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Phase2a > Neurology > Flashcards

Neurology Flashcards

1
Q

Why can the parasympathetic fibres of the oculomotor nerve become paralysed without the motor fibres?

A

They lie on the outside of the nerve.

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2
Q

Why are 3rd cranial nerve palsies common?

A

The nerve lies over the apex of the petrous part of the temporal bone.

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3
Q

What are the signs of a 3rd parasympathetic nerve palsy?

A

Fixed dilated pupil.

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4
Q

What separates the posterior cranial fossa (cerebellum) from the cerebrum?

A

Tentorium

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5
Q

What is the consequence of the foramen of Magendie or the foramina of Lushka getting blocked?

A

Obstructive hydrocephalus

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6
Q

Give two signs of cerebellar syndrome.

A
  • Ataxia

- Nystagmus

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7
Q

If the cerebellum is injured, is the deficit ipsilateral or contralateral?

A

Ipsilateral

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8
Q

What is the brainstem bound by superiorly and inferiorly?

A

SUPERIORLY
- thalamus and internal capsule

INFERIORLY
- spinal cord

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9
Q

How is the cerebellum ‘connected’ to the rest of the brain?

A

Via peduncles connecting to the brainstem.

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10
Q

Which dorsal column carries sensation from the lower limbs?

A

Fasiculus gracilis (medial)

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11
Q

Which dorsal column carries sensation from the upper limbs?

A

Fasiculus cuneatus (lateral)

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12
Q

What sensations does the DCML pathway carry?

A
  • Proprioception
  • Fine touch
  • Vibration
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13
Q

Where does the DCML decussate?

A

Medulla

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14
Q

What sensations does the spinothalamic tract carry?

A

ANTERIOR
- Crude touch

LATERAL

  • Pain
  • Temperature
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15
Q

Where do the spinothalamic tracts decussate?

A

2-3 levels above entry to the spinal cord

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16
Q

Where does the corticospinal tract decussate?

A

ANTERIOR
- Just before they exit the spinal cord

LATERAL
- Pyramids of medulla

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17
Q

What does the anterior corticospinal tract innervate?

A

Proximal muscles (trunk)

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18
Q

What does the lateral corticospinal tract innervate?

A

Muscles of the limbs

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19
Q

What does the corticobulbar tract innervate?

A

Head and neck muscles

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20
Q

Give five functions of the reticular activating system.

A
  • Alertness
  • Sleep/wake
  • REM/nonREM sleep
  • Respiratory centre
  • Cardiovascular drive
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21
Q

Give two brain structures associated with the reticular activating system.

A
  • Peri-aqueductal grey

- Floor of fourth ventricle

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22
Q

Give seven criteria for brainstem death.

A
  • Absent pupillary reflexes
  • Absent corneal reflex
  • Absent caloric vestibular reflex
  • Absent cough reflex
  • Absent gag reflex
  • Absent respirations
  • No response to pain
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23
Q

Describe Aa nerve fibres (size, myelination, what information do they carry?).

A
  • Large
  • Myelinated
  • Proprioception
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24
Q

Describe Ab nerve fibres (size, myelination, what information do they carry?).

A
  • Large
  • Myelinated
  • Light touch, pressure, vibration
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25
Q

Describe Adelta nerve fibres (size, myelination, what information do they carry?).

A
  • Small
  • Myelinated
  • Cold and pain
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26
Q

Describe C nerve fibres (size, myelination, what information do they carry?).

A
  • Small
  • Unmyelinated
  • Warmth and pain
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27
Q

Give six mechanisms of nerve damage.

A
  • Demyelination
  • Axonal damage
  • Wallerian degeneration
  • Compression
  • Infarction
  • Infiltration
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28
Q

What would a nerve conduction study show in demyelinated nerves?

A

Slower conduction velocities

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29
Q

What would a nerve conduction study show in axonal damage?

A

Reduced amplitudes of potentials

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30
Q

Is demyelination or axonal damage more common?

A

Axonal damage

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31
Q

What causes wallerian nerve degeneration?

A

Section of a nerve

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32
Q

What does nerve compression result in?

A

Focal demyelination

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33
Q

Describe what causes infarction of a nerve and give two conditions in which it occurs.

A

Infarction of vasa nervosum in vasculitis and diabetes.

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34
Q

Give seven general causes of axonal peripheral neuropathies.

A
  • Systemic diseases
  • Inflammatory
  • Infectious
  • Ischaemic
  • Metabolic
  • Hereditary
  • Toxins
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35
Q

Give 11 systemic diseases that can cause axonal damage.

A
  • Diabetes mellitus
  • B12 deficiency
  • Coeliac disease
  • Chronic kidney disease
  • Excessive alcohol
  • Hypothyroidism
  • Amyloidosis
  • Connective tissue disease
  • Paraproteinaemia
  • Paraneoplastic syndrome
  • Critical illness polyneuropathy
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36
Q

Give three infections that may cause axonal peripheral neuropathies.

A
  • Hepatitis
  • HIV
  • Lyme
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37
Q

Give a condition which makes mononeuropathies more common.

