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2A revision > Neuro > Flashcards

Neuro Flashcards

1
Q

What is a TIA?

A

ischaemic neurological event with symptoms lasting <24h

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2
Q

Causes of TIA

A

atherothromboembolism
cardioembolism (post-mi etc)
hyperviscosity (polycythaemia, sickle-cell anaemia, myeloma)
vasculitis (rare, non-embolic cause)

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3
Q

assessing risk of stroke: what does the ABCD2 score stand for?

A 
A- age >60 (1pt)
B- BP>140/90mmHg (1pt)
C-clinical features (unilateral weakness 2pt, speech disturbance without weakness 1pt)
D-duration (>60min 2pt)
D- diabetes (1pt)
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4
Q

Factors for high risk of stroke

A

ABCD2 score>4
atrial fibrillation
>1 TIA in a week
TIA whilst on anticoagulant

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5
Q

what is amaurosis fugax

A

renal artery is occluded causing unilateral progressive vision loss (like curtain descending)

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6
Q

investigations for TIA

A 
bloods
CXR
ECG
carotid doppler
CT angiography
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7
Q

management of TIAs

A
  • control CV risk factors
  • antiplatelet drug = aspirin 300mg for 2 weeks then switch to clopidogrel 75mg
  • carotid endarterectomy to remove plaque build up in carotid
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8
Q

Causes of stroke

A
  • thrombus in situ
  • cardiac emboli
  • atherothroboembolism
  • CNS bleeds
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9
Q

risk factors for stroke

A
  • high BP
  • smoking
  • DM, heart disease, peripheral vascular disease
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10
Q

clinical manifestations of stroke

A
  • worst at onset
  • pointers to bleeding = meningism, severe headache, coma
  • pointers to ischaemia = carotid bruit, AF, past TIA, IHD
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11
Q

signs of cerebral infarcts

A
  • depends on site
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12
Q

signs of brainstem infarcts

A
  • varied

- quadriplegia, visual/gaze disturbance, locked-in syndrome (aware but unable to respond)

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13
Q

where are lacunar infarcts and what are the 5 syndromes associated?

A
  • basal ganglia, internal capsule, thalamus, pons

- 5 syndromes= ataxic hemiparesis, pure motor, pure sensory, sensorimotor, dysarthria/clumsy hand

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14
Q

signs of MCA occlusion

A

motor weakness, hemiplegia (paralysis of one side of body)
sensory disturbances
receptive and affective aphasia

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15
Q

signs of ACA occlusion

A

frontal lobe, drowsiness, changes in logical thinking and personality

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16
Q

signs of PCA occlusion

A

contralateral hemianopia

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17
Q

differential diagnosis for stroke

A

head injury
hypo/hypercalcaemia
subdural haemorrhage
tumours, migraine

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18
Q

investigations for stroke

A
  • FAST
  • CT/MRI
  • ECG (AF)
  • CXR (LV hypertrophy)
  • Carotid doppler US (stenosis of carotid)
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19
Q

treatment for ischaemic stroke

A
  • thrombolysis = IV alteplase
  • aspirin 2 weeks then switch to clopidogrel
  • rehab and modify risk factors
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20
Q

treatment for haemorrhagic stroke

A
  • control BP = beta blocker (atenolol)

- surgery = clot evation

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21
Q

acute management of stroke

A
  • protect airway
  • maintain homeostasis
  • CT/MRI within 1h
  • antiplatelets (aspirin 300mg) and thrombolysis (IV alteplase) once haemorrhagic stroke excluded
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22
Q

primary prevention of strokes

A

control risk factors

lifelong anticoagulant in AF and prosthetic heart valves

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23
Q

what does aspirin do

A
  • blocks cyclooxygenase (COX)

- anti-platelet

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24
Q

what does clopidogrel do

A
  • anti-platelet

- makes platelets less ‘sticky’

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25
Q

causes of subarachnoid haemorrhage

A
  • rupture of berry aneurysm
  • arterio-venous malformations
  • encephalitis, vasculitis, tumour invading blood vessels, idiopathic
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26
Q

what is a berry aneurysm

A

arise at site of bifurcations around Circle of Willis and may rupture causing subarachnoid haemorrhage

