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My Phase 3a Revision > NEURO > Flashcards

NEURO Flashcards

1
Q

STROKE
What is a stroke?

A

Rapid onset of neurological deficit due to a vascular lesion lasting >24 hours and associated with infarction of central nervous tissue

poor blood flow to the brain causes cell death

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2
Q

STROKE
What are the two main classifications of stroke?

A
  • Ischaemic (85%) – cerebral ischaemia leads to infarction of neural tissue + so loss of functionality
  • Haemorrhagic (15%) – ruptured blood vessel leads to reduced blood flow
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3
Q

STROKE
What are the causes of ischaemic strokes?

A

small vessel occlusion by thrombus
atherothromboembolism (e.g. from carotid artery)
cardioembolism (post MI, valve disease, IE)
hyper viscosity
hypoperfusion
vasculitis
fat emboli from a long bone fracture
venous sinus thrombosis

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4
Q

STROKE
What are the causes of haemorrhagic stroke?

A

Bleeding from the brain vasculature

  1. Hypertension - stiff and brittle vessels, prone to rupture
  2. Secondary to ischaemic stroke - bleeding after reperfusion
  3. Head trauma
  4. Arteriovenous malformations
  5. Vasculitis
  6. Vascular tumours
  7. Carotid artery dissection
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5
Q

STROKE
Give an example of how chronic HTN can cause a stroke.

A
  • Charcot-Bouchard aneurysms most often in the basal ganglia
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6
Q

STROKE
What are the risk factors for ischaemic strokes?

A

Age
Male
Hypertension
Smoking
Diabetes
Recent/past TIA
Heart disease - IHD, AF, valve disease
Combined oral contraceptive

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7
Q

STROKE
What are some important differentials of stroke?

A
  • Metabolic (hypo or hyperglycaemia, electrolytes)
  • Intracranial tumours, hemiplegic migraine
  • Infection (meningitis)
  • Head injury, seizure (focal > Todd’s paralysis)
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8
Q

STROKE
What classification system can be used for strokes?

A
  • Oxford stroke (Bamford) classification
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9
Q

STROKE
What are the various classifications of strokes?

A
  • Total anterior circulation stroke (TACS)
  • Partial anterior circulation stroke (PACS)
  • Posterior circulation syndrome (POCS)
  • Lacunar syndrome (LACS)
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10
Q

STROKE
How would an ACA stroke present?

A
  1. Leg weakness - contralateral
  2. Sensory disturbance in legs
  3. Gait apraxia
  4. Incontinence
  5. Drowsiness
  6. Akinetic mutism - decrease in spontaneous speech (in a stupor)
  7. truncal ataxia - can’t sit or stand unsupported
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11
Q

STROKE
How would a MCA stroke present?

A
  1. Contralateral arm and leg weakness and sensory loss
  2. Hemianopia
  3. Aphasia
  4. Dysphasia
  5. Facial droop
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12
Q

STROKE
How would a PCA stroke present?

A

visual issues

  1. Contralateral homonymous hemianopia
  2. Cortical blindness
  3. Visual agonisa
  4. Prosopagnoisa
  5. Dyslexia
  6. Unilateral headache
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13
Q

STROKE
How would a brainstem/basilar artery infarct present?

A
  • Locked in syndrome – complete paralysis BUT eye movement + awareness preserved
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14
Q

STROKE
What tools can be used to identify stroke?

A
  • FAST = Facial drooping, Arms floppy, Slurred speech, Time critical (999)
  • ROSIER = Recognition Of Stroke In Emergency Room
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15
Q

STROKE
What investigation is crucial for the management of stroke and why?

A
  • Non-contrast CT head to exclude haemorrhagic before treatment given.
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16
Q

STROKE
How would an ischaemic stroke appear on CT head?

A
  • Hypodensity in region affected with hyperdense vessel
  • Loss of grey-white matter differentiation + sulcal effacement (squishing) in cortical infarction
  • Hypodense basal ganglia may be seen in deep vessel infarcts
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17
Q

STROKE
How would a haemorrhagic stroke appear on CT head?

A
  • Acute = hyperdense
  • Subacte = isodense
  • Chronic = hypodense
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18
Q

STROKE
What are the pros of CT head imaging?

A
  • Quick, readily available, can distinguish site affected + if ischaemic or haemorrhagic
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19
Q

STROKE
What is the gold standard imaging for stroke if nothing can be seen on CT head?

A
  • Diffusion-weighted MRI head as shows changes within minutes + higher sensitivity for infarcts
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20
Q

STROKE
What bloods may be taken in suspected stroke?

A
  • FBC, ESR + clotting screen (polycythaemia, vasculitis, thrombocytopenia)
  • U+Es, creatinine, LFTs, Ca2+ (electrolytes)
  • Blood glucose (hypo)
  • TFTs, lipid profile (hypercholesterolaemia)
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21
Q

STROKE
What other investigations may you do in stroke?

A
  • ECG 72h tape to look for paroxysmal AF, MI.
  • ECHO to check for endocarditis or CHD
  • CTA/MRA or carotid doppler USS to look for dissection or carotid stenosis
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22
Q

STROKE
What are some potential complications following a stroke?

A
  • Raised ICP, aspiration pneumonia due to dysphagia, pressure sores
  • Cognitive impairment, long-term disability, depression
  • VTE due to immobility
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23
Q

STROKE
What is the treatment for an ischaemic stroke?

A

Immediate management:

  • CT/MRI to exclude haemorrhagic stroke
  • aspirin 300mg

Antiplatelet therapy

  • aspirin 300mg for 2 weeks
  • clopidogrel daily long term

Anticoagulation (e.g. warfarin) for AF

thrombolysis

  • within 4.5 hrs of onset
  • IV alteplase
  • lots of contraindications (can cause massive bleeds)

mechanical thromboectomy
- endovascular removal of thrombus

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24
Q

STROKE
What is the timeframe for thrombolysis for ischaemic strokes?

A
  • Within 4.5 hours of the onset of symptoms
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25
Q

STROKE
what is the mechanism of action for alteplase / streptokinase (thrombolysis drugs for ischaemic stroke)?

A
  • Converts plasminogen > plasmin so promotes breakdown of fibrin clot
  • Alteplase (tPA) or can use streptokinase
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26
Q

STROKE
What must be done after alteplase treatment?

A
  • Repeat CT head after 24h to check for haemorrhagic transformation
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27
Q

STROKE
What are the benefits of alteplase?

A
  • Improves chance of independence on discharge,
  • benefit decreases with time (time=brain),
  • risk of death same
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28
Q

STROKE

What are the risks of alteplase?

A
  • Haemorrhage (1 in 20), reaction to tPA
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29
Q

STROKE
What are some contraindications to treatment with alteplase?

A
  • Haemorrhagic stroke
  • Recent surgery
  • GI bleeding
  • Pregnancy
  • Hx of intracranial haemorrhage
  • Active cancer
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30
Q

STROKE
What other treatment can be given in ischaemic stroke either alongside alteplase or after the time frame?

A
  • Thrombectomy (mechanical retrieval of clot)
  • Proximal anterior circulation stroke within 6h (with IV alteplase if <4.5h) or within 24h if potential to salvage brain tissue
  • Proximal posterior circulation stroke within 24h (with IV alteplase if <4.5h) if potential to salvage brain tissue
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31
Q

STROKE
What other management is given for ischaemic strokes?

A
  • Control BP
  • 300mg aspirin OD 2w post-stroke + then lifelong 75mg clopidogrel
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32
Q

STROKE
What is the management of a haemorrhagic stroke?

A
  • Stop anticoagulants if on any + warfarin reversal with vitamin K + beriplex
  • Aggressive BP control (140–160mmHg systolic)
  • Surgical decompression (either endovascular clipping or coiling)
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33
Q

STROKE
What lifestyle advice should be given post-stroke?

A
  • Smoking + alcohol cessation
  • Improve diet + exercise
  • Cannot drive for 1m post-stroke or 1y if HGV driver
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34
Q

STROKE
What medication and general management may be given in stroke prevention?

A
  • Antiplatelets (lifelong clopidogrel or aspirin + dipyridamole if cardiac disease)
  • Anticoagulation if have AF but wait 2w post-stroke
  • Manage co-morbidities (HTN, DM)
  • Cholesterol >3.5mmol/L diet + 80mg atorvastatin
  • VTE assessment + monitor for infection
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35
Q

STROKE
When assessing whether to anticoagulate a patient, what scores could you use?

A
  • CHA2DS2-VaSc (risk of stroke due to AF)
  • HAS-BLED (risk of serious bleeding)
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36
Q

STROKE
What is the CHA2DS2-VaSc score

A
  • Congestive heart failure
  • HTN
  • Age 65-74 (1), ≥75 (2)
  • Diabetes
  • Prev stroke/TIA (2)
  • Vascular disease
  • Sex female
  • 1 = consider anticoagulation, ≥2 = anticoagulate
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37
Q

STROKE
What is the HAS-BLED score?

A
  • HTN >160mmHg
  • Abnormal liver/renal function
  • Stroke
  • Bleeding Hx or predisposition
  • Labile INR
  • Elderly >65y
  • Drug/alcohol use
  • ≥3 = high risk of bleeding
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38
Q

STROKE
what is the primary prevention of strokes?

A

Risk factor modifcaiton

  • Antihypertensives for HTN
  • Statins for hyperlipiaemia
  • Smoking cessation
  • Control DM
  • AF treatment = warfarin/NOAC’s
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39
Q

STROKE
what is the secondary prevention of strokes?

A

2 weeks of aspirin –> long term clopidogrel

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40
Q

STROKE
what non-pharmaceutical treatment options are there for people after a stroke?

A
  1. Specialised stroke units
  2. Swallowing and feeding help
  3. Phsyio and OT
  4. Neurorehab - physio + speech therapy
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41
Q

TIA
What is a transient ischaemia attack (TIA)?

A

sudden onset, brief episode of neurological deficit due to temporary, focal cerebral ischaemia
symptoms are maximal at onset and lasts 5-15 mins (<24hrs)

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42
Q

TIA
what are the signs of a carotid TIA?

A

Amaurosis fugax = retinal artery occlusion –> vision loss
Aphasia
Hemiparesis
Hemisensory loss
hemianopia

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43
Q

TIA
What are the causes of a transient ischaemia attack (TIA)?

A
  • Artherothromboembolism of the carotid - main cause (can hear carotid bruit)
  • Cardioembolism - in AF, after MI, valve disease/prosthetic valve
  • Hyperviscosity - polycythaemia, sickle cell, high WBCC
  • hypoperfusion - postural hypotension, decreased flow
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44
Q

TIA
what is the pathophysiology of TIA?

A

Cerebral ischaemia due to lack of O2 and nutrients –> cerebral dysfunction without infarction (no irreversible cell death)

symptoms are maximal at onset -> usually last 5-15 mine (<24hrs)

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45
Q

TIA
What is a crescendo TIA?

A
  • ≥2 TIAs within a week (high risk of stroke)
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46
Q

TIA
what are the signs of a vertebrobasilar TIA?

A

Diplopia, vertigo, vomiting
Choking and dysarthria
Ataxia
Hemisensory loss
Hemianopic/bilateral visual loss
tetraparesis
loss of consciousness

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47
Q

TIA
what are the differential diagnosis’s for a TIA

A

Migraine aura
Epilepsy
Hypoglycaemia
Hyperventilation
retinal bleed
syncope - due to arrhythmia

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48
Q

TIA
What investigations would you do in someone who you suspect to have a TIA?

A

first line = diffusion weighted MRI or CT

second line = carotid imaging (doppler ultrasound followed by angiography if stenosis is found)

Bloods

FBC - look for polycythaemia
ESR - raised in vasculitis
U&Es, glucose
ECG

echocardiogram

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49
Q

TIA
What is it essential to do in someone who has had a TIA?

A

Assess their risk of having stroke in the next 7 days = ABCD2 score

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50
Q

TIA
what is the ABCD2 score?

A

Assesses risk of stoke in the next 7 days for those who have had a TIA

age
BP
clinical features - unilateral weakness, speech disturbance
duration of TIA
presence of diabetes mellitus

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51
Q

TIA
What do the scores from ABCD2 mean?

A
  • ≥4 or crescendo TIAs = specialist assessment within 24h (give aspirin 300mg OD)
  • ≤3 = specialist assessment within 1 week, ?brain imaging
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52
Q

TIA
What is the treatment for a TIA?

A

immediate treatment = aspirin 300mg and refer to specialist within 24hrs

control CV risk factors

BP control - ACEi (RAMIPRIL) or ARB (CANDESARTAN)
smoking cessation
statin - SIMVASTATIN
no driving for 1 month
antiplatelet therapy
- ASPIRIN 75mg daily (With Dipyridamole)
or
- CLOPIDOGREL daily

anticoagulation (e.g. WARFARIN) for patients with AF

carotid endarterectomy

if >70% carotid stenosis
reduces stroke/TIA risk by 75%

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53
Q

TIA
What treatment may be considered after a TIA?

A
  • Carotid endarterectomy if >70% carotid artery stenosis within 2w of Sx (TIA/stroke)
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54
Q

TIA
How would you assess suitability for a carotid endarterectomy after a TIA??

A
  • Carotid doppler USS
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55
Q

SAH
What is the pathophysiology of a subarachnoid haemorrhage (SAH)?

A
  1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
  2. raised ICP - fast flowing arterial blood is pumped into the cranial space
  3. space occupying lesion - puts pressure on the brain
  4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
  5. vasospasm - bleeding irritates other vessels -> ischaemic injury
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56
Q

SAH
What are the causes of SAH?

A
  • Traumatic injury
  • Berry aneurysm rupture
    (70-80%) - at common points round Circle of Willis
  • Arteriovenous malformations (15%) - abnormal tangle of blood vessels connecting arteries and veins
  • Idiopathic (15-20%)
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57
Q

SAH
What conditions are linked to SAH?

A
  • Polycystic kidneys
  • coarctation of aorta
  • Ehlers-Danlos syndrome
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58
Q

SAH
What are some risk factors for SAH?

A

Hypertension
Known aneurysm
Previous aneurysmal SAH

Smoking
Alcohol
Family history
Bleeding disorders

  • associated with berry aneurysms:
    • Polycystic Kidney Disease
    • Coarctation of aorta
    • Ehlers-Danlos syndrome & Marfan syndrome
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59
Q

SAH
What are some symptoms of SAH?

A
  • sudden onset excruciating headache - thunderclap, worst headache, typically occipital
  • sentinel headache - before main rupture, sign of warning leak
  • nausea
  • vomiting
  • collapse
  • loss of/depressed consciousness
  • seizures
  • vision changes
  • coma - can last for days
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60
Q

SAH
What are some signs of SAH?

A
  • signs of meningeal irritation
    1. Kernig’s sign (can’t straighten leg past 135 degrees)
    2. neck stiffness
    3. Brudzinski’s sign (Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed)
  • retinal, subhyaloid and vitreous bleeds
    • worse prognosis
    • with/without papilloedema
  • neurological signs - e.g. 3rd nerve palsy
  • increased BP
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61
Q

SAH
What are some complications of SAH?

A
  • 50% die suddenly or soon after haemorrhage
  • Rebleeding (20% within first few days)
  • Cerebral ischaemia due to vasospasm can cause permanent CNS deficit (most common cause of morbidity)
  • Obstructive hydrocephalus due to blockage of arachnoid granulations (requires ventricular or lumbar drain)
  • Hyponatraemia (IV 0.9% NaCl saline)
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62
Q

SAH
What is often associated with better outcomes in SAH?

A
  • GCS >12 on arrival
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63
Q

SAH
What are the investigations for SAH?

