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2a - Systems Based Clinical Sciences > Neuro 1 > Flashcards

Neuro 1 Flashcards

1
Q

what area of the brain is involved with comprehension and understanding of speech? where in the brain is this? what is its main blood supply?

A

Wernicke’s area.
superior temporal gyrus of the dominant hemisphere.
middle cerebral artery.

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2
Q

what area of the brain is involved with the production of speech? where in the brain is this? what is its main blood supply?

A

Broca’s area.
frontal lobe of the dominant hemisphere.
middle cerebral artery.

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3
Q

how would an ischaemic stroke of the anterior cerebral artery present?

A

tends to affect feet, legs, up to bowel problems.

leg weakness, sensory disturbance in leg, gait apraxia, truncal ataxia, incontinence, drowsiness, akinetic mutism

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4
Q

what is akinetic mutism?

A

worst form of ACA stroke - decrease in spontaneous speech, stuporous state, completely mute and don’t move.

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5
Q

a patient presents with leg weakness, incontinence, drowsiness, and some missing sensations in his legs. in what artery is the ischaemic stroke likely to have occurred?

A

anterior cerebral artery

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6
Q

how would an ischaemic stroke of the middle cerebral artery present?

A

tends to be more arm and face.

contralateral arm and leg weakness, contralateral sensory loss, aphasia, dysphasia, facial droop.

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7
Q

how would a posterior cerebral artery stroke present?

A

contralateral homonymous hemianopia, cortical blindness with bilateral involvement of the occipital lobe branches.
visual agnosia (can see, but can’t interpret visual information).
prospagnosia - can’t recognise faces (parietal lobe).
dyslexia, anomic aphasia, colour naming and discrimination problems.

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8
Q

what clinical features might a patient have with a posterior circulation stroke (vertebral/basilar arteries)?

A 
motor deficits e.g. hemiparesis or tetraparesis and facial paresis.
dysarthria and speech impairment.
vertigo, nausea and vomiting.
visual disturbances.
altered consciousness.
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9
Q

at what point do symptoms become a stroke, rather than a TIA?

A

if they last over 24h.

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10
Q

name 2 causes of a TIA, other than atherosclerosis/emboli

A

vasculitis, sickle cell anaemia, polycythaemia, myeloma - causes of hyperviscosity!

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11
Q

what specific investigation would you carry out if you suspected that atherosclerosis had caused your patient’s TIA? what treatment would you consider?

A

carotid Doppler and carotid endarterectomy.

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12
Q

name 3 risk factors for a TIA

A

hypertension, smoking, obesity, diabetes, high alcohol intake

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13
Q

what is amaurosis fugax?

A

progressive loss of vision in one eye - “like a curtain descending over my field of view” - due to emboli passing into the retinal artery

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14
Q

name 2 differential diagnoses of a TIA

A

hypoglycaemia, migraine aura, focal epilepsy, hyperventilation, retinal bleeds

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15
Q

what is the ABCD2 score and what is it used for?

A

used to predict progression to full stroke:
Age >60yo
BP >140/90
Clinical features - unilateral weakness, speech disturbance without weakness.
Duration of symptoms - >1h or 10-59min.
Diabetes.

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16
Q

how would you treat a TIA?

A

control hypertension/hyperlipidaemia/diabetes.
smoking cessation.
antiplatelet drugs - clopidogrel/aspirin/warfarin.
± carotid endartectomy.

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17
Q

how does warfarin work to reduce platelet aggregation?

A

inhibits vitamin K dependent synthesis of clotting factors 2, 7, 9 and 10

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18
Q

list 4 risk factors for stroke

A

hypertension, smoking, diabetes, heart/peripheral vascular disease, past TIA/stroke, hyperlipidaemia, alcohol, increased clotting/clotting disorders, the Pill, syphilis, carotid bruit

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19
Q

what are the 2 main types of stroke?

A

ischaemic and haemorrhagic

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20
Q

list 5 causes of haemorrhagic stroke

A

hypertension, trauma, aneurysm rupture, anticoagulation, thrombolysis, carotid artery dissection, subarachnoid haemorrhage

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21
Q

what might be some pointers in the presentation of stroke, to whether it is due to haemorrhage or ischaemia?