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27
Q

risk factors for subarachnoid haemorrhage

A
  • previous aneurysm
  • smoking/alcohol
  • hypertension
  • bleeding disorders
  • polycystic kidneys, aortic coarctation, Ehlers-Danlos syndrome = associated with berry aneurysm
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28
Q

clinical presentation of subarachnoid haemorrhage

A
  • thunder-clap headache
  • precipitated by exertion
  • mat be LOC or instant death
  • symptoms = vomiting, collapse, seizures, come/drowsiness, photophobia
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29
Q

signs of subarachnoid haemorrhage

A
  • neck stiffness
  • Kernig’s sign (stiffness of hamstrings - cant straighten leg when hip flexed)
  • retinal, sub-hyaloid, vitreous bleeds
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30
Q

investigations for subarachnoid haemorrhage

A
  • urgent CT
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31
Q

management of subarachnoid haemorrhage

A
  • re-examine CNS often
  • keep well hydrated
  • nimodipine (CCB) reduces vasospasm so reduces ischaemia
  • mannitol to reduce ICP
  • surgery = endovascular coiling or surgical clipping
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32
Q

complications of subarachnoid haemorrhage

A
  • re-bleeding
  • cerebral ischaemia due to vasospasm
  • hydrocephalus due to blockage of arachnoid granulations (needs lumbar drain)
  • hyponatraemia
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33
Q

what can skull fractures cause

A
  • may cause contusions and haematomas

- base of skull fracture = LCN palsies or CSF discharge from nose or ear

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34
Q

what are cerebral contusions, what causes them and what can they cause

A
  • bruises on brain surface
  • from brain suddenly moving in cranial cavity and being crushed
  • causes oozing of blood into brain parenchyma and can cause cerebral oedema and raised ICP
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35
Q

what is a subdural haemorrhage

A
  • between dura and arachnoid mater
  • bleeding from bridging veins between cortex and venous sinuses
  • blood spreads freely in subdural space so crescent shape
  • starts to break down weeks later causing increase in oncotic pressure leading to water being pulled in and growing in size
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36
Q

causes of subdural haemorrhage

A

minor trauma up to 9 months prior

dural metastases, lowered ICP

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37
Q

symptoms and signs of subdural haemorrhage

A
  • fluctuating consciousness
  • physical/intellectual slowing
  • sleepiness, headache, personality change, unsteadiness
  • raised ICP
  • seizures
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38
Q

differential diagnoses for subdural haemorrhage

A
  • dementia
  • stroke
  • CNS masses
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39
Q

investigations for subdural haemorrhage

A
  • CT/MRI

- crescent shaped collection of blood over one hemisphere

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40
Q

management of subdural haemorrhage

A
  • reverse clotting abnormalities
  • IV mannitol to reduce ICP
  • surgical removal
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41
Q

what is an extradural haemorrhage

A
  • bleeding from middle meningeal artery after fracture of squamous temporal bone. (temple)
  • accumulation of blood is slow
  • characteristic lucid period
  • any tear in a dural venous sinus can also cause
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42
Q

Clinical presentation of extradural haemorrhage

A
  • appear well for several hours/days then deteriorate quickly
  • low GCS from rising ICP
  • increasingly severe headache, vomiting, confusion, seizure
  • ipsilateral pupil dilates, coma deepens, bilateral limb weakness, breathing becomes deep and irregular
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43
Q

differential diagnosis for extradural haemorrhage

A
  • epilepsy
  • carotid dissection
  • carbon monoxide poisoning
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44
Q

management for extradural haemorrhage

A
  • urgent surgery
  • IV mannitol
  • care of airway
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45
Q

what is epilepsy

A

recurrent tendency to spontaneous episodes of abnormal electrical activity within the brain which manifests as seizures

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46
Q

what are partial seizures (simple and complex)

A
  • localised part of one hemisphere
  • simple = consciousness is not affected
  • complex = consciousness is impaired
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47
Q

what are generalised seizures

A
  • no features referable to one hemisphere
  • consciousness always impaired
  • absence seizures
  • tonic-clonic (LOC with stiffening then jerking movements)
  • myoclonic (sudden jerking)
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48
Q

what are focal seizures

A
  • one hemisphere, often with underlying structural disease
  • without LOC
  • with LOC = usually from temporal lobe, postictal confusion
  • evolving to a bilateral, convulsive seizure (turns into generalised seizure)
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49
Q

presentation of temporal lobe seizure

A

emotional disturbances, dysphagia, hallucinations, bizzare associations

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50
Q

presentation of frontal lobe seizure

A

motor features (peddling movements), motor arrest, dysphagia or speech arrest, post-ictal Todd’s palsy (limb paralysis for hours after)

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51
Q

presentation of parietal lobe seizure

A

sensory = tingling, numbness, pain

motor

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52
Q

presentation of occipital lobe seizure

A

visual phenomena = spots, lines, flashes

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53
Q

investigations for seizure

A
  • look for provoking causes
  • EEG
  • MRI for structural lesions
  • drug levels
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54
Q

what AED (anti-epileptic drug) is used for focal seizures

A

carbamazepine

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55
Q

what AED for generalised seizures (tonic-clonic, abscence, myoclonic, tonic)

A

sodium valproate

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56
Q

management of epilepsy

A
  • monotherapy or combination therapy with AEDs

- epilepsy surgery = vagal nerve stimulator = palliative treatment

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57
Q

what is Parkinson’s disease

A

-neurodegenerative hypokinetic movement disorder characterised by parkinsonism, neuronal loss and Lewy bodies concentrated in substantia nigra

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58
Q

pathology of parkinsons

A
  • normal = neurones from substantia nigra connect to the putamen and globus pallidus where they release dopamine and control movement
  • lack of dopamine release and loss of dopaminergic neurones in SN
  • other parts of nervous system involved
  • most are sporadic but can be many genetic loci
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59
Q

clinical manifestation of parkinsonism (classical triad)

A

1) tremor = worse at night
2) rigidity = hypertonia
3) bradykinesia (parkinsonism) = slow to initiate movement = shuffling, pitched forward gait
- autonomic dysfunction, cognitive/behavioural disturbance, sleep disfunction (rapid eye movement sleep disorder)

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60
Q

what may patients with parkinsons develop

A
  • dysphagia
  • depression
  • dementia
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61
Q

investigations for parkinsons disease

A
  • clinical
  • clinical response to dopaminergic therapy is supportive
  • signs worse on one side
  • MRI = atrophy of substantia nigra
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62
Q

management of parkinsons disease

A
  • dopaminergic drugs (eg levodopa) for symptom easing but longterm use can cause seveer dyskinesias
  • co-careldopa = levodopa + carbidopa
  • dopamine receptor agonists = pramiprexole
  • tremor management with anti-cholinergics (amantadine)
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63
Q

what is Huntington’s chorea

A
  • inherited autosomal dominant neurodegenerative disorder caused by mutation of the HTT gene
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64
Q

genetics of Huntingtons chorea

A
  • HHT gene mutation on chromosome 4
  • > 36 trinucleotide repeats (CAG) = higher the number, the fuller the penetrance and earlier the onset.
  • anticipation = expansion of repeats in each successive generation
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65
Q

pathology of huntingtons

A
  • huntingtin = protein coded by HHT, expressed in all cells but highest concentration in brain and testis.
  • mutated huntingtin is cytotoxic to certain cells = neurones in caudate nucleus and putamen
  • atrophy and neuronal loss of striatum and cortex.
  • loss of neurotransmitters
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66
Q

what neurotransmitters are lost in huntingtons

A
  • GABA, ACh, glutamate
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67
Q

clinical manifestations of huntingtons

A
  • chorea (uncontrolled, random , jerky movements) caused by decrease of GABA and unbalanced dopamine
  • motor, neuropsychiatric and cognitive decline
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68
Q

what does huntingtons chorea always result in

A

dementia

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69
Q

differential diagnoses for huntingtons

A

SLE

MS

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70
Q

investigations for huntingtons

A
  • clinical
  • abnormal eye movements
  • chorea = random, unpredictable movements
  • often parkinsonism = regidity and slowness of fine finger movements
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71
Q

management of huntingtons

A
  • chorea and aggression= risperidone (dopamine receptor antagonist)
  • depression = sertraline (selective serotonin reuptake inhibitors)
  • psychosis = haloperidol (neuroeptics)
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72
Q

primary headaches

A

migraine, cluster, tension

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73
Q

secondary headaches

A
  • meningitis
  • subarachnoid haemorrhage
  • giant cell arteritis
  • idiopathic intracranial hypertension
  • medication overuse headache
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74
Q

what symptoms of headache need urgent referral

A
  • thunderclap
  • seizure or new headache
  • suspected encephalitis
  • red eye (acute glaucoma)
  • headache and new focal neurology (papilledema)
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75
Q

headache red flags

A

new onset and history of cancer
papilledema
cluster headache

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76
Q

headache exam

A

fever
altered consciousness
neck stiffness/ kernig’s sign
focal neurology signs

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77
Q

clinical presentation of migraine

A
  • unilateral, throbbing headache +/- aura
  • nausea/vomiting
  • sensory disturbances
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78
Q

diagnostic criteria for migraine

A

> 5 headches lasting 4-72h + nausea + unilateral/pulsating/ impairs routine activity

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79
Q

management of migraines

A
  • propranolol (beta blocker) to reduce frequency (prophylactic).
  • oral triptan (severe) + NSAID/paracetamol during attack
  • non-pharmaceutical therapies = cold packs etc
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80
Q

what is a tension headache

A
  • very common

- bilateral, tightening, mild/moderate pain, not aggravated by physical activity, no nausea

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81
Q

cause of tension headache

A

missed meals, conflict, stress, clenched jaw, overexertion, lack of sleep, depression

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82
Q

clinical manifestations of cluster headache

A
  • rapid onset of excruciating pain around one eye that may become watery, bloodshot, lid swelling, lacrimation, facial flushing.
  • unilateral
  • last 15 min - 3h (once/twice a day)
  • clusters last 4-12 weeks and are followed by pain free periods of months to years
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83
Q

management of cluster headaches

A
  • treatment = 100% oxygen for 15 min + sumatriptan sc 6mg

- preventative = avoid triggers, corticosteroids short term, verapamil (CCB)

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84
Q

how do triptan drugs work

A
  • used for migraines and cluster headaches
  • serotonin receptor agonists
  • vasoconstriction of pain sensitive intracranial vessels
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85
Q

what is the criteria for a drug overuse headache

A
  • > 15 days/month

- use of drug for >3months (ergotamine, triptans, opioids)

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86
Q

what is the treatment for drug overuse headache

A

withdraw drug

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87
Q

what is giant cell arteritis

A

vasculitis of medium/large vessels mostly head and neck arteries in >50s

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88
Q

clinical manifestations of giant cell arteritis

A
  • over weeks/months with fever, anorexia, weightloss
  • temporal artery = headache, scalp tenderness, jaw claudication
  • ocular vessels = blindness
  • aortic involvement = thoracic or abdominal aortic aneurysm formation
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89
Q

investigations for giant cell arteritis

A
  • positive temporal artery biopsies (lymphohistiocytic infiltrate and giant cells)
  • ESR/CRP raised, raised platelets, low Hb
  • criteria = >50y/o, new headache, temporal artery tenderness and decreased pulsation, ESR>50, abnormal biopsy
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90
Q

management of giant cell arteritis

A
  • prednisolone PO immediately or IV methylprednisolone if evolving vision loss
    main cause of death = long term steroid treatment
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91
Q

what is trigeminal neuralgia

A

neuralgia involving one+ of the branches of the trigeminal nerves (CNV) causing severe pain

92
Q

triggers of trigeminal neuralgia

A
  • washing face, shaving, eating, talking, dental prostheses
93
Q

secondary causes of trigeminal neuralgia

A
  • compression of trigeminal root by tumour
  • hypertension
  • chronic meningeal inflammation
  • ms
  • skull base malformation (chiari)
94
Q

clinical manifestation of trigeminal neuralgia

A
  • paroxysms of intense, stabbing pain, lasts seconds (1-180), unilateral, face screws up with pain
95
Q

investigations for trigeminal neuralgia

A

MRI to exclude secondary causes

clinical

96
Q

management of trigeminal neuralgia

A
  • carbamazepine (anticonvulsant)

- surgery

97
Q

causes of spinal cord compression

A
  • secondary malignancy

- rare = infection, cervical disk prolapse, heamatoma

98
Q

clinical manifestations of cord compression

A
  • bilateral leg weakness, back pain, bladder and anal sphincter involvement
  • normal findings above the level of the lesion
  • LMN signs at level
  • UMN signs below the level
99
Q

investigations for cord compression

A

MRI = definitive
biopsy of and masses
CXR for lung malignancy
bloods (FBC, ESR, B12, syphilis serology, U&E, LFT, PSA)

100
Q

treatment for cord compression

A
  • urgent dexamethasone in malignancy
  • radio/chemotherapy
  • epidural abscesses must be surgically decompressed and Abx
101
Q

what is cauda equina syndrome

A
  • spinal cord compression at the site of the corda equina (normally starts at L1/2)
102
Q

causes of cauda equina syndrome

A

same as cord compression + congenital lumbar disc disease and lumbosacral nerve lesions

103
Q

signs of cauda equina syndrome

A
  • back pain, radiates down legs
  • sensory loss in root distribution
  • decreased anal sphincter tone and bladder/bowel incontinence
104
Q

treatment for cauda equina syndrome

A

lumbar decompression surgery

105
Q

what is multiple sclerosis

A

demyelinating disease of the CNS in which episodes of neurological disturbance affect different parts of the CNS at different times

106
Q

pathology of ms

A
  • episodes of demyelination leads to attacks of acute neurological deficit over a few days and remain for a few weeks before symptom recovery.
  • in early stages the recovery is complete/almost.
  • eventually, extensive axonal death results in permanent neurological disability
107
Q

clinical presentation of ms

A
  • variable depending on lesion site.

- symptoms worsen with heat = Uhthoff’s phenomenon

108
Q

presentation of MS plaque in cerebral hemispheres

A
  • large variety of symptoms and many silent lesions
109
Q

presentation of MS plaque in the spinal cord

A

weakness, paraplegia, spasticity, tingling, numbness, Lhermitte’s sign (electric shock sensation down back into legs), bladder and sexual dysfunction

110
Q

presentation of MS plaques in the optic nerves

A

impaired vision, eye pain

111
Q

presentation of MS in the medulla and pons

A

dysarthria, double vision, vertigo, nystagmus

112
Q

presentation of MS in the cerebellar white matter

A

dysarthria (slur words), nystagmus, intention tremor, ataxia (slurred speach, stumbling, falling, incoordination)