A

Diabetes

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38
Q

Give three mononeuropathies, and the nerves which are involved.

A
  • Carpel tunnel syndrome (median nerve)
  • Ulnar neuropathy (ulnar nerve)
  • Peroneal neuropathy (peroneal nerve)
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39
Q

Which cranial nerves most common are affected in mononeuropathies?

A

III and VII

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40
Q

What is the most common cause of a mononeuropathy?

A

Focal demyelination

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41
Q

What do the sensory symptoms of a peripheral neuropathy depend on?

A

Which fibres (Aa, Ab, Adelta, C) are lost

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42
Q

What is ataxia?

A

Poor balance

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43
Q

What two methods can cause ataxia?

A
  • Sensory (loss of Aa proprioception)

- Cerebellar

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44
Q

How can you tell the difference between sensory and cerebellar ataxia?

A

When sensory, ataxia gets worse with the eyes closed or in the dark.

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45
Q

Give five motor symptoms of peripheral neuropathy.

A
  • Muscle cramps
  • Weakness
  • Fasciculations
  • Atrophy
  • Absent reflexes
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46
Q

What is a radiculopathy?

A

A neuropathy affecting the nerve roots.

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47
Q

Give three patterns of peripheral neuropathies.

A
  • Symmetrical sensorimotor
  • Asymmetrical sensory
  • Asymmetrical sensorimotor
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48
Q

Which is the most common pattern of peripheral neuropathies?

A

Symmetrical sensorimotor

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49
Q

Which nerve fibres are affected first in symmetrical sensorimotor neuropathies?

A

Long fibres

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50
Q

Describe the presentation of symmetrical sensorimotor neuropathies.

A

Initially starts with sensory features affecting fingers and toes, and eventually motor symptoms develop.

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51
Q

What is another name for asymmetrical sensory neuropathies?

A

Sensory ganglionopathy

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52
Q

Describe where the symptoms are felt in asymmetrical sensory neuropathies.

A

Patchy distribution

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53
Q

What nerve structure is affected in asymmetrical sensory neuropathies?

A

Dorsal root ganglia

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54
Q

Give three conditions that are associated with asymmetrical sensory neuropathies.

A
  • Paraneoplastic syndromes
  • Sjogren’s
  • Coeliac disease
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55
Q

Give another name for asymmetrical sensorimotor neuropathy.

A

Mononeuritis multiplex

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56
Q

Give four conditions that are associated with asymmetrical sensory motor neuropathies.

A
  • Vasculitis
  • Diabetes
  • Sarcoidosis
  • Amyloidosis
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57
Q

What three aspects of the clinical examination are important in peripheral neuropathies?

A
  • Reduced or absent tendon reflexes
  • Sensory deficit
  • Weakness/muscle atrophy
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58
Q

What special investigation can be used to assess peripheral neuropathies?

A

Neurophysiological examination (nerve conduction studies)

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59
Q

Give three features of chronic idiopathic axonal polyneuropathy.

A
  • Develops over at least 6 months
  • No aetiology can be identified
  • Axons are affected (most commonly in proportion to length)
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60
Q

Give two examples of immune-mediated chronic demyelinating peripheral neuropathies.

A
  • Chronic inflammatory demyelinating polyneuropathy (CIDP)

- Multifocal motor neuropathy (MMN)

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61
Q

Give two examples of genetic chronic demyelinating peripheral neuropathies.

A
  • Charcot Marie Tooth Disease

- Hereditary sensory and autonomic neuropathies

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62
Q

What is Charcot Marie Tooth disease also known as?

A

Peroneal muscular atrophy

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63
Q

Name an acute polyneuropathy.

A

Gullian Barre syndrome

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64
Q

What mechanism usually causes Gullian Barre syndrome?

A

Usually demyelinating, but occasionally can be axonal.

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65
Q

What causes Gullian Barre syndrome?

A

Immune mediated, usually after GI infection (eg. Campylobacter)

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66
Q

Describe the clinical presentation of Gullian Barre syndrome.

A

Rapid ascending paralysis and sensory deficits, usually occurring over a few days.

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67
Q

What is the treatment for Gullian Barre Syndrome?

A

IMMEDIATE IV Ig or plasma exchange.

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68
Q

Give three approaches to the treatment of peripheral neuropathies.

A
  • Treat pain
  • Treat cramps
  • Improve balance
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69
Q

What can be used to treat cramps in peripheral neuropathies?

A

Quinine

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70
Q

What is the treatment for chronic inflammatory demyelinating polyneuropathy?

A

IV Ig/plasma exchange in flare ups, + long term steroids.

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71
Q

What is meningitis?

A

Inflammation of the meninges

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72
Q

Give three non-infective causes of meningitis.

A
  • Paraneoplastic
  • Drug side effects
  • Autoimmune (vasculitis, SLE)
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73
Q

Give three causative organisms of meningitis in neonates.

A
  • Listeria
  • Group B Strep
  • E.coli
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74
Q

Give three causes of meningitis in children.

A
  • Neisseria meningitidis
  • Strep.pneumoniae
  • Hib
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75
Q

Give two causes of meningitis in adults.

A
  • Neisseria meningitidