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My Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

Give an example of a primary headache.

A
  1. Migraine.
  2. Tension headache.
  3. Cluster headache.
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2
Q

Give an example of a secondary headache.

A
  1. Meningitis.
  2. Subarachnoid haemorrhage.
  3. Giant cell arteritis.
  4. Medication overuse headache.
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3
Q

Give 6 questions that are important to ask when taking a history of headache.

A
  1. Time: onset, duration, frequency, pattern.
  2. Pain: severity, quality, site and spread.
  3. Associated symptoms e.g. nausea, vomiting, photophobia, phonophobia.
  4. Triggers/aggravating/relieving factors.
  5. Response to attack: is medication useful?
  6. What are symptoms like between attacks?
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4
Q

Give 5 red flags for suspected brain tumour in a patient presenting with a headache.

A
  1. New onset headache and history of cancer.
  2. Cluster headache.
  3. Seizure.
  4. Significantly altered consciousness, memory, confusion.
  5. Papilloedema (swollen optic disc).
  6. Other abnormal neuro exam.
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5
Q

How long do migraine attacks tend to last for?

A

Between 4 and 72 hours.

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6
Q

Describe the pain of a migraine.

A
  1. Unilateral.
  2. Throbbing.
  3. Moderate/severe pain.
  4. Aggravated by physical activity.
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7
Q

Would a patient with migraine experience any other symptoms?

A

Photophobia and/or phonophobia are common complaints. May have nausea but not vomiting.

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8
Q

How can migraines be subdivided?

A
  1. Episodic with (20%)/without (80%) aura.

2. Chronic migraine.

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9
Q

What would a patient experiencing migraine with aura complain of?

A
  • Visual disturbances e.g. flashing lights, zig-zag lines.
  • Sensory disturbances e.g. tingling in hands and feet.
  • Language aura and motor aura.
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10
Q

Describe the treatment for migraines.

A
  1. Ensure an accurate diagnosis.
  2. Lifestyle modification and trigger management.
  3. Psychological and behavioural treatment.
  4. Abortive treatment: PO triptan and NSAIDs.
  5. Anti-emetics.
  6. Preventative treatment: propranolol, acupuncture, amitriptyline.
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11
Q

What is the most common type of primary headache?

A

Tension headache.

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12
Q

How long do tension headaches usually last for?

A

From 30 minutes to 7 days.

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13
Q

Describe the pain of a tension headache.

A
  1. Bilateral.
  2. Pressing/tight.
  3. Mild/moderate pain.
  4. Not aggravated by physical activty.
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14
Q

Would a patient with a tension headache experience any other symptoms?

A

No!

Nausea, vomiting, photo/phonophobia would not be associated.

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15
Q

What is the most common type of secondary headache?

A

Medication overuse headache.

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16
Q

What is the diagnostic criteria for medication overuse headache?

A
  1. Headache present for >15 days/month.
  2. Regular use for >3 months of >1 symptomatic treatment drugs.
  3. Headache has developed or markedly worsened during drug use.
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17
Q

Describe the pain of a cluster headache.

A
  1. Severe/very severe pain.
  2. Pain around the eye/temporal area.
  3. Unilateral.
  4. Headache is accompanied by cranial autonomic features.
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18
Q

How long do cluster headaches usually last for?

A

15 minutes to 3 hours.

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19
Q

Name a type of headache that is accompanied with cranial autonomic features.

A

Cluster headache.

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20
Q

Describe the pain of trigeminal neuralgia.

A
  1. Unilateral face pain.
  2. Pain commonly in V3 distribution.
  3. Very severe.
  4. Electric shock like/shooting/sharp.
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21
Q

How long does the pain associated with trigeminal neuralgia usually last for?

A

A few seconds.

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22
Q

What features might be present in the history of a headache that make you suspect meningitis?

A
  1. Pyrexia.
  2. Photophobia.
  3. Neck stiffness.
  4. Non-blanching purpura rash.
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23
Q

What investigations might you do if you suspect someone has meningitis?

A
  1. Bloods.
  2. Blood cultures.
  3. Throat swab.
  4. Blood for serology and PCR.
  5. CT head.
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24
Q

How would you describe the headache associated with sub-arachnoid haemorrhage?

A

Thunderclap headache - maximum severity within seconds.

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25
Q

Name 2 investigations you could do to determine whether someone has a subarachnoid haemorrhage?

A
  1. CT of the head.

2. Cerebral angiography.

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26
Q

Describe the treatment/management for subarachnoid haemorrhage.

A
  1. Resuscitation.
  2. Nimodipine (CCB).
  3. Early intervention and close monitoring will improve prognosis.
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27
Q

What muscle is essential for correcting the extorsion action of lateral rectus when walking downstairs?

A

Super oblique (Cn 4 innervation).

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28
Q

What muscle needs to be working in order to test the action of superior and inferior rectus?

A

Lateral rectus.

To test superior and inferior rectus the patient is asked to abduct their eye 30 degrees first, this requires lateral rectus.

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29
Q

Superior and inferior oblique can never have isolated action. How can they be tested?

A

Position the eye so that superior and inferior recti are giving maximal rotation and look for complete correction.

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30
Q

Name 3 organisms that can cause meningitis in adults.

A
  1. N.meningitidis (g-ve diplococci).
  2. S.pneumoniae (g+ve cocci chain).
  3. Listeria monocytogenes (g+ve bacilli).
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31
Q

Name 3 organisms that can cause meningitis in children.

A
  1. E.coli (g-ve bacilli).
  2. Group B streptococci e.g. s.agalactiae.
  3. Listeria monocytogenes.
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32
Q

Give 5 symptoms of meningitis.

A
  1. Non-blanching petechial rash.
  2. Neck stiffness.
  3. Headache.
  4. Photophobia.
  5. Papilloedema.
  6. Fever.
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33
Q

How would you describe the rash that is characteristic of meningitis?

A

Non-blanching petechial rash.

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34
Q

What investigations might you do in someone who you suspect has meningitis.

A
  1. Blood cultures.
  2. Bloods: FBC, U+E, CRP, serum glucose, lactate.
  3. Lumbar puncture.
  4. CT head.
  5. Throat swabs.
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35
Q

What antibiotic is commonly given for the treatment of meningitis?

A

Cefotaxime.

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36
Q

What is the treatment of meningitis?

A

Cefotaxime.
+ amoxicillin if L.monocytogenes infection.
+ steroids to reduce inflammation in S.pneumoniae infection.

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37
Q

When is a child vaccinated against meningitis B?

A

At 8 weeks and 16 weeks.

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38
Q

When is a child vaccinated against meningitis C?

A

At 12 weeks and 1 year.

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39
Q

When is a child vaccinated against meningitis ACWY?

A

At age 14.

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40
Q

For which bacteria is meningitis prophylaxis effective against?

A

N.meningitidis.

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41
Q

What can be given as prophylaxis against N.meningitidis infection?

A

Ciprofloxacin.

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42
Q

At what vertebral level would you do a lumbar puncture?

A

L4/5.

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43
Q

Give 4 potential adverse effects of doing a lumbar puncture.

A
  1. Headache.
  2. Damage to spinal cord.
  3. Paraesthesia.
  4. CSF leak.
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44
Q

What investigations would you do on a CSF sample?

A
  • Protein and glucose levels.
  • MCS.
  • Bacterial and viral PCR.
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45
Q

What is the most common cause of viral meningitis?

A

Enterovirus.

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46
Q

What is the colour of the CSF in someone with bacterial infection?

A

Cloudy.

It is normally clear.

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47
Q

In what group of people is encephalitis common?

A

The immunocompromised.

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48
Q

Give 4 symptoms of encephalitis.

A
  1. Fever.
  2. Headache.
  3. Lethargy.
  4. Behavioural change.
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49
Q

A lumbar puncture is done and a CSF sample is obtained from someone who is suspected to have encephalitis. Describe what the lymphocyte, protein and glucose levels would be like in someone with encephalitis.

A
  • Lymphocytosis (raised lymphocytes).
  • Raised protein.
  • Normal glucose.
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50
Q

What is the treatment for encephalitis?

A

Acyclovir.

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51
Q

Give 4 symptoms of rabies.

A
  1. Fever.
  2. Anxiety.
  3. Confusion.
  4. Hydrophobia.
  5. Hyperactivity.
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52
Q

Name the organism responsible for causing tetanus.

A

Clostridium tetani (gram positive anaerobe).

It infects via dirty wounds.

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53
Q

Give 3 symptoms of tetanus.

A
  1. Trismus (lockjaw).
  2. Sustained muscle contraction.
  3. Facial muscle involvement.
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54
Q

Name the organism responsible for causing botulism.

A

Clostridium botulinum.

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55
Q

Give 3 symptoms of botulism.

A
  1. Diplopia (double vision).
  2. Dysphagia.
  3. Peripheral weakness.
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56
Q

If a patient has aphasia what region in the brain has been affected?

A

Broca’s area.

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57
Q

If a patient has receptive dysphasia what region in the brain has been affected?

A

Wernicke’s area.

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58
Q

Name 3 intra-cranial haemorrhages.

A
  1. Extra-dural.
  2. Sub-dural.
  3. Sub-arachnoid.
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59
Q

What can cause a sub-arachnoid haematoma?

A

Rupture of a berry aneurysm around the circle of willis.

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60
Q

Give 5 symptoms of a sub-arachnoid haemorrhage.

A
  1. Sudden onset ‘thunderclap’ headache.
  2. Photophobia.
  3. Reduced conciousness.
  4. Neck stiffness.
  5. Nausea and vomiting.
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61
Q

What investigations might you do to see if someone has a sub-arachnoid haemorrhage?

A
  1. CT scan of head - would show blood in sulci.
  2. Lumbar puncture.
  3. MRA.
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62
Q

What is the treatment for a sub-arachnoid haematoma?

A
  • Bed rest and BP control.
  • CCB to prevent cerebral artery spasm.
  • IV saline.
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63
Q

What can cause a sub-dural haematoma?

A

Head injury -> vein rupture.

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64
Q

Describe the natural history of a sub-dural haematoma.

A

Latent period after the head injury. 8-10 weeks later the clot starts to break down and there is a massive increase in oncotic pressure, water is sucked up into the haematoma -> signs and symptoms develop. There is a gradual rise in ICP.

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65
Q

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

A

The clot starts to break down and there is a massive increase in oncotic pressure, water is sucked up by osmosis into the haematoma.

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66
Q

Give 3 symptoms of a sub-dural haematoma.

A
  1. Headache.
  2. Drowsiness.
  3. Confusion.
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67
Q

What is the treatment for a sub-dural haematoma?

A

Surgical removal.

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68
Q

What can cause an extra-dural haematoma?

A

Trauma to the temporal bone -> bleeding from the middle meningeal artery.

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69
Q

What do the ventricles do to prolong survival in someone with an extra-dural haemorrhage?

A

The ventricles get rid of their CSF to prevent the rise in inter-cranial pressure.

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70
Q

What is the treatment for an extra-dural haematoma?

A

Immediate surgical drainage.

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71
Q

What proportion of strokes are due to intracerebral haemorrhages?

A

10-15%.

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72
Q

Give 2 primary causes of intra-cerebral haemorrhage.

A
  1. Hypertension -> Berry or Charcot-Bouchard aneurysms -> rupture.
  2. Lobar (amyloid angiopathy).
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73
Q

Give 5 secondary causes of intra-cerebral haemorrhage.

A
  1. Tumour.
  2. Arterio-venous malformations (AVM).
  3. Cerebral aneurysm.
  4. Anticoagulants e.g. warfarin.
  5. Haemorrhagic transformation infarct.
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74
Q

Give 3 potential complications of Charcot-Bouchard aneurysms.

A
  1. Rupture (haemorrhage).
  2. Thrombosis.
  3. Leakage (microbleeds).
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75
Q

What is the likely cause of bleeds in the basal ganglia, pons and/or cerebellum?

A

Hypertension.

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76
Q

Describe the treatment for anti-coagulant related intra-cerebral haemorrhage.

A

Check warfarin INR and consider reversal with vitamin K.

If low platelets, platelet transfusion.

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77
Q

Define stroke.

A

Rapid onset of neurological deficit which is the result of a vascular lesion and is associated with infarction of central nervous tissue.

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78
Q

What can cause a stroke?

A
  1. Cerebral infarction due to embolism or thrombosis (85%).

2. Intracerebral or sub-arachnoid haemorrhage (15%).

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79
Q

Give 5 risk factors for stroke.

A
  1. Hypertension.
  2. Diabetes mellitus.
  3. Cigarette smoking.
  4. Hyperlipidaemia.
  5. Obesity.
  6. Alcohol.
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80
Q

Give 5 signs of an ACA stroke.

A
  1. Lower limb weakness and loss of sensation to the lower limb.
  2. Gait apraxia (unable to initiate walking).
  3. Incontinence.
  4. Drowsiness.
  5. Decrease in spontaneous speech.
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81
Q

Give 5 signs of a MCA stroke.

