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Phase 2a flashcards (Alec's) > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a transient ischemic attack?

A

Ischemia, without infarction which resolves within 24 hours

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2
Q

Which artery supplies the anterior circulation and which the posterior of the brain?

A
  • Anterior = internal carotid
  • Posterior = vertebral arteries
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3
Q

Which circulation do the majority (90%) of TIAs affect?

A

Anterior circulation (embolism travels through internal carotid)

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4
Q

What are some risk factors for stroke (8)?

A
  • Old
  • Smoking
  • T2DM
  • Hypertension
  • Obesity
  • Hypercholestrolaemia
  • AF
  • VSD + other heart defects
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5
Q

What deficit is seen in an occluded anterior cerebral artery?

A

Weak/ numb contralateral leg

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6
Q

What deficits are seen in an occluded middle cerebral artery (2)?

A
  • Weakness/ numbness contralateral body/ face
  • Dysphasia (can’t speak properly -temporal)
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7
Q

What deficits are seen in an occluded posterior cerebral artery (1)?

A

Contralateral visual changes

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8
Q

What part of the vision is often spared and why during a PCA occlusion?

A

Macular sparring - macular is represented at the occipital pole and can receive collateral blood flow from middle cerebral artery

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9
Q

What deficits are seen in an occluded vertebral artery (2)?

A
  • Cranial nerve lesions (3-12)
  • Limb ataxia (clumsiness)
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10
Q

What is amaurosis fugax?

A

Transient vision loss in one or both eyes

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11
Q

When would amaurosis fugax occur (3)?

A
  • Vascular origin (ophthalmic artery blocked - comes off internal carotid)
  • Occular origin
  • Neurological origin (nerve lesion)
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12
Q

How is a TIA investigated?

A
  • Clinically by symptoms, usually quite obvious, resolves within 10-15 minutes (can’t differentiate from stroke till after recovery)
  • CT head - rule out haemorrhagic stroke
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13
Q

How is TIA treated?

A
  • Acutely = aspirin 300mg
  • Long term prophylaxis = clopidogrel + atorvastatin
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14
Q

What is a stroke?

A

Focal neurological deficit lasting 24+ hours with infarction

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15
Q

What percentage of strokes are ischemic?

A

85%

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16
Q

Which “brain bleeds” are considered strokes?

A
  • Intracererbal
  • Subarachnoid
    (Sub/epi dural not considered strokes)
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17
Q

What are some risk factors for an ischemic stroke (9)?

A
  • Old
  • Smoking
  • T2DM
  • Hypertension
  • Obesity
  • Hypercholestrolaemia
  • AF
  • VSD + other heart defects
  • TIA
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18
Q

What are the symptoms of a stroke?

A

Same as TIA

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19
Q

What is a lacunar stroke?

A

Block in arteries that supply deep brain structures e.g. thalamus, pons

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20
Q

What are the symptoms of a lacunar stroke (1)?

A

Weakness/ lack of coordination on one side of body

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21
Q

How is an ischemic stroke diagnosed?

A
  • CT head
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22
Q

How is an ischemic stroke treated?

A
  • If within 4.5 hours –> thrombolytic
  • Aspirin for 2 weeks
  • Prophylactic clopidogrel + atorvastatin
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23
Q

What thrombolytic is given for ischmemic strokes?

A

Alteplase

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24
Q

How does alteplase break down clots?

A

Tissue plasminogen activator (activates plasminogen to plasmin)

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25
Q

What are some risk factors for intracerebral bleeds (5)?

A
  • Trauma
  • Hypertension
  • Aneurisms
  • Tumours
  • Anticoagulants (e.g. warfarin)
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26
Q

How is a haemorrhagic stroke investigated generally (2)?

A
  • CT head - midline shift, high ICP
  • Lumbar puncture - if CT negative
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27
Q

What are some signs/ symptoms of intracerebral bleed (4)?

A
  • Seizures
  • Weakness
  • Vomiting
  • Reduced consciousness
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28
Q

What scale accesses conciseness?

A

Glasgow coma scale (3-15)

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29
Q

How is intracererbal haemorrhage treated?

A

Neuro referal - usually surgery

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30
Q

What are the layers of the skull and brain?

A

Skin –> periosteum –> cranium –> dura –> arachnoid –> pia

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31
Q

Where is CSF located in the meninges?

A

Sub-arachnoid space

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32
Q

Which vessels lie in the subarachnoid space?

A

Circle of willis

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33
Q

What is a berry aneurysm?

A

Round out pouching of an artery at the base of the brain (in the circle of willis)

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34
Q

What is the most common site for a berry aneurysm?

A

Anterior communicating artery

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35
Q

What are some risk factors for subarachnoid haemorrhages (7)?

A
  • Marfans/ EDS
  • Hypertension
  • PKD
  • Trauma
  • Older
  • Family history
  • Alcohol/ cocaine
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36
Q

What are the signs/ symptoms of subarachnoid headache (5)?

A
  • Thunderclap headache (sudden occipital)
  • Meningism
  • N + V
  • Reduced GCS
  • CN 3/6 palsies
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37
Q

What sometimes occurs before a subarachnoid haemorrhage?

A

Sentinel headache - days/ weeks before rupture

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38
Q

How is subarachnoid haemorrhage investigated (3)?

A
  • CT head - shows bleed
  • Lumbar puncture
  • CT angiogram - localise point of bleeding
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39
Q

What shape is a subarachnoid haemorrhage?

A

Spider web in centre of brain

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40
Q

What is performed if the CT head is negative for bleeding in a SAH?

A

Lumbar puncture

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41
Q

What would a lumbar puncture show if there was a subarachnoid haemorrhage (2)?

A
  • Xanthochromia (bilirubin in CSF due to breakdown of RBCs)
  • Raised RBC count
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42
Q

How is a subarachnoid haemorrhage treated?

A

Neurosurgey

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43
Q

What is a common surgical treatment for subarachnoid haemorrhage?

