
carbon monoxide poisoning
subdural haematoma
subarachnoid haemorrhage

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96
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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97
Q

What are the causes of amaurosis fugax

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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98
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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99
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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100
Q

What is the aetiology of MS?

A

unclear but thought to be a combination of:
- multiple genes
- Epstein-Barr virus
- Low vitamin D
- Smoking
- Obesity

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101
Q

What are the risk factors for MS?

A

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

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102
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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103
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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104
Q

What are the atypical symptoms of MS?

A

aphasia, hemianopia, extrapyramindal movement disorders, severe muscle wasting, muscle fasciculation

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105
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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106
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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107
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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108
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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109
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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110
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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111
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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112
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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113
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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114
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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115
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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116
Q

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

A

carotid or vertebral dissection

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117
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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118
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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119
Q

WHat are the eligibility criteria for mechanical thrombectomy?

A

previously independent (MRS <3 able to walk unaided)
large proximal arterial occlusion (internal carotid or M1 or proximal M2)
procedure can be achieved within 6 hours of onset (or up to 24hrs if sufficient penumbra on CT perfusion imaging)

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120
Q

What are the eligibility criteria for mechanical thrombectomy?

A

previously independent (MRS <3 able to walk unaided)
large proximal arterial occlusion (internal carotid or M1 or proximal M2)
procedure can be achieved within 6 hours of onset (or up to 24hrs if sufficient penumbra on CT perfusion imaging)

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121
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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122
Q

What is the incidence of brain tumours?

A

18 per 100,000

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123
Q

What percentage of brain tumours are malignant?

A

55%

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124
Q

What is the aetiology of brain tumours?

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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125
Q

What are the risk factors for brain tumours?

A

ionising radiation
FHx
other cancer
immunosuppression
older age
obesity

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126
Q

What are the prognostic factors for low grade gliomas?

A

histology type
age
size of tumour
rate of growth
location
cross midline
presenting features
performance status

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127
Q

What is the median age for low grade glioma diagnosis?

A

35 yrs old

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128
Q

What is the average survival length for low grade glioma patients?

A

10 yrs

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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 the prognosis for high grade lymphoma?

A

6 months (no treatment)
18 months (with treatment)

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132
Q

What is the median survival for low grade lymphoma?

A

10 years with early treatment

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133
Q

What is a glioblastoma multiforme?

A

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

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134
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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135
Q

What are the key presentations of brain tumours?

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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136
Q

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

A

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

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137
Q

What are the investigations for brain tumours?

A

1st line - contrast CT
GS - MRI
other - functional MRI

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138
Q

What is the management for high grade brain tumours?

A

Steroids - reduce oedema
Palliative care
Chemotherapy - temozolamide, PCV
Radiotherapy - mainstay, radical vs palliative
Surgery - biopsy or resection

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139
Q

What is the management for low grade brain tumour?

A

Surgery - early resection
Radiotherapy and early chemotherapy

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140
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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141
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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142
Q

What is status epilepticus?

A

medical emergency defined as seizures lasting more than 5 minutes or more than 3 seizures in one hour

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143
Q

What is epilepsy?

A

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

144
Q

What are seizures>

A

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

145
Q

What is a focal seizure?

A

originates in one hemisphere, retained awareness or impaired awareness, usually 2 minutes or less

146
Q

What are examples of focal seizures?

A

focal aware seizure, focal impaired awareness seizure

147
Q

What are examples of generalised seizures?

A

tonic-clonic, absence, myoclonic, tonic, atonic

148
Q

What are the risk factors for epilepsy?

A

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

149
Q

What are the stages of an epileptic seizure?

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)

150
Q

What are the positive ictal symptoms?

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

151
Q

What are examples of post-ictal symptoms?

A

confusion
amnesia
drowsiness
hypertension
headache
nausea

152
Q

What are some other common features of epileptic seizures?

A

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

153
Q

What are the investigations for epilepsy?

A

EEG, ECG, CT head + MRI

154
Q

How many seizures must a patient have had for epilepsy diagnosis to be considered?

A

2+

155
Q

What is the management for epilepsy?

A

aim is to be seizure free on the minimum anti-epileptic medications
1st line = sodium valproate

156
Q

What are the features of generalised tonic-clonic seizures?

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

157
Q

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

A

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

158
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

159
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

160
Q

What are the characteristic features of focal seizures?

A

originate in temporal lobes
affect hearing, speech, memory and emotions
present with hallucinations, memory flashbacks, deja vu, doing strange things on autopilot

161
Q

What are the features of a frontal focal seizure?

A

Jacksonian march + Todd’s palsy

162
Q

What are the features of a temporal focal seizure?

A

aura, dysphagia, post-ictal period

163
Q

what are the features of an occipital seizure?

A

vision changes

164
Q

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

A

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

165
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

166
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

167
Q

What are functional/dissociative seizures?

A

paroxysmal event in which changes in behaviour sensation and cognitive function caused by mental processes triggered by internal or external aversive stimuli

168
Q

What are the characteristics of functional/dissociative seizures?

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

169
Q

What are the characteristics of syncope?

A

Situational
Presyncopal changes (sweating, nausea, pallor, prolonged standing position, hyperventilation, increased heart rate)
Typically from sitting or standing
Rarely from sleep
Presyncopal symptoms
Duration 5-30 seconds
Recovery within 30 seconds
Cardiogenic syncope (less warning, history of heart disease)

170
Q

What is Parkinson’s disease?

A

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

171
Q

What are the risk factors for Parkinson’s?

A

FHx
increased age
male

172
Q

What is the pathophysiology of Parkinson’s disease?

A

The substantia nigra in the basal ganglia produces dopamine which is essential for the correct functioning of the basal ganglia
In parkinson’s disease there is a gradual but progressive fall in the production of dopamine

173
Q

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

A

resting tremor, rigidity, bradykinesia

174
Q

What are the tremor features of Parkinson’s?

A

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

175
Q

What are the rigidity features of 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

176
Q

What are some other symptoms of Parkinson’s?

A

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

177
Q

How is Parkinson’s diagnosed

A

clinical dianosis based on symptoms and examination

178
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

179
Q

What is Motor Neuron Disease?

A

Neurodegenerative disease which causes upper and lower motor neuron signs

180
Q

What are the 4 diagnoses encompassed in MND?

A

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

181
Q

What are the risk factors for MND?

A

FHx
Smoking
Exposure to heavy metals and certain pesticides

182
Q

What are the key presentations of MND?

A

Insidious progressive weakness of the muscle 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

183
Q

What are the signs of LMN disease?

A

muscle wasting
hypotonia
fasciculations
hyporeflexia

184
Q

What are the signs of UMN disease?

A

hypertonia
spasticity
hyperreflexia
plantar responses

185
Q

What are the investigations for MND?

A

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

186
Q

What is the management for MND?

A

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

187
Q

What are some potential complications of MND?

A

respiratory failure, aspiration pneumonia, swallowing failure

188
Q

What is Guillain-barre syndrome?

A

acute paralytic polyneuropathy affecting the peripheral nervous system

189
Q

What is the cause of Guillain-Barre syndrome?

A

campylobacter jejuni + viruses; CMV, EBV, HSV

190
Q

What are the risk factors for Guillain-Barre Syndrome?

A

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

191
Q

What is the pathophysiology of G-B syndrome?

A

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

192
Q

What are the key presentations of G-B syndrome?

A

post-infection , presents with :
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

193
Q

What are the investigations for G=B syndrome?

A

lumbar puncture at L3/4 –> raised protein + normal WCC (=inflammation but no infection)
nerve conduction studies (GS)

194
Q

What is the management for G-B syndrome?

A

IV Ig for 5 days + plasma exchange
supportive care
venous thromboembolism prophylaxis
severe case + resp failure –> need intubation, ventilation and ITU admission

195
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

196
Q

What are the risk factors for Wernicke’s encephalopathy?

A

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

197
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.

198
Q

What are the presentations of Wernicke’s encephalopathy?

A

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

199
Q

What are the investigations for Wernicke’s encephalopathy?

A

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

200
Q

What is the management for Wernicke’s encephalopathy?

A

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

201
Q

What is Korsakoff syndrome?

A

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

202
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

203
Q

What is the cause of DMD?

A

X-linked recessive mutated dystrophin gene

204
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

205
Q

What are the key presentations of DMD?

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

206
Q

What is Gower’s sign for DMD?

A

specific technique to stand up from a lying position

207
Q

What are the investigations for DMD?

A

Serum creatine kinase
genetic testing
clinical presentation
electromyogram
muscle biopsy

208
Q

What are the differential diagnoses for DMD?

A

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

209
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)

210
Q

What is the life expectancy of DMD patients?

A

25-35 yrs

211
Q

What are examples of primary brain tumours?

A

originate from cells within the brain - gliomas, germ cell tumours, meningiomas

212
Q

Where do brain tumours commonly metastasise from?

A

lungs
breast
colorectal
testicular
renal cell
malignant melanoma

213
Q

What is the incidence of brain tumours?

A

18 per 100,000

214
Q

What are the risk factors for brain tumours?

A

ionising radiation
FHx
Other cancer
immunosuppression
obesity

215
Q

What is the most common primary brain tumour?

A

glioma (=tumour of glial cells - astrocytes, oligodendrocytes, ependymal cells)

216
Q

What is the most common primary brain tumour?

A

glioma (=tumour of glial cells - astrocytes, oligodendrocytes, ependymal cells)

217
Q

What are the key presentations of brain tumours?

A

varied 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 (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 changes/behaviour, memory disturbance, confusion)
signs of ↑ICP - altered mental state, visual field defects, seizures, unilateral ptosis, 3rd and gth nerve palsies, papilloedema (on fundoscopy)

218
Q

What are the key presentations of brain tumours?

A

varied 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 (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 changes/behaviour, memory disturbance, confusion)
signs of ↑ICP - altered mental state, visual field defects, seizures, unilateral ptosis, 3rd and 6th nerve palsies, papilloedema (on fundoscopy)

219
Q

What are the investigations for brain tumours?

A

Contrast CT Head
MRI (GS)
Functional MRI (while person speaking, finger tapping etc.) - helps guide management

220
Q

What are the investigations for brain tumours?

A

Contrast CT Head
MRI (GS)
Functional MRI (while person speaking, finger tapping etc.) - helps guide management

221
Q

WHat is the management for high grade brain tumours?

A

Steroids - reduce oedema
Palliative care
Chemotherapy - temozolamide, PCV
Radiotherapy - mainstay, radical vs palliative
Surgery - biopsy or resection

222
Q

What is the management for low grade brain tumours?

A

Surgery - early resection
Radiotherapy and early chemotherapy

223
Q

What are the red flags for brain tumours?

A

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

224
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

225
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

226
Q

What is the aetiology of Brown-Sequard syndrome?

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

227
Q

What is the pathophysiology of B-S syndrome:

A

caused by lateral hemisection of the spinal cord severs the pyramidal tract (already crossed in the medulla), the uncrossed dorsal columns and the crossed spinothalamci tract

228
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

229
Q

What are the investigations for B-S syndrome?

A

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

230
Q

WHat are the differential diagnoses for B-S syndrome?

A

MND
Progressive spinal muscular atrophy
Primary lateral sclerosis
Stroke

231
Q

What is the management for B-S syndrome?

A

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

232
Q

What are the complications of B-S syndrome?

A

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

233
Q

What is Charcot-Marie-Tooth syndrome?

A

inherited sensory + motor PNS polyneuropathy

234
Q

What is the incidence of CMT syndrome?

A

1 in 25000

235
Q

What is the mutation which causes CMT syndrome?

A

autodominant mutation on chromosome 17;PUP 22 gene

236
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

237
Q

What are the key presentations of CMT syndrome?

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

238
Q

What are the investigations for CMT syndrome?

A

Clinical evaluation

E<Gs, motor conduction veolcities, DNA bloods

239
Q

What is the management for CMT syndrome?

A

Supportive treatment
Orthotics
Physiotherapy
Surgical treatment

240
Q

What are the types of peripheral neuropathy?

A

motor neuropathy
sensory neuropathy
autonomic nerve neuropathy
combination neuropathies

241
Q

What are the causes of peripheral neuropathy?

A

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

242
Q

What are the mechanisms of peripheral neuropathy?

A

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

243
Q

What are the key presentations of peripheral neuropathy?

A

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

244
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

245
Q

What is the management for peripheral neuropathies?

A

treat underlying condition (e.g. diabetes)
analgesia

246
Q

What are the causes of mononeuritis multiplex?

A

Wegeners
AIDS/amyloidosis
RA
DMT2
Sarcoidosis
Polyarteritis nodosa
Leprosy
Carcinomas

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?

A

Female
Hypothyroidism
Acromegaly
Pregnancy
RA
Obesity
Diabetes
Perimenopause
Repetitive strain

249
Q

What are the risk factors for carpal tunnel syndrome?

A

Female
Hypothyroidism
Acromegaly
Pregnancy
RA
Obesity
Diabetes
Perimenopause
Repetitive strain

250
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.

251
Q

What are the key presentations of carpal tunnel syndrome?

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

252
Q

What is the phaeln test for CTS?

A

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

253
Q

What is the phaeln test for CTS?

A

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

254
Q

What is the tinel test for CTS?

A

tapping wrist causes tingling

255
Q

What is the gold standard test for CTS?

A

EMG (electromyography)

256
Q

What is the management for CTS

A

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

257
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

258
Q

What nerve palsy causes claw hand?

A

ulnar nerve
treatment = splint , simple analgesia

259
Q

What nerve palsy causes foot drop?

A

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

260
Q

What are the functions of the cerebellum?

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

261
Q

What is ataxia?

A

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

262
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)

263
Q

What is Friedrich’s ataxia?

A

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

264
Q

What are the symptoms of cerebellar dysfunction?

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

265
Q

What are the clinical signs of ataxia?

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
tone/reflexes

266
Q

What are the levels of clinical severity of ataxia?

A

mild - mobilising independently or with one walking aid

moderate - mobilising with 2 walking aids or walking frame

severe - predominantly wheelchair dependent

267
Q

Which blood tests are used in ataxia diagnosis?

A
  • FBC, U&E, extended LFT’s
  • HbA1c, B12, folate, TSH
  • ESR, CRP
  • gluten related serology* (can only be requested in sheffield)
268
Q

What is MRI used for in ataxia?

A

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

269
Q

What is the bamford classification?

A

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

270
Q

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

A

TACS, PACS, POCS, Lacunar stroke

271
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

272
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)

273
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

274
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)

275
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)

276
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

277
Q

What is a lacunar stroke?

A

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

278
Q

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

A

pure sensory stroke
pure motor stroke
sensori-motor
ataxic hemiparesis

279
Q

What is dementia?

A

chronic neurodegenerative disorder which causes decreased cognitive function over time

280
Q

What percentage of dementia cases are Alzheimer’s disease?

A

60%

281
Q

What are the questions in the 6 CIT test for dementia?

A

What year is it?
What month is it?
Give an address with 5 parts (John, Smith, 42, High, St, Bedford)
Count 20-1
Say months of year in reverse
Repeat address

282
Q

What is Alzheimer’s?

A

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

283
Q

What is vascular dementia?

A

dementia resulting from cerebrovascular damage and stroke

284
Q

What are the types of vascular dementia?

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

285
Q

What are the risk factors for dementia?

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

286
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

287
Q

What is the pathophysiology of vascular dementia

A

reduced blood flow to neurons leading to ischemia and cell death

288
Q

What is the pathophysiology of lewy body dementia?

A

spherical intracellular deposits formed from a-synuclein + ubiquitin

289
Q

What is the pathophysiology of frontotemporal dementia?

A

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

290
Q

What are the key presentations of alzheimer’s?

A

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

291
Q

What are the key presentations of vascular dementia?

A

stepwise deterioration, impaired planning, organising, judgement which present early

292
Q

What are the key presentations of lewy body dementia?

A

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

293
Q

What is the presentation of polyneuropathy?

A

glove and stocking loss of sensation

294
Q

What are the key presentations of frontal temporal dementia?

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

295
Q

What are the investigations for dementia?

A

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

296
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

297
Q

What are the causes of neuropathy

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

298
Q

What are the types of primary headaches?

A

migraine, cluster, tension type

299
Q

what are the causes of secondary headaches?

A

meningitis, subarachnoid haemorrhage, GCA, idiopathic intracranial hypertension, medication overuse headaches

300
Q

What are the red flags for headaches>

A

thunderclap headache (SAH)
seizure + new headache
suspected meningitis
suspected encephalitis
red eye (acute glaucoma)
headache + new focal neurology
significantly altered consciousness, memory, confusion, coordination

301
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

302
Q

What is the aetiology 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

303
Q

What are the key presentations of LEMS?

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

304
Q

What is post-tetanic potentiation?

A

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

305
Q

What are the investigations for LEMS?

A

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

306
Q

What are the differential diagnoses for LEMS?

A

Acute/chronic inflammatory demyelinating polyradiculopathy
Dermatomyositis
Multiple sclerosis

307
Q

What is the management for LEMS?

A

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

308
Q

What is myasthenia gravis?

A

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

309
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.

310
Q

What are the key presentations of myasthenia gravis?

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

311
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)

312
Q

What is the management for myasthenia gravis?

A

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

313
Q

What is a myasthenic crisis?

A

acute worsening of symptoms which can lead to resp failure

314
Q

What is huntington’s disease?

A

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

315
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

316
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

317
Q

what are the risk factors for huntington’s?

A

polyglutamine composition of the toxic fragments predisposes them to cross-link, forming aggregates that resist degradation and interfere with a variety of normal cellular functions, particularly mitochondrial energy metabolism

318
Q

What are the key presentations of Huntington’s?

A

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

319
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

320
Q

What is the prognosis of Huntington’s?

A

15-20 years after symptom onset

321
Q

What are the triggers of migraines?

A

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

322
Q

What is a migraine?

A

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

323
Q

What are the stages of migraines?

A

prodrome (days before attack) - mood changes, cravings, yawning
Aura (part of attack, minutes before headache) - visual phenomena - zigzag lines
Throbbing headache (lasting 4-72hrs)

324
Q

What are the key presentations of migraines?

A

2≤ of:
Unilateral pain
Throbbing
Motion-sickness
MOD-severity intense
1 ≤ of:
Nausea and vomiting
Photophobia
With normal neuro exam

325
Q

What is the management for migraines?

A

Acute = oral triptan (sumatriptan) or aspirin 900mg
Prophylaxis - Bb (propranolol) or Topiramate (anti-convulsant) if asthmatic or TCA e.g. amitriptyline (2nd line)

326
Q

What are cluster headaches?

A

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

327
Q

What are the risk factors for cluster headaches?

A

Male
Smoking
Genetics

328
Q

What are the key presentations of cluster headaches?

A

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

329
Q

What confirms diagnosis of cluster headache?

A

5 ≤ similar attack

330
Q

What is the management for cluster headaches?

A

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

331
Q

What are tension headaches?

A

bilateral generalised headaches which radiate to neck

332
Q

What are the risk factors for tension headaches?

A

Stress
Sleep deprivation
Bad posture
eyestrain
Depression
Alcohol
Skipping meals
dehydration

333
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

334
Q

What is the treatment for tension headaches?

A

simple analgesia

335
Q

What is trigeminal neuralgia?

A

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

336
Q

What are the triggers of trigeminal neuralgia?

A

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

337
Q

What are the risk factors for trigeminal neuralgia?

A

MS (20x more likely)
Increased age
Female

338
Q

What does trigeminal neuralgia feel like?

A

electric shock pain lasting up to 2 mins

339
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)

340
Q

What is cauda equina syndrome?

A

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

341
Q

What are the causes of cauda equina syndrome?

A

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

342
Q

What are the risk factors for cauda equina syndrome?

A

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

343
Q

What are the key presentations of cauda equina syndrome?

A

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

344
Q

What is the gold standard investigation for cauda equina syndrome?

A

Spinal MRI + testing nerve roots/reflexes

345
Q

What is the management for cauda equina syndrome?

A

Emergency decompression surgery to prevent permanent neurological dysfunction

346
Q

What are the red flags for cauda equina syndrome?

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

347
Q

What is spinal cord compression?

A

compression of C1-L1/2

348
Q

What are the risk factors for spinal cord compression?

A

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

349
Q

What are the key presentations of spinal cord compression?

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)

350
Q

What is the gold standard investigation for spinal cord compression?

A

MRI, CXR if malignancy suspected

351
Q

What is the management for spinal cord compression?

A

neurosurgery - laminectomy, microdisectomy

352
Q

What is sciatica?

A

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

353
Q

What are the causes of sciatica?

A

herniated disc, sponylolisthesis, spinal stenosis

354
Q

What are the risk factors for sciatica?

A

Age
Obesity
Occupation
Prolonged sitting
Diabetes

355
Q

What is the pathophysiology of sciatica?

A

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

356
Q

What is the management for sciatica?

A

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

Phase 2A (18 decks)

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