A
  1. urgent Head CT = star pattern (diagnostic)
  2. Lumbar Puncture = xanthochromia -> RBC breakdown (only if normal ICP and after 12 hrs)
  3. MR/CT angiography - to establish source of bleeding
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64
Q

SAH
what is the appearance of SAH on CT head?

A

white star-shaped lesion as blood fills gyro patterns around brain + ventricles

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65
Q

SAH
What is the management of SAH?

A
  • NIMOPIDINE for 3 weeks -> CCB which prevents vasospasm so reduces cerebral ischaemia
  • surgery = endovascular coiling
  • IV fluids - maintain cerebral perfusion
  • ventricular drainage for hydrocephalus
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66
Q

SAH
give 3 possible complications of a subarachnoid haemorrhage

A
  1. Rebleeding (common = death)
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
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67
Q

EDH
What is the pathophysiology of extra-dural haematoma (EDH)?

A
  • Often fractured temporal/parietal bone leads to blood accumulating between bone + dura mater over minutes to hours

After a lucid interval there is:
- rapid rise in ICP
pressure on the brain
- midline shift
- tentorial herniation
- coning

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68
Q

EDH
Which vessels most commonly are affected in extradural haematomas?
which other vessels can be affected?

A
  • Middle meningeal artery
  • 25% venous if fracture disrupts the venous sinuses
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69
Q

EDH
What do the ventricles do to prolong survival in someone with an extradural haematoma?

A
  • Ventricles get rid of their CSF to prevent the rise in ICP
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70
Q

EDH
What causes an EDH?

A

Traumatic head injury (typically to temple, just lateral to eye e.g. punch) - often the temproal bone

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71
Q

EDH
What is the clinical presentation of EDH?

A
  • initial injury followed by lucid period
  • period of rapid deterioration
  • rapid decline in GCS
  • increasing severe headache
  • vomiting
  • seizures
  • hemiparesis
  • coma
  • UMN signs
  • ipsilateral pupil dilation
  • bilateral limb weakness
  • deep and irregular breathing - due to coning
    late signs = bradycardia and raised BP (cushing’s reflex)
  • death from respiratory arrest
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72
Q

EDH
what are the signs of ICP ± focal neurology in EDH?

A
  • Increasingly severe headache,
  • vomiting,
  • confusion + seizures ± hemiparesis with brisk reflexes
  • upgoing plantars
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73
Q

EDH
what is Cushing’s reflex?

A

Bradycardia and increased BP

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74
Q

EDH
What are some differentials for EDH?

A
  • Epilepsy,
  • CO poisoning,
  • carotid dissection
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75
Q

EDH
What are some complications of EDH?

A
  • Brainstem compression can cause deep + irregular breathing,
  • death may follow period of coma due to respiratory arrest
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76
Q

EDH
What are the investigations for EDH?

A

Non-contrast CT head

Skull x-ray - may show fracture lines

LP is contraindicated

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77
Q

EDH
what is the appearance of EDH on non-contrast head CT?

A

lens shaped haematoma = LEMON SHAPE
doesn’t cross suture lines
shows midline shift

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78
Q

EDH
What investigation is contraindicated in EDH and why?

A
  • Lumbar puncture
  • Drop in CSF pressure in spinal column will speed up brain herniation through the foramen magnum as CSF + brain mass may shift towards low pressure outlet > brainstem compression + respiratory arrest
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79
Q

EDH
What is the management for EDH?

A

STABILISE PATIENT

URGENT SURGERY

clot evacuation
ligation of bleeding vessel
IV MANNITOL
- to reduce ICP

airway care
- intubation and ventilation

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80
Q

SDH
What is the most common cause of subdural haematoma (SDH)?

A
  • Rupture of a vein running from hemisphere to the sagittal sinus of the dural venous sinuses (bridging veins) that’s beneath the dura leading to haematoma between arachnoid + dura mater
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81
Q

SDH
What is the pathophysiology of a SDH?

A
  1. bleeding from bridging veins into the subdural space forms a haematoma
  2. then bleeding stops
  3. weeks/months later the haematoma starts to autolyse - massive increase in oncotic and osmotic pressure. Water is sucked in and haematoma enlarges
  4. gradual rise in ICP over weeks
  5. midline structures shift away from side of clot - causes tentorial herniation and coning
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82
Q

SDH
What causes water to be sucked up into a subdural haematoma 8-10 weeks after a head injury?

A

Clot starts to break down and there is massive increase in oncotic pressure –> water is sucked up by osmosis into the haematoma

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83
Q

SDH
what are the risk factors of SDH?

A
  • Elderly - brain atrophy, dementia
  • Frequent falls - epileptics, alcoholics
  • Anticoagulants
  • babies - traumatic injury (“shaking baby syndrome”)bridging veins stretched so more likely to rupture,
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84
Q

SDH
What are the symptoms of SDH?

A
  • Fluctuating GCS
  • Headache
  • Confusion - may fluctuate
  • Drowsiness
  • physical and intellectual slowing
  • personality change
  • unsteadiness
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85
Q

SDH
What are some signs of SDH?

A
  • raised ICP - seizures
  • localising neurological signs (unequal pupils, hemiparesis)
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86
Q

SDH
what are the differential diagnoses for a subdural haematoma?

A

stroke
dementia
CNS masses (tumour vs abscess)

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87
Q

SDH
What are the investigations for SDH?

A

Non-contrast CT head
MRI scan

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88
Q

SDH
what is the appearance of SDH on non-contrast head CT?

A

crescent shaped haematoma = BANANA SHAPE (clot turns from white to grey over time)
unilateral
shows midline shift

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89
Q

SDH
What is the management of SDH?

A

SURGERY
1* = irrigation via burr-hole craniostomy
2* = craniotomy

IV MANNITOL - to reduce ICP

address cause of trauma

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90
Q

EPILEPSY
Define epilepsy

A

Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures

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91
Q

EPILEPSY
Define seizure

A

Paroxysmal event in which changes of behaviour, sensation, cognition + consciousness caused by excessive, hypersynchronous neurological discharges in the brain

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92
Q

EPILEPSY
Define ictal phase

A

Early phase w/ +ve Sx (excessive/jerky actions)

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93
Q

EPILEPSY
Define post-ictal phase

A

Later phase w/ -ve Sx (weakness, drowsy)

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94
Q

EPILEPSY
What are the causes of epilepsy?

A
  1. Idiopathic (2/3)
  2. cortical scarring
  3. tumour
  4. stroke
  5. alzheimers dementia
  6. alcohol withdrawal
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95
Q

EPILEPSY
What is a focal/partial seizure?

A
  • Confined to one area of cortex with recognisable pattern, usually unilateral meaning 1 hemisphere affected, may affect one body part
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96
Q

EPILEPSY
What is a simple-partial seizure?

A

Consciousness + awareness is preserved (e.g. foot twitch)

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97
Q

EPILEPSY
What is a complex-partial seizure?

A

Without consciousness or awareness

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98
Q

EPILEPSY
What is a secondary generalised seizure?

A

Seizures starts in 1 hemisphere but spreads to both (focal > general)

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99
Q

EPILEPSY
How would a partial seizure present in the frontal lobe?

A

strange smells,
motor movements,
Jacksonian march

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100
Q

EPILEPSY
How would a partial seizure present in the temporal lobe?

A

déjà/jamais-vu, automatisms (chewing, lip smacking), hallucinations,
aura/sensations,
amnesia

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101
Q

EPILEPSY
How would a partial seizure present in the parietal lobe?

A

contralateral altered sensation (tingling, numbness, crawling, electric-shock)

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102
Q

EPILEPSY
How would a partial seizure present in the occipital lobe?

A

flashing lights, eyelid fluttering, eye movements

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103
Q

EPILEPSY
What is Jacksonian march?

A

Starts on one side of body then “marches” over a few seconds to affect larger parts of body like entire hand, foot or facial muscles + may generalise

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104
Q

EPILEPSY
What is Todd’s paresis?

A

Focal weakness in a part or all of the body after a seizure

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105
Q

EPILEPSY
What is a generalised seizure?

A
  • Activity in both hemispheres, diffuse throughout the brain with bilateral movement abnormalities
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106
Q

EPILEPSY
What are the 4 main types of generalised seizure?

A
  • Absence seizures,
  • tonic-clonic seizures,
  • myoclonic seizures
  • atonic (akinetic) seizures/drop attacks
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107
Q

EPILEPSY
Explain what an absence seizure is.

A
  • Brief <30s pauses where activity stops (still, no talking, stares)
  • Begins in childhood, may progress to tonic-clonic later in life
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108
Q

EPILEPSY
How might epilepsy present in terms of…

i) patient?
ii) triggers?
iii) prodrome?
iv) ictal?
v) post-ictal?

A

i) Any age, ?CNS lesion, FHx of epilepsy
ii) Alcohol, decreased sleep, illness, hyperventilation, none
iii) No warning or ?aura, staring/vacant, vocalisation (cry out), posturing
iv) Tonic>clonic, symmetrical, few minutes, eyes open, incontinence, lateral tongue biting
v) Slow recovery, amnesia, confused, drowsy, agitated

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109
Q

EPILEPSY
Explain what a tonic clonic seizure is.

A
  • Tonic = vague warning, rigid, pt falls + may make sound, LOC + may stop breathing
  • Clonic = convulsions, bilateral rhythmic muscle jerks, irregular breathing, may bite tongue (lateral) or urinary incontinence
  • Post-ictal = drowsy, confused, irritable or depressed
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110
Q

EPILEPSY
Explain what a myoclonic seizure is.

A
  • Brief, sudden muscle contractions like jerk of a limb, face or trunk
  • Usually remains awake, can occur in juvenile myoclonic epilepsy
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111
Q

EPILEPSY
Explain what an atonic (akinetic) seizure/drop attack is.

A
  • Brief, sudden loss of muscle tone causing a fall but no LOC
  • Typically begin in childhood, ?indicate Lennox-Gastaut syndrome
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112
Q

EPILEPSY
What are some differentials of epilepsy?

A
  • Cardiac = postural or cardiogenic syncope
  • Non-epileptic attack disorder, hypoglycaemia, TIA
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113
Q

EPILEPSY
What investigations would you do in epilepsy?

A
  • Mostly clinical Dx, witnessed seizure Hx crucial

Electroencephalogram (EEG) = supports diagnosis

MRI/ CT head = rule out space-occupying lesions

Bloods
FBC, Ca2+, electrolytes, U&Es, LFTs, blood glucose = rule out metabolic disturbances

Genetic testing
If suspected genetic cause -> juvenile myoclonic epilepsy

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114
Q

EPILEPSY
what is the diagnostic criteria for eilespy?

A

At least 2 or more unprovoked seizures occurring >24 hours apart

One unprovoked seizure + probability of future seizures

Epileptic syndrome diagnosis

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115
Q

EPILEPSY
What is the emergency treatment for epilepsy?

A

ABCDE
check glucose
RECTAL/IV DIAZEPAM or LORAZEPAM
IV PHENYTOIN loading
mechanical ventilation

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116
Q

EPILEPSY
What is the general management in the ictal phase?

A
  • Ensure little harm as possible, maintain airway, do not restrain
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117
Q

EPILEPSY
what is the treatment for generalised tonic-clonic epilepsy?

A

1st line = Sodium Valproate for Males & women unable to childbear,

2nd line = Lamotrigine to females of childbearing potential for myoclonic

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118
Q

EPILEPSY
what is the treatment for generalised tonic/atonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Lamotrigine to females of childbearing potential

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119
Q

EPILEPSY
what is the treatment for generalised myoclonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Levetiracetam/Topiramate to females of childbearing potential

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120
Q

EPILEPSY
what is the treatment for absence (petit mal) epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Ethosuximide to females of childbearing potential

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121
Q

EPILEPSY
What is the management of epilepsy if anti-epileptic drugs fail to control it?

A

Vagal stimulation,
surgery (hemispherectomy or non-dominant lobectomy)

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122
Q

EPILEPSY
how do lamotrigine and carbamazepine work?

A

Inhibit pre-synaptic Na+ channels so prevent axonal firing

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123
Q

EPILEPSY
how does sodium valproate work?

A

Inhibits voltage gated Na+ channels and increases GABA production

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124
Q

EPLILEPSY
give 4 potential side effects of anti-epileptic drugs (AEDs)

A
  1. Cognitive disturbances
  2. Heart disease
  3. Drug interactions
  4. Teratogenic
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125
Q

EPILEPSY
What driving advice should be given to patients regarding seizures and established epilepsy?

A
  • Cannot drive for 6m following seizure + must inform DVLA
  • Established epilepsy must be seizure free for 12m before driving
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126
Q

STATUS EPILEPTICUS
What is status epilepticus?

A
  • Medical emergency where a seizure does not self-limit – seizures lasting >5m or ≥2 within a 5-minute period
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127
Q

STATUS EPILEPTICUS
What are some causes of status epilepticus?

A
  • Poor adherence #1
  • Infections (meningitis, encephalitis)
  • Worsening of primary cause of epilepsy (e.g. brain tumour growing)
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128
Q

STATUS EPILEPTICUS
When might status epilepticus be the first presentation of epilepsy?

A

First presentation in alcohol abuse (most commonly) or acute brain problem (stroke, trauma, infections, hypoglycaemia)

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129
Q

STATUS EPILEPTICUS
What is the clinical presentation of status epilepticus?

A
  • Convulsions tend to occur for 2–3m
  • Followed by slow activity or rest period + then more convulsions
  • The whole process continues although individual seizures do not
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130
Q

STATUS EPILEPTICUS
What are the complications of status epilepticus?

A
  • 10% mortality
  • Long-term morbidity after episode, esp. if hypoxic brain injury occurred (rhabdomyolysis, metabolic acidosis, renal failure)
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131
Q

STATUS EPILEPTICUS
What is the initial management for status epilepticus?

A
  • ABCDE approach (Secure airway, high conc oxygen, assess cardiorespiratory function)
  • Establish IV access
  • Measure capillary glucose + correct immediately
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132
Q

STATUS EPILEPTICUS
What investigations might you do for aetiologies of status epilepticus?

A
  • FBC, U+Es, Ca2+, Mg+, LFTs, INR, AED levels, CK
  • Blood cultures
  • Toxicology screen
  • CT head to rule out organic causes
  • LP if imaging -ve
  • EEG useful
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133
Q

STATUS EPILEPTICUS
What is the step-wise management of status epilepticus?

A
  • IV lorazepam 4mg if fitting >5m – repeat after 10m if persists
  • IV phenytoin (regular ECG/BP), phenobarbital or sodium valproate
  • No response to step 2 within 30m then anaesthesia + ICU admission as anaesthesia will stop but v dangerous
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134
Q

STATUS EPILEPTICUS
What considerations should be made in status epilepticus?

A
  • Community – buccal midazolam or rectal diazepam as step 1
  • If ?alcohol related treat with IV thiamine or Pabrinex
  • If medication not working or no response ?non-epileptic
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135
Q

LOC
What is LOC?

A

Partial or complete loss of perception of yourself + surroundings

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136
Q

LOC
What are the potential causes of LOC?

A

CRASH
- Cardiogenic (more alarming)
- Reflex (neurally mediated)
- Arterial
- Systemic
- Head

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137
Q

LOC
How might cardiogenic LOC present/causes?

A
  • Transient arrhythmias (SVT, WPW, Brugada, long QT)
  • Bradyarrhythmias like complete heart block > asystole
  • Structural (aortic stenosis, hypertrophic cardiomyopathy) where may have palpitations, dyspnoea + CP
    BLACKOUT ON EXERCISE IS CARDIOGENIC UNTIL PROVEN OTHERWISE
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138
Q

LOC
How might reflex LOC present?

A
  • Vasovagal syncope = intense fear like watching surgery, needles > faint
  • Situational syncope = coughing, post-micturition
  • Carotid sinus syncope = hypersensitive baroreceptors cause excessive reflexive bradycardia on minimal stimulation (turn head, shaving, reaching high)
  • Postural hypotension (iatrogenic autonomic failure)
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139
Q

LOC
What are some important questions to ask in LOC?

A
  • Collateral Hx/witness account is crucial
  • Head banging
  • Triggers, before, during, after (how they felt, warning signs, incontinence, injury like tongue biting, sleepy or muscle aches)
  • Previous episodes
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140
Q

SYNCOPE
What is syncope?

A

Transient global cerebral hypoperfusion

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141
Q

SYNCOPE
How might syncope present in terms of…

i) patient?
ii) triggers?
iii) prodrome?
iv) ictal?
v) post-ictal?

A

i) Older, co-morbidities or young + FHx of young deaths
ii) Posture, exertion, metabolic
iii) Pale, clammy, palpitations, CPs, ‘going dark’
iv) Floppy, seconds, eye closed ± few jerks
v) Rapid recovery, seconds

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142
Q

NEAD
What is NEAD?

A

Episodes of movement, sensation or experience that resemble epileptic seizures but without ictal cerebral discharges, physical manifestation of psychological distress

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143
Q

NEAD
How might NEAD present in terms of…

i) patient?
ii) triggers?
iii) prodrome?
iv) ictal?
v) post-ictal?

A

i) Younger, F>M, social/personal stressors, psych Hx, deprivation, abuse
ii) Heightened emotion, stress or panic
iii) No warning, upset/panic, aware of impending seizure
iv) Thrashing/asymmetrical, long (up to 1h), pelvic thrusting, violent, back arching, eyes + mouth forcibly closed, crying, ?distractible, tongue biting (tip), waxing/waning
v) unusually rapid, emotional ± amnesia

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144
Q

NEAD
How can NEAD and a true epileptic seizure be differentiated?

A
  • Vital signs including lying-standing BP
  • FBC, U+Es, glucose, LFTs, TFTs (normal CK + prolactin in NEAD)
  • 24h 12-lead ECG + ECHO
  • EEG + CT/MRI if necessary
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145
Q

NEAD
what is the management of NEAD?

A

correct Dx vital,
speak to pt,
reassure them,
wait for seizure to pass,
CBT,
avoid AEDs as can be fatal if mistreated excessively (respiratory depression)

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146
Q

PARKINSON’S DISEASE
Define Parkinson’s disease

A

Degenerative movement disorder caused by a reduction in dopamine in the pars compacta of the substantia nigra

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147
Q

PARKINSONS DISEASE
what is the pathway for dopamine production?

A

Tyrosine –> L-dopa –> Dopamine

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148
Q

PARKINSON’S DISEASE
What is the pathophysiology of Parkinson’s disease?

A

destruction of dopaminergic neurones (in substantia nigra) –> reduced dopamine supply –> thalamus inhibits –> decrease in movement + symptoms
Lewy body formation in basal ganglia

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149
Q

PARKINSON’S DISEASE
What are the causes of Parkinson’s disease?

A
  • Unknown, some genetic link, typically 70y/o M
  • Haloperidol (dopamine blockade)
  • Metoclopramide + domperidone (anti-emetics which blockade dopamine)
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150
Q

PARKINSON’S DISEASE
what can exacerbate parkinson’s disease?

A

Anticholinergics can precipitate confusion

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151
Q

PARKINSON’S DISEASE
What are the cardinal features of Parkinson’s disease?

A
  • BRADYKINESIA (slow, difficult initiating movement, small movements)
  • RIGIDITY (pain, problems turning in bed) – cogwheel rigidity with tension in arm that gives way to movement in small increments (little jerks)
  • RESTING TREMOR – ‘pill-rolling’
  • Shuffling gait, small steps + postural instability (stooped)
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152
Q

PARKINSON’S DISEASE
what are the clinical features of Parkinson’s disease

A

● Often an insidious onset

impaired dexterity,
fixed facial expressions,
foot drag
● Common associated symptoms:

dementia,
depression,
urinary frequency,
constipation,
sleep disturbances
- Smaller writing (micrographia)
- Hypomimia

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153
Q

PARKINSON’S DISEASE
Would you describe the symptoms of Parkinson’s disease as symmetrical or asymmetrical?

A

Asymmetrical = One side is always worse than the other

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154
Q

PARKINSON’S DISEASE
In terms of tremor, what is an intention tremor?

A

Worse at end of movement (past-pointing) indicative of cerebellar issue

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155
Q

PARKINSON’S DISEASE
In terms of tremor, what is resting tremor?

A

Tremor seen in Parkinson’s disease

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156
Q

PARKINSON’S DISEASE
In terms of tremor, what is postural tremor?

A

Anxiety, increased adrenaline, salbutamol, valproate, lithium, benign essential tremor

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157
Q

PARKINSON’S DISEASE
How can you differentiate Parkinson’s resting tremor from benign essential tremor ?

A
  • Asymmetrical vs symmetrical
  • 4–6Hz vs 5–8Hz
  • Worse at rest vs improves at rest
  • Improves with intentional movement vs worse with intentional movement
  • No change with alcohol vs improves with alcohol (also Rx = propranolol)
  • Parkinson’s vs. autosomal dominant condition
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158
Q

PARKINSON’S DISEASE
What are 4 differential diagnoses to consider in Parkinson’s disease?

A

Parkinson’s plus syndromes –
- Progressive supranuclear palsy
- Multiple system atrophy
- Lewy Body dementia
- Corticobasal degeneration

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159
Q

PARKINSON’S DISEASE
What is progressive supranuclear palsy?

A
  • Early falls, cognitive decline or both sides being equally affected
  • Occurs above nuclei of CN3, 4 + 6 so difficulty moving eyes
  • Impaired vertical gaze (down worse = issues reading or descending stairs)
  • Ocular cephalic reflex present (caused by supranuclear issue) where they tilt/turn their head to look at things rather than moving eyes
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160
Q

PARKINSON’S DISEASE
What is multiple system atrophy?

A
  • Neurones in multiple systems in the brain degenerate
  • Degeneration in basal ganglia > Parkinsonism
  • Degeneration in other areas > early autonomic (postural hypotension + falls, bladder/bowel dysfunction) + cerebellar (ataxia) dysfunction
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161
Q

PARKINSON’S DISEASE
What is Lewy Body dementia associated with?

A
  • Associated with Sx of visual hallucinations, delusions, REM sleep disorders, fluctuating consciousness, progressive cognitive decline + Parkinsonism
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162
Q

PARKINSON’S DISEASE
What is corticobasal degeneration?

A
  • Early myoclonic jerks, gait apraxia, agnosia + alien limb
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163
Q

PARKINSON’S DISEASE
What investigations would you do in Parkinson’s disease?

A

DaTscan

Functional neuroimaging - PET

Can confirm by reaction to levodopa

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164
Q

PARKINSON’S DISEASE
Give 2 histopathological signs of Parkinson’s disease

A
  1. Loss of dopaminergic neurones in the substantia nigra
  2. Lewy bodies
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165
Q

PARKINSON’S DISEASE
What are some complications of Parkinson’s disease?

A
  • Infections
  • Falls
  • Depression
  • Aspiration pneumonia
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166
Q

PARKINSON’S DISEASE
What is the management of Parkinson’s disease?

A
  • Lifestyle: education, exercise, physio, MDT

young onset + fit
- Dopamine agonist (ropinirole)
- MAO-B inhibitor (rasagiline)
- L-DOPA (co-careldopa)

frail + co-morbidities
- L-DOPA (co-careldopa)
- MAO-B inhibitor (rasagiline)

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167
Q

PARKINSON’S DISEASE
What surgical treatment methods are there for Parkinson’s disease?

A

Deep brain stimulation of the sub-thalamic nucleus

Surgical ablation of overactive basal ganglia circuits

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168
Q

HUNTINGTON’S DISEASE
What is the pathophysiology of Huntington’s disease?

A
  • Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
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169
Q

HUNTINGTON’S DISEASE
What is the inheritance pattern of Huntington’s disease?

A
  • Autosomal dominant inheritance with 100% penetrance
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170
Q

HUNTINGTON’S DISEASE
What is the triplet code that is repeated in Huntington’s disease?

A

Trinucleotide expansion repeat of CAG in HTT gene on chromosome 4
- >35 = HD

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171
Q

HUNTINGTON’S DISEASE
Huntington’s disease shows anticipation.
What does this mean?
When do symptoms typically occur?

A
  • Successive generations have more repeats leading to earlier age of onset + increased severity of disease
  • Around middle age
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172
Q

HUNTINGTON’S DISEASE
How does Huntington’s disease present?

A

● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination
● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety

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173
Q

HUNTINGTON’S DISEASE
what are the signs of Huntington’s disease?

A

Abnormal eye movements
Dysarthria
Dysphagia
Rigidity
Ataxia

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174
Q

HUNTINGTON’S DISEASE
What is the life expectancy from Sx onset?

A

15–20y + death mostly respiratory disease

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175
Q

HUNTINGTON’S DISEASE
What investigations would you do for Huntington’s disease?

A
  • GENETIC TESTING - with pre- + post-test counselling (cannot give to children have to be old enough to decide themselves), high risk of suicide with diagnosis
  • MRI HEAD - shows atrophy of striatum
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176
Q

HUNTINGTON’S DISEASE
What is the management of Huntington’s disease?

A

poor prognosis - no treatment
● Benzodiazepines/valproic acid - chorea
● SSRIs = depression
● Haloperidol = psychosis

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177
Q

HEADACHES
What are the two types of headaches and give some examples?

A
  • Primary (no underlying cause) such as migraine, cluster + tension (most common)
  • Secondary due to an underlying cause.
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178
Q

HEADACHES
What do these red flags for headaches indicate…

i) fever, photophobia, neck stiffness, rash?
ii) sudden onset occipital?
iii) vomiting, worse on coughing or straining?
iv) Hx of trauma + may resist analgesia?
v) dizziness or new neuro Sx?
vi) visual disturbance?
vii) pregnancy?
viii) subacute or sudden with papilloedema?
ix) travel Hx + flu-like illness?

A

i) Meningitis/encephalitis
ii) SAH
iii) Raised ICP (?SOL)
iv) Head injury or haemorrhage
v) Stroke
vi) GCA or glaucoma
vii) Pre-eclampsia
viii) Venous sinus thrombosis
ix) Malaria

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179
Q

HEADACHES
How does a cluster headache present and how long does it last?

A
  • 15m–3h
  • Rapid onset excruciating pain around one eye
  • Pain is unilateral, often nocturnal
  • Eye may be bloodshot, lid swelling, miosis, ptosis + lacrimation
  • ‘Cluster’ of attacks in a day then remission for weeks/months
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180
Q

HEADACHES
How can you diagnose cluster headaches?

A

≥5 classical headaches

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181
Q

HEADACHES
What is the acute management of cluster headaches?

A
  • S/c triptans
  • 15L 100% oxygen via non-rebreathe mask for 15 minutes
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182
Q

HEADACHES
What is the prophylactic management of cluster headaches?

A

1st line = Verapamil
- avoid triggers (alcohol)
- short course prednisolone may break cycle during clusters

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183
Q

HEADACHES
How does a tension headache present?

A
  • 30m– 7 days
  • Bilateral, non-pulsatile headache ± scalp tenderness
  • Pressing/tight-band like sensation
  • Mild–moderate intensity
    (Med overuse headache is similar)
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184
Q

HEADACHES
How can you diagnose tension headaches?

A

Clinical Dx

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185
Q

HEADACHES
What is the management of tension headaches?

A
  • Reassure, stress relief (Exercise, avoid triggers, massage)
  • Simple analgesia like paracetamol (<15d/m) or complex analgesia (<10d/m)
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186
Q

HEADACHES
How does a sinusitis headache present?

A
  • Facial pain behind nose, forehead + eyes, pain on leaning forward
  • Tenderness over affected sinus
  • Post-nasal drip, common with coryza
  • Pain lasts 1–2w, viral
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187
Q

HEADACHES
What is the management of sinusitis headache?

A
  • Nasal irrigation w/ saline
  • Prolonged Sx with steroid nasal spray
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188
Q

HEADACHES
How does acute glaucoma present?

A
  • Constant aching pain rapidly develops around 1 eye, radiates to forehead, markedly reduced vision, visual halos, N+V
  • Signs = red, congested eye, cloudy cornea, dilated non-responsive eye (may be oval shaped)
  • Can be precipitated by dilating eye-drops, emotions or sitting in dark
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189
Q

HEADACHES
What is the management of acute glaucoma?

A
  • Immediate expert help + IV acetazolamide (carbonic anhydrase inhibitor)
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190
Q

HEADACHES
What is the most common type of secondary headache?

A

Medication overuse headache - episodic headache becomes daily chronic headache

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191
Q

HEADACHES
How can you diagnose medication overuse headaches?

A
  • Present >15d/month,
  • regular use for >3m of >1 symptomatic treatment drugs
  • headache developed or worsened during drug use
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192
Q

HEADACHES
What is the management of medication overuse headache?

A
  • Withdrawal of analgesia (may be challenging if pt thinks necessary for headache)
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193
Q

TRIGEMINAL NEURALGIA
What is the pathophysiology of trigeminal neuralgia?
What is affected?

A
  • Compression of trigeminal nerve results in demyelination + excitation of the nerve resulting in erratic pain signalling
  • Affects all 3 ophthalmic (V1), maxillary (V2) + mandibular (V3) branches but V3 mostly
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194
Q

TRIGEMINAL NEURALGIA
What are the causes of trigeminal neuralgia?

A

Compression of trigeminal nerve by a loop of vein or artery
Aneurysms
Meningeal inflammation
Tumours

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195
Q

TRIGEMINAL NEURALGIA
What is the epidemiology?

A

peak age = 50-60yrs
women > men

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196
Q

TRIGEMINAL NEURALGIA
What are some triggers?

A

Washing affected area, shaving, eating, talking + dental prostheses

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197
Q

TRIGEMINAL NEURALGIA
What is the clinical presentation of trigeminal neuralgia?

A
  • Paroxysms of intense, stabbing pain, lasting seconds in the trigeminal nerve distribution (knife-like shooting pain with no neuro deficit)
  • Mostly unilateral, face screws up in pain
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198
Q

TRIGEMINAL NEURALGIA
How would you diagnose trigeminal neuralgia?

A
  • Clinically with ≥3 attacks with pain in ≥1 division + classical Sx
  • ?CT/MRI head to exclude secondary causes
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199
Q

TRIGEMINAL NEURALGIA
How would you manage trigeminal neuralgia?

A

Carbamazepine - suppresses attacks
Less effective options = phenytoin, gabapentin and lamotrigine
Surgery = microvascular decompression, gamma knife surgery

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200
Q

MIGRAINE
What is the pathophysiology of migraines?

A
  • Changes in brainstem blood flow leads to unstable trigeminal nerve nucleus + nuclei in basal thalamus
  • Leads to release of vasoactive neuropeptides CGRP + substance P > neurogenic inflammation > vasodilation + plasma protein extravasation leading to pain propagating all over the cerebral cortex
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201
Q

MIGRAINE
What are the triggers of migraines?

A

CHOCOLATE –
- Chocolate
- Hangovers
- Orgasms
- Cheese/caffeine
- Oral contraceptives
- Lie-ins
- Alcohol
- Travel
- Exercise

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202
Q

MIGRAINE
How long do they last for and who are they more common in?

A

4–72h, F>M

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203
Q

MIGRAINE
What are the stages of migraine?

A
  • Prodromal (up to 3d before with fatigue + mood change)
  • Aura
  • Headache
  • Resolution (headache fades or resolved by vomiting/sleep)
  • Postdromal
    (Not typical, some experience a few stages)
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204
Q

MIGRAINE
What is a prodrome for migraines?

A

Precedes migraine by hours-days

yawning
food cravings
changes in sleep, appetite or mood

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205
Q

MIGRAINE
what is a migraine aura?

A

Precedes migraine attacks and can be a variety of symptoms
- Visual = lines, dots, zig-zags
- somatosensory = paraesthesia, pins and needles
Dysphagia
Ataxia

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206
Q

MIGRAINE
what is a migraine aura?

A

Precedes migraine attacks and can be a variety of symptoms
- Visual = lines, dots, zig-zags
- somatosensory = paraesthesia, pins and needles
Dysphagia
Ataxia

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207
Q

MIGRAINE
What are the 4 main types of migraine?

A
  • Migraine without aura (most common)
  • Migraine with aura
  • Silent migraine
  • Hemiplegic migraine
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208
Q

MIGRAINE
Describe the pain of a migraine

A
  • Unilateral
  • Throbbing
  • Moderate/severe pain
  • Aggravated by physical activity
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209
Q

MIGRAINE
What other symptoms may a patient with a migraine experience other than pain?

A

Nausea
Photophobia
Phonophobia
Aura

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210
Q

MIGRAINE
How does a migraine with aura present?

A

Same as without but –
- Sparks/zig-zag lines in vision, blurred vision or loss of different visual fields
- Aura usually unilateral + lasts up to 60m before headache

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211
Q

MIGRAINE
What investigations would you do in migraine?

A
  • Mostly clinical Dx
  • Exclude other causes with bloods, CRP/ESR, CT/MRI head, LP if any red flag concerns
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212
Q

MIGRAINE
What is the diagnostic criteria for a migraine?

A

classified as with or without aura
at least 2 of:
unilateral pain (usually 4-72hrs)
throbbing-type pain
moderate > severe intensity
motion sensitivity
plus at least 1 of:

  • nausea/vomiting
    -photophobia/phonophobia

there must also be a normal examination and no attributable cause

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213
Q

MIGRAINE
What is the acute management of migraines?

A
  • PO (or nasal in paeds) triptan like sumatriptan plus paracetamol or NSAID
  • Antiemetic like metoclopramide or prochlorperazine if vomiting occurs
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214
Q

MIGRAINE
How does triptan work?

A

Selectively stimulates 5-hydroxytryptamine (serotonin) receptors in the brain

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215
Q

MIGRAINE
What is the prophylaxis for migarines?

A
  • Propranolol or topiramate are first line
  • Topiramate is teratogenic + can reduce efficacy of hormonal contraceptives though
  • Also, amitriptyline, botulinum toxin or acupuncture.
  • 400mg OD of riboflavin (B2) may help
  • NOT gabapentin
  • Avoid indentified triggers (?headache diary)
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216
Q

MND
does MND affect UMN or LMN?

A

both UMN and LMN can be affected

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217
Q

MND
does MND affect eye movement?

A

Never affects eye movements (clinical feature of myasthenia gravis)

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218
Q

MND
Does MND cause sensory loss or sphincter disturbance?

A

No (clinical feature of MS)

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219
Q

MND
What is the pathophysiology of motor neurone disease (MND)?

A
  • Relentless + unexplained destruction/degeneration of UMN + anterior horn cells in the brain + spinal cord
  • Motor cortex = UMN signs
  • Anterior horn cells = LMN signs
  • Cranial nerve nuclei = mixed signs
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220
Q

MND
What is the cause of MND?

A
  • Most spontaneous + idiopathic with no FHx
  • Rare familial cases with SOD-1 implication (suggests free radicals like smoking, pesticides + heavy metals) can cause MN destruction
  • M>F, 60y/o, associated with frontotemporal dementia
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221
Q

MND
What are the 4 types of MND?
Best and worse prognosis?

A
  • Amyotrophic lateral sclerosis (ALS)
  • Progressive bulbar palsy (worst prognosis)
  • Progressive muscular atrophy (best prognosis)
  • Primary lateral sclerosis
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222
Q

MND
What is ALS?
What is a long-term consequence?

A
  • Loss of motor neurones in motor cortex + anterior horn of cord so mixed signs
  • Long term consequence is progressive spastic tetraparesis
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223
Q

MND
What is progressive bulbar palsy?
What does it affect?
What does it need to be differentiated from?

A
  • Only affects CN 9–12 (brainstem motor nuclei) so LMN of them
  • Primarily affects muscles of talking, chewing, tongue palsy + swallowing
  • Progressive pseudobulbar palsy = destruction of UMN so same as bulbar but small spastic tongue with no fasciculations
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224
Q

MND
What is…

i) progressive muscular atrophy?
ii) primary lateral sclerosis?

A

i) Anterior horn cells affected so LMN signs only, distal > proximal
ii) Loss of cells in motor cortex so UMN signs only

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225
Q

MND
What is the general clinical presentation of MND?

A
  • Insidious + progressive muscle weakness affecting limbs, trunk, face + speech
  • Often first noticed in upper limbs, may be fatigue when exercising
  • May have stumbling spastic gait, weak grip + clumsiness
  • Dysarthria, dysphagia, emotional lability in pseudobulbar palsy
  • NO SENSORY SYMPTOMS
226
Q

MND
What are UMN signs?

A

Hypertonia or spasticity,
brisk reflexes
upgoing plantars,
muscle wasting

227
Q

MND
What are LMN signs?

A

Hypotonia + muscle wasting,
reduced reflexes,
fasciculations (particularly tongue)

228
Q

MND
What are some important differentials of MND and how can they be differentiated?

A
  • Cervical spine lesion as may present with UMN signs
  • Myasthenia gravis but MND NEVER affects eye movements
  • Multiple sclerosis but MND NEVER affects sphincters or sensation
229
Q

MND
What are some investigations for MND?

A

Head/spine MRI
Blood tests = muscle enzymes, autoantibodies
Nerve conduction studies
EMG
Lumbar Puncture

230
Q

MND
What is the diagnostic criteria for MND?

A

LMN + UMN signs in 3 regions

El Escorial criteria

Presences of LMN and UMN degeneration and progressive history
Absence of other disease processes

231
Q

MND
How rapidly does MND progress?

A

Half of patients die <3y from onset, monitor FVC closely for respiratory distress as most die from bulbar palsy respiratory failure

232
Q

MND
What are some complications of MND?

A
  • UTI, pneumonia + respiratory failure (common cause of death), constipation, pressure sores
233
Q

MND
What medication may be given in MND?

A
  • RILUZOLE – Na+ blocker inhibits glutamate release
  • Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
  • Dysphagia: NG tube
  • Spasms: ORAL BACLOFEN
  • Non-invasive ventilation
  • Analgesia e.g. NSAIDs - DICLOFENAC
234
Q

MND
What MDT management is given for MND?

A
  • NG/PEG tube for feeding, blend food if dysphagia (SALT)
  • Exercise for spasticity (physio, orthotics)
  • Non-invasive ventilation at home to support breathing at night
  • Palliative care (advanced directives, EOL planning)
235
Q

MULTIPLE SCLEROSIS
what is MS?

A

A chronic autoimmune, T-cell mediated inflammatory condition of the CNS characterised by multiple plaques of demyelination within the brain and spinal cord, occurring sporadically over years

236
Q

MULTIPLE SCLEROSIS
What is the pathophysiology of MS?

A
  • Inflammation leads to infiltration of immune cells + damages the myelin causing focal loss
  • Demyelination heals poorly leaving thinner, inefficient myelin
  • Initially relative preservation of axons but as neurodegenerative, eventually axonal loss leading to fixed + progressive deficits
237
Q

MULTIPLE SCLEROSIS
What are some classic sites for MS?

A
  • Periventricular white matter lesions
  • Predilection for distinct sites – optic nerves, corpus callosum, brainstem + cerebellar peduncles
238
Q

MULTIPLE SCLEROSIS
What is the aetiology of MS?

A
  • Unknown as autoimmune but influenced by genes, EBV, lifestyle factors such as low vitamin D, smoking + obesity
239
Q

MULTIPLE SCLEROSIS
What is the epidemiology of MS?

A

Commonly presents in young females living further away from equator

240
Q

MULTIPLE SCLEROSIS
What is a clinically isolated syndrome?

A
  • First episode of demyelination + neuro Sx – not diagnosis as does not meet criteria
  • More likely to develop MS if lesions on MRI
241
Q

MULTIPLE SCLEROSIS
What are the 4 types of MS?

A
  • Relapsing remitting (most common)
  • Secondary progressive
  • Primary progressive
  • Benign
242
Q

MULTIPLE SCLEROSIS
What is relapsing remitting MS?

A
  • Characterised by episodes of Sx in attacks (relapses)
  • Followed by periods of stability (remission)
  • May accumulate disability if don’t fully recover
243
Q

MULTIPLE SCLEROSIS
What is secondary progressive MS?

A

Initially RR but now progressive worsening of Sx + incomplete remissions

244
Q

MULTIPLE SCLEROSIS
What is primary progressive MS?

A

Gradually worsening of disease from point of diagnosis without any RR

245
Q

MULTIPLE SCLEROSIS
What is benign MS?

A

Relapses + Remissions but overall progress will never worsen

246
Q

MULTIPLE SCLEROSIS
What is the diagnostic criteria for MS?

A

McDonald criteria –
- Multiple CNS lesions (≥2)
- Sx that last >24h
- Disseminated in space (Clinically or on MRI) and time (>1m apart)

247
Q

MULTIPLE SCLEROSIS
What are the symptoms of MS?

A

DEMYELINATION –
- Diplopia (CN VI)
- Eye movement pain (optic neuritis, v common)
- Motor weakness
- nYstagmus
- Elevated temp worsens
- Lhermitte’s sign
- Intention tremor
- Neuropathic pain
- Ataxia
- Talking slurred (dysarthria)
- Impotence
- Overactive bladder
- Numbness

248
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is the pattern of motor weakness?

A

i) Pyramidal pattern so extensors weaker than flexors in upper limb, flexors weaker than extensors in lower

249
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Uhthoff’s phenomenon?

A

symptoms worsening in heat e.g. in the shower/exercise

250
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Lhermitte’s sign?

A

Neck flexion causes electric shock sensation down spine

251
Q

MULTIPLE SCLEROSIS
What are some signs of MS?

A
  • UMN = spastic paraparesis, brisk reflexes, hypertonia
  • Sensory = loss of sensation, cerebellar signs
  • Relative afferent pupillary defect
  • Internuclear ophthalmoplegia
  • Optic atrophy (pale optic disc) in chronic MS
252
Q

MULTIPLE SCLEROSIS
What is relative afferent pupillary defect?

A
  • Seen on swinging light test (retina or optic nerve lesion –afferent issue)
  • The affected and normal eye appears to dilate when light is shone on the affected eye
253
Q

MULTIPLE SCLEROSIS
What is internuclear ophthalmoplegia?

A
  • CN VI/medial longitudinal fasciculus lesion
  • Disorder of conjugate lateral gaze with;
    – Decreased adduction of ipsilateral eye
    – Nystagmus on abduction of contralateral eye
254
Q

MULTIPLE SCLEROSIS
What are the differential diagnosis’s of MS

A

SLE
Sjogren’s
AIDS
Syphilis

255
Q

MULTIPLE SCLEROSIS
What are the investigations for MS?

A
  • MRI head + spinal cord to show demyelination plaques = diagnostic
  • Lumbar puncture may show oligoclonal bands of IgG on CSF electrophoresis
  • Evoked potentials = delayed visual, auditory + somatosensory potentials
256
Q

MULTIPLE SCLEROSIS
What is the management of MS relapses?
How does this affect disease prognosis?

A
  • IV methylprednisolone
  • Shortens acute relapses but no overall effect on prognosis
257
Q

MULTIPLE SCLEROSIS
What is the management of MS remissions?

A
  • First line = beta-interferons (1b) to decrease # relapses + lesions on MRI but SEs = depression, flu Sx + miscarriage
  • 2nd line = DMARDs (monoclonal antibody) - natalizumab, dimethyl fumarate
258
Q

MULTIPLE SCLEROSIS
What is the criteria for treatment of MS remissions?

A
  • 2 relapses in past 2y
259
Q

MULTIPLE SCLEROSIS
What is the general symptomatic management for MS?

A

Spasticity
- BACLOFEN (GABA analogue, reduces Ca2+ influx)
- TIZANIDINE (alpha-2 agonist)
- BOTOX INJECTION (reduces ACh in neuromuscular junction)

urinary incontinence = catheterisation

incontinence
- DOXAZOSIN (anti-cholinergic alpha blocker drugs

260
Q

MENINGITIS
What is meningitis?

A
  • Inflammation of the meninges which line the brain + spinal cord
261
Q

MENINGITIS
How does it occur?

A

Microorganisms can reach the meninges either by direct extension from ears, nasopharynx or via blood

262
Q

MENINGITIS
What are the bacterial causes of meningitis?

A

N. meningitidis
S. pneumoniae
H. influenzae

263
Q

MENINGITIS
What are the bacterial causes of meningitis in neonates?

A

E.coli
Group B strep - strep agalactiae

264
Q

MENINGITIS
What are the viral causes of meningitis?

A

Enterovirus (most common viral)
HSV
CMV
Varicella zoster virus

265
Q

MENINGITIS
What can cause meningitis in immunocompromised patients?

A

CMV
Cryptococcus
TB
HIV
herpes simplex

266
Q

MENINGITIS
What are the aseptic causes of meningitis?

A

MS.
HSV2, SLE, sarcoidosis + skull # can cause recurrent aseptic meningitis

267
Q

MENINGITIS
What are the symptoms of meningitis?

A

Neck stiffness
Photophobia
Papilloedema (due to increased ICP)
Petechial non-blanching rash
Headache
Fever
Decreased GCS

268
Q

MENINGITIS
How does viral meningitis present?

A

benign + self-limiting, no rash but blurred vision or headache

269
Q

MENINGITIS
What are the clinical signs of meningitis?

A
  • Meningism
  • +ve Kernig’s = pain or unable to extend leg at knee when it’s bent
  • +ve Brudzinski = involuntary flexion of hips + knees when neck flexed
  • Non-blanching purpuric rash = later sign in meningococcal septicaemia
270
Q

MENINGITIS
How would you describe the rash associated with meningococcal sepsis?

A

Petechial non-blanching rash

271
Q

MENINGITIS
What are some differentials of meningitis?

A
  • Malaria
  • Encephalitis
  • SAH
  • Septicaemia
  • Tetanus
  • Dengue fever
272
Q

MENINGITIS
What investigations would you do for meningitis?

A

Blood cultures (pre LP)
Bloods - FBC, U+E, CRP, ESR, serum glucose, lactate
Lumbar puncture (contraindicated with raised ICP)
CT head - exclude lesions
Throat swabs - bacterial and viral

273
Q

MENINGITIS
What would you expect the lumbar puncture result for meningitis to be in bacterial causes for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Cloudy/turbid
ii) ++
iii) ––
iv) ++ neutrophils
v) Gram stain

274
Q

MENINGITIS
What would you expect the lumbar puncture result for meningitis to be in viral causes for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Clear
ii) Mild + or normal
iii) Mild – or normal
iv) ++ lymphocytes
v) PCR

275
Q

MENINGITIS
What would you expect the lumbar puncture result for meningitis to be in TB causes for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Fibrin web
ii) ++
iii) ––
iv) ++ lymphocytes
v) Acid fast bacilli

276
Q

MENINGITIS
When is a lumbar puncture contraindicated in meningitis?

A
  • Drowsy, signs of raised ICP + in meningococcal septicaemia due to risk of coning of cerebellar tonsils
277
Q

MENINGITIS
What are some complications following meningitis?

A
  • Hearing loss is key complication
  • Seizures + epilepsy
  • Sepsis or abscess
  • Hydrocephalus
  • Cognitive impairment + learning disability
278
Q

MENINGITIS
You see a patient in General Practice with a non-blanching petechial rash and suspect meningococcal septicaemia.
What immediate treatment should be given whilst awaiting for hospital transfer?

A
  • IM benzylpenicillin
279
Q

MENINGITIS
What is the management of bacterial meningitis

A
  • IV cefotaxime
    • amoxicillin to cover listeria (potential contraction in birth) in <3m
  • Dexamethasone to reduce frequency + severity of neurological sequelae
  • Adjust treatment according to sensitivities
280
Q

MENINGITIS
What is the management of viral meningitis?

A
  • Supportive therapy mainly
  • IV aciclovir for HSV
281
Q

MENINGITIS
What can be given as prophylaxis against meningitis?

A

IV CIPROFLOXACIN (all ages and pregnancy) and IV RIFAMPICIN (all ages but NOT pregnancy)

282
Q

MENINGITIS
Who must you notify about cases of meningitis?

A
  • Public Health England immediately as notifiable disease
283
Q

MENINGITIS
Give 4 potential adverse effect of a lumbar puncture

A

Headache
Paraesthesia
CSF leak
Damage to spinal cord

284
Q

ENCEPHALITIS
What is encephalitis?

A
  • Infection + inflammation of the brain parenchyma (cortex, white matter, brainstem, basal ganglia)
285
Q

ENCEPHALITIS
In what group of people is encephalitis common?

A

Immunocompromised

the infections are most frequent in children and elderly

286
Q

ENCEPHALITIS
What are the viral causes of encephalitis?

A

Herpes simplex (most common)
CMV
Epstein Barr
varicella zoster
HIV
measles
mumps

287
Q

ENCEPHALITIS
What are the non-viral causes of encephalitis?

A

Bacterial meningitis
TB
Malaria
Lyme’s disease

288
Q

ENCEPHALITIS
Name the main triad of symptoms of encephalitis

A

Fever + headache + altered mental state

289
Q

ENCEPHALITIS
What is the clinical presentation of encephalitis?

A

begins with features of viral infection:
- fever, headaches, myalgia, fatigue, nausea

progresses to:

personality & behavioural changes
decreased consciousness, confusion, drowsiness
focal neurological deficit - hemiparesis, dysphagia
seizures
raised ICP and midline shift
coma

290
Q

ENCEPHALITIS
What are the differentials of encephalitis

A
  • Meningitis
  • Stroke
  • Brain tumour
  • Hypoglycaemia, SLE, hypoxic brain injury, DKA
291
Q

ENCEPHALITIS
What investigations would you do for encephalitis?

A
  • Blood culture + CSF serology for viral PCR
    MRI - shows areas of inflammation, may be midline shifting
    EEG - periodic sharp and slow wave complexes
    lumbar puncture
292
Q

ENCEPHALITIS
What would the CSF look like in encephalitis for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?

A

i) Clear
ii) Raised
iii) Normal/low
iv) + lymphocytes

293
Q

ENCEPHALITIS
What is the management of encephalitis?

A

IV Acyclovir immediately - even before investigation results
Primidone = anti-seizure medication if needed
IV benzylpenicillin if meningitis is suspected

294
Q

BRAIN ABSCESS
What are the most common causative organisms?

A
  • Staph. aureus + strep. pnuemoniae
295
Q

BRAIN ABSCESS
What is a brain abscess?

A
  • Pus-filled swelling in the brain
296
Q

BRAIN ABSCESS
What are the aetiologies of brain abscesses?

A
  • Local infection spread (otitis media, sinusitis, mastoiditis)
  • Penetrating head injuries, trauma or surgery to the scalp
  • Haematogenous spread (more common in immunocompromised) from CHD (esp. R>L shunt), pneumonia, embolic events from infective endocarditis
297
Q

BRAIN ABSCESS
What is the clinical presentation of a brain abscess?

A
  • Fever, headache (raised ICP Sx) + focal neurology are the classic triad
  • If in critical area (motor cortex) will present earlier
  • Often have considerable mass effect in brain + raised ICP common
298
Q

BRAIN ABSCESS
What are the investigations for brain abscess?

A
  • CT head shows ring-enhancing lesion ± surrounding oedema
  • LP is contraindicated due to raised ICP
299
Q

BRAIN ABSCESS
What is the management of brain abscess?

A
  • CT guided aspiration via burr hole or craniotomy + abscess cavity debridement
  • Craniotomy usually if no response to aspiration or if reoccurs
  • Abx with IV ceftriaxone + metronidazole, ICP Mx with dexamethasone
300
Q

BRAIN DEATH + COMA
What is a coma?

A

Unarousable unresponsiveness

301
Q

BRAIN DEATH + COMA
What is a persistent vegetative state?

A

State of wakefulness with sleep-wake cycles but no detectable awareness

302
Q

BRAIN DEATH + COMA
What is brain death?

A

Irreversible cessation of all brain function, usually from widespread injury to brain indicated by lack of brainstem signs

303
Q

BRAIN DEATH + COMA
What are some neurological causes of brain death and coma?

A
  • Trauma, tumours
  • Infection (meningitis, encephalitis)
  • Vascular (stroke, haemorrhages)
  • Epilepsy (status epilepticus, post-ictal)
304
Q

BRAIN DEATH + COMA
What are some metabolic causes of brain death + coma?

A
  • Drugs, poisoning (alcohol, TCAs, CO, opiates)
  • Hyperglycaemia (DKA, HHS) or hypoglycaemia
  • Septicaemia
  • Hypothermia
  • Hepatic/uraemia encephalopathy due to liver/renal failure
  • CO2 narcosis in COPD where too much oxygen leads to hypoxic drive slowing down so CO2 builds up
305
Q

BRAIN DEATH + COMA
In terms of clinical presentation in brain death and coma, what are some…

i) focal neurological deficits?
ii) brainstem signs?

A

i) Asymmetry of motor function, tendon reflexes + plantar responses
ii) Pupil size (pinpoint vs. dilated + pupillary reactions), eye movements, corneal reflexes, cough + gag reflexes, ice cold water in ears > nystagmus

306
Q

BRAIN DEATH + COMA
What are lateralising signs?
Give an example of one

A
  • Signs that occur from one hemisphere of the brain but not the other, helps to localise pathology
  • Fixed dilated pupil (CN3 palsy)
307
Q

BRAIN DEATH + COMA
Explain the pathophysiology of a third nerve palsy?

A
  • CN3 comes out of brainstem + goes over apex of petrous part of temporal bone as it goes through cavernous sinus to supply eye so susceptible to damage if brain swollen, bleeding + trauma.
  • Outside CN3 are parasympathetic fibres which constrict pupil so if damaged > fixed + dilated
308
Q

BRAIN DEATH + COMA
What is the main differential of a third nerve palsy?
How can they be differentiated?

A
  • Blind eye
  • Blind eye will not give contralateral responsiveness but other causes will + if you shine light in good eye then dilated pupil will restrict
309
Q

BRAIN DEATH + COMA
What are some investigations for brain death and coma?

A
  • Bloods – FBC, cultures, U+Es, Ca2+, phosphate, LFTs, glucose, clotting screen, toxicology (+ alcohol), ABG
  • CT/MRI head, EEG + LP for infection
310
Q

BRAIN DEATH + COMA
What is the Glasgow Coma Scale (GCS)?
What is it based on?
What scores should prompt action?

A
  • Universal consciousness assessment tool
  • BEST eye, verbal + motor response – 15 max, 3 min
  • ‘GCS ≤8 = intubate’ secure airway as may be unable to maintain on own
  • GCS >8 is greatest prognostic indicator in patients with traumatic brain injury
311
Q

BRAIN DEATH + COMA
What are the components of ‘eyes’ in GCS?

A

E4 = opens spontaneously
E3 = opens to verbal command
E2 = opens to pain
E1 = no response

312
Q

BRAIN DEATH + COMA
What are the components of ‘verbal’ in GCS?

A

V5 = orientated in TPP, answers appropriately
V4 = confused conversation, odd answers
V3 = inappropriate words (random, abusive)
V2 = incomprehensible sounds (groans)
V1 = no response

313
Q

BRAIN DEATH + COMA
What are the components of ‘motor’ in GCS?

A

M6 = obeys commands
M5 = localises pain
M4 = withdraws away from painful stimulus
M3 = flexion to pain
M2 = extension to pain
M1 = no response

314
Q

BRAIN DEATH + COMA
What is abnormal flexion to pain?
What does it indicate?

A
  • Decorticate posturing – arm adducted + flexed, wrist flexed, internal rotation, plantar flexed + stiff appearance
  • Indicates significant damage to cerebral hemispheres, internal capsule + thalamus
315
Q

BRAIN DEATH + COMA
What is abnormal extension to pain?
What does it indicate?

A
  • Decerebrate posturing – arms + legs extended, head extension, plantar flexion, internal rotation, pt rigid with teeth clenched
  • Indicates brainstem damage + so lesions in cerebellum or midbrain
316
Q

BRAIN DEATH + COMA
What does the progression from decorticate to decerebrate posturing suggest?

A
  • Uncal (transtentorial) or tonsillar brain herniation ‘coning’
317
Q

BRAIN DEATH + COMA
What is the management of brain death + coma?

A
  • ABCDE as emergency
  • Measure vitals, GCS, neuro signs (pupils) + re-check
  • IV access
  • Stabilise c-spine if trauma
  • Management in ICU
318
Q

MYASTHENIA GRAVIS
What is myasthenia gravis?

A
  • Autoimmune disorder against acetylcholine receptors in the neuromuscular junction
319
Q

MYASTHENIA GRAVIS
What is the pathophysiology of myasthenia gravis?

A
  • Anti-ACh receptor antibodies (IgG) interfere with NMJ via depletion of working post-synaptic receptor sites for ACh to bind to leading to fewer action potentials firing, blocking excitatory effect of ACh on receptors (all or nothing principle)
  • Both B + T cells implicated
320
Q

MYASTHENIA GRAVIS
What is the aetiology of myasthenia gravis?

A
  • Associated with autoimmune disease (RA, SLE)
  • If <40y: F>M, thymic hyperplasia
  • If >60y: M>F, thymoma
321
Q

MYASTHENIA GRAVIS
What is the main symptom of myasthenia gravis?

A
  • Fatiguable weakness of muscles which improves with rest
  • Affects ocular, bulbar + proximal limb muscles
  • Dysphagia + dysarthria (bulbar)
322
Q

MYASTHENIA GRAVIS
What is the natural course of myasthenia gravis?

A
  • Eventually leads to atrophy
  • Fluctuating relapsing + remitting pattern
323
Q

MYASTHENIA GRAVIS
What will patients with myasthenia gravis struggle with?

A
  • Hairs, chairs + stairs (proximal muscle weakness)
  • Speech, mastication, face + neck weakness
  • Resp muscles (breathing difficulty + dysphagia dangerous features which indicates advancing disease)
324
Q

MYASTHENIA GRAVIS
What are the signs of myasthenia gravis?

A
  • Ptosis, diplopia (extra-ocular muscle weakness)
325
Q

MYASTHENIA GRAVIS
What medications can exacerbate myasthenia gravis?

A

Abx, CCBs, beta-blockers, lithium + statins

326
Q

MYASTHENIA GRAVIS
What can weakness due to myasthenia gravis be worsened by?

A

Pregnancy
Hypokalaemia
Infection
Emotion
Exercise
Drugs

327
Q

MYASTHENIA GRAVIS
What are some clinical signs of myasthenia gravis?

A
  • Repeated blinking = ptosis
  • Repeated abduction of one arm 20x + compare to other side
328
Q

MYASTHENIA GRAVIS
What antibodies are implicated in myasthenia gravis?

A
  • Anti-AChR antibodies (90%)
  • Muscle-specific tyrosine kinase (MuSK, esp. males)
  • Low density lipoprotein receptor-related protein 4 (rare)
329
Q

MYASTHENIA GRAVIS
What investigations would you do for myasthenia gravis?

A

mostly clinical examination
positive tensilon test
anti-AChR antibodies
TFTs
EMG
CT of thymus
crushed ice test - ice is applies to ptosis for 3 mins, if it improves it is likely to be myasthenia gravis

330
Q

MYASTHENIC CRISIS
What is the main complication of myasthenia gravis?

A
  • Myasthenic crisis
331
Q

MYASTHENIC CRISIS
What are the clinical features?

A
  • Resp failure or death
332
Q

MYASTHENIC CRISIS
what are the complications?

A

Resp failure or death

333
Q

MYASTHENIC CRISIS
What are the causes of myasthenic crisis?

A
  • Infection (resp), natural disease cycle, under/overdosing meds
334
Q

MYASTHENIC CRISIS
What is the management of myasthenic crisis?

A
  • Urgent review by neurologists + anaesthetists
  • Monitor breathing with serial FVC measurements
  • NIV, BiPAP or intubation + ventilation
  • Immunomodulatory therapies (IVIg or plasmapheresis)
335
Q

MYASTHENIA GRAVIS
What is the management of myasthenia gravis?

A
  • Acetylcholinesterase inhibitors like pyridostigmine or rivastigmine
  • Immunosuppression with prednisolone (acute) or azathioprine to suppress antibody production
  • Thymectomy if thymoma or anti-AChR +ve disease
  • Plasmapheresis for severe relapsing cases
336
Q

GUILLAIN-BARRE
What is Guillain-Barré syndrome (GBS)?

A
  • Acute inflammatory demyelinating polyneuropathy which targets Schwann cells
337
Q

GUILLAIN-BARRE
What is the pathophysiology of GBS?

A
  • B cells produce antibodies against the antigens on the pathogen causing the preceding infection and these antibodies also match proteins on the nerve cells leading to demyelination and potentially axonal degeneration
338
Q

GUILLAIN-BARRE
What is Miller-Fisher syndrome?

A
  • GBS variant which affects CNS + eye muscles
  • Characterised by ophthalmoplegia + ataxia
339
Q

GUILLAIN-BARRE
What are the causes of GBS?

A
  • Often triggered by preceding illness 4w before symptoms

Bacteria
- Camplylobacter jejuni
- Mycoplasma

Viruses
- CMV
- EBV
- HIV
- Herpes zoster

340
Q

GUILLAIN-BARRE
What is the clinical presentation of GBS?

A
  • Acute symmetrical, progressive, ascending muscle weakness.
  • Peripheral neuropathy or neuropathic pain
  • Absent tendon reflexes early in disease
  • Back or leg pain is very common in initial stages
  • Proximal muscles (trunk, resp) more affected + cranial nerves (esp. VII)
  • Autonomic –urinary retention, diarrhoea, sweating, BP changes
341
Q

GUILLAIN-BARRE
What are some differentials for GBS?

A
  • Other causes of neuromuscular paralysis = hypokalaemia, polymyositis, botulism
  • Cord compression, transverse myelitis
342
Q

GUILLAIN-BARRE
What are the investigations for GBS?

A

Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction
Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation)
bloods - FBC, U&E, LFT, TFT
Spirometry = respiratory involvement
ECG

343
Q

GUILLAIN-BARRE
What is the prognosis of GBS?

A
  • 80% fully recover
  • 15% recover with neurological disability
  • 5% die, mostly from PE, resp failure or infection
344
Q

GUILLAIN-BARRE
What is the main treatment for GBS?

A
  • IVIg reduces duration + severity of paralysis but C/I if IgA deficiency as would cause anaphylaxis
  • Plasma exchange
  • Intubation, ventilation + ICU admission in severe cases in resp failure
345
Q

GUILLAIN-BARRE
When is IV immunoglobulin contraindicated in the treatment for Guillain-Barre syndrome?

A

If a patient has IgA deficiency - can cause severe allergic reaction

346
Q

GUILLAIN-BARRE
What is the supportive therapy for GBS?

A
  • VTE prophylaxis with heparin
  • Physio to prevent contractures
  • NG or PEG feeding if swallowing issues
347
Q

BRAIN TUMOURS
What is a brain tumour?
What is the prognosis?
Where do they come from?

A
  • Abnormal growths in the brain
  • Poor (12m median survival time)
  • Most commonly secondary (lungs > breast > melanoma > GI tract > kidney)
348
Q

BRAIN TUMOURS
Give 4 examples of different brain tumours

A
  • Gliomas
  • Meningiomas
  • Pituitary tumours
  • Acoustic neuromas (vestibular Schwannomas)
349
Q

BRAIN TUMOURS
What are gliomas?
Give some examples

A
  • Glial cell in origin in the brain or spinal cord
  • Graded 1–4 (1 = most benign ?cure, 4 = most malignant glioblastomas)
  • Astrocytomas like glioblastoma multiforme most common (90%), oligodendrogliomas + ependymoma
350
Q

BRAIN TUMOURS
What are meningiomas?

A
  • Benign tumours growing from cells of the meninges in the brain + spinal cord
351
Q

BRAIN TUMOURS
What are pituitary tumours?

A
  • Often benign, if large can press on optic chiasm causing bitemporal hemianopia
  • Can cause hypopituitarism or release excessive hormones > acromegaly, Cushing’s, hyperthyroidism
352
Q

BRAIN TUMOURS
What are acoustic neuromas?
What are they associated with?

A
  • Tumours of Schwann cells that occur around cerebellopontine angle surrounding the auditory nerve that innervates inner ear
  • Slow growing but eventually grow large enough to produce Sx
  • Usually unilateral, bilateral associated with neurofibromatosis type 2
353
Q

BRAIN TUMOURS
How do acoustic neuromas present?

A

Classic Sx = hearing loss, tinnitus, balance issues, decreased facial sensation

354
Q

BRAIN TUMOURS
What are the 3 cardinal signs of brain tumours?

A
  • Progressive focal neurological deficit depending on location of tumours
  • Sx of raised ICP
  • Seizures/epilepsy (focal rather than generalised, recent new onset suggest sinister aetiology)
355
Q

BRAIN TUMOURS
Why is the neurological deficit progressive in brain tumours?

A
  • Mass effect of tumour + surrounding cerebral oedema as it grows
356
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the frontal lobe?

A

Personality + intellect change, hemiparesis, expressive dysphasia

357
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the temporal lobe?

A

Receptive dysphasia, amnesia

358
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the parietal lobe?

A

Hemisensory loss, dysphasia

359
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the occipital lobe?

A

Contralateral visual defects

360
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the cerebellum?

A

Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia (DANISH)

361
Q

BRAIN TUMOURS
What are some symptoms of raised ICP?

A
  • Headache – worse in morning, coughing, bending forwards or lying
  • Drowsiness, confusion, vomiting
  • Papilloedema (cardinal sign = swollen optic disc) on fundoscopy
362
Q

BRAIN TUMOURS
What investigations would you perform for brain tumours?

A
  • CT/MRI head (MRI gold standard)
  • LP C/I if Sx of raised ICP until after imaging
  • Audiogram + gadolinium enhanced MRI head for acoustic neuroma
  • MR angiography may be useful to define site or blood supply of mass
363
Q

BRAIN TUMOURS
When would surgery be indicated as management in brain tumours?

A
  • Single mets in younger pts with controlled primary with aim to improve QOL
  • Meningiomas may be removed entirely without unacceptable damage to surrounding structures
364
Q

BRAIN TUMOURS
Other than surgery, what management is there for brain tumours?

A
  • Radio/chemotherapy – stereotactic radiotherapy (gamma knife)
  • Medical – dexamethasone or mannitol to reduce cerebral oedema but can cause insomnia so give in mornings
  • AEDs for seizures
  • Palliative care involvement
365
Q

NEUROPATHY
What is a neuropathy?

A
  • Dysfunction/disease of the nerves typically causing weakness or numbness
366
Q

NEUROPATHY
What are the peripheral nerve causes of muscle weakness?

A
  • Peripheral neuropathy = lots of nerves affects all over body, often symmetrical + systemic causes
  • Mononeuropathy = 1 nerve affected, usually due to entrapment
  • Mononeuritis multiplex = various, individual nerve defects all over the place, randomly
367
Q

NEUROPATHY
What is the pathophysiology of mononeuritis multiplex?

A
  • Inflammation of vasa nervorum can block off blood supply to nerve causing sudden deficit
368
Q

NEUROPATHY
What can cause mononeuritis multiplex?

A

Inflammatory or immune mediated vasculitis like granulomatosis with polyangiitis, polyarteritis nodosa, RA or sarcoidosis

369
Q

NEUROPATHY
What are the causes of peripheral neuropathy?

A

ABCDE –
- Alcohol
- B12 deficiency
- Cancer + CKD
- Diabetes + drugs (isoniazid, amiodarone)
- Every vasculitis

370
Q

NEUROPATHY
In terms of peripheral neuropathy, what conditions show a…

i) mostly motor loss?
ii) mostly sensory loss?

A

i) GBS, chronic inflammatory demyelination polyneuropathy (chronic GBS), Charcot-Marie-Tooth disease
ii) DM, CKD, deficiencies

371
Q

NEUROPATHY
What is Charcot-Marie-Tooth disease?

A
  • Autosomal dominant condition.
  • Characterised by high-arched feet, distal muscle weakness + atrophy (inverted champagne bottle legs), hyporeflexia, foot drop + hammer toes
372
Q

NEUROPATHY
What is the generic clinical presentation of mononeuropathy?

A

Individual nerve deficits in isolation, mostly upper limb nerves affected at compression points

373
Q

NEUROPATHY
What is the generic clinical presentation of mononeuritis multiplex?

A

Subacute presentation (months rather than years), painful, asymmetrical sensory + motor neuropathy

374
Q

NEUROPATHY
What is the generic clinical presentation of peripheral neuropathy?

A
  • Chronic + slowly progressive
  • Starts in legs + longer nerves first (furthest from heart)
  • Sensory/motor/both
  • Glove + stocking distribution
375
Q

NEUROPATHY
What is the most common mononeuropathy?

A
  • Carpal tunnel syndrome
376
Q

NEUROPATHY
What is the pathophysiology of carpal tunnel syndrome?

A

Inflammation of carpal tunnel leads to entrapment of the median nerve

377
Q

NEUROPATHY
What are the causes of carpal tunnel syndrome?

A

Idiopathic but associated with local tumours, DM + RA

378
Q

NEUROPATHY
What muscles does the median nerve innervate?

A

LLOAF –
- Lateral lumbricals x2
- Opponens pollicis
- Abductor pollicis brevis
- Flexor pollicis brevis

379
Q

NEUROPATHY
What is the clinical presentation of carpal tunnel syndrome?

A
  • Aching pain in hand + arm (especially at night)
  • Paraesthesia in radial 3.5 digits relieved by dangling hand over edge of bed + shaking (wake + shake)
  • Difficulty with precision grip
  • Sensory loss (radial 3.5 digits palmar + fingertips dorsally)
  • Wasting of thenar eminence (APB, FPB + OP)
380
Q

NEUROPATHY
What investigations can you do for carpal tunnel syndrome?

A
  • Phalen’s test = inverse prayer sign, can only maximally flex wrist for 1m
  • Tinel’s test = tapping on nerve at wrist induces tingling
  • Nerve conduction studies
381
Q

NEUROPATHY
What is the management of carpal tunnel syndrome?

A
  • Splinting
  • Analgesia
  • Local steroid injection ± decompression surgery
382
Q

NEUROPATHY
What does a CN1 lesion cause?

A
  • Anosmia
383
Q

NEUROPATHY
In terms of the optic nerve, what does a…

i) L optic nerve lesion
ii) Optic chiasma lesion
iii) L optic tract lesion
iv) L Baum’s loop lesion
v) L Meyer’s loop lesion

cause?

A

i) No vision through L eye
ii) Bitemporal hemianopia
iii) Contralateral (R) homonymous hemianopia
iv) Inferior R homonymous quadrantanopia
v) Superior R homonymous quadrantanopia

384
Q

NEUROPATHY
Where is Baum’s loop located?
Where is Meyer’s loop located?
How can you remember which is superior/inferior?

A
  • Parietal lobe
  • Temporal lobe
  • PITS – Parietal Inferior Temporal Superior
385
Q

NEUROPATHY
What does a CN3 lesion cause?

A
  • Tramps’ palsy (eye down + out)
  • Ptosis
  • Fixed dilated pupil (loss of parasympathetic outflow, exclude a surgical 3rd nerve)
386
Q

NEUROPATHY
What does a CN4 lesion cause?

A
  • Vertical diplopia noticed when reading book or going downstairs
  • Defective downward gaze as innervates superior oblique
387
Q

NEUROPATHY
What does a CN5 lesion cause?

A
  • Loss of sensation to face
  • Weak muscles of mastication
  • Loss of corneal reflex (afferent)
  • Jaw deviation to weak side
388
Q

NEUROPATHY
What does a CN6 lesion cause?

A
  • Issues abducting eye beyond midline as innervates lateral rectus
389
Q

NEUROPATHY
What does a CN7 lesion cause?

A

Face, ear, taste, tear –
- Muscles of expression
- Stapedius
- Anterior 2/3rd tongue
- Parasympathetic fibres to lacrimal + salivary glands

390
Q

NEUROPATHY
What is Bell’s palsy?

A
  • CN7 lesion with complete facial paralysis, hyperacusis,
  • Differentiate from stroke as no forehead sparring as LMN
  • Often post-viral (HSV), treat with pred + eye care
391
Q

NEUROPATHY
What does a CN8 lesion cause?

A
  • Sensorineural deafness
  • Tinnitus, vertigo, nystagmus
392
Q

NEUROPATHY
What does a CN9/10 lesion cause?

A
  • Swallow, gag + cough issues
  • Uvula deviated away from side of lesion
393
Q

NEUROPATHY
What does a CN11 lesion cause?

A
  • Weakness turning head to contralateral side
394
Q

NEUROPATHY
What does a CN12 lesion cause?

A
  • Tongue deviation towards side of lesion
395
Q

NEUROPATHY
What are the investigations used in neuropathy?

A
  • Neuropathy screen (symmetrical) = FBC, CRP/ESR, U+E, glucose, TFT, B12 + folate
  • Vasculitis screen (asymmetrical) = first 3 + ANA, ANCA, anti-dsDNA, RhF, complement
  • EMG + nerve conduction studies
396
Q

NEUROPATHY
What is the management of neuropathy?

A
  • Sx relief with neuropathic analgesia (gabapentin, pregabalin, amitriptyline)
  • Treat underlying cause
  • Inflammatory = pred + steroid-sparing agents like azathioprine (+ IVIg or plasmapheresis in CIDP)
  • Vasculitis = rapid pred + immunosuppressant (cyclophosphamide) to avoid irreversible damage
397
Q

CORD COMPRESSION
What is myelopathy?

A

Injury to the spinal cord due to severe compression resulting in UMN signs + specific symptoms based on compression

398
Q

RADICULOPATHY
What is radiculopathy?

A

Sx caused by pinching of a nerve root as they exit the spinal cord

399
Q

RADICULOPATHY
How does radiculopathy present?

A
  • Sharp, shooting pain within distribution of nerve, weakness + loss of sensation
400
Q

RADICULOPATHY
what are the causes?

A
  • intervertebral disc prolapse
  • degenerative diseases of the spine
  • fracture (trauma or pathological)
  • malignancy (metastatic)
  • infection (extradural abscesses, osteomyelitis)
401
Q

RADICULOPATHY
what is the management?

A

analgesia - amitryptyline, pregabalin, gabapentin
physiotherapy
surgery in emergencies

402
Q

RADICULOPATHY
What is the most common radiculopathy?

A

Sciatica (L5) = lower back pain that travels to buttocks + down back of thigh to calf

403
Q

CORD COMPRESSION
What are the aetiologies of spinal cord compression?

A
  • Malignancy (mostly secondary, 5Bs = breast, bronchus, byroid, bidney, brostate)
  • Infection (epidural abscess), spinal osteophytes
  • Disc prolapse (slower onset), haematoma (warfarin)
  • Lumbar degeneration due to trauma or age (conservative Mx or steroid injections)
  • Myeloma
404
Q

CORD COMPRESSION
What are the symptoms of spinal cord compression?

A
  • Weakness of legs with UMN signs (contralateral spasticity + hyperreflexia)
  • Sudden/progressive onset weakness = emergency
  • Sensory loss below certain level
  • Numbness/tingling may have stabbing pain
  • Bladder + anal sphincter involvement is a later manifestation (hesitancy, frequency, painless retention)
405
Q

CORD COMPRESSION
What are the signs of spinal cord compression?

A
  • Motor, reflex + sensory level = normal ABOVE lesion
  • LMN signs = AT level
  • UMN signs = BELOW level
  • Tone + reflexes usually reduced in acute cord compression
  • ?Sign of infection like tender spine, pyrexia
406
Q

CORD COMPRESSION
How does degenerative cervical myelopathy present?

A
  • Pain, loss of motor or sensory function affecting neck, upper or lower limbs
  • Loss of autonomic function
  • Hoffman’s sign +ve
407
Q

CORD COMPRESSION
What are the differentials for spinal cord compression?

A
  • Transverse myelitis (inflammation of both sides of one section of spinal cord)
  • MS
  • Trauma
  • Dissecting aneurysm
408
Q

CORD COMPRESSION
What are the investigations of spinal cord compression?

A
  • PR to assess loss of sphincter control
  • Screening bloods (FBC, CRP/ESR, B12, LFT, U+Es)
  • MRI spine gold standard
  • If mass, ?biopsy/surgical exploration
409
Q

CORD COMPRESSION
What is the main complication of spinal cord compression?

A
  • Cauda equina syndrome
  • Cord compression below the level of the termination of the spinal cord at L1/2 vertebral level = medical emergency
410
Q

CORD COMPRESSION
What can cause cauda equina syndrome?
How does it present?

A
  • Mostly malignancy, disc prolapse (L4/5, L5/S1), trauma
  • Back pain, early urinary retention + constipation, saddle anaesthesia, decreased sphincter tone, mixed UMN/LMN leg weakness, erectile dysfunction, asymmetrical paralysis of legs
411
Q

CORD COMPRESSION
What is spinal stenosis?

A
  • Narrowing of lower spinal canal almost always due to degeneration
412
Q

CORD COMPRESSION
How does spinal stenosis present?

A
  • Spinal claudication > pain in buttocks/legs when walking
  • pain eased by bending forward as canal opens
  • negative straight leg raise
413
Q

CORD COMPRESSION
How is spinal stenosis managed?

A

MRI + canal decompression surgery

414
Q

CORD COMPRESSION
What is the management of spinal cord compression?

A
  • Malignancy = stat dexamethasone + consider chemo, radio, surgery
  • Epidural abscess = surgical decompression + Abx
  • Cauda equina = surgery for emergency pressure relief
  • Degenerative cervical myelopathy = urgent spinal surgery referral for surgical decompression
415
Q

SPINAL CORD INJURY
What is Brown-Sequard syndrome?

A
  • Lateral hemisection of spinal cord
  • Ipsilateral weakness below the lesion (lateral corticospinal)
  • Ipsilateral loss of fine touch, proprioception + vibration (DCML)
  • Contralateral loss of pain + temp (lateral spinothalamic)
416
Q

ANTERIOR CORD SYNDROME
What is anterior cord syndrome?

A
  • Anterior spinal artery occlusion or compression
  • Bilateral spastic paresis (lateral corticospinal)
  • Bilateral loss of pain + temp (lateral spinothalamic)
417
Q

ANTERIOR CORD SYNDROME
what are the causes?

A
  • iatrogenic - thoracic and thoracoabdominal AA repair
  • aortic dissection
  • atherothrombotic disease
  • emboli
  • vasculitis
418
Q

ANTERIOR CORD SYNDROME
what are the symptoms?

A
  • acute motor dysfunction
  • loss of pain and temperature sensation below level of infarction
  • autonomic dysfunction - neurogenic bowel/bladder
  • acute onset back pain
419
Q

ANTERIOR CORD SYNDROME
what are the investigations?

A

MRI - ‘owls eyes’ hyperintensities in anterior horns

lumbar puncture, CSF testing, blood and urine to rule out other causes

420
Q

ANTERIOR CORD SYNDROME
what is the treatment?

A
  • IV fluids to increase intravascular volume
  • vasopressor medications to increase systemic vascular resistance
  • lumbar drain to remove CSF

symptomatic management
- mechanical ventilation
- catheterisation

421
Q

SPINAL CORD INJURY
What is posterior cord syndrome?

A
  • Trauma or posterior spinal artery occlusion
  • Loss of fine touch, proprioception + vibration (DCML)
422
Q

SPINAL CORD INJURY
What is central cord syndrome?

A
  • Hyperextension injury, often elderly with underlying cervical disease
  • Sensory + motor deficit (upper extremities > lower)
423
Q

MYOPATHY
What are myopathies?

A
  • Neuromuscular disorders where the primary Sx is muscle weakness due to dysfunction of muscle fibres
424
Q

MYOPATHY
What are dystrophies?

A

If they’re inherited = dystrophies

425
Q

MYOPATHY
How do myopathies compare to neuropathies?

A

Weakness is proximal in muscle disease (nerves = distal)

426
Q

MYOPATHY
What are the aetiologies of myopathies?

A
  • inflammatory
  • metabolic
  • inherited
  • polio
  • drugs - steroids, statins
427
Q

MYOPATHY
How do myopathies present?

A
  • Symmetrical proximal pattern of muscle weakness (hairs, stairs + chairs)
  • Weakness > wasting
  • Reflexes + sensation normal, no fasciculations
428
Q

MYOPATHY
what is myotonic dystrophy?

A

autosomal dominant genetic condition causing progressive muscle weakness
most common form of muscular dystrophy to occur in adults

429
Q

MYOPATHY
what are the causes of myotonic dystrophy type 1 and 2?

A

type 1 - DMPK gene mutation on chromosome 19

type 2 = ZNF9 gene on chromosome 3

430
Q

MYOPATHY
How does myotonic dystrophy present?

A
  • type 1 = distal weakness more prominent
  • type 2 = proximal weakness more prominent.
  • May have cataracts, testicular atrophy, cardiac lesions (heart block, cardiomyopathy), DM
431
Q

MYOPATHY
What are the investigations for myopathies?

A
  • CRP/ESR, creatinine kinase elevated
  • Autoantibodies (anti-Jo-1), EMG, genetics + muscle biopsy
432
Q

MYOPATHY
What is the management of myopathies?

A
  • Remove causative agent (statins, steroids)
  • Immunosuppression (steroids, azathioprine) if inflammatory cause.
433
Q

MYOPATHY
What is the general supportive management of myopathies?

A
  • OT = aids + adaptations to help live with condition
  • Physio = prevent contractures
  • Renal protection = myoglobin can cause kidney damage
  • Diet = ideally low BMI with good nutrition
434
Q

HYDROCEPHALUS
What are the 3 types of hydrocephalus?

A
  • Obstructive (non-communicating) = structural pathology blocking flow of CSF with dilatation superior to site of obstruction
  • Non-obstructive (communicating) = imbalance of CSF production/absorption
  • Normal pressure = unknown, can develop after head injury or stroke, >60s
435
Q

HYDROCEPHALUS
What are the 3 types of hydrocephalus?

A
  • Obstructive (non-communicating) = structural pathology blocking flow of CSF with dilatation superior to site of obstruction
  • Non-obstructive (communicating) = imbalance of CSF production/absorption
  • Normal pressure = unknown, can develop after head injury or stroke, >60s
436
Q

HYDROCEPHALUS
What is hydrocephalus?

A
  • Abnormal build-up of CSF around the brain causing compression to nearby brain tissue as the ventricles dilate
437
Q

HYDROCEPHALUS
What is the purpose of CSF?

A
  • Protects brain from damage
  • Removes waste products from the brain
  • Provides brain with nutrients to function properly
438
Q

HYDROCEPHALUS
What is the usual flow of CSF in the brain?

A
  • Lateral ventricles
  • Foramen of Munro
  • 3rd ventricle
  • Cerebral aqueduct
  • 4th ventricle
  • Subarachnoid space (Medially by foramen of Magendie, Laterally by Luschka)
  • Dural sinus via arachnoid granulations
439
Q

HYDROCEPHALUS
What are the 3 types of hydrocephalus?

A
  • Obstructive (non-communicating)
  • Non-obstructive (communicating)
  • Normal pressure
440
Q

HYDROCEPHALUS
What is the pathophysiology of obstructive (non-communicating) hydrocephalus?

A

due to a structural pathology blocking the flow of cerebrospinal fluid. Dilatation of the ventricular system is seen superior to site of obstruction

441
Q

HYDROCEPHALUS
What is the pathophysiology of non-obstructive (communicating) hydrocephalus?

A

due to an imbalance of CSF production absorption

442
Q

HYDROCEPHALUS
What are some causes of obstructive hydrocephalus?

A

Tumour,
acute haemorrhages,
developmental abnormalities (aqueduct stenosis)

443
Q

HYDROCEPHALUS
What are some causes of non-obstructive hydrocephalus?

A
  • Commonly failure of reabsorption of arachnoid granulations (meningitis, post-haemorrhage)
  • increased CSF production (choroid plexus tumour) but very rare
444
Q

HYDROCEPHALUS
How does hydrocephalus present?

A
  • Signs of raised ICP
  • Headache (worse in morning or lying down)
  • N+V, papilloedema, blurred vision
445
Q

HYDROCEPHALUS
what are the causes of normal pressure hydrocephalus?

A

excess fluid builds up in the ventricles, which enlarge and press on nearby brain tissue

  • injury
  • bleeding
  • infection
  • brain tumour
  • brain surgery
446
Q

HYDROCEPHALUS
How does normal pressure hydrocephalus present?

A

‘Wet, wacky, wobbly’ –
- Urinary incontinence, dementia + abnormal gait (apraxia)
Trouble walking (feels like the feet are stuck to the ground)
Poor balance
Falling
Changes in the way you walk
Forgetfulness and confusion
Mood changes
Depression
Difficulty responding to questions
Loss of bladder control

  • Sx come on gradually + similar to Alzheimer’s so difficult to diagnose
447
Q

HYDROCEPHALUS
What are the investigations for hydrocephalus?

A
  • CT head = enlarged ventricles
  • MRI head if suspected underlying lesion
  • LP is both diagnostic + therapeutic (caution in obstructive as difference in cranial/spinal pressures can cause brain herniation)
448
Q

HYDROCEPHALUS
What is the management of hydrocephalus?

A
  • An external ventricular drain (EVD) is used in acute, severe hydrocephalus and is typically inserted into the right lateral ventricle and drains into a bag at the bedside
  • Ventriculoperitoneal shunt = surgically implanted into brain to drain excess fluid (may become blocked or infected)
  • Endoscopic third ventriculostomy = hole made in floor of 3rd ventricle to allow trapped CSF to escape to be reabsorbed
449
Q

IIH
What is idiopathic intracranial hypertension (IIH)?

A
  • Build up of CSF pressure around the brain causing signs of raised ICP
  • Associated with obese young women
450
Q

IIH
What are the causes of IIH?

A
  • Primary = idiopathic
  • Secondary (often causing chronic intracranial HTN) = brain tumour, chronic SDH, meningitis/encephalitis, venous sinus thrombosis, drugs (nitrofurantoin, vitamin A)
451
Q

IIH
What is the clinical presentation of IIH?

A
  • Presents as if mass but none found
  • Signs of raised ICP (headache, papilloedema + enlarged blind spot)
  • Blurred vision, narrowed visual fields ± diplopia
  • Consciousness + cognition preserved
452
Q

IIH
What are the investigations for IIH?

A
  • Routine bloods + CT head to exclude organic causes
  • LP to exclude infection = increased opening pressure (can be therapeutic)
453
Q

IIH
What is the management of IIH?

A
  • # 1 weight loss (topiramate can be used + has benefit of weight loss)
  • Acetazolamide
  • Surgery = optic nerve sheath decompression + fenestration to prevent damage
  • Lumboperitoneal or ventriculoperitoneal shunt
454
Q

NEURO PHARMACOLOGY
Give some examples of anti-epileptic drugs (AEDs).
What is their mechanism of action?

A
  • Carbamazepine, valproate, lamotrigine, levetiracetam, phenytoin, ethosuximide.
  • Inhibit voltage-gated Na+ channels which prevents excitability of neurones > reduced firing > stops seizure, some promote GABA release
455
Q

NEURO PHARMACOLOGY
What are some side effects and important information for…

i) carbamazepine?
ii) valproate?
iii) lamotrigine

A

i) Blurred vision, headache, drowsiness – agranulocytosis, aplastic anaemia, P450 inducer
ii) Teratogenic, hepatitis, hair loss, tremor, weight gain – some interactions with antidepressants
iii) Blurred vision, headache, drowsiness – Steven-Johnson syndrome + risk of leukopenia

456
Q

NEURO PHARMACOLOGY
What are some side effects and important information for…

i) phenytoin?
ii) levetiracetam?
iii) ethosuximide?

A

i) Megaloblastic anaemia (folate), osteomalacia, teratogenic, P450 interactions – Steven-Johnson syndrome
ii) Headache, drowsiness – some interactions with antidepressants
iii) Night terrors, rashes

457
Q

NEURO PHARMACOLOGY
What is the mechanism of action of Levodopa?

A
  • Levodopa is dopamine precursor which can cross BBB to be converted to dopamine by dopa-decarboxylase
  • Must be combined with peripheral dopa-decarboxylase inhibitor like carbidopa so levodopa can reach brain
458
Q

NEURO PHARMACOLOGY
What are the side effects of Levodopa?

A
  • Postural hypotension
  • Confusion
  • Dyskinesias (abnormal movements)
  • Effectiveness decreases with time (even with dose increase)
  • On-off effect
  • Psychosis
459
Q

NEURO PHARMACOLOGY
A side effect of high dopamine are dyskinesias.
What is dystonia?
What is chorea?
What is athetosis?

A
  • Excessive muscle contraction > abnormal postures/movements
  • Abnormal involuntary movements may be jerky
  • Involuntary twisting or writhing movements, usually in fingers/hands/feet
460
Q

NEURO PHARMACOLOGY
Give some examples of dopamine receptor agonists.
What is the mechanism of action?
What are some side effects?
What monitoring is required?

A
  • Bromocriptine, cabergoline, ropinirole
  • Increases amount of dopamine in CNS
  • Hallucinations (more than levodopa), postural hypotension
  • ECHO, ESR, creatinine + CXR prior to Rx
461
Q

NEURO PHARMACOLOGY
What are some adverse effects of dopamine receptor agonists?

A
  • Pulmonary retroperitoneal + cardiac fibrosis
  • Bromocriptine associated with gambling + other inhibition disorders (e.g. sexual)
462
Q

NEURO PHARMACOLOGY
What are COMT + MAO-B inhibitors?
What is the mechanism of action?

A
  • Catechol-o-methyltransferase (COMT) inhibitor = entacapone
  • Monoamine oxidase-B (MAO-B) inhibitor = selegiline
  • Inhibit enzymatic breakdown of dopamine
463
Q

NEURO PHARMACOLOGY
Why are dopamine receptor agonists + COMT/MAO-B inhibitors used in Parkinson’s disease?

A
  • Delay use of levodopa + then used in combination to reduce levodopa dose as levodopa is most effective treatment
464
Q

NEURO PHARMACOLOGY
Examples of triptans.
Mechanism of action?
Used for?

A
  • Sumatriptan, naratriptan
  • 5-HT (serotonin) receptor agonists + act on smooth muscle in arteries > vasoconstriction, peripheral pain receptors > inhibit activation of pain receptors (vasoactive peptides) + reduce neuronal activity in CNS
  • Abort migraines when start to develop
465
Q

NEURO PHARMACOLOGY
What are some SEs + C/Is of triptans?

A
  • Dizziness, dry mouth, sleepy, nausea
  • C/I in CVD
466
Q

DIZZINESS/VERTIGO
What is vertigo?
What is it characterised by?

A
  • Hallucination of movement, often rotary, of the pt/their surroundings
  • Spinning, tilting, veering sideways, feeling as if being pushed/pulled
  • Always worse with movement, relief on lying or sitting still
  • Difficulty walking or standing
  • N+V, pallor, sweating
467
Q

DIZZINESS/VERTIGO
What is benign paroxysmal positional vertigo (BPPV)?
What is it caused by?
What is the treatment?

A
  • Brief vertigo on head movements (rolling in bed) due to disruption of debris in semi-circular canal of ears (canalolithiasis)
  • Idiopathic, secondary to head trauma, labyrinthitis
  • Reassurance, Epley manoeuvre
468
Q

ACUTE LABYRINTHITIS
What is acute labyrinthitis?

A
  • Inflammation of labyrinth + damage to vestibular + auditory end organs
469
Q

ACUTE LABYRINTHITIS
How does it present?

A
  • Abrupt onset severe vertigo, N+V, may have hearing loss or tinnitus + nystagmus towards side opposite to lesion
  • Severe vertigo subsides in days, full recovery 3-4w
470
Q

ACUTE LABYRINTHITIS
What are the causes?

A

Usually viral, ?vascular lesion

471
Q

MENIERE’S DISEASE
What is Ménières disease?

A
  • Increased pressure in endolymphatic system due to increased volume of inner ear.
472
Q

MENIERE’S DISEASE
How does it present?

A

Recurrent attacks in clusters of vertigo lasting >20m, fluctuating/perm sensorineural hearing loss (uni/bilateral), tinnitus + sense of fullness or pressure in one or both ears

473
Q

MENIERE’S DISEASE
what is the classical triad of symptoms?

A

vertigo
hearing loss - worse during attacks
tinnitus

474
Q

MENIERE’S DISEASE
What causes it?

A

Idiopathic, trauma, endo

475
Q

MENIERE’S DISEASE
How is it managed?

A

Bed rest, reassurance

476
Q

DIZZINESS/VERTIGO
How does traumatic damage present?

A
  • Trauma affecting petrous temporal bone or cerebellopontine angle then auditory nerve may be damaged > vertigo, deafness ± tinnitus.
477
Q

DIZZINESS/VERTIGO
What are other causes of dizziness/vertigo?

A
  • Alcohol
  • Motion sickness
  • Ototoxicity (aminoglycoside Abx like gentamicin, thiazide diuretics, lithium)
  • Vestibular neuronitis – recent viral, recurrent vertigo attacks, no hearing loss.
478
Q

DIZZINESS/VERTIGO
What is the management of dizziness/vertigo?

A
  • Tilt-table test + Dix-Hallpike manoeuvre
  • FBC, ESR/CRP, U+Es, LFTs, TFTs to exclude causes
  • MRI head if ?acoustic neuroma or other brain issue
  • Sx relief with anti-emetic (prochlorperazine), dizziness use antihistamine cinnarizine
479
Q

SHINGLES
what is the cause of shingles?

A

reactivation of herpes varicella zoster virus

480
Q

SHINGLES
what are the risk factors for shingles?

A
  • increasing age
  • immunocompromised
  • HIV, hodgkins lymphoma, bone marrow transplants
481
Q

SHINGLES
what is the pathophysiology of shingles?

A
  • latent virus is reactivated in the dorsal root ganglia + travels down affected nerve via sensory root
  • affects one dermatome
482
Q

SHINGLES
what is the clinical presentation?

A
  • rash - restricted to same dermatome
  • neuritic pain
  • malaise, myalgia, headache and fever
483
Q

SHINGLES
how is it diagnosed?

A

clinical diagnosis

484
Q

SHINGLES
what is the management?

A
  • acyclovir
  • analgesia for pain
485
Q

SHINGLES
what are the complications?

A
  • post herpetic neuralgia - pain which lasts >4 months
  • damage to opthalmic branch of trigeminal nerve - results in sight loss
486
Q

CEREBELLAR DISEASE
what are the signs of cerebellar dysfunction?

A

DANISH
dysdiadochokinesia
ataxia
nystagmus
intention tremor
slurred speech
hypotonia

487
Q

CEREBRAL PALSY
what are the causes?

A
  • antenatal = prematurity, multiple births, TORCH
  • perinatal = asphyxia during delivery
  • postnatal = hyperbilirubinaemia, neonatal sepsis, resp distress, meningitis, head injuries, seizures
488
Q

CEREBRAL PALSY
what are the symptoms?

A
  • delay in motor/speech/cognitive development
  • retention of primitive reflexes
  • spasticity/clonus
  • toe walking/knee hyperextension
  • scissoring
  • crouched gait
  • contractures
489
Q

CEREBRAL PALSY
what are the investigations?

A

MRI brain - periventricular leukomalacia, congenital malformation, stroke or haemorrhage

490
Q

CEREBRAL PALSY
what is the management?

A
  • OT, physio and speech therapy
  • orthoses
  • adaptive equipment
491
Q

BELL’S PALSY
what are the causes?

A

viral infection - reactivation of herpes simplex virus 1 (HSV1)

this leads to swelling of CN VII

492
Q

BELL’S PALSY
what is the pathophysiology?

A

reactivation of HSV-1 results in destruction of ganglion cells and infection of schwann cells leading to demyelination and neural inflammation

493
Q

BELL’S PALSY
what are the symptoms?

A

unilateral LMN facial weakness
altered taste
post auricular pain - pain behind ears

494
Q

BELL’S PALSY
how do you tell the difference between bell’s palsy and a stroke?

A
  • stroke = forehead still innervated - forehead sparing
  • Bell’s palsy = both forehead and lower face are affected on one side
495
Q

BELL’S PALSY
what is the management?

A
  • corticosteroid
  • eye drops
  • ?antivrials
496
Q

BELL’S PALSY
what are the investigations?

A
  • can be clinical diagnosis
  • ENoG
  • needle EMG
497
Q

NEUROFIBROMATOSIS
what are the clinical signs of NF1?

A
  • cafe-au-lait spots on the skin
  • pea-sized lumps under skin
  • skeletal abnormalities
  • tumour on optic nerve
498
Q

NEUROFIBROMATOSIS
what are the clincial signs of NF2?

A
  • acoustic neuromas
  • family history
  • meningioma, schwannoma, juvenile cortical cataracts or glioma
499
Q

NEUROFIBROMATOSIS
what are the causes of neurofibromatosis 1 and 2?

A

NF1 = neurofibromin 1 (autosomal dominant)
NF2 = neurofibromin 2 (autosomal dominant)

500
Q

NEUROFIBROMATOSIS
what is the treatment for NF1 and NF2?

A
  • no cure
  • pain management
  • growths can be surgically removed
501
Q

NARCOLEPSY
what are the clinical features?

A
  • excessive daytime sleepiness/sleep attacks
  • cataplexy
  • hypnagogic/hypnopompic hallucinations
  • sleep paralysis
  • excessive fatigue/impaired memory
502
Q

NARCOLEPSY
what are the investigations?

A
  • actigraphy and sleep diary
  • overnight polysomnography
  • multiple sleep latency test (MSLT)
503
Q

NARCOLEPSY
what is the management?

A

1st line = sleep hygiene + lifestyle changes
can also consider pharmacotherapy
- modafinil
- pitolisant
- sodium oxybate

504
Q

RADICULOPATHY
what is the management?

A

analgesia - amitryptyline, pregabalin, gabapentin
physiotherapy
surgery in emergencies

505
Q

WERNICKE-KORSAKOFF SYNDROME
what is it?

A
  • includes wernicke’s encephalopathy and korsakoff’s syndrome
  • it is a spectrum (wernicke’s = acute, korsakoff’s = chronic)
506
Q

WERNICKE-KORSAKOFF SYNDROME
what are the clinical signs?

A
  • mental confusion/amnesia
  • vision problems
  • coma
  • tremor
  • ataxia
  • hypothermia
  • low blood pressure
507
Q

WERNICKE-KORSAKOFF SYNDROME
what is the cause?

A

vitamin B1 (thiamine) deficiency - most commonly caused by alcoholism

508
Q

WERNICKE-KORSAKOFF SYNDROME
what is the management?

A

B1 (thiamine) replacement and proper nutrition/hydration

509
Q

CATAPLEXY
what is it?

A

sudden muscle weakness triggered by strong emotions such as laughter, anger and surprise

510
Q

CATAPLEXY
what happens during an attack?

A
  • slurred speech
  • impaired eyesight (double vision, unable to focus)
  • hearing and awareness are undisturbed (remain conscious)
511
Q

CATAPLEXY
what are the causes?

A
  • 75% of people with narcolepsy have cataplexy
  • it is rare for cataplexy to be only symptom
512
Q

CATAPLEXY
what is the management?

A

sodium oxybate
tricyclic antidepressants (clomipramine)
SSRIs

513
Q

HORNER’S SYNDROME
what is the pathophysiology of horner’s syndrome?

A

unilateral damage to the sympathetic chain

514
Q

HORNER’S SYNDROME
what is the pathophysiology of horner’s syndrome?

A

unilateral damage to the sympathetic chain

515
Q

HORNER’S SYNDROME
what are the causes of 1st order horner’s syndrome?

A

stroke, tumours of hypothalamus, spinal cord lesions

516
Q

HORNER’S SYNDROME
what are the causes of 2nd order horner’s syndrome?

A

tumours of upper chest cavity, trauma to the neck

517
Q

HORNER’S SYNDROME
what are the causes of 3rd order horner’s syndrome?

A

lesions to carotid artery, middle ear infections, injury to base of the skull

518
Q

HORNER’S SYNDROME
what are the clinical features of horner’s syndrome?

A

MAPLE

Miosis
Anhydrosis
Ptosis
Loss of ciliospinal reflex
Endophthalmos (sunken eyeball)

519
Q

HORNER’S SYNDROME
what are the investigations for horner’s syndrome?

A

clinical examination

MRI - detect lesions

520
Q

HORNER’S SYNDROME
what is the treatment for horner’s syndrome?

A

treat underlying cause

521
Q

BULBAR PALSY
what is it?

A

refers to a set of signs and symptoms linked to the impaired function of the lower cranial nerves, typically caused by damage to their lower motor neurons or to the lower cranial nerve itself
CN 9, 10, 11 and 12

522
Q

BULBAR PALSY
what ar ethe causes?

A
  • brainstem tumours and strokes
  • ALS
  • GBS
523
Q

BULBAR PALSY
what are the causes?

A
  • brainstem tumours and strokes
  • ALS
  • GBS
524
Q

BULBAR PALSY
what are the symptoms?

A
  • dysphagia
  • reduced/absent gag reflex
  • slurred speech
  • aspiration of secretions
  • dysphonia
  • dysarthria
  • drooling
  • difficulty chewing
  • nasal regurgitation
  • atrophic tongue
    weak jaw/facial muscles
525
Q

BULBAR PALSY
what are the investigations?

A

MRI
lumbar puncture

526
Q

BULBAR PALSY
what is the treatment?

A
  • no known treatment
  • drooling = riluzole
  • feeding tube
  • SaLT - help chewing
527
Q

STRABISMUS
what is it?

A

where there is misalignment of the visual axes of the eyes; it may be latent or manifest and, if manifest, it may be constant or intermittent

528
Q

STRABISMUS
what are the causes?

A
  • congenital
  • graves (restricted eye movement)
  • myasthenia gravis
  • intra-cranial process (mass, raised ICP, CNS infarction, inflammation of CNS)
529
Q

STRABISMUS
what are the symptoms?

A
  • diplopia
  • eye misalignment
  • amblyopia (decreased vision in an anatomically normal eye)
  • abnormal eye movements
  • visual confusion
  • asthenopia (ocular discomfort)
530
Q

STRABISMUS
what are the risk factors?

A

FHx of strabismus
prematurity
low birth weight
maternal smoking during pregnancy

531
Q

STRABISMUS
what are the investigations?

A
  • cover test
  • simultaneous prism and cover test (SPCT)
  • uncover test (UCT)
  • alternate prism cover test (APCT)
  • Hirschberg test
  • Krimsky test
532
Q

STRABISMUS
what is the management?

A

definitive treatment = extraocular muscle surgery

correction of refractive errors

treatment of amblyopia - eye patch

treatment for diplopia - patch, prisms, high prescription, orthoptic exercises

533
Q

SCIATICA
what is it?

A

nerve pain from an injury or irritation to sciatic nerve which originates in buttock/gluteal region

534
Q

SCIATICA
how is the pain from sciatica described?

A
  • burning
  • electric
  • stabbing

can be constant or it can come and go
worse when sat down
usually unilateral

535
Q

SCIATICA
what are the risk factors?

A
  • previous injury
  • overweight
  • lack of core strength
  • physically demanding job
  • diabetes
  • osteoarthritis
  • inactivity
  • smoking
536
Q

SCIATICA
what are the causes?

A
  • herniated/slipped disc - puts pressure on nerve root
  • degenerative disc disease
  • spinal stenosis
  • spondylolisthesis
  • osteoarthritis
  • trauma
  • cauda equina syndrome
537
Q

SCIATICA
what are the symptoms?

A
  • moderate pain in lower back, buttock and leg
  • numbness/weakness in lower back, buttock, leg or feet
  • pain gets worse with movement
  • pins and needles in legs, toes, or feet
  • loss of bladder or bowel control (due to cauda equina)
538
Q

SCIATICA
what are the investigations?

A
  • physical exam - straight leg raises
  • spinal x-ray
  • MRI/CT
  • nerve conduction velocity
  • electromyography
  • myelogram
539
Q

SCIATICA
what is the management?

A
  • apply ice/hot packs
  • over the counter medications
    • NSAIDs
    • aspirin
    • paracetamol
  • prescription medications
    • muscle relaxants (cyclobenzaprine)
    • tricyclic antidepressants (amitryptyline)
    • gabapentin/pregabalin
  • physical therapy
540
Q

RAISED ICP
what are the causes?

A
  • tumour
  • abscess
  • haemorrhage
  • hydrocephalus
  • strokes that cause brain swelling
541
Q

RAISED ICP
what are the symptoms?

A
  • high BP
  • irregular or slow pulse
  • severe headache
  • weakness
  • cardiac arrest
  • LOC, coma
  • loss of brainstem reflexes (blinking, gagging, pupils reacting to light)
  • respiratory arrest
  • dilated pupils + no movement in one/both eyes
542
Q

RAISED ICP
what are the investigations?

A
  • x-ray of skull + neck
  • head CT
  • MRI head
  • blood tests
543
Q

RAISED ICP
what is the management?

A
  • drain to remove CSF
  • mannitol to reduce swelling
  • intubation
  • surgery to remove part of skull
544
Q

RAISED ICP
what is the prognosis for brain herniation?

A

high chance of brain damage/death

545
Q

CHRONIC FATIGUE SYNDROME
what is it?

A

It is a disorder characterized by extreme fatigue or tiredness that doesn’t go away with rest and can’t be explained by an underlying medical condition.

546
Q

CHRONIC FATIGUE SYNDROME
What are the causes?

A

unknown - could be:
- viruses (EBV, rubella, RRV)
- a weakened immune system
- stress
- hormonal imbalances

547
Q

CHRONIC FATIGUE SYNDROME
what are the risk factors?

A
  • sex (female)
  • genetic predisposition
  • allergies
  • stress
  • environmental factors
548
Q

CHRONIC FATIGUE SYNDROME
what are the symptoms?

A
  • severe fatigue that interferes with daily life for >6 months
  • sleep problems
    • feeling unrefreshed after night’s sleep
    • chronic insomnia
  • memory loss
  • reduced concentration
  • orthostatic intolerance
  • muscle pain
  • frequent headaches
  • multi-joint pain without redness or swelling
  • frequent sore throat
549
Q

CHRONIC FATIGUE SYNDROME
what are the differentials?

A

mononucleosis
lyme disease
MS
SLE
hypothyroidism
fibromyalgia
depression
sleep disorders

550
Q

CHRONIC FATIGUE SYNDROME
what are the investigations?

A

rule out all other causes
- bloods - FBC, U+Es, CRP, ESR, TFTs

551
Q

CHRONIC FATIGUE SYNDROME
what is the management?

A

no cure
- pacing activities
- reduce caffeine, nicotine and alcohol
- create sleep routine
- antidepressant medications
- complementary/alternative medicines

552
Q

ESSENTIAL TREMOR
what is it?

A

Progressive, mainly symmetrical, rhythmic, involuntary oscillation movement disorder of the hands and forearms (69% of patients) that is usually absent at rest and present during posture and intentional movements.
it can also involve the voice, head and jaw

553
Q

ESSENTIAL TREMOR
what is the presentation?

A
  • slowly progressive
  • difficulties with writing, eating, drinking, dressing
  • tremor only present with movement
554
Q

ESSENTIAL TREMOR
what are the investigations?

A

clinical diagnosis
- bilateral tremor with normal muscle tone and speed of movement

555
Q

ESSENTIAL TREMOR
what is the management?

A
  • medication - propranolol, primidone
  • deep brain stimulation
  • focused ultrasound thalamotomy with MRI guidance
556
Q

MENIERE’S DISEASE
what is it?

A

It is an auditory disease characterised by an episodic sudden onset of vertigo, low-frequency hearing loss (in the early stages of the disorder), low-frequency roaring tinnitus, and sensation of fullness in the affected ear

557
Q

MENIERE’S DISEASE
what are the investigations?

A

pure tone air and bone conduction with masking
speech audiometry
tympanometry
oto-acoustic emissions (OAE)

558
Q

MENIERE’S DISEASE
what is the management?

A
  • dietary changes - salt restriction, limit caffeine, alcohol, smoking
  • reduce stress
  • audiological counselling
  • endolymphatic sac surgery
  • vestibular nerve section
  • labyrinthectomy
559
Q

DIABETIC NEUROPATHY
what is the distribution of sensory loss?

A

glove and stocking - usually lower legs are affected first

560
Q

DIABETIC NEUROPATHY
what is the management of neuropathic pain?

A
  • 1st line = amitriptyline, duloxetine, gabapentin or pregabalin (if one doesn’t work try another)
  • tramadol for rescue therapy
  • topical capsaicin
561
Q

DIABETIC NEUROPATHY
what are the effects on the GI system?

A
  • gastroparesis
  • chronic diarrhoea (particularly at night)
  • GORD
562
Q

DIABETIC NEUROPATHY
what is the management for gastroparesis?

A

metoclopramide, domperidone or erythromycin

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