A

Endovascular coiling (catheter through arterial system)

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44
Q

What medication is used to prevent vasospasm in subarachnoid haemorrhage?

A

Nimodipine (CCB)

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45
Q

The rupture of which vessel is the most common cause of subdural haemorrhage?

A

Bridging veins

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46
Q

What are 2 risk factors/ causes of subdural haemorrhage?

A
  • Trauma
  • Atrophy of brain - e.g. in dementia (weakens vessels and widens subdural space)
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47
Q

What are the signs/ symptoms of subdural haemorrhage (4)?

A
  • Headache that keeps getting worse
  • N + V
  • Lower GCS
  • High ICP symptoms
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48
Q

Is a subdural haemorrhage fast or slow onset and why?

A

Slower because bridging vein is lower pressure than arteries

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49
Q

What are some symptoms/ signs of high ICP (3)?

A
  • Cushings triad
  • Papilloedema
  • CN3/6 palsy
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50
Q

What are the three parts of Cushing’s triad?

A
  • Bradycardia
  • Increased pulse pressure
  • Irregular breathing
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51
Q

What shape is a subdural haemorrhage on a CT?

A

Banana shape

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52
Q

How can you tell on CT if a subdural haemorrhage is acute, subacute or chronic?

A
  • Acute = hyperdense
  • Subacute = isodense (same colour as brain tissue)
  • Chronic = hypodense
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53
Q

How is subdural haemorrhage treated?

A

Surgery (craniotomy/ burr hole) to allow swelling

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54
Q

What medication is used to treat high ICP?

A

Mannitol

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55
Q

Rupture of which vessel often causes extradural haemorrhage?

A

Middle meningeal artery

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56
Q

What age does extradural haemorrhage typically affect?

A

Younger adults (20-30)
dura more firmly adhered in older people

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57
Q

Why does risk of extradural haemorrhage decrease as you age?

A

Dura more firmly adhered to the skull

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58
Q

What is the cause of most extradural haemorrhage?

A

Trauma

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59
Q

What are some signs/ symptoms of extradural haemorrhage?

A
  • Headache that keeps getting worse
  • N + V
  • Lower GCS
  • High ICP symptoms
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60
Q

What is a typical presentation after trauma for people who develop extradural haemorrhage?

A

They feel fine –> then ICP builds up and they feel acutely unwell

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61
Q

How does a haematoma result in increased ICP?

A

Clot haemolysed –> becomes osmotically active –> water moves into brain + swells

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62
Q

How can high ICP lead to respiratory arrest?

A

Cerebellar tonsil herniation –> compression of respiratory centre in PONS

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63
Q

What shape does an extradural haemorrhage form on a CT?

A

Lemon shaped (biconvex)

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64
Q

How is an extradural haemorrhage treated (2)?

A
  • Surgery
  • Mannitol
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65
Q

Give 3 types of primary headaches?

A
  • Tension
  • Migraine
  • Cluster
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66
Q

Give 6 causes of secondary headaches?

A
  • Giant cell arteritis
  • Infection
  • Sub-arachnoid haemorrhage
  • Trauma
  • Cerebrovascular diseases (e.g. strokes, aneurysms)
  • ENT problems
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67
Q

What is the most common type of recurrent headache?

A

Migraine

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68
Q

Which gender is most commonly affected by migraines?

A

Females

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69
Q

What age range is most commonly affected by migraines?

A

< 40

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70
Q

What are the 3 stages in the development of a migraine?

A

Prodrome –> Aura –> Throbbing headache

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71
Q

What is prodrome in the development of a migraine?

A

Change in mood before attack

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72
Q

What is an aura in the development of a migraine?

A

Visual/ sensory changes minutes before an attack

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73
Q

What are some symptoms of migraines (5)?

A
  • Unilateral moderate-severe throbbing pain
  • Motion sickness
  • N + V
  • Photophobia/ phonophobia
  • Facial weakness
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74
Q

As well as presence of symptoms, what is also important to be done for a diagnosis of migraine?

A

Negative neurological examination

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75
Q

How are migraines treated acutely (2)?

A
  • Triptan (serotonin receptor agonists)
  • Other analgesics
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76
Q

How are migraines treated prophylactically (2)?

A
  • Propanolol (topiramate in asthmatics)
  • TCA e.g. amitriptyline = 2nd line
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77
Q

What is important to check in women of child bearing age with migraines?

A

Take them off oral contraceptive pill (increases risk of stroke)

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78
Q

Give some examples of triggers for migraines (5)?

A
  • Over/under sleeping
  • Caffeine
  • Alcohol
  • Dehydration
  • Bright lights
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79
Q

What are some risk factors for cluster headaches (3)?

A
  • Male
  • Smoking
  • Genetics/ family history
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80
Q

What sort of pain and where is it felt in a cluster headache?

A

Unilateral excruciating periorbital (around eye) pain

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81
Q

What are some other features of a cluster headache?

A
  • Ptosis
  • Red swollen watering eye
  • Rinorrhoea (watery nose)
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82
Q

How frequently do cluster headaches attack and how long do they last, typically?

A
  • 15 min - 3 hours
  • 3-4 attacks a day then pain free period
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83
Q

How many cluster headache attacks are often required for diagnosis?

A

5 or more

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84
Q

How are cluster headaches treated?

A
  • Acutely = triptan (serotonin receptor agonist)
  • Prophylaxis = verapamil
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85
Q

What class of drug is verapamil?

A

CCB

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86
Q

What is the most common primary headache disorder?

A

Tension headache

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87
Q

What are 2 triggers for tension headaches?

A
  • Stress
  • Stagnant head/ neck position
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88
Q

What pain is felt in tension headaches?

A

Bilateral, tight, band like pain around forehead, temples and back of head/neck

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89
Q

Are other symptoms such as motion sickness and N+V present in those with tension headaches?

A

NOOOOOO

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90
Q

How are tension headaches treated?

A

Analgesics

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91
Q

What cause shooting/ stabbing pain in the face?

A

Trigeminal neuralgia

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92
Q

What are three risk factors for trigeminal neuralgia?

A
  • Multiple sclerosis
  • Older age
  • Female
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93
Q

Where can trigeminal neuralgia affect?

A

Any combination of trigeminal nerve branches: ophthalmic (V1), mandibular (V3), maxillary (V2)

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94
Q

What medication is used to treat trigeminal neuralgia?

A

Carbamazepine (anticonvulsant)

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95
Q

What is another treatment for trigeminal neuralgia?

A

Surgery (decompression)

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96
Q

What type of disease is giant cell arteritis?

A

Large vessel vasculitis

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97
Q

What are some signs/ symptoms of giant cell arteritis (3)?

A
  • Unilateral tender scalp/ temples
  • Intermittent jaw claudication
  • Amaurosis fugax
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98
Q

What features would be present in a biopsy positive for giant cell arteritis?

A

Granulomatous non-caseating inflammation of media + intima with skip lesions

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99
Q

What blood findings are common in those with GCA?

A
  • Anaemia (normocytic, normochromic)
  • High ESR/ CRP
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100
Q

How is GCA treated?

A

PREDNISOLONE

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101
Q

What is a seizure?

A

Transient episode of abnormal electrical activity in the brain?

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102
Q

What are 9 causes for seizures?

A
  • Vascular
  • Infection
  • Trauma
  • Autoimmune - e.g. SLE
  • Metabolic
  • Idiopathic
  • Neoplasms
  • Dementia/ drugs
  • Eclampsia (pre-eclampsia + seizures)
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103
Q

What specific type of seizure is classed as epilepsy?

A

Idiopathic seizure

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104
Q

What is required for a diagnosis of epilepsy to be made?

A

2 seizures < 24 hours apart (without a cause)

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105
Q

What are two risk factors for epilepsy?

A
  • Family history
  • Dementia
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106
Q

What are three ways an epileptic seizure can be differentiated from a non-epileptic seizure?

A

In epileptic seizures…
* Eyes are often open
* Synchronous movements
* Happen at night

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107
Q

What is thought may be the cause of epilepsy?

A

Imbalances between GABA (inhibitory) and glutamate (stimulatory) - increased glutamate compared to GABA

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108
Q

How long does an epileptic seizure typically last?

A

< 2 minutes

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109
Q

What are the 4 phases of epileptic seizures?

A

Prodrome –> Aura –> Ictal event –> Post-ictal period

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110
Q

How does an aura before an epileptic fit often present (2)?

A
  • Deja vu
  • Lip smacking (automatism)
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111
Q

How are epileptic seizures classified depending on the part of the brain affected?

A
  • Generalised - bilateral + loss of consciousness
  • Focal - features confined to one region
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112
Q

What are 5 types of generalised epileptic seizures?

A
  • Tonic-clonic (grand mal)
  • Absence (petit mal)
  • Tonic
  • Myoclonic
  • Atonic
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113
Q

What are the features of a tonic-clonic seizure (3)?

A
  • Tonic phase (1st) = rigidity, fall to floor
  • Clonic phase (2nd) = jerking of limbs
    + incontinence, tongue bitten
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114
Q

What is the main feature of an absence seizure?

A

Moment of staring off into space (seconds to minutes)

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115
Q

What age do absence seizures most commonly affect?

A

Children

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116
Q

What feature is seen on an EEG in absence seizures?

A

3 Hz spike

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117
Q

What is the main feature of tonic seizures?

A

Rigid body

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118
Q

What is the main feature of myoclonic seizures?

A

Just jerking limbs

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119
Q

What is the main feature of atonic seizures?

A

Sudden floppy limbs + muscles

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120
Q

What are the two types of focal seizure?

A
  • Simple focal
  • Complex focal
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121
Q

What is the difference between simple and complex focal seizures?

A

Simple maintain conciseness, complex loose conciseness

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122
Q

What are the symptoms of a focal seizure in each hemisphere of the brain?

A
  • Temporal = aura + dysphasia
  • Frontal = repeated muscle twitching/ paralysis
  • Parietal = parenthesis in limbs
  • Occipital = vision changes
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123
Q

What are two neurological phenomena that occur with frontal lobe seizure?

A
  • Jacksonian marching (repeated twitching)
  • Todds palsy (paralysis)
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124
Q

What extra brain structure is usually involved in complex focal seizures when the patient loses consciousness?

A

Basal ganglia

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125
Q

How is epilepsy investigated?

A
  • MRI (check for structural issues)
  • Bloods (check for metabolic/ infection causes)
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126
Q

What is the first line drug for generalised seizures?

A

Sodium valproate

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127
Q

What is the first line drug for focal seizures?

A

Carbamazepine

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128
Q

Who must sodium valproate not be given to?

A

Pregnant women (teratogenic - interferes with folic acid)

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129
Q

What epileptic drug is used for those who are pregnant?

A

Lamotrigine

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130
Q

What is a complication of epilepsy?

A

Status epilepticus

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131
Q

What is status epileptics defined as?

A
  • Seizures > 5 minutes
  • > 3 seizures in one hour
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132
Q

How is status epileptics treated?

A
  • Lorazepam (benzodiazepine)
  • If not worked, then phenytoin
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133
Q

What is the second most common neurodegenerative condition after dementia?

A

Parkinsons disease

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134
Q

What causes Parkinson’s disease?

A

Loss of dopaminergic neurones from the substantial nigra pars compactica

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135
Q

What are 3 risk factors for Parkinson’s disease?

A
  • Family history
  • Males
  • Older age
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136
Q

What is protective against Parkinson’s disease?

A

SMOKING

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137
Q

Draw out the direct and indirect pathways in the basal ganglia

A

Direct: cortex (+) –> striatum (-) –> GPi and SNpr (-) –> thalamus (+) –> cortex
Indirect: cortex (+) –> striatum (-) –> GPe (-) –> STN (+) –> SNpr and GPi (-) –> thalamus (+) –> cortex

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138
Q

How does substantial nigra pars compactica affect the indirect/ direct pathways?

A
  • Direct = stimulatory (via D1 neurones)
  • Indirect = inhibitory (via D2 neurones)
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139
Q

What is the effect of the indirect and direct pathway on muscle movement?

A
  • Direct = stimulator
  • Indirect = inhibitory
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140
Q

Therefore a lack of dopaminergic neurones will increase or decrease muscle inhibition?

A

Increase muscle inhibition therefore more difficult to initiate movement

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141
Q

What are 4 typical features of parkinsons?

A
  • Bradykinesia
  • Unilateral resting tremor
  • Rigidity
  • Postural instability
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142
Q

What are some features of bradykinesia when walking (3)?

A
  • Stooped posture
  • Reduced arm swing
  • Shuffling gait
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143
Q

Does Parkinson’s typically affect both or one side?

A

One side (particularly at the beginning)

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144
Q

How is parkinsons diagnosed?

A

Clinically, by a specialist

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145
Q

How is parkinsons treated when moderate-severe?

A

L-DOPA (levodopa)

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146
Q

How is parkinsons treated in more mild disease?

A
  • Da agonist
  • Monoamine oxidase - B inhibitors
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147
Q

What condition is often confused with parkinsons?

A

Benign essential tremor

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148
Q

What is a significant difference between benign essential tremor and parkinsons (in terms of the tremor)?

A

Bilateral in benign essential tremor

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149
Q

Which dementia often causes Parkinson like symptoms?

A

Lewy body dementia

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150
Q

What are the 4 main types of dementia?

A
  • Alzheimers (60%)
  • Vascular
  • Lewy body
  • Frontotemporal
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151
Q

How does Alzheimers cause dementia?

A

Beta amyloid proteins accumulate as plaques and tau neurofibrillary triangles –> death of brain cells

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152
Q

What are two risk factors for Alzheimers?

A
  • Downs syndrome (inevitable due to gene mutation)
  • Family history
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153
Q

What are some symptoms of Alzheimer’s (3)?

A

Affects whole brain
* Agnosia - can’t recognise
* Apraxia - can’t move
* Aphasia - cant speak

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154
Q

How is Alzheimers treated?

A

Cholinesterase inhibitors (e.g. galantamine)

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155
Q

What causes vascular dementia?

A

Lots of small (or big) infarcts of brain tissue

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156
Q

What is the pattern of deterioration in vascular dementia?

A

Stepwise - as more tissue damaged e.g. by TIA

157
Q

What causes levy body dementia?

A

Lewy body accumulation in cortex

158
Q

What is the main constituent of Lewy bodies?

A

Alpha synuclein

159
Q

What are the symptoms of Lewy body dementia (2)?

A
  • Cognitive decline
  • Parkinsonism
160
Q

The collection of what protein leads to fronto-temporal dementia?

A

Tau protein/ pick body

161
Q

What sometimes causes frontotemporal dementia?

A

Autosomal dominant mutation in tau protein

162
Q

What are the symptoms of frontotemporal dementia (2)?

A
  • Frontal = thinking + memory affected
  • Temporal = speech + language affected
163
Q

What tool helps with dementia diagnoses?

A

Mini mental state exam (normal > 25)

164
Q

What investigation is sometimes done I those with dementia?

A

MRI head

165
Q

What other conditions can also cause dementia (4)?

A
  • SLE
  • Infection
  • Neoplasm
  • Hydrocephalus
    Many others
166
Q

What pattern is Huntington’s chorea inherited?

A

Autosomal dominant

167
Q

What gene is affected in Huntington’s chorea?

A

HTT gene on chromosome 4

168
Q

What is the mutation found in people with Huntingtons?

A

Trinucleotide repeat disorder of CAG

169
Q

How many repeats of CAG are required for a person to develop huntingtons?

A

35 <

170
Q

What changes in the development of huntingtons disease are seen from generation to generation?

A

Anticipation - symptoms present:
* Earlier
* More severely

171
Q

How often is the genotype expressed in the phenotype for Huntington’s chorea?

A

100% FULL penetrance

172
Q

What are the signs/ symptoms of Huntington’s chorea (5)?

A
  • Chorea (limb jerking)
  • Dementia
  • Psychiatric issues
  • Depression
  • Dysphagia + dysarthria (speech problems)
173
Q

How is Huntingtons chorea diagnosed?

A
  • Family history + clinically
  • Genetic testing (if wanted)
174
Q

How can chorea be treated in those with huntingtons?

A
  • Valproic acid
  • Benzodiazepines (diazepam)
175
Q

How can depression be treated in huntingtons?

A

SSRIs (fluoxetine)

176
Q

How is psychosis treated in those with huntingtons chorea?

A

Risperidone

177
Q

What is multiple sclerosis?

A

Chronic and progressive demyelination of neurones in the CNS

178
Q

What are the two types of myelin producing cells?

A
  • CNS = oligodendrocytes
  • PNS = Schwann cells
179
Q

Which type of cell does multiple sclerosis affect and which protein that is produced by this cell?

A

Oligodendrocytes (myelin basic protein)

180
Q

What sort of hypersensitivity reaction is MS?

A

Type 4 (cell mediated)

181
Q

What are some risk factors for MS (5)?

A
  • Female
  • Other autoimmune diseases
  • Family history
  • EBV
  • 20-40
182
Q

What are the four patterns of MS disease?

A
  • Clinically isolated syndrome
  • Relapsing-remitting
  • Primary progressive
  • Secondary progressive
183
Q

What is the difference between primary and secondary progressive MS?

A

Secondary were initially presenting as relapsing-remitting at point of diagnosis

184
Q

How are MS lesions/ progression of the disease often described?

A

Disseminated in time and space

185
Q

What are the symptoms of MS (5)?

A
  • Parasthesia
  • Blurred vision
  • Eye movement disorder
  • Weakness
  • Ataxia
186
Q

What are some signs of MS (4)?

A
  • Optic neuritis
  • UMN signs
  • Lhermittes sign
  • Charcot neurological triad
187
Q

What is Lhermittes sign?