A

haemorrhagic - meningism, severe headache, coma within hours.
ischaemic - carotid bruit, AF, past TIA, IHD.

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22
Q

what would be the clinical features of a brainstem infarct?

A

quadriplegia, disturbances of gaze and vision, locked-in syndrome

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23
Q

what are the 5 different syndromes produced by lacunar infarcts?

A

ataxic hemiparesis, pure motor, pure sensory, sensorimotor, dysarthria/clumsy hands

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24
Q

if a patient presented with vertigo, headache, ataxia and vomiting, what structure has been affected and what vessel has caused it?

A

cerebellar syndrome - due to occlusion of superior, anterior inferior or posterior inferior cerebellar artery

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25
Q

what is the essential investigation to carry out before you start specific stroke treatments?

A

urgent CT head

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26
Q

give 3 differential diagnoses of stroke

A

head injury, hypo/hyperglycaemia, subdural haemorrhage, intracranial tumours, hemiplegic migraine, epilepsy, CNS lymphoma, pneumocephalus, Wernicke’s encephalopathy, hepatic encephalopathy, mitochondrial cytopathies, abscesses, mycotic aneurysm

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27
Q

if CT showed that the stroke was caused by an infarct, how would you treat it?

A

thrombolysis - aspirin and alteplase - recombinant tissue plasminogen activator (tPA)

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28
Q

give 2 examples of primary prevention of stroke

A

treat hypertension, control DM, statins for hyperlipidaemia, regular physical exercise, smoking cessation, anticoagulation of patients with rheumatic/prosthetic heart valves on left

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29
Q

give 2 examples of secondary prevention of stroke

A

control risk factors (hypertension, diabetes, hyperlipidaemia).
aspirin or clopidogrel (unless haemorrhagic stroke)

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30
Q

list the causes of subarachnoid haemorrhage

A

rupture of saccular (Berry) aneurysms - 80%.
AV malformations - 15%.
idiopathic.

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31
Q

list 3 risk factors for subarachnoid haemorrhage

A

smoking, alcohol misuse, hypertension, bleeding disorders, mycotic aneurysm

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32
Q

what are some common sites for Berry anuerysms?

A

junction of posterior communicating artery with internal carotid.
junction of anterior communicating artery with anterior cerebral artery.
bifurcation of middle cerebral artery.

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33
Q

what 3 things are Berry aneurysms associated with?

A

polycystic kidneys, coarctation of the aorta, Ehlers-Danos syndrome

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34
Q

describe the symptoms of subarachnoid headache

A

THUNDERCLAP HEADACHE.
sudden, devastating occipital headache (I thought I’d been kicked in the head).
vomiting, collapse, seizures, coma.

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35
Q

give some signs of subarachnoid haemorrhage

A

neck stiffness, Kernig’s sign (inability to straighten knee with flexed hip).
retinal, subhyaloid and vitreous bleeds.

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36
Q

give 2 differential diagnoses of subarachnoid haemorrhage

A

meningitis, migraine, intracerebral bleeds, cortical vein thrombosis

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37
Q

what would you see on CT head in a subarachnoid haemorrhage?

A

no clear bleed - blood pools in available spaces, showing up white.
“star sign” - blood pooled in ventricles appears as white star.

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38
Q

what clinical features would indicate you should avoid doing a lumbar puncture and why?

A

headache, unilateral pupillary dilatation, vomiting, papilloedema, reduced mental state.
these are signs of raised ICP - risk herniation of brain and coning leading to death.

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39
Q

how would the CSF look if you performed a lumbar puncture on a person with subarachnoid haemorrhage?

A

CSF is bloody early on, then becomes yellow due to bilirubin - finding xanthochromia (yellow CSF) confirms SAH

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40
Q

how would you manage a subarachnoid haemorrhage?

A

hydrate, aim for systolic BP of 160 in order to maintain cerebral perfusion.
nimodipine - CCB, reduces vasospasm.
endovascular coiling, surgical clipping, intracranial stents, balloon remodelling.