A
  1. Upper limb weakness and loss of sensation to the upper limb.
  2. Hemianopia.
  3. Aphasia.
  4. Dysphasia.
  5. Facial drop.
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82
Q

Give 5 signs of a PCA stroke.

A
  1. Visual field defects.
  2. Cortical blindness.
  3. Visual agnosia.
  4. Prosopagnosia.
  5. Dyslexia.
  6. Unilateral headache.
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83
Q

What is visual agnosia?

A

An inability to recognise or interpret visual information.

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84
Q

What is prosopagnosia?

A

An inability to recognise a familiar face.

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85
Q

A patient presents with upper limb weakness and loss of sensory sensation to the upper limb. They also have aphasia and facial drop. Which artery is likely to have been occluded?

A

The middle cerebral artery.

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86
Q

A patient presents with lower limb weakness and loss of sensory sensation to the lower limb. They also have incontinence, drowsiness and gait apraxia. Which artery is likely to have been occluded?

A

The anterior cerebral artery.

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87
Q

A patient presents with a contralateral homonymous hemianopia. They are also unable to recognise familiar faces and complain of a headache on one side of their head. Which artery is likely to have been occluded?

A

The posterior cerebral artery.

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88
Q

What investigation could you do to determine whether someone has had a haemorrhagic or an ischaemic stroke?

A

A CT scan of the head.

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89
Q

What is the treatment for an ischaemic stroke?

A

Thrombolysis e.g. alteplase - IV infusion to break up the clot.

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90
Q

What non pharmacological treatment options are there for people after a stroke?

A
  1. Specialised stroke units.
  2. Swallowing and feeding help.
  3. Physiotherapy.
  4. Home modifications.
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91
Q

What is MS?

A

A chronic auto-immune disorder of the CNS. It is an inflammatory and demyelinating disease characterised by progressive disability.

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92
Q

Describe the epidemiology of MS.

A
  • Presents between 20-40 y/o.
  • Females > males.
  • Rare in the tropics.
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93
Q

Describe the aetiology of MS.

A
  • Environment e.g. EBV infection is shown to be associated.
  • Genetic predisposition.
  • Chance.
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94
Q

Briefly describe the pathophysiology of MS.

A

Genetic susceptibility + environmental trigger -> T cell activation -> B cell and macrophage activation -> inflammation, demyelination and axon destruction.

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95
Q

Where would MS plaques be seen histologically?

A

Around blood vessels: perivenular.

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96
Q

Does myelin regenerate in someone with MS?

A

Yes but it is much thinner which causes inefficient nerve conduction.

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97
Q

Give 3 major features of an MS plaque.

A
  1. Inflammation.
  2. Demyelination.
  3. Axon loss.
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98
Q

Describe the relapsing/remitting course of MS.

A

The patient has random attacks over a number of years. Between attacks there is no disease progression.

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99
Q

Describe the chronic progressive course of MS.

A

Slow decline in neurological functions from the onset.

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100
Q

What can exacerbate the symptoms of MS?

A

Heat - typically a warm shower.

Symptoms can be relieved by cool temperatures.

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101
Q

Give 5 signs of MS.

A
  1. Spasticity.
  2. Nystagmus and double vision.
  3. Optic neuritis: impaired vision and pain.
  4. Weakness.
  5. Sensory symptoms.
  6. Paraesthesia.
  7. Bladder and sexual dysfunction.
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102
Q

Give 3 atypical symptoms of MS e.g. if a patient presents with these they are unlikely to have MS.

A
  1. Aphasia.
  2. Hemianopia.
  3. Muscle wasting.
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103
Q

What is the diagnostic criteria for MS?

A
  1. > 2 CNS lesions disseminated in time and space.

2. Exclusion of conditions that may give a similar clinical presentation.

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104
Q

Name 3 conditions in the differential diagnosis of MS.

A
  1. SLE.
  2. Sjögren’s.
  3. AIDS.
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105
Q

What investigations might you do in someone to see if they have MS?

A
  1. MRI of brain and spinal cord - lesions may be seen around ventricles.
  2. Lumbar puncture - CSF.
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106
Q

What might electrophoresis of CSF show for someone with MS?

A

Oligoclonal IgG bands.

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107
Q

What medication might you give to someone to reduce the relapse severity of MS?

A

Short course steroids e.g. methylprednisolone.

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108
Q

Describe the pharmacological treatment for MS.

A
  1. Beta interferon (anti-inflammatory).
  2. Natalizumab.
  3. Stem cell transplant.
  4. Muscle relaxants for spasticity and other symptom relief.
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109
Q

Describe the non-pharmacological treatment for MS.

A
  1. Psychological therapies and counselling.
  2. Speech therapists.
  3. Physiotherapy and occupational therapy.
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110
Q

What is a UMN?

A

A neurone that is located entirely in the CNS. Its cell body is located in the primary motor cortex.

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111
Q

Give 4 signs of UMN weakness.

A
  1. Spasticity.
  2. Increased muscle tone.
  3. Hyper-reflexia.
  4. Minimal muscle atrophy.
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112
Q

Give 3 causes of UMN weakness.

A
  1. MS.
  2. Brain tumour.
  3. Stroke.
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113
Q

What is a LMN?

A

A neurone that carries signals to effectors. The cell body is located in the brain stem or spinal cord.

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114
Q

Give 5 signs of LMN weakness.

A
  1. Flaccid.
  2. Reduced muscle tone.
  3. Hypo-reflexia.
  4. Muscle atrophy.
  5. Fasciculations.
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115
Q

What is epilepsy?

A

The tendency to have seizures.

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116
Q

Define seizure.

A

A convulsion caused by paroxysmal discharge of cerebral neurones.

Abnormal and excessive excitability of neurones.

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117
Q

Give 5 causes of transient loss of consciousness.

A
  1. Syncope.
  2. Epileptic seizures.
  3. Non-epileptic seizures.
  4. Intoxication e.g. alcohol.
  5. Ketoacidosis/hypoglycaemia.
  6. Trauma.
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118
Q

Give 5 causes of epilepsy.

A
  1. Flashing lights.
  2. Cerebrovascular disease e.g. stroke.
  3. Genetic predisposition.
  4. CNS infection e.g. meningitis.
  5. Trauma.
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119
Q

Give a definition for an epileptic seizure.

A

Excessive, unsynchronised neuronal discharges in the brain cause paroxysmal changes in behaviour, sensation or cognitive processes.

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120
Q

Give 5 signs of an epileptic seizure.

A
  1. 30-120s in duration.
  2. ‘Positive’ symptoms e.g. tingling and movement.
  3. Tongue biting.
  4. Head turning.
  5. Muscle pain.
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121
Q

Define syncope.

A

Insufficient blood or oxygen supply to the brain causes paroxysmal changes in behaviour, sensation and cognitive processes.

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122
Q

Give 5 signs that a transient loss of consciousness is due to syncope.

A
  1. Situational.
  2. 5-30s in duration.
  3. Sweating.
  4. Nausea.
  5. Pallor.
  6. Dehydration.
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123
Q

Give a definition for a non-epileptic seizure.

A

Mental processes associated with psychological distress cause paroxysmal changes in behaviour, sensation and cognitive processes.

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124
Q

Give 5 signs of a non-epileptic seizure.

A
  1. Situational.
  2. 1-20 minutes in duration (longer than epileptic).
  3. Eyes closed.
  4. Crying or speaking.
  5. Pelvic thrusting.
  6. History of psychiatric illness.
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125
Q

Which is likely to last for longer, an epileptic or a non-epileptic seizure?

A

A non-epileptic seizure can last from 1-20 minutes whereas an epileptic seizure lasts for 30-120 seconds.

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126
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient had their eyes closed, was speaking and there was waxing/waning/pelvic thrusting. They say the seizure lasted for about 5 minutes. Is this likely to be an epileptic or a non-epileptic seizure?

A

This is likely to be a non-epileptic seizure.

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127
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient was moving their head and biting their tongue. They say the seizure lasted for just under a minute. Is this likely to be an epileptic or a non-epileptic seizure?

A

This is likely to be an epileptic seizure.

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128
Q

A patient complains of having a ‘black out’. They tell you that before the ‘black out’ they felt nauseous and were sweating. They tell you that their friends all said they looked very pale. Is this likely to be due to a problem with blood circulation or a disturbance of brain function?

A

This is likely to be due to a blood circulation problem e.g. syncope.

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129
Q

What 2 categories can epileptic seizures be broadly divided into?

A
  1. Focal epilepsy - only one portion of the brain is involved.
  2. Generalised epilepsy - the whole brain is affected.
130
Q

Give 3 examples of focal epileptic seizures.

A
  1. Simple partial seizures with consciousness.
  2. Complex partial seizures without consciousness.
  3. Secondary generalised seizures.
131
Q

Give 3 examples of generalised epileptic seizures.

A
  1. Absence seizures.
  2. Myoclonic seizures.
  3. Generalised tonic clonic seizures.
132
Q

Describe a generalised tonic clonic seizure.

A

Sudden onset rigid tonic phase followed by a convulsion (clonic phase) in which the muscles jerk rhythmically.

The episode lasts up to 120s and is associated with tongue biting and incontinence.

133
Q

Give 2 features of absence seizures.

A
  1. Commonly present in childhood.

2. Child ceases activity and stares for a few seconds.

134
Q

Describe a myoclonic seizure.

A

Isolated muscle jerking.

135
Q

What is the treatment for focal epileptic seizures?

A

Carbamazepine.

136
Q

How does carbamazepine work as an AED?

A

It inhibits pre-synaptic Na+ channels and so prevents axonal firing.

137
Q

What is the treatment for generalised epileptic seizures?

A

Sodium valporate.

138
Q

What is the major side effect of sodium valporate?

A

It is teratogenic!

139
Q

Give 4 potential side effects of AED’s e.g. sodium valporate and carbamazepine.

A
  1. Cognitive disturbances.
  2. Heart disease.
  3. Drug interactions.
  4. Teratogenic.
140
Q

Name 3 viruses that can cause encephalitis?

A
  • Herpes simplex virus.
  • Varicella zoster virus.
  • HIV.
141
Q

Describe the CSF cell count for someone with viral meningitis.

A
  1. High lymphocytes.
  2. Normal/high protein.
  3. Normal glucose.
142
Q

Describe the CSF cell count for someone with bacterial meningitis.

A
  1. High neutrophils.
  2. High protein.
  3. Low glucose.
143
Q

Describe the appearance of listeria monocytogenes on a gram film?

A

Gram positive bacilli.

144
Q

Describe the treatment for meningitis caused by listeria monocytogenes.

A

Cefotaxime and amoxicillin.

145
Q

What would the CSF of someone with meningitis look like?

A

Purulent, cloudy.

146
Q

What can be the affect of non missile trauma to the scalp?

A

Contusions and lacerations.

147
Q

What can be the affect of non missile trauma to the skull?

A

Fracture.

148
Q

Give 2 risks associated with skull fracture.

A
  1. Haematoma.

2. Infection.

149
Q

What can be the affect of non missile trauma to the meninges?

A

Haemorrhage and infection (due to skull fracture).

150
Q

What can be the affect of non missile trauma to the brain?

A

Contusions, lacerations, haemorrhage and infection (due to skull fracture).

151
Q

Describe the aetiology of diffuse traumatic axonal injury.

A

Acceleration/deceleration -> shearing rotational forces -> axons tear.

152
Q

Give a sign of diffuse vascular injury due to non missile trauma.

A

Multiple petechial haemorrhages.

153
Q

What is more severe: diffuse traumatic axonal injury or diffuse vascular injury?

A

Diffuse vascular injury is MUCH more severe. It can result in near immediate death.

154
Q

Describe the mechanism behind acceleration/deceleration damage.

A

A force to the head can cause differential brain movements -> shearing, traction and compressive stresses -> risk of axon tear and blood vessel damage.

155
Q

What is contusion?

A

Superficial ‘bruises’ of the brain.

156
Q

What is laceration?

A

When a contusion is severe enough to tear the pia mater.

157
Q

What is the cause of chronic traumatic encephalopathy?

A

Often seen following repetitive mild traumatic brain injury.

158
Q

Give 3 initial symptoms of chronic traumatic encephalopathy.

A
  1. Irritable.
  2. Impulsive.
  3. Aggressive.
  4. Depressed.
159
Q

Give 3 later symptoms of chronic traumatic encephalopathy.

A
  1. Dementia.
  2. Gait and speech problems.
  3. PD symptoms.
160
Q

Give 3 signs of chronic traumatic encephalopathy.

A
  1. Atrophy of deep brain structures.
  2. Enlarged ventricles.
  3. Tau deposited in sulci.
161
Q

Describe the diagnosis of migraine without aura.

A

> 5 attacks lasting between 4 and 72 hours with nausea/vomiting or photophobia/phonophobia. And >2 of:

  • Unilateral pain.
  • Throbbing pain.
  • Pain aggravated by physical activity.
  • Moderate/severe pain.
162
Q

Give 5 triggers of migraine.

A
  1. Cheese.
  2. OCP.
  3. Alcohol.
  4. Caffeine.
  5. Anxiety.
  6. Travel.
  7. Exercise.
163
Q

Briefly describe the pathophysiology of cauda equina syndrome.

A

Spinal compression at or distal to the L1 nerve root disrupts sensation and movement. It is a surgical emergency.

164
Q

Give 5 signs of cauda equina syndrome.

A
  1. Bilateral sciatica (pain radiates down the leg to the foot).
  2. Saddle anaesthesia.
  3. Bladder/bowel dysfunction.
  4. Erectile dysfunction.
  5. Variable leg weakness.
165
Q

What investigation might you do to see if someone has cauda equina syndrome?

A

MRI of spine.

166
Q

Define spondyloisthesis.

A

Slippage of vertebra over the one below.

167
Q

Define spondylosis.

A

Degenerative disc disease.

168
Q

Define myelopathy.

A

Spinal cord disease; UMN problem. Surgery is often indicated to prevent deterioration.

169
Q

Define radiculopathy.

A

Spinal nerve root disease; LMN problem.

170
Q

Is myelopathy or radiculopathy an UMN problem?

A

Myelopathy is a spinal cord disease and therefore is an UMN problem.

171
Q

Is myelopathy or radiculopathy a LMN problem?

A

Radiculopathy is a spinal nerve root disease and therefore is a LMN problem.

172
Q

What is the treatment for sciatica without neurological signs?

A

Conservative management e.g. physio and NSAIDs.

173
Q

You see a patient who you suspect has meningitis. It is noted that they have raised ICP. Would you do a lumbar puncture?

A

NO! You would not do a lumbar puncture in someone with raised ICP due to the risk of coning.

174
Q

Give 4 signs of raised intra-cranial pressure.

A
  1. Papilloedema.
  2. Focal neurological signs.
  3. Loss of consciousness.
  4. New onset seizures.
175
Q 
What drug is prescribed in sub-arachnoid haematoma to prevent arterial spasm and subsequent ischaemia? 
What class of drugs does this come from?
A

Nimodipine – CCB.

176
Q

Give 3 differences in the presentation of a patient with a subdural haemorrhage in comparison to an extradural haemorrhage.

A
  1. Time frame: extra-dural symptoms are more acute.
  2. GCS: sub-dural GCS will fluctuate whereas GCS will drop suddenly in someone with an extra-dural haematoma.
  3. CT: extra-dural haematoma will have a rounder more contained appearance.
177
Q

What is the most common cause of spinal cord compression?

A

Secondary malignancy from lung, breast, prostate, kidney etc.

178
Q

Give 3 activities that can trigger trigeminal neuralgia.

A
  1. Washing your face.
  2. Eating.
  3. Shaving.
  4. Talking.
179
Q

Define weakness.

A

Impaired ability to move a body part in response to will.

180
Q

Define paralysis.

A

The ability to move a body part in response to will is completely lost.

181
Q

Define ataxia.

A

Willed movements are clumsy and uncontrolled.

182
Q

Define involuntary movements.

A

Spontaneous movement independent of will.

183
Q

Define apraxia.

A

The ability to carry out familiar purposeful movements is lost in the absence of paralysis or other sensory or motor impairments.

184
Q

Give 3 things that modulate LMN action potential transmission to effectors.

A
  1. Cerebellum.
  2. Basal ganglia.
  3. Sensory feedback.
185
Q

Where are LMN’s located?

A

LMN cell bodies are found in the spinal cord or in the cranial nerve nuclei in the brainstem.

186
Q

Give 5 potential sites of damage along the ‘final common pathway’.

A
  1. Cranial nerve nuclei.
  2. Motor neurones.
  3. Spinal ventral roots.
  4. Peripheral nerves.
  5. NMJ.
  6. Muscles.
187
Q

Give 3 diseases that are associated with motor neurone damage.

A
  1. Motor neurone disease.
  2. Spinal atrophy.
  3. Poliomyelitis.
  4. Spinal cord compression.
188
Q

Give 3 pathologies that are associated with ventral spinal root damage.

A
  1. Tumours.
  2. Prolapsed intervertebral discs.
  3. Cervical/lumbar spondylosis (wear and tear).
189
Q

Name a disease that is associated with NMJ damage.

A

Myasthenia Gravis.

190
Q

What investigations could you do to see if someone has damage to their LMN’s?

A
  1. EMG.
  2. MRI.
  3. Muscle enzymes.
  4. Lumbar puncture -> CSF.
191
Q

What are muscle spindles innervated by?

A

Gamma motor neurones.

192
Q

What is the function of muscle spindles?

A

Muscle spindles control muscle tone and tell you how much a muscle is stretched.

193
Q

Describe the pyramidal pattern of weakness in the upper limb.

A

Flexors are stronger than extensors.

194
Q

Describe the pyramidal pattern of weakness in the lower limb.

A

Extensors are stronger than flexors.

195
Q

Give 4 potential sites of UMN damage.

A
  1. Motor cortex lesions.
  2. Internal capsule.
  3. Brainstem.
  4. Spinal cord.
196
Q

Give 3 clinical patterns of motor neurone disease.

A
  1. Muscular atrophy: anterior horn cell lesion - LMN. Fasciculations, weakness, wasting.
  2. Amyotrophic lateral sclerosis: loss of neurones in the motor cortex and the anterior horn of the spinal cord - LMN and UMN signs -> progressive spastic tetra-paresis.
  3. Progressive bulbar palsy: destruction of Cn 9-12.
197
Q

Progressive bulbar palsy is a clinical pattern of MND. What symptoms might someone present with?

A
  1. Dysarthria (slurred speech).
  2. Dysphagia.
  3. Wasting and fascitulations of the tongue.
198
Q

What is the long term consequence of amyotrophic lateral sclerosis?

A

Progressive spastic tetraparesis.

199
Q

What is the treatment for motor neurone disease?

A
  • Riluzole - inhibits glutamate release and slows disease progression.
  • Ventilatory support.
  • Feeding by a PEG.
200
Q

Does hereditary spastic paraplegia affect UMN’s or LMN’s?

A

UMN’s.

201
Q

Give 5 signs/symptoms of hereditary spastic paraplegia.

A
  1. Abnormal gait - knees knocking, walking on toes.
  2. Bladder problems.
  3. High arched feet.
  4. Increased tone in legs and minimal muscle wasting.
  5. Family history.
202
Q

What are the 3 cardinal presenting symptoms of brain tumours?

A
  1. Raised ICP.
  2. Progressive neurological deficit.
  3. Epilepsy.
203
Q

Give 3 symptoms of raised ICP.

A
  1. Headache.
  2. Drowsiness.
  3. +/- vomiting.
204
Q

You ask a patient with a brain tumour about any factors that aggravate their headache. What might they say?

A
  1. Worst first thing in the morning.

2. Worst when coughing, straining or bending forward.

205
Q

What is the cardinal physical sign of raised ICP?

A

Papilloedema.

Due to obstruction of venous return from the retina.

206
Q

Where might secondary brain tumours arise from?

A
  1. Lung (NSCC).
  2. Breast.
  3. Malignant melanoma.
  4. Kidney.
  5. Gut.
207
Q

Describe the treatment for secondary brain tumours.

A
  1. Surgery and adjuvant radiotherapy.
  2. Chemotherapy.
  3. Supportive care.
208
Q

From what cell do primary brain tumours originate?

A

Glial cells:

  • Astrocytoma (90%).
  • Oligodendroglioma (<5%).
209
Q

Which primary brain tumour do you associate with genetic defects in chromosomes in 1 and 19?

A

Oligodendroglioma.

210
Q

Give 3 features of oligodendroglioma’s.

A
  1. Genetic defects in chromosomes 1 and 19.
  2. All IDH1 mutation positive.
  3. Chemo sensitive.
  4. 10-15 year survival.
211
Q

Describe the WHO glioma grading.

A
  1. Grade 1: benign paediatric tumour.
  2. Grade 2: pre-malignant tumour.
  3. Grade 3: ‘anaplastic astrocytoma’ - cancer.
  4. Grade 4: glioblastoma multiforme (GBM).
212
Q

Describe the epidemiology of grade 2 gliomas.

A

Disease of young adults.

213
Q

What is often the first symptom that someone with a grade 2 glioma presents with?

A

Seizures.

214
Q

Give 3 causes of grade 2 glioma deterioration.

A
  1. Tumour transformation to a malignant phenotype.
  2. Progressive mass effect due to slow growth.
  3. Progressive neurological deficit from functional brain destruction.
215
Q

Describe the common pathway to GBM.

A

Initial genetic error of glucose glycolysis -> IDH 1 mutation -> excessive build up of 2-hydroxyglutarate -> genetic instability in glial cells triggered.

216
Q

Give 5 good prognostic factors for GBM.

A
  1. <45 y/o.
  2. Aggressive surgical therapy.
  3. Good performance post surgery.
  4. Secondary GBM.
  5. MGMT ‘mutant’ - will respond well to chemo.
217
Q

Give 5 poor prognostic factors for GBM.

A
  1. > 50 y/o.
  2. Poor neurological function after surgery.
  3. Non-radical surgery treatment.
  4. Primary GBM.
  5. MGMT ‘wild type’ - no response to chemo.
218
Q

Describe the treatment for GBM.

A
  1. Resective surgery.
  2. Adjuvant chemotherapy with Temozolomide.
  3. Palliative care.
219
Q

What drug is used as adjuvant chemotherapy for people undergoing GBM resection?

A

Temozolomide.

220
Q

Define dementia.

A

A set of symptoms that may include memory loss and difficulties with thinking, problem solving or language. There is a progressive decline in cognitive function.

221
Q

Describe the epidemiology of dementia.

A

10% of people over 65 and 20% of people over 80 have dementia.

222
Q

Give 3 causes of dementia.

A
  1. Alzheimer’s disease (65%).
  2. Fronto-temporal.
  3. Vascular.
  4. Lewy bodies.
  5. Vitamin deficiency e.g. B12.
223
Q

Frontal lobe atrophy is seen on an MRI. What kind of dementia is this patient likely to have?

A

Fronto-temporal.

224
Q

Give 3 symptoms of fronto-temporal dementia.

A
  1. Behaviour variants: personality and behavioural change.
  2. Language variants.
  3. Often there is overlap with MND.
225
Q

Which disease is fronto-temporal dementia often associated with?

A

Motor neurone disease.

226
Q

Give 3 functions of the temporal lobe.

A
  1. Hearing.
  2. Language comprehension.
  3. Memory.
  4. Emotion.
227
Q

What lobe of the brain is affected in Alzheimer’s disease?

A

Temporal lobe.

228
Q

Give 4 symptoms of Alzheimer’s disease.

A
  1. Selective attention.
  2. Language impairments - difficulty in naming and understanding.
  3. Apraxia.
  4. Global deficits.
229
Q

What is often the first cognitive marker of AD?

A

Short term memory impairment.

230
Q

Give 2 histological signs of AD.

A
  1. Plaques of amyloid.

2. Neuronal reduction.

231
Q

How is AD diagnosed?

A

When criteria (Braak staging) for intermediate or high likelihood AD are met AND the patient has a clinical history of dementia.

232
Q

25% of all patients with AD will develop what?

A

Parkinsonism.

233
Q

What lobe of the brain is affected in semantic dementia?

A

Symmetrical temporal lobe atrophy.

234
Q

What is functional memory dysfunction?

A

Acquired dysfunction of memory that significantly affects a person’s professional/private life in the absence of an organic cause.

235
Q

How could you determine whether someone has functional memory dysfunction or a degenerative disease?

A

When asked the question ‘when was the last time your memory let you down?’, someone with functional memory dysfunction would give a good detailed answer whereas someone with degenerative disease would struggle to answer.

236
Q

What investigations can you do in primary care to determine whether someone might have dementia?

A
  1. Good history of symptoms.
  2. 6CIT.
  3. Blood tests.
237
Q

What questions are asked in 6CIT?

A
  1. What year is it?
  2. What month is it?
    (Give an address).
  3. Count backwards from 20.
  4. Say the months of the year in reverse.
  5. Repeat the address.
238
Q

Why might you do a blood test in someone who you suspect has dementia?

A

To look at the vitamin levels that may suggest a reversible cause e.g. dementia due to B12 deficiency.

239
Q

Dementia: what secondary care investigation could you do to look at brain structure?

A

MRI of the brain.

240
Q

What secondary care investigation could you do to look at the pathology of dementia?

A

Amyloid and tau histopathology.

241
Q

Name the staging system that classifies the degree of pathology in AD.

A

Braak staging.

242
Q

Describe Braak staging.

A
  • Stage 5/6 - high likelihood of AD.
  • Stage 3/4 - intermediate likelihood.
  • Stage 1/2 - low likelihood.
243
Q

Dementia: what secondary care investigation could you do to assess brain function.

A

PET scans and functional MRI.

244
Q

Give 5 ways in which dementia can be prevented.

A
  1. Stop smoking.
  2. Healthy diet.
  3. Regular exercise.
  4. Healthy weight.
  5. Low alcohol intake.
245
Q

What medications might you use in someone with dementia?

A

Acetylcholine esterase inhibitors.

246
Q

How long do you wait for before doing a lumbar puncture in someone with a suspected SAH?

A

At least 12 hours! You need to wait for the Hb to break down and then CSF will become yellow, this is a sign that there is bleeding in the sub-arachnoid space - xanthochromia.

247
Q

Will GCS drop rapidly or slowly in someone with an extra-dural haematoma?

A

GCS will drop suddenly - there is a rapid deterioration in consciousness with focal neurological signs.

248
Q

A 60-year-old man has just had surgery on his carotids and is complaining of difficulty speaking and swallowing. OE his tongue is deviated to the right. Which nerve has most likely been damaged during the operation?

A

Right hypoglossal.

249
Q

What is a TIA?

A

An acute loss of cerebral or ocular function with symptoms lasting <24 hours and with a complete clinical recovery. It is caused by an inadequate cerebral blood supply due to low blood flow, ischaemia or embolism.

250
Q

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

A

Assess their risk of having a stroke in the next 7 days - ABCD2 score.

251
Q

What is the ABCD2 score?

A

It is used in patients who have had TIA’s to assess their risk of stroke in the next 7 days.

  • Age > 60.
  • BP > 140/90mmHg.
  • Clinical features: unilateral weakness, speech disturbance.
  • Duration?
  • Diabetes?
252
Q

What is the management for someone who has had a TIA?

A

Give statins and aspirin/clopidogrel. Control BP.

253
Q

What is the function of the cerebellum?

A

The cerebellum is responsible for precise control, fine adjustment and co-ordination of motor activity based on continual sensory feedback. The cerebellum decides HOW you do something. It computes motor error, adjusts commands and projects this information back to the motor cortex.

254
Q

What are the 3 layers of the cerebellum?

A
  • Molecular layer.
  • Purkinje layer.
  • Granular layer.
255
Q

Give 5 signs of cerebellar dysfunction.

A
  1. Dysdiadochokinesis.
  2. Ataxia.
  3. Nystagmus.
  4. Intention tremor.
  5. Slurred speech.
  6. Hypotonia.
256
Q

How can the severity of ataxia be classified?

A
  • Mild: patient is independent or requires 1 walking aid.
  • Moderate: patient requires 2 walking aids.
  • Severe: patient is wheelchair dependent.

SARA scale can also be used, looks at gait, stance, sitting and speech.

257
Q

What investigations might you do in someone who is presenting with signs of cerebellar dysfunction?

A

MRI - will show cerebellar atrophy and will exclude other causes e.g. CV, tumour, hydrocephalus.

258
Q

Give an example of an AR inherited cerebellar ataxia.

A

Friedreich’s ataxia (FA) - presents early in childhood. Motor and sensory problems. Patients are at increased risk of diabetes/CV problems.

259
Q

Give an example of an AD inherited cerebellar ataxia.

A

Spino-cerebellar ataxia 6 (SCA6) and episodic ataxia (presents with difficulty focusing and migraines).

260
Q

Give 4 causes of acquired cerebellar ataxia.

A
  1. Toxic e.g. alcohol, lithium.
  2. Idiopathic.
  3. Neurodegenerative.
  4. Immune mediated.
261
Q

Give 3 examples of immune mediated cerebellar ataxia.

A
  1. Post-infection cerebellitis.
  2. Gluten ataxia.
  3. Para-neoplastic cerebellar degeneration (secondary from lung or breast, look for a tumour on MRI. Rapid onset).
  4. Primary autoimmune cerebellar ataxia.
262
Q

Briefly describe the physiology of muscle contraction.

A

Ca2+ is released from the sarcoplasmic reticulum -> T-tubules -> binds to troponin C. Troponin C moves tropomyosin to expose myosin binding site. Myosin binds to specific sites on actin (requires ATP) and there is a cross bridge formation and detachment cycle.

263
Q

What is the function of dystrophin?

A

Dystrophin links the ECM to the cytoskeleton of the muscle fibre.

264
Q

What protein is affected to produce the signs and symptoms seen in duchenne muscular dystrophy?

A

Dystrophin.

265
Q

Describe the inheritance pattern of Duchenne muscular dystrophy.

A

X linked recessive. (Xp21).

266
Q

At what age do people present with duchenne muscular dystrophy?

A

<5 y/o. There are delayed milestones and the patient is often in a wheelchair by the time they are 13.

267
Q

What cardiac problems might someone with duchenne muscular dystrophy have?

A
  • Arrhythmias.
  • Conduction block.
  • Cardiomyopathy.
268
Q

What would you see histologically in someone with duchenne muscular dystrophy?

A

Muscle cell nuclei all over the place (not just around the edge of the cell). Muscle cells all different shapes and sizes. Absence of dystrophin.

269
Q

Describe the pathophysiology of duchenne muscular dystrophy.

A

Large deletions, duplications and mutations disrupt the reading frame -> ‘out of frame’ mutations -> dystrophin not produced -> DMD phenotype.

270
Q

What is the treatment for duchenne muscular dystrophy?

A
  • Supportive - physio, OT, home adaptations.
  • Scoliosis corrective surgery.
  • Manage cardiac problems.
  • Steroids.
  • Gene therapy.
271
Q

Describe the inheritance pattern of Becker muscular dystrophy.

A

X linked recessive - milder form of Duchenne.

272
Q

At what age do people present with becker muscular dystrophy?

A

5-15 y/o. Most are still ambulant in their 20’s.

273
Q

What cardiac problems might someone with becker muscular dystrophy have?

A
  • Arrhythmia.

- Cardiomyopathy.

274
Q

Describe the pathophysiology of becker muscular dystrophy.

A

In frame mutations mean dystrophin is still produced but it is defective/shortened.

275
Q

Describe the inheritance pattern of myotonic dystrophy.

A

Autosomal dominant.

276
Q

Describe the pathophysiology of myotonic dystrophy.

A

Tri-nucleotide repeats: CTG expansion in non-coding region of DMPK -> down-steam affects -> mis-splicing of proteins -> Cl channel gene (CLCN1) affected -> myotonia.

Myotonic dystrophy is a SPLICEOPATHY!

277
Q

Give 5 adult onset symptoms of myotonic dystrophy.

A
  1. Myotonia - delayed relaxation after contraction, hard to release grasp after shaking hands.
  2. DISTAL muscle weakness.
  3. Cataracts.
  4. Male hypogonadism.
  5. Frontal baldness.
  6. Diabetes.
  7. Cardiac problems.
278
Q

What is the treatment for myotonic dystrophy?

A
  • Supportive care.
  • Treat cardiac problems.
  • Anti-convulsants for myotonia.
279
Q

What is myotonia?

A

Delayed muscle relaxation after contraction. Characteristic sign - unable to release grasp after shaking hands.

280
Q

What is dopamine produced from?

A

Tyrosine -> L-dopa -> dopamine.

281
Q

Describe the pathophysiology of parkinson’s disease.

A

There is a loss of dopamine producing neurones in the substantia nigra.

282
Q

Where does the substantia nigra project to?

A

The striatum.

283
Q

Describe the symptoms of parkinson’s disease.

A
  1. Bradykinesia - problems with doing up buttons, writing smaller, small steps/shuffling, walking slowly, reduced arm swing.
  2. Rigidity - pain, problems turning in bed.
  3. Resting tremor.
  4. Postural instability.
  5. Depression, psychiatric problems, dementia.
284
Q

Would you describe the symptoms of parkinson’s disease as symmetrical or asymmetrical?

A

One side is always worse than the other - the symptoms are asymmetrical.

285
Q

You ask a patient who you suspect might have PD to walk up and down the corridor so that you can assess their gait. What features would be suggestive of PD?

A
  • Stooped posture.
  • Asymmetrical arm swing.
  • Small steps.
  • Shuffling.
286
Q

Describe the treatment for PD.

A

Symptomatic treatment - compensate for the loss of dopamine.

  • L-dopa.
  • Dopamine agonists.
  • COMT/MAO inhibitors.
287
Q

What site does brain stimulation affect?

A

The sub-thalamic nucleus.

288
Q

Give 3 signs of normal pressure hydrocephalus.

A
  1. Magnetic gait.
  2. Incontinence.
  3. Dementia.
289
Q

Describe the treatment for essential tremor.

A
  • Beta blockers.

- Primidone.

290
Q

Describe the inheritance pattern seen in huntington’s disease.

A

AD inheritance.

291
Q

In huntington’s disease, what area of the basal ganglia and what neurotransmitter are affected?

A
  • Striatum (caudate nucleus).

- GABA.

292
Q

Name a thrombolytic drug that can be used in the treatment of ischaemic stroke.

A

Alteplase.

293
Q

How does alteplase work?

A

It converts plasminogen to plasmin and so promotes the break down of a fibrin clot.

294
Q

What is alteplase used for?

A

Thrombolysis in someone with an ischaemic stroke.

295
Q

When can you do thrombolysis in someone with an ischaemic stroke?

A

Up to 4.5 HOURS post onset of symptoms.

296
Q

Give 2 histopathological signs of Parkinson’s disease.

A
  1. Lewy bodies.

2. Loss of dopaminergic neurones in the substantia nigra.

297
Q

Give an example of a dopamine agonist.

A

Ropinirole, cabergoline.

298
Q

Give an example of a MAO inhibitor.

A

Selegiline.

299
Q

Name 3 groups of people who are at increased risk of a sub-dural haematoma.

A
  1. Elderly people.
  2. Alcoholics.
  3. Shaken babies.
300
Q

Why are elderly people and alcoholics at increased risk of a sub-dural haematoma?

A

Both of these groups have cerebral atrophy which leads to an increased tension on cerebral veins.

301
Q

What triplet code is repeated in Huntington’s disease?

A

CAG triplet repeat.

> 39 repeats = HD.

302
Q

Give 2 early signs of Huntington’s disease.

A
  1. Irritability.
  2. Depression.
  3. Personality change.
303
Q

Give 3 later signs of Huntington’s disease.

A
  1. Chorea - fidgety.
  2. Psychiatric problems.
  3. Dementia.
304
Q

Describe the pathophysiology behind myasthenia gravis.

A

Myasthenia gravis is an autoimmune disorder. Auto-antibodies (IgG) attach to Ach receptors and destroy them -> fewer action potentials fire -> muscle weakness and fatigue.

305
Q

Give 2 symptoms of myasthenia gravis.

A

Muscle weakness and fatigue.

306
Q

What investigations might you do it see if someone has myasthenia gravis?

A
  1. Serum anti-Ach receptor antibodies.

2. Ask the patient to count to 50.

307
Q

Give an example of an acute neuroapthy.

A

Guillain-barré syndrome.

308
Q

What can cause Guillain-barré syndrome?

A

Often post-infection e.g. following CMV, EBV, campylobacter jejuni infection.

309
Q

Describe the symptoms seen in Guillain-barré syndrome.

A

ASCENDING muscle weakness, changes in sensation/pain.

310
Q

What nerve is affected in carpal tunnel syndrome?

A

The median nerve.

311
Q

Give 3 risk factors for carpal tunnel syndrome.

A
  1. Pregnancy.
  2. Obesity.
  3. RA.
  4. Hypothyroidism.
  5. Acromegaly.
312
Q

What investigations might you do in someone who you suspect has carpal tunnel syndrome?

A

Tinnel’s and Phalen’s test.

313
Q

What are the 4 stages of a seizure?

A
  1. Prodromal - often emotional signs.
  2. Aura.
  3. Ictal.
  4. Post-ictal - often drowsy and confused.
314
Q

Give an example of a polyneuropathy.

A

Guillain-barré syndrome.

315
Q

MND: give 3 limb onset symptoms.

A
  1. Weakness.
  2. Clumsiness.
  3. Wasting of muscles.
  4. Foot drop.
  5. Tripping.
316
Q

MND: give 3 bulbar onset symptoms.

A
  1. Dysarthria.
  2. Slurred speech.
  3. Dysphagia.
  4. Wasting and fasciculation of the tongue.
317
Q

MND: give 3 respiratory onset symptoms.

A
  1. Dyspnoea.
  2. Orthopnoea.
  3. Poor sleep.
318
Q

What is the treatment for Alzheimer’s disease?

A

Supportive care.

AChE inhibitors e.g. galantamine.

319
Q

What is the treatment for raised ICP?

A

Osmotic diuresis with mannitol.

320
Q

What are the 4 main signs seen in PD?

A
  1. Resting tremor.
  2. Bradykinesia.
  3. Postural instability.
  4. Rigidity.
321
Q

What auto antibodies might be present in someone with myasthenia gravis?

A
  1. Anti-AChR antibodies.

2. Antibodies against tyrosine kinase - anti-MuSK antibodies.

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