113
Q

what are the categories of MS

A
  • relapsing/remitting course
  • chronic progressive (often follows R/R)
  • benign (few relapses, little disability)
114
Q

differential diagnoses for MS

A
  • lyme disease

- autoimmune = SLE, primary Sjogren’s syndrome

115
Q

investigations for MS

A
  • MRI
  • CSF = oligoclonal bands of IgG on electrophoresis
  • clinical
116
Q

diagnostic criteria for MS

A
  • 2+ CNS lesions disseminated in time and space

- exclusion of other conditions

117
Q

management of MS

A
  • lifestyle = exercise, stop smoking, avoid stress
  • dimethyl fumarate for mild/moderate relapsing/remitting MS
  • Altemtuzumab = anti-T cell
    Natalizumab = inhibits VLA-4 receptor so immune cells can’t cross BBB
118
Q

treatment for MS relapses

A

IV methylprednisolone

119
Q

symptom control in MS

A

spasticity = baclofen
tremor = botulinum toxin type A injections for arms
bladder dysfunction = self-catheterisation
fatigue = amantadine, CBT, exercise

120
Q

what is myasthenia gravis

A
  • NMJ disorder
  • autoimmune disease = production of auto Abs against various antigens of the NMJ
  • nicotinic ACh receptor, rarely MuSK, very rarely LRPP4
121
Q

What do 75%of people with myasthenia gravis from nAChR have

A

abnormality of thymus = thymoma or hyperplasia

122
Q

pathology of myasthenia gravis

A
  • nAChR is the receptor at the motor endplate
  • auto-Abs binding to receptors limit depolarisation at the end plate and impair muscular contraction
  • MuSK is involved with clustering of nAChR which is important for normal functioning
123
Q

clinical manifestations of myasthenia gravis

A
  • muscular fatigability
  • muscle groups affected = extraocular, bulbar face, neck, limb girdle, trunk
  • can be subtle
  • Lambert-eaton syndrome= paraneoplastic syndrome with auto Abs against calcium channel on nerve terminal causing gait difficulties, autonomic involvement and hyporeflexia
124
Q

investigations for myasthenia gravis

A
  • Abs = anti-AChR Abs, MuSK Abs
  • EMG = decremental muscle response to repetitive nerve stimulation.
    CT to exclude thymoma
125
Q

management of myasthenia gravis

A
  • acetylcholinesterase inhibitors (pyridostigmine)

- immunosuppression = treat relapses with prednisolone

126
Q

what is myasthenic crisis and how to treat it

A
  • life threatening weakness of respiratory muscles
  • monitor forced vital capacity
  • ventilatory support
  • plasmapheresis or IV Ig
  • identify and treat trigger (infection/ meds etc)
127
Q

what is motor neurone disease

A

group of neurodegenerative diseases characterised by selective loss of motor neurones.

128
Q

what are the 4 clinical patterns of MND

A

1) ALS/ amyotrophic lateral sclerosis
2) progressive bulbar palsy
3) progressive muscular atrophy
4) primary lateral sclerosis

129
Q

MND: what is amyotrophic lateral sclerosis

A
  • loss of motor neurones in the motor cortex and anterior horn of the cord
  • combined UMN + LMN signs
130
Q

MND: what is progressive bulbar palsy

A
  • affects cranial nerves IX - XII
131
Q

MND: what is progressive muscular atrophy

A
  • anterior horn cell lesion
  • LMN signs only
  • distal muscle groups first
132
Q

MND: what is primary lateral sclerosis

A
  • rare
  • loss of Betz cells in motor cortex
  • mainly UMN signs - spastic leg weakness and pseudobulbar palsy
  • no cognitive decline
133
Q

pathology of MND

A

little known

- defects in RNA metabolism due to lack of RNA binding proteins (TDP-43 and FUS)

134
Q

clinical manifestations of MND

A
  • asymmetric weakness, wasting, fasciculations and spasticity of limb muscles
  • difficulty swallowing, chewing, speaking, coughing and breathing
  • cognitive changes
135
Q

clinical features of LMN lesions

A
  • muscle tone reduced = flaccid
  • muscle wasting
  • fasciculations (visible spontaneous contraction of motor units)
  • hyporeflexia
  • everything goes DOWN!
136
Q

clinical features of UMN

A
  • muscle tone increased (spasticity)
  • hyperreflexia (jaw jerk)
  • Babinski sign = extensor plantar response (toes fan out)
  • upper limb extensors weaker
  • lower limb flexors weaker
  • emotional liability
  • everything goes UP!
137
Q

investigations for MND

A
  • no diagnostic test
  • brain/cord MRI to exclude structural causes
  • neurophysiology can detect subclinical denervation
138
Q

management of MND

A
  • progressive and fatal within years
  • multidisciplinary
  • riluzole = inhibits glutamate release
  • augmentive and alternative communication equipment
  • palliative care
139
Q

what is guillian-barre syndrome

A

classical GBS is an acute demyelinating polyneuropathy which usually follows 1-2 weeks after an upper resp tract or GI infection

140
Q

common triggers of GBS

A
  • clostridium jejuni, mycoplasma, CMV, HIV, VZV, EBV

- vaccination, surgery, malignancy

141
Q

pathology of GBS

A
  • immune response mounted to an antigen on a pathogen cross-reacts with components of the peripheral nerve (myelin)
  • demyelination
142
Q

clinical manifestations of GBS

A
  • few weeks after an infection a symmetrical ascending muscle weakness starts
  • sudden onset of tingling and numbness of fingers and toes
143
Q

investigations for GBS

A

lumbar puncture shows raised CSF protein with normal cell count

144
Q

management of GBS

A

IV Ig

145
Q

acute and chronic peripheral neuropathies

A
  • acute = evolve rapidly and patients seek A&E

- chronic = small fibre or large fibre (axonal or demyelinating)

146
Q

common peripheral mononeuropathies

A
  • carpal tunnel syndrome (median nerve)
  • ulnar neuropathy (entrapment at cubital tunnel)
  • peroneal neuropathy (entrapment at the fibular head)
  • cranial (III or VII cranial nerve palsy)
147
Q

what is ataxia

A

poor balance
sensory (loss of proprioception) or cerebellar
if sensory, ataxia worsens when eyes closed

148
Q

motor symptoms of peripheral neuropathies

A
  • muscle cramps
  • weakness
  • fasciculations
  • atrophy
  • high arched feet
149
Q

symmetrical peripheral neuropathy presentation

A
  • longer fibres affected first
  • initially sensory then sensorimotor
  • most common
150
Q

asymmetrical sensory peripheral neuropathy presentation

A
  • patchy distribution of symptoms

- dorsal root ganglia are affected

151
Q

asymmetrical sensorimotor peripheral neuropathy presentation

A
  • very uncommon
  • multiple nerve involvement
  • mononeuritis complex
152
Q

difference between demyelinating and axonal neuropathies

A
  • demyelinating = slow conduction velocities

- axonal = reduced amplitudes of the potentials

153
Q

causes of axonal PN

A
  • associated with systemic disease (diabetes, B12 deficiency, coeliac, chronic renal disease, alcohol, hypothyroid, amyloidosis, paraneoplastic, connective tissue disease, paraproteinemia)
  • inflammatory
  • infectious (hepatitis, HIV, Lyme)
  • ischaemic (vasculitis)
  • metabolic
  • hereditary (CMT, HLPP)
  • toxins (B6, environmental toxins)
154
Q

chronic demyelinating PN

A
  • immune mediated = CIDP (chronic inflammatory demyelinating polyneuropathy), multifocal motor neuropathy
  • genetic = Charcot Marie Tooth disease (foot drop, hammer toe, leg muscle wasting)
155
Q

acute polyneuropathies

A
  • Guillain Barre syndrome (rapidly ascending paralysis and sensory deficits after disease)
156
Q

treatment for PN

A
  • symptomatic = quinine (cramps), pain, physio

- identify reversible cause

157
Q

signs of median nerve C6-T1 lesion/neuropathy

A

unable to grip

158
Q

signs of ulnar nerve C7-T1 lesion/neuropathy

A
  • vulnerable to elbow trauma

- sensory loss of medial 1.5 fingers

159
Q

signs of radial nerve C5-T1 lesion/neuropathy

A

wrist and finger drop

unable to open fist

160
Q

signs of brachial plexus lesion/neuropathy

A

pain/paraesthesia and weakness in affected arm

161
Q

signs of phrenic nerve C3-C5 lesion/neuropathy

A

orthopnoea (SOB while laying flat) with raised diaphragm on CXR

162
Q

signs of lateral cutaneous nerve of the thigh L2-3 lesion/neuropathy

A

paraesthesia

163
Q

signs of sciatic nerve L4-5 lesion/neuropathy

A
  • foot drop

- loss of sensation below the knee

164
Q

signs of common perineal nerve L4-S1 lesion/neuropathy

A
  • foot drop
  • weak ankle
  • sensory loss of foot
165
Q

signs of tibial nerve L4-S3 lesion/neuropathy

A

inability to stand of tiptoe, invert foot or flex toes

166
Q

upper motor nerve lesions

A
  • damage to motor pathways (corticospinal tract)
  • affects muscle groups
  • nerve cells in precentral gyrus of frontal cortex - internal capsule - brainstem and cord - synapse with the anterior horn cells in the cord
167
Q

signs of upper motor nerve lesions

A
  • no muscle wasting
  • loss of fine finger movement
  • spasticity in arm flexors and leg extensors
  • hyperreflexia
  • upgoing plantars
  • +/- clonus (rhythmic beat of foot on dorsiflexion)
  • +/- Hoffman’s reflex (flexion on thumb and index finger in pincer movement following a flick to the middle finger)
168
Q

lower motor nerve lesions

A
  • ## damage anywhere from anterior horn cells in cord, nerve roots, plexi or peripheral nerves
169
Q

signs of LMN lesions

A
  • wasting and fasciculations in affected muscles
  • hypotonia/flaccidity
  • hyporeflexia
  • plantars remain flexed
170
Q

causes of cranial nerve lesions

A
  • diabetes mellitus
  • stroke
  • MS
  • tumours
  • sarcoidosis
  • vasculitis
  • syphilis
171
Q

CN I lesion

A
  • olfactory
  • anosmia
  • from resp tract infection, trauma, meningitis, frontal lobe tumour
172
Q

CN II lesion

A
  • optic
  • monocular blindness
  • bilateral blindness
  • bitemporal hemianopia
  • homonymous hemianopia (affects visual field contralateral to lesion)
  • optic neuritis
  • ischaemia papillopathy (from stenosis of posterior ciliary artery)
  • papilloedema
  • optic atrophy (pale optic disc)
173
Q

CN III lesion

A
  • oculomotor

- ptosis, large pupil, eye down and out

174
Q

CN IV lesion

A
  • trochlear

- horizontal diplopia

175
Q

CN V lesion

A
  • trigeminal
  • jaw deviated to side of lesion
  • sensory loss
176
Q

CN VI lesion

A
  • abducens

- nystagmus

177
Q

CN VII lesion

A
  • FACIAL
  • lower 2/3 of face will droop if UMN lesion
  • one side of face drops if LMN
  • loss of taste
178
Q

CN VIII lesions

A
  • vestibulocochlear

- problems with hearing, balance and vertigo

179
Q

CN IX and X lesions

A
  • glossopharyngeal and vagus
  • gag reflex problems
  • brainstem lesions
180
Q

CN XI lesions

A
  • acccessory
  • unable to shrug shoulders against resistance or turn head
  • innervates trapezius and sternocleidomastoid
181
Q

CN XII lesion

A
  • hypoglossal

- tongue deviates to side of lesion

182
Q

3 presenting signs of brain tumour

A
  • raised ICP (headache, reduced consciousness, nausea and vomiting)
  • progressive neurological deficit
  • epilepsy
183
Q

features of the raised ICP headache

A
  • worst on waking in the morning
  • increased by coughing, straining and bending forwards
  • sometimes relieved by vomiting
184
Q

cardinal physical signs of brain tumour

A
  • papilledema due to obstruction of venous return from the retina
  • loss of crisp optic nerve head
  • venous engorgement
  • retinal oedema
  • haemorrhages
185
Q

secondary brain tumours

A
  • more common

- most from lung

186
Q

primary brain tumours

A
  • most glial cell origin = astrocytoma, oligodendroglioma
187
Q

grading of gliomas

A
  • I = pilocytic astrocytoma (paediatric)
  • II = benign premalignant tumour
  • III = anaplastic astrocytoma
  • IV = glioblastoma multiforme (gbm)
  • all gliomas would eventually become GBM
188
Q

treatment of glioblastomas

A
  • resective surgery if possible
  • adjuvant chemo (temozolomide) with RT then followed by more chemo
  • dexamethasone improves brain function and decreases inflammation
  • gene therapy (inoculation of tumour with replication deficient HSV-1 retrovirus)
189
Q

what is an astrocytoma

A
  • CNS tumour formed by glial cells showing astrocytic differentiation
  • most frequent primary brain tumour in adults
  • diffuse astrocytoma’s WHO grade II
  • anaplastic astrocytoma WHO grade III
  • glioblastoma WHO grade IV
190
Q

what is an oligodendroglioma

A
  • diffusely infiltrative CNS tumour formed by glial cells showing oligodendroglial differentiation
  • can be classical (II) or anaplastic (III)
  • calcification on scan
  • from neural stem or progenitor cells
191
Q

what is an ependymoma

A
  • CNS tumour composed of neoplastic ependymal cells from the ependymal-linked ventricular system or the spinal cord.
  • classical or anaplastic (III)
  • genetic mutations on chromosome 22
192
Q

what is a meningioma

A
  • tumour from meningothelial cells which is attached to the inner surface of the dura matter
  • majority are benign (I) and sporadic
  • slow growing
  • anaplastic meningiomas are aggressive malignant tumours
193
Q

what is a medulloblastoma

A

primitive embryonal tumour of the cerebellum (IV)
highly malignant
children

194
Q

what are primary CNS lymphomas

A
  • primary extra nodal lymphomas arising in the CNS

- immunocompromised at increased risk (EBV plays role)

195
Q

what is meningitis

A

infection of subarachnoid space and inflammation of the meninges

196
Q

what viruses can cause meningitis

A

echoviruses, EBV, herpes simplex, mumps

197
Q

what bacteria can cause meningitis

A
  • neisseria meningitidis or streptococcus pneumonia

- neonates = e.coli and group B streptococci

198
Q

pathophysiology of meningitis

A

1) blood - CSF - brain barrier
2) bacteria in CSF isolated from immune cells
3) replication
4) blood vessels become leaky
5) inflammation

199
Q

clinical manifestations of meningitis

A 
headache
fever
neck stiffness
photophobia
more sever in bacterial infection 
non-blanching purpuric rash
200
Q

investigations for meningitis

A
  • examination of CSF from lumbar puncture (DO NOT do if symptoms of raised ICP)
  • predominance of lymphocytes in viral
  • many neutrophils in bacterial
201
Q

management of viral meningitis

A

usually runs a mild course with complete recovery

202
Q

management of bacterial meningitis

A

life threatening
antibiotics (cefotaxime or ceftriaxone)
IV dexamethasone

203
Q

immediate hospital management of meningitis

A
  1. assess GCS
  2. blood cultures
  3. broad spec Abx (cefotaxime)
  4. steroids : IV dexamethasone
  5. lumbar puncture (microscopy, gram stain, culture, protein, glucose, viral PCR)
204
Q

what is encephalitis

A

infection of the brain parenchyma and inflammation of the brain

205
Q

causes of encephalitis

A
  • HSV most common cause
  • autoimmune, paraneoplastic
  • bacterial meningitis
  • TB
  • Malaria
  • lyme disease
206
Q

pathology of HSV encephalitis

A
  • following reactivation of the virus in the trigeminal ganglion where it passes into the temporal lobe
207
Q

clinical manifestation of encephalitis

A
  • precedes flu symptoms
  • confusion
  • behavioral changes
  • low GCS or coma
  • seizures
208
Q

investigations for encephalitis

A
  • bloods
  • MRI of brain
  • lumbar puncture = viral PCR on lymphocytic CSF sample
  • urgent EEG
209
Q

management of encephalitis

A
  • urgent antivirals (acyclovir)

- symptomatic and supportive treatment

210
Q

pathology of herpes zoster (shingles)

A
  • varicella-zoster virus (VZV) highly infectious and causes chickenpox in children
  • transmitted by respiratory droplets
  • infection is lifelong due to viral latency within sensory ganglia
  • reactivation of virus in adults leads to shingles
211
Q

clinical manifestations of chicken pox

A 
fever
malaise
headache
abdominal pain
pruritic rash = erythematous macules for vesicles and crust
212
Q

clinical manifestation of shingles

A
  • band like vesicular eruption along the distribution of a sensory nerve (macular = dermatomal distribution)
  • painful, hyperaesthetic area
  • infectious until scabs appear
213
Q

investigations for shingles

A
  • clinical

- in immunocompromised use viral PCR, culture, immunofluorescence

214
Q

treatment of shingles

A
  • acyclovir/valaciclovir (IV in immunosuppressed)

- vaccination in elderly to prevent reactivation

215
Q

what is dementia

A
  • neurodegenerative
  • progressive decline in several cognitive domains
  • alzheimer’s, lewy body, vascular, fronto-temporal
216
Q

what is frontotemporal dementia

A
  • frontal and temporal atrophy
  • loss of >70% of spindle neurons
  • behavioural/personality change, disinhibition, hyperorality, emotional unconcern
217
Q

investigations for dementia

A
  • look for reversible causes (raised TSH, low B12/folate)
  • check MSU, FBC, ESR, U&E, LFT and glucose
  • MRI
  • functional imaging
218
Q

pathology of vascular dementia

A
  • small vessel disease may cause chronic ischaemia and diffuse white matter injury
  • multiple infarcts from vascular occlusion
219
Q

presentation of vascular dementia

A
  • impairment of executive function and slowing of mental processing
  • stepwise progression and focal neurology
220
Q

pathology of Lewy body dementia

A
  • accumulations of Lewy bodies within neurones of cortical grey matter and subcortical nuclei leads to damage and cell loss
221
Q

presentation of Lewy body dementia

A
  • progressively worsening dementia similar to Alzheimer’s
  • fluctuating levels of cognition, recurrent visual hallucinations, parkinsonism, hypersensitivity to neuroleptics
  • autonomic nervous system problems and sleep disorders
222
Q

what is Alzheimer’s

A
  • dementia

- neuronal loss in the cerebral cortex associated with amyloid plaques and neuro-fibrillary tangles

223
Q

aetiology of Alzheimer’s

A
  • accumulation of beta-amyloid peptide and tau protein results in neurofibrillary tangles, amyloid plaques and loss of ACh
  • mostly in hippocampus, amygdala, temporal neocortex, and subcortical nuclei.
224
Q

temporal lobe

A
  • hearing (superior temporal lobe)
  • language comprehension (superior temporal lobe)
  • semantic knowledge (anterior temporal lobe)
  • memory (hippocampus)
  • emotional/effective behaviour (limbic system)
225
Q

clinical presentation of Alzheimer’s

A
  • memory loss
  • increasing disability to perform daily tasks
  • agnosia (can’t recognise self in mirror)
  • psychotic symptoms
  • loss of motor skills
  • agitation, restlessness, wandering, disinhibition
  • terminal stages= reduced speech, immobility, incontinence
226
Q

management of Alzheimer’s (medications)

A
  • acetyl choline esterase inhibitors (rivastigmine)
  • memantine (anti-glutamate)
  • antipsychotics if very severe

2A revision (10 decks)

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