A

Electric shock sensation with neck flexion (in MS)

188
Q

What is Charcot neurological triad?

A
  • Dysarthria
  • Nystagmus
  • Intention tremor
    For MS
189
Q

What is usually the first presenting sign/ symptom of MS?

A

Optic neuritis (blurred vision)

190
Q

What diagnostic criteria is used for MS?

A

McDonald criteria

191
Q

What investigations are often does for those with MS?

A

MRIs

192
Q

How are relapses of MS treated?

A

Methylprednisolone

193
Q

What medications are used for long term prophylaxis for MS?

A

DMARD/ biologic (e.g. beta interferon)

194
Q

What are UMN lesion signs/ symptoms (4)?

A
  • Hyper-reflexia
  • Weakness
  • Spasticity/ hypertonia
  • Positive Babinski sign
195
Q

What is Babinski sign?

A

Toes extend when foot stoked

196
Q

What is spasticity?

A

Muscles rigid with movement

197
Q

What are LMN lesion signs/ symptoms (5)?

A
  • Hypo-reflexia
  • Weakness
  • Muscle waisting/ hypotonia
  • Negative Babinski sign
  • Fasciculations
198
Q

What is a fasciculation?

A

Muscle twitching

199
Q

What is motor neurone disease?

A

Progressive degeneration of upper and lower motor neurones (with a variety of causes, many unknown)

200
Q

What is the main tract responsible for movement?

A

Corticospinal tract

201
Q

What part of the brain is responsible for idea of movement?

A

Association cortexes e.g. premotor cortex

202
Q

Where does activation of the upper motor neurone originate from?

A

Motor cortex

203
Q

Which parts of the brain modulate motor control (2)?

A
  • Basal ganglia - turn signals on/ off
  • Cerebellum - fine control of movement
204
Q

What are some risk factors for MND?

A
  • Family history/ genetics (5-10% inherited)
  • Male
205
Q

What gene has been associated with MND?

A

SOD-1 gene mutation

206
Q

What parts of the body/ functions are never affected by MND (3)?

A
  • Eyes
  • Sensory function
  • Sphincters
207
Q

What are 4 types of MND?

A
  • ALS - 80% (amyotrophic lateral sclerosis)
  • Progressive bulbar palsy
  • Progressive muscular atrophy
  • Primary lateral sclerosis
208
Q

What are 3 features of amyotrophic lateral sclerosis?

A
  • UMN + LMN lesions
  • Can have corticobulbar involvement
  • SOD-1 mutation (associated)
209
Q

Which cranial nerves are affected in progressive bulbar palsy?

A

CN 9-12
(Upper + lower involvement)

210
Q

What are the main symptoms of progressive bulbar palsy?

A

Breathing/ swallowing/ talking difficulties

211
Q

What neurones are affected in progressive muscular atrophy?

A

Lower motor neurones - distal muscles affected first

212
Q

Which neurones are affected in primary lateral sclerosis?

A

Upper motor neurones

213
Q

How is MND diagnosed?

A

Clinically (electromyography shows fibrillation potentials - in muscles)

214
Q

What medication can be used to slow the progression of motor neurone disease?

A

Riluzole

215
Q

What is meningitis?

A

Inflammation of the meninges

216
Q

What action do you need to take as a doctor if a patient has meningitis?

A

Notify public health England

217
Q

What is the most common class of pathogen in infective meningitis?

A

Viruses

218
Q

What are 3 viruses that infect the meninges?

A
  • Enteroviruses
  • Herpes simplex virus - 2
  • Varicella zoster virus
219
Q

What is an example of an enterovirus?

A

Coxsackie

220
Q

What are 2 bacteria that infect the meninges the most in people over 3 months?

A
  • S. pneumoniae
  • N. meningitidus
221
Q

What bacteria often infects the meninges of older (over 60) and younger (under 3 months)?

A

Listeria

222
Q

What is the most common meningitis causing bacteria in neonates (0-3 months)?

A

Group B alpha haemolytic strep (s. agalactiae)

223
Q

What 4 bacteria often causes meningitis in neonates?

A
  • E. coli
  • S. pneumoniae
  • Group B alpha haemolytic strep
  • Listeria
224
Q

What bacteria has decreased in the prevalence of meningitis due to vaccinations?

A

H. influenzae

225
Q

What sort of bacteria is N. meningitidus?

A

Gram -ve diplococcus

226
Q

What sort of rash does N. meningitidus cause?

A

Non-blanching purpuric rash

227
Q

What sort of bacteria is S. pneumoniae?

A

Gram + ve diplococcus in chains

228
Q

What sort of bacteria is group b alpha haemolytic strep?

A

Gram +ve coccus in chains

229
Q

Why is group b alpha haemolytic strep the most common cause of neonatal meningitis?

A

It colonises the maternal vagina

230
Q

What sort of bacteria is listeria?

A

Gram +ve bacillus

231
Q

What are the main 3 symptoms of meningitis?

A
  • Headache
  • Neck stiffness
  • Photophobia
232
Q

What are 3 signs of meningitis?

A
  • Kernig sign
  • Brudzinski sign
  • Pyrexia
233
Q

What is kerning sign?

A

Can’t extend knee when hip is flexed

234
Q

What is brudzinski sign?

A

Knees + hips automatically flex when neck flexed

235
Q

How is meningitis diagnosed?

A

Lumbar puncture + CSF analysis

236
Q

Where is a lumbar puncture done?

A

L3/L4

237
Q

When is a lumbar puncture contraindicated?

A

High ICP

238
Q

What is the appearance of bacterial viral and fungal/TB meningitis?

A
  • Bacterial = cloudy yellow
  • Viral = normal
  • Fungal/ TB = cloudy fibrous
239
Q

What leukocytes are common in bacterial viral and fungal/TB meningitis?

A
  • Bacterial = neutrophilia
  • Viral = lymphocytosis
  • Fungal/ TB = lymphocytosis
240
Q

What is the protein levels in bacterial, viral and fungal/TB meningitis?