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41
Q

give 2 possible complications of SAH

A

rebleeding.
cerebral ischaemia due to vasospasm - permanent CNS deficit.
hydrocephalus due to blockage of arachnoid granulations.

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42
Q

explain the process behind subdural haemorrhage

A

bleeding from bridging veins between cortex and venous sinuses - accumulating haematoma between dura and arachnoid - ICP gradually rises - midline structures shifted away from side of clot - eventual tentorial herniation and coning unless treated

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43
Q

who is at risk of subdural haemorrhage?

A

(those with small brains) - trauma patients, the elderly.
those prone to falls (epileptics, alcoholics).
those on anticoagulants.

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44
Q

how would a subdural haemorrhage present?

A

fluctuating consciousness level ± insidious physical/intellectual slowing.
sleepiness, headache, personality change, unsteadiness.
raised ICP, seizures.

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45
Q

what would you see on head CT/MRI of a patient with a subdural haemorrhage?

A

clot ± midline shift.

crescent shaped collection of blood over one hemisphere.

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46
Q

how would you manage a subdural haemorrhage?

A

mannitol for ICP.
irrigation/evacuation - burr twist drill/burr hole craniostomy.
craniotomy.

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47
Q

what causes an extradural haemorrhage?

A

MIDDLE MENINGEAL ARTERY most common.
any tear in dural venous sinus.
fractured temporal or parietal bone - causes laceration of middle meningeal artery and vein, typical after trauma to temple just lateral to eye.

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48
Q

what is a common clinical presentation of extradural haemorrhage?

A

‘lucid interval’ - walks away from road traffic accident seeming fine, then after a few hours/days, there’s a decrease in GCS from rising ICP.

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49
Q

after a lucid interval, what will be the clinical features of an extradural haemorrhage?

A

increasingly severe headache, vomiting, confusion, fits ± hemiparesis.
then - ipsilateral pupil dilates, coma deepens, bilateral weakness develops, deep and irregular breathing (brainstem compression)

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50
Q

how would an extradural haematoma appear on head CT?

A

round shape, rather than the sickle shape seen in subdural haematoma.

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51
Q

how would an extradural haematoma be treated?

A

mannitol for ICP.

neurosurgery - clot evacuation ± ligation of bleeding vessel

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52
Q

what treatment is contraindicated in all cerebral haemorrhages?

A

antiplatelets and anticoagulants

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53
Q

what 2 medical treatments can help reduce the risk of complications in intracranial haemorrhages?

A

dexamethasone (glucocorticoid) - reduces cerebral oedema, stabilises BBB.
nimodipine - CCB, reduces vasospasm

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54
Q

define a seizure, and define epilepsy

A

seizure = convulsion or transient event caused by a paroxysmal discharge of cerebral neurones.

epilepsy = continued tendency to have seizures.

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55
Q

what do the terms tonic, myoclonic and akinetic mean in terms of seizures?

A 
tonic = intense stiffening of body with no convulsions.
myoclonic = isolated muscle jerking (rapid repetitions of this = clonic).
akinetic = cessation of movement, falling and loss of consciousness
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56
Q

what may be features of the post-ictal state?

A

headache, confusion, myalgia, sore tongue.

temporary weakness following focal seizure in motor cortex / dysphasia following seizure in temporal lobe.

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57
Q

list 4 causes of epilepsy

A

idiopathic/familial - 2/3rds!
cortical scarring, developmental, space-occupying lesion, stroke, hippocampal sclerosis, vascular malformations, tuberous sclerosis, sarcoidosis, SLE, PAN

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58
Q

list 4 non-epileptic causes of seizures

A

trauma, stroke, haemorrhage, raised ICP, alcohol/benzodiazepine withdrawal, metabolic disturbance, liver disease, fever.
infection - HIV, meningitis, encephalitis, syphilis.
drugs - tricyclics, cocaine, tramdol, theophylline

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59
Q

describe the features of a simple partial seizure

A

awareness unimpaired.
focal motor, sensory, autonomic or psychic symptoms.
no post-ictal symptoms.

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60
Q

describe the features of a complex partial seizure

A

impaired awareness.
may have simple partial onset (aura).
arise from temporal lobe.
post-ictal confusion.

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61
Q

what happens in a partial seizure with secondary generalisation?

A

electrical disturbance that began focally spreads widely causing a secondary generalised seizure - usually convulsive

62
Q

what occurs in the brain during a primary generalised seizure?

A

simultaneous onset of electrical discharge throughout cortex with no localised features

63
Q

describe the features of absence seizures

A

brief pauses, e.g. stops mid-sentence then carries on - presents in childhood

64
Q

describe the features of tonic-clonic seizures

A

loss of consciousness.
limbs stiffen (tonic) then jerk (clonic).
may have one without the other.
post-ictal - confusion, drowsiness.

65
Q

describe the features of myoclonic seizures

A

sudden jerk of a limb, face or trunk.

patient may be thrown to the ground suddenly, or have a violently disobedient limb.

66
Q

describe the features of atonic (akinetic) seizures

A

sudden loss of muscle tone causing a fall, no loss of consciousness

67
Q

list some features of a focal seizure that would localise it to the temporal lobe

A

automatisms - motor phenomena with impaired awareness and no recollection afterwards - lip smacking, chewing, fumbling, fiddling - even complex acts - singing, kissing, driving a car, violence.
abdo rising sensation/pain.
dysphasia.
memory phenomena (deja vu/jamais vu).
hippocampal involvement = emotional disturbance.
uncal involvement = hallucinations of smell or taste.
auditory cortex involvement - auditory hallucinations.

68
Q

give some features of a focal seizure that would localise it to the frontal lobe

A 
motor - posturing, versive movements of head and eyes, peddling of legs.
jacksonian march.
motor arrest.
subtle behaviour disturbances.
dysphasia or speech arrest.
69
Q

give some features of a focal seizure that would localise it to the parietal lobe

A

sensory disturbances - tingling, numbness, pain.

motor symptoms - spread to pre-cental gyrus.

70
Q

give some features of a focal seizure that would localise it to the occipital lobe

A

visual phenomena - spots, lines, flashes

71
Q

how would you diagnose an epileptic seizure?

A

clinically - detailed description of attack from eye witness.
EEG - electroencephalogram and CT/MRI.

72
Q

how would you treat generalised tonic-clonic seizures?

A

sodium valproate or lamotrigine.

2nd line - carbamazepine or topiramate.

73
Q

how would you treat absence seizures?

A

sodium valproate or lamotrigine or ethosuximide

74
Q

how would you treat tonic, atonic and myoclonic seizures? what should be avoided?

A

as for tonic-clonic but avoid carbamazepine.

so, sodium valproate/lamotrigine, with topiramate as 2nd line.

75
Q

how would you treat partial seizures ± secondary generalisation?

A

carbamazepine.

76
Q

give a side effect for each of the main 3 anti-epileptic drugs

A

sodium valproate - nausea, diarrhoea, weight gain.
lamotrigine - Stevens-Johnsons syndrome, diplopia, blurred vision.
carbamazepine - Stevens-Johnson syndrome, hyponatraemia, impaired balance.

77
Q

what is the cardinal Parkinsonism triad comprised of?

A

bradykinesia (Parkinsonian gait), cogwheel rigidity, pill-rolling tremor

78
Q

explain the pathophysiology of Parkinson’s disease. the presence of what feature in the brain is diagnostic?

A

degeneration of dopaminergic neurons in the substantia nigra pars compacta, associated with presence of Lewy bodies.
causes decrease in striatal dopamine levels leading to cell loss and akinesia.

79
Q

give 3 non-motor symptoms of Parkinson’s disease

A

depression, dementia, dribbling, anosmia, hallucinations, constipation, dysphagia, heartburn, urinary difficulties, micrographia.

80
Q

what one main risk factor for other diseases, is protective in Parkinson’s disease?

A

smoking

81
Q

explain what you are likely to observe if you were to ask a Parkinson’s patient to walk up and down for you

A

stooping, shuffling gait. struggles to start walking. narrow base making falls common. obstacles, doors etc make them freeze and struggle to restart.

82
Q

what is the typical age of onset of Parkinson’s disease?

A

65yrs

83
Q

describe the medical management of Parkinson’s disease

A

dopamine agonists (ropinirole, pramipexole) and MAO-B inhibitor (rasagiline, selegiline) allows delay of starting L-Dopa.

start levodopa late - becomes ineffective after several years so start late and at a low dose then increase as needed.
prescribe with a decarboxylase inhibitor (carbidopa, besnerazide) to reduce peripheral side effects (esp. nausea).

84
Q

why can’t Parkinson’s patient just be treated with dopamine?

A

it cannot cross the blood-brain barrier - levodopa is a precursor of dopamine and is able to cross the BBB and the be converted to dopamine within the brain.

85
Q

what non-pharmacological treatment options are available for Parkinson’s?

A

deep brain stimulation, surgical ablation of overactive basal ganglia circuits.

86
Q

what is Huntington’s chorea?

A

autosomal dominant, incurable, progressive, neurodegenerative disease.

87
Q

define chorea

A

abnormal involuntary movements - brief, abrupt, irregular, unpredictable, non-stereotyped - may appear purposeful - patient appears fidgety/clumsy

88
Q

describe the features of the prodromal phase of Huntington’s disease

A

irritability, depression, incoordination - personality changes, self-neglect (doesn’t wash, doesn’t care about work), fidgeting, tic.

89
Q

describe the features of Huntington’s chorea

A

chorea, dementia ± fits and death.

90
Q

what is the underlying pathology of Huntington’s chorea?

A

atrophy and neuronal loss of striatum and cortex.

91
Q

what are the changes in neurotransmitters seen in Huntington’s chorea?

A

reduced ACh synthesis, depleted GABA and ACE in substantia nigra.
high somatostatin levels in corpus striatum.
dopamine remains normal.

92
Q

what would an MRI scan of the brain of a patient with Huntington’s chorea show?

A

caudate nucleus atrophy

93
Q

how would you treat Huntington’s chorea?

A

nothing will stop progression - symptomatic treatment only.

phenothiazines - sulpiride - antipsychotic drug, selective dopamine antagonist against receptors D2 and D3.

Tetrabenazine - used in hyperkinetic movement, promotes degradation of dopamine, helps chorea.

94
Q

name 3 precipitating factors of a tension headache

A

loud noise, worry, fumes, concentrated efforts

95
Q

how might a patient describe the pain of a tension headache?

A

bilateral, ‘tight band’, non-pulsatile, scalp tenderness.

96
Q

how would you manage a patient with tension headaches?

A

reassurance. stress relief.

can prescribe NSAIDs, paracetamol or aspirin - watch for analgesic overuse headache

97
Q

what causes tension headaches?

A

neurovascular irritation, referred to scalp muscles and soft tissues.

98
Q

what other symptoms may accompany the pain of a tension headache?

A

vomiting, sensitivity to head movement

99
Q

what are the clinical features that affect the eye in cluster headaches?

A

lacrimation, transient ipsilateral Horner’s, lid swelling, unilateral eye pain

100
Q

describe the timeline of cluster headaches

A

recurrent bouts of the headache a couple of times a day, coming on a few times a month, then disappears for a few months and then returns unexpectedly

101
Q

describe the pain of a cluster headache

A

rapid onset excrutiating pain around one eye. strictly unilateral - affects same side each time.

102
Q

how would you treat an acute attack of a cluster headache?

A

100% O2 for 15min via non-rebreathe mask.

sumatriptan (SC) - 5HT receptor agonist, acts on serotonin receptors.

103
Q

what preventatives are available to be used for cluster headaches?

A

suboccipital steroid injections.
intranasal civamide.
both are controversial.

also verapamil (CCB)

104
Q

give 4 migraine triggers

A

chocolate, cheese, oral contraceptives, caffeine, alcohol, anxiety, travel, exercise, lie ins, loud noise

105
Q

give 3 possible features of a migraine aura

A

flashing lights, tingling and weakness down one side, visual disturbance, ataxia, dysphasia

106
Q

give 2 possible features of a migraine prodrome

A

yawning, cravings, mood/sleep change

107
Q

describe the pain of migraine

A

severe unilateral throbbing headache, with nausea, vomiting ± photophobia/phonophobia.

108
Q

what are the diagnostic criteria for migraine without aura?

A

> 5 headaches lasting 4-72h + nausea/vomiting (or photo/phonophobia) + 2 of:
unilateral, pulsating, impairs (or worsened by) routine activity.

109
Q

give 3 differential diagnoses of migraine

A

cluster or tension headache, cervical spondylosis, hypertension, intracranial pathology, sinusitis/otitis media, TIA (may mimic migraine aura)

110
Q

how might you pharmacologically treat a migraine?

A

NSAIDs - ketoprofen, aspirin.

triptans (5HT agonists) - riztriptan, sumatriptan.

111
Q

what drugs might be used to prevent migraines?

A

1st line - propranolol, amitriptyline, topiramate, CCBs.

2nd line - valproate, pizotifen, gabapentin, pregabalin.

112
Q

what rheumatological disease is giant cell arteritis associated with?

A

polymyalgia rheumatica

113
Q

describe the 3 main clinical features of giant cell arteritis, and what causes them

A

headache - inflamed superficial temporal/occipital artery that hurts to touch and can become tortuous and thickened (I can’t even comb my hair!)
facial pain - inflammation of facial maxillary and lingual branches of external carotid artery, worse on eating (jaw claudication) - I can’t eat steak anymore!
visual disturbance - arterial inflammation and occlusion causing monocular painless visual loss (amaurosis fugax).

114
Q

what is the risk if treatment of giant cell arteritis is delayed?

A

irreversible bilateral visual loss.

115
Q

how would you diagnose giant cell arteritis? what should be done first?

A

raised ESR/CRP.

temporal artery biopsy - start steroids first!!

116
Q

how would you treat giant cell arteritis?

A

immediate high dose oral prednisolone.

117
Q

list 3 secondary causes of trigeminal neuralgia

A 
compression of trigeminal root by anomalous/aneurysmal intracranial vessels or a tumour.
chronic meningeal inflammation.
MS.
herpes zoster.
skull base malformation.
118
Q

describe the clinical features of trigeminal neuralgia

A

paroxysms of intense, stabbing pain, lasting seconds in the trigeminal nerve distribution.

unilateral, affecting mandibular or maxillary divisions.
face screwed up in pain.

119
Q

give 2 examples of triggers of trigeminal neuralgia

A

washing affected area, shaving, eating, talking, dental prostheses

120
Q

how would you treat trigeminal neuralgia?

A

carbamazepine, lamotrigine, phenytoin or gabapentin.

some surgical options.

121
Q

give 3 causes of spinal cord compression

A

secondary malignancy - breast, lung, prostate, thyroid, kidney.
TB - Pott’s disease (destruction of vertebral bodies and disc spaces).
epidural haemorrhage or haematoma
prolapsed disc.

122
Q

where do the corticospinal tracts decussate? what do they control?

A

85% - pyramids of medulla - lateral corticospinal tract, muscles of arms and legs.
15% - at the spinal level they leave at - control postural muscles, only present in thoracic levels.

123
Q

which tract controls pain and temperature? where does it decussate?

A

spinothalamic - goes up 2-3 levels, then decussates

124
Q

what tract controls “nice sensations” where does it decussate?

A

dorsal columns - touch, vibration, proprioception.
gracile fasciculus - legs, cuneatus fasciculus - arms.
decussate in upper medulla.

125
Q

what imaging would you use to investigate the cause of the symptoms in spinal cord compression?

A

MRI

126
Q

in Brown-Sequard syndrome, there is a hemisection of the spinal cord, on what side is there a loss of proprioception, vibration, power, pain and temperature?

A

contralateral loss of pain and temperature.

ipsilateral loss of proprioception, vibration and power.

127
Q

what is the T10 dermatome?

A

umbilical level

128
Q

what is the L1 dermatome?

A

inguinal ligament

129
Q

what is the L2-3 dermatome?

A

anterior and inner leg

130
Q

what is the C3-4 dermatome?

A

clavicles

131
Q

what is the C6-7 dermatome?

A

lateral arm/forearm

132
Q

what is the T1 dermatome?

A

medial side of the arm

133
Q

what is the T4 dermatome?

A

nipple level

134
Q

how would you treat spinal cord compression due to malignancy?

A

dexamethasone IV ± radio/chemotherapy

135
Q

what is the cauda equina?

A

a bundle of spinal nerves and spinal nerve roots that consists of L2-5 and S1-5, they innervate the lower limbs and pelvic organs.
they also supply the sensory innervation to the perineum and parasympathetic supply to the bladder.

136
Q

what causes damage to the cauda equina?

A

damage to spine at or distal to L1

137
Q

what are the clinical features of cauda equina syndrome?

A

flaccid leg weakness and areflexic paralysis of legs.

back pain, radicular pain down legs, sensory loss in a root distribution, decreased sphincter tone

138
Q

how would you manage cauda equina syndrome?

A

surgical decompression within 48h

139
Q

explain the pathogenesis of multiple sclerosis

A

inflammatory process in the white matter of the brain and cord mediated by CD4 T cells.
there are discrete plaques of demyelination at multiple CNS sites.
demyelination leads to axonal damage.
heals incompletely causing relapsing and remitting disease.

140
Q

describe the 4 possible disease courses in MS. what is necessary for diagnosis?

A

need lesions disseminated in time and space.

relapsing and remitting - disease relapses followed by full recovery, or at least partial recovery - clear period of time with no disease activity, followed by another relapse.

primary progressive - disease progresses from onset, with occasional plateaus/temporary improvements.

secondary progressive - initially relapsing/remitting, then following progressive phase.

progressive/relapsing - progressive disease from onset, with clear acute relapses that recover then continue to progress.

141
Q

describe the epidemiology of MS

A

prevalence increases with distance from equator - possible role of vitamin D?
more common in women, mean age of onset 30yrs.

142
Q

give some clinical features of MS

A

unilateral optic neuritis - pain on eye movement, rapid worsening of central vision.
numbness or tingling limbs.
leg weakness.
brainstem/cerebellar symptoms (diplopia, ataxia).
sensory - paraesthesiae, trigminal neuralgia.
motor - spastic weakness, myelitis.
GU - ED, urine retention, incontinence.
GI - swallowing disorders, constipation.
eye - diplopia, hemianopia, visual phenomena, pupil defects.
cognitive decline - amnesia, mood swings, decreased executive functioning.

143
Q

what commonly makes symptoms of MS worse?

A

raised body temp - HOT BATHS

144
Q

what 2 investigations would you carry out in MS and what would you expect to see?

A

MRI - visible plaques.
CSF - oligoclonal IgG bands on electrophoresis.

lesions disseminated in time and space

145
Q

how would you treat MS?

A

acute - IV methylprednisolone (doesn’t affect prognosis, just treats relapse symptoms).
prevention of relapses - beta-interferon, azathioprine.

146
Q

what is the gold standard investigation for stroke?

A

CT

147
Q

why do you get a lucid interval in extradural haematomas?

A

because the patient is bleeding very slowly - due to how tightly the dura mater is adherent to the skull.
venous bleed.

148
Q

what is the genetic basis of Huntington’s chorea? how many repeats may a patient have before they develop Huntington’s?

A

expansion of CAG repeat on chromosome 4 - overexpression of the huntingtin gene.

> 27 repeats is abnormal.
40 almost definitely will get Huntington’s.
the more repeats, the worse the symptoms.

149
Q

what is giant cell arteritis?

A

systemic immune mediated vasculitis affecting medium and large sized arteries

150
Q

what 3 clinical features make up Cushing’s triad of signs of raised ICP?

A

irregular resps.
bradycardia.
hypertension.

2a - Systems Based Clinical Sciences (18 decks)

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