A
  • Bacterial = high
  • Viral = normal
  • Fungal/ TB = high
241
Q

Why is protein high in bacterial and fungal/ TB meningitis?

A

Waste product of those pathogens

242
Q

What are the glucose levels in bacterial, viral and fungal/ TB meningitis?

A
  • Bacterial = low
  • Viral = normal
  • Fungal/ TB = low
243
Q

How is meningitis treated in hospital?

A

Ceftriaxone/ cefotaxime + steroids (dexamethasone)

244
Q

What antibiotic is given for meningitis if listeria is suspected?

A

Amoxicillin

245
Q

What antibiotic is given IM to people in the GP if meningitis is suspected?

A

Benzylpenicillin

246
Q

What antiviral is used for the treatment of some meningitis?

A

Aciclovir

247
Q

What prophylactic antibiotic is given to those deemed closed contacts of those diagnosed with meningitis?

A

Ciprofloxacin

248
Q

What are some complications of meningitis (3)?

A
  • Meningococcal septicaemia (DIC) - causes rash
  • Hearing loss
  • Adrenal insufficiency
249
Q

What is the most common cause of encephalitis?

A

Viral infections

250
Q

What are some other less common causes of encephalitis (3)?

A
  • Parasitic
  • Autoimmune
  • Fungal
    Rarely bacterial
251
Q

What is a parasite that can cause encephalitis?

A

Toxoplasma gondii (toxoplasmosis - from CATS 🐱)

252
Q

Who is most at risk of encephalitis?

A

Immunocompromised + very young/ old

253
Q

What are some symptoms of encephalitis (4)?

A
  • Fever
  • Headache
  • Focal neuropathy (e.g. aphasia)
  • Seizures
254
Q

How is encephalitis investigated (2)?

A
  • Lumbar puncture = lymphocytosis
  • MRI head
255
Q

How is the viral cause of encephalitis found?

A

PCR testing of CSF

256
Q

How is encephalitis treated?

A

Aciclovir

257
Q

What are 4 types of brain tumour?

A
  • Astrocytoma (90%)
  • Oligodendrocytoma
  • Meningioma
  • Schwannoma
258
Q

Which cancers most commonly metastasise to brain (3)?

A
  • Lung cancers
  • Breast cancer
  • Melanoma
259
Q

How are astrocytomas graded?

A

1-4 (by WHO)

260
Q

What is grade 4 astrocytoma known as?

A

Glioblastoma

261
Q

What is a glioma?

A

Cancer of glial cells (oligodendrocytes, microglial cells or astrocytes)

262
Q

What are the signs/ symptoms of a brain tumour (5)?

A
  • Cushing’s triad (high ICP)
  • Seizures
  • Lethargy + weight loss
  • Focal neurology
  • Occipital headaches (due to high ICP)
263
Q

How is a brain tumour diagnosed?

A

MRI

264
Q

How are brain tumours treated (3)?

A
  • Surgery
  • Chemo
  • Steroids (reduce tumour size)
265
Q

What are the three types of paralysis and what sort of lesion would cause them??

A
  • Hemiplegia = lesion in the brain (half the body paralysed)
  • Paraplegia = lesion in the spinal cord (legs paralysed)
  • Quadriplegia = lesion in spinal cord (both legs + arms)
266
Q

Where does the spinal cord end?

A

L1/2

267
Q

What is found at the end and after the spinal cord (3 anatomical things)?

A
  • Conus medularis
  • Cauda equina
  • Filum teminale
268
Q

What are the main ascending tracts?

A
  • DCML
  • Spinothalamic
  • Spinocerebellar
269
Q

What does DCML carry?

A
  • Fine touch
  • Vibration
  • Proprioception
270
Q

Describe the pathway of the DCML?

A
  • 1st order –> medulla (in gracile (T6 below legs) and cuneatus (arms) fasiculata)
  • 2nd order –> decussate –> thalamus
  • 3rd order –> sensory cortex
271
Q

What does spinothalamic carry?

A
  • Anterior = crude touch + pressure
  • Lateral = pain + temperature
272
Q

Describe the pathway of the spinothalamic tract?

A
  • 1st order –> ipsilateral dorsal horn
  • 2nd order –> decussate immediately –> contralateral thalamus
  • 3rd order –> sensory cortex
273
Q

What does the spinocerebellar tract carry?

A

Unconscious proprioception

274
Q

What are the main descending tracts?

A
  • Corticospinal
  • Corticobulbar
275
Q

What do the descending tracts carry?

A

Motor information

276
Q

Describe the path of the corticospinal tract?

A
  • Upper neurones - lateral tract (decussate in medulla); anterior tract (decussate just before point of synapse)
  • Lower neurones - travel to muscle
277
Q

What is the difference in terms of the muscles supplied by the lateral and anterior corticospinal tracts?

A
  • Anterior = axial muscles
  • Lateral = extremities
278
Q

What is the corticobulbar tract?

A

The cranial nerves

279
Q

Where does the knee jerk reflex go to in the spinal cord?

A

L3/4

280
Q

Where does the big toe jerk reflex go to in the spinal cord?

A

L5

281
Q

Where does the ankle jerk reflex go to in the spinal cord?

A

S1

282
Q

What is brown squared syndrome?

A

Hemisection of the spinal cord

283
Q

What are the symptoms of brown sequard syndrome?

A
  • Ipsilateral motor control loss
  • Ipsilateral proprioception + 2 point discrimination loss
  • Contralateral pain + temp loss
284
Q

What is myelopathy?

A

Spinal cord compression

285
Q

What are two causes of myelopathy?

A
  • Neoplasms
  • Disco prolapse/ herniation
    Lots of other spinal pathologies
286
Q

What are some signs/symptoms of myelopathy?

A
  • Progressive leg weakness
  • UMN signs
  • Sensory loss below lesions
287
Q

How are myelopathies investigated?

A

MRI spine

288
Q

How are myelopathies treated?

A

Surgery

289
Q

What two surgical procedures are used to treat myelopathies?

A
  • Microdiscectomy (removal of small part of disc)
  • Laminectomy (removal of some of vertebral bone)
290
Q

What is cauda equina syndrome?

A

Compression below conus medularis

291
Q

What can cause cauda equina syndrome (4)?

A
  • Herniated disc
  • Tumours
  • Trauma
  • Abscess
292
Q

What do the nerves of the cauda equina supply?

A
  • Motor/ sensory function of lower limbs
  • Parasympathetic to bladder and rectum
293
Q

What are the signs/ symptoms of cauda equina (4)?

A
  • Leg weakness
  • LMN signs
  • Saddle anaesthesia (perianal numbness)
  • Bladder/ bowel dysfunction + sphincter involvement
294
Q

How is cauda equina diagnosed?

A

MRI cord

295
Q

How is cauda equina treated?

A

Treat underlying cause, e.g:
* Spinal fixation
* Microdiscectomy

296
Q

What is peripheral neuropathy?

A

Nerve damage/ pathology outside of the CNS

297
Q

What are the mechanisms that can damage nerves?

A
  • Demyelination
  • Axonal damage
  • Nerve compression
  • Infarction
  • Wallerian degeneration
298
Q

What is Wallerian degeneration?

A

Nerve lesion, dies distally

299
Q

What is mononeuritis multiplex?

A

Several individual nerves affected

300
Q

What are some causes of mononeuritis multiplex (4)?

A
  • T2DM
  • Vasculitis
  • RA
  • Infections
301
Q

What is carpal tunnel syndrome?

A

Pressure on median nerve passing through the carpal tunnel

302
Q

What are the nerve roots of the median nerve?

A

C6 - T1

303
Q

What are some risk factors/ causes of carpal tunnel syndrome (5)?

A
  • Hypothyroidism
  • Acromegally
  • Obesity
  • RA
  • Strain
304
Q

What are the symptoms of carpal tunnel (3)?

A
  • Hand weakness
  • Thenar eminence waisting
  • Parasthesia
305
Q

How is carpal tunnel investigated?

A
  • Tinsel test
  • Phalen test
  • Electymyography (EMG)
306
Q

What is tinsels test?

A

Tapping wrist where median nerve is causes pain/ tingling

307
Q

What is Phalens test?

A

Flexing wrist (wrists opposite of praying) causes numbness/ pain

308
Q

How is carpal tunnel syndrome treated?

A
  • Wrist splint at night (extent wrist)
  • Steroid injections
  • Surgery decompression
309
Q

What would cause wrist drop?

A

Radial nerve palsy (C5 - T1)

310
Q

Which muscles does the radial nerve innervate which causes wrist drop?

A

Extensor muscles

311
Q

What causes claw hand?

A

Ulna nerve palsy (C8 - T1)

312
Q

How are ulna and radial nerve palsy treated?

A

Splints

313
Q

What is sciatica?

A

Irritation/ damage to sciatic nerve

314
Q

What are the sciatic nerve roots?

A

L4 - S3

315
Q

What can cause sciatica (4)?

A
  • IV disc herniation/ prolapse
  • Piriformis syndrome
  • Tumours
  • Trauma
316
Q

What is piriformis syndrome?

A

Muscle in buttock spasms and irritates sciatic nerve

317
Q

What are the symptoms/ signs of sciatica (2)?

A

*Shooting pain down from buttock to lateral leg
* Weakness in leg + foot

318
Q

How is sciatica investigated?

A
  • Clinically - can’t do strait leg raise
  • MRI - check for possible causes
319
Q

How is sciatica treated (3)?

A
  • Analgesia + steroids
  • Amitriptyline
  • Surgery
320
Q

Where do polyneuropathies typically affect?

A

Peripheries (glove and stocking distribution)

321
Q

What causes a mostly motor polyneuropathy?

A

Guillain barre syndrome

322
Q

What causes a mostly sensory polyneuropathy?

A

Diabetic neuropathy

323
Q

What bacteria is a common cause of guillain barre syndrome?

A

Campylobacter jejuni

324
Q

What is thought to cause diabetic neuropathy (2)?

A
  • Microvascular disease
  • Oxygen free radicals
325
Q

What are some other causes of polyneuropathies (2)?

A
  • Vasculitis
  • Vitamin B12 deficiency (damage myelin sheaf)
    GBS and diabetes on previous cards
326
Q

What would a CN3 lesion present as (3)?

A
  • Ptosis
  • Down + out eye position
  • Fixed dilated pupil
327
Q

What would a CN4 lesion present as (1)?

A

Can’t look down (and inwards)
Rare, due to trauma

328
Q

What would a CN5 lesion present as (3)?

A
  • Jaw deviates towards affected side
  • Loss of corneal reflex
  • Trigeminal neuralgia
329
Q

What would a CN6 lesion present as (1)?

A

Can’t abduct eye
Sign of high ICP

330
Q

What would CN7 lesion present as (1)?

A

Drooping of one side of face (no forehead sparing)

331
Q

What may cause a CN7 lesion?

A

Bells palsy

332
Q

What would a CN8 lesion present as (2)?

A
  • Hearing loss
  • Loss of balance
333
Q

What often causes a CN8 lesion?

A

Skull change - compression of internal acoustic meatus

334
Q

What would a CN 9+10 lesion present as (2)?

A
  • Impaired gag reflex
  • Uvula deviation
335
Q

What would CN11 lesion present as (1)?

A

Can’t shrug shoulders/ turn head against resistance

336
Q

What would CN12 lesion present as (1)?

A

Tongue deviation towards side of lesion

337
Q

What is myasthenia gravis?

A

Autoimmune response at neuro-muscular junction against post synaptic receptor

338
Q

What type of hypersensitivity reaction is myasthenia gravis?

A

Type 2

339
Q

Who is most commonly affected by myasthenia gravis (2 groups)?

A
  • Women under 40
  • Men over 60
340
Q

What has myasthenia gravis been connected to?

A

Thyoma (thymus tumour) - stimulate production of auto-antibodies

341
Q

What two types of antibodies are found in those with myasthenia gravis?

A
  • Anti nicotinic Ach-R antibodies
  • Anti MuSK (muscle specific kinase) antibodies
342
Q

How do Anti Ach-R antibodies cause pathology in myasthenia gravis (2)?

A
  • Competitively bind to Ach nicotinic receptors
  • Activate compliment system –> receptor destruction
343
Q

How do Anti MuSK antibodies cause pathology in myasthenia gravis?

A
  • Activate compliment system –> receptor destruction
  • MuSK helps synthesise Ach-R –> less Ach-R expression
344
Q

When is myasthenia gravis worse in the day?

A

At the end of the day (worse with exertion - as more Ab binding)

345
Q

Where do symptoms of myasthenia gravis usually begin?

A

Head and neck –> lower body

346
Q

What are some signs/ symtpoms of myasthenia gravis (4)?

A
  • Diplopia (due to eye muscle weakness)
  • Ptosis
  • Swallowing + speech difficulties
  • Lopsided smile
347
Q

How is myasthenia gravis diagnosed (2)?

A
  • Serology (Ab presence detected)
  • Edrophonium (tensilon) test
348
Q

What is the edrophonium (tensilon) test - how does it work?

A

Edrophonium administered –> inhibits breakdown Ach-ase –> more Ach available –> weakness relieved

349
Q

How is myasthenia gravis treated (2)?

A
  • Ach-ase inhibitors (neostigmine)
  • Immunosurpression (steroids)
350
Q

What is an example of an ACH-ase inhibitor?

A

Neostigmine
pyridostigmine

351
Q

What is a complication of myasthenia gravis?

A

Myasthenia crisis - muscle weakness –> resp failure

352
Q

How is myasthenic crisis treated (2)?

A
  • Plasma exchange
  • IV Ig
    both remove harmful Abs from circulation
353
Q

What is a differential diagnosis of myasthenia gravis?

A

Lambert eaton syndrome

354
Q

What are the differences between Lambert eaton syndrome and myasthenia gravis (3)?

A

Lambert eaton …
* Pre-synaptic Ca++ channel autoimmune pathology
* Improves with exertion
* Start at extremities

355
Q

What is the treatment for Lambert eaton syndrome?

A

Similar treatment (steroids + immunosuppression)

356
Q

What is Guillain barre syndrome?

A

Destruction of Schwann cells in PNS (basically MS in PNS)

357
Q

What pathogens commonly cause GBS?

A
  • Campylobacter jejuni (MOST common)
  • CMV
  • EBV
358
Q

How does infection cause GBS?

A

Molecular mimicry (organism and schwann cell antigens similar)

359
Q

What is the presentation of GBS (2)?

A
  • Ascending symmetrical muscle weakness
  • Reduced reflexes
360
Q

What is a dangerous complication of GBS?

A

Respiratory failure

361
Q

How is GBS investigated?

A
  • Nerve conduction studies - reduced impulses
  • CSF analysis
362
Q

What is found in CSF analysis in GBS (2)?

A
  • High protein levels (=inflammation)
  • No WBC
363
Q

How is GBS managed (3)?

A
  • IV Ig (target schwann cell Abs)
  • Plasma exchange
  • Intubation if difficulty breathing
364
Q

What is wernickes encephalopathy?

A

Lesions in the CNS caused by vitamin B1 (thiamine) deficiency

365
Q

What causes wernickes encephalopathy?

A

High alcohol consumption

366
Q

What are 3 classical symtpoms of wernickes encephalopathy?

A
  • Ataxia
  • Confusion
  • Opthalmoplegia (lesions in eye movement nerves)
367
Q

How is wernickes encephalopathy diagnosed (2)?

A
  • Clinically
  • Supported by microcytic anaemia + deranged LFTs
368
Q

How is wernickes encephalopathy treated?

A

Pabrinex (vit B1 + others)

369
Q

What is a complication of wernickes encephalopathy?

A

Korsakoff syndrome (irreversible damage - memory disorder)

370
Q

How is duchennes muscular dystrophy inherited?

A

X-linked recessive
Pystrophin gene

371
Q

What is the pathophysiology of DMD?

A

Muscle replaced with adipose tissue

372
Q

Who is affected by DMD?

A

Almost exclusively boys

373
Q

What are 2 symptoms of DMD?

A
  • Difficulty getting up
  • Skeletal deformities
374
Q

How is DMD diagnosed?

A

Genetic testing (often prenatally)

375
Q

What is charcot marie tooth syndrome?

A

Inherited autosomal dominant that causes sensory + motor polyneuropathy

376
Q

What gene is affected by Charcot marie tooth syndrome?

A

Duplicated PUP 22 gene (chromosome 17)

377
Q

What are the symptoms of Charcot Marie tooth syndrome (3)?

A
  • Foot drop + weaknesses
  • Thin calves
  • Hammer toe!!!
378
Q

How is charcot marie tooth diagnosed?

A
  • Genetic testing
  • Nerve biopsy
379
Q

What sort of bacteria is clostridium tetani?

A

Gram +ve bacilli

380
Q

How can you get tetanus?

A

Dirty soil + rusty metal

381
Q

How does tetanus cause tetany?

A

Tetanospasmin toxin produced –> travels retrogradely up axons –> muscle spasms

382
Q

How is tetanus prevented?

A

Vaccine !!!

383
Q

What virus causes chicken pox?

A

Varicella zoster virus

384
Q

What causes shingles?

A

Reactivation of varicella zoster virus (usually in adulthood)

385
Q

What causes sensory defects in shingles?

A

Dorsal root of peripheral nerves attacked

386
Q

What are the main symptoms of shingles?

A
  • Painful erythromatous blistering rash (confined to dermatome)
  • Tingling + pain in area of rash
387
Q

How can shingles/ chicken pox be treated?

A

Aciclovir

388
Q

What causes creutzfeldt Jakob disease?

A

Prions (misfiled proteins)

Phase 2a flashcards (Alec's) (13 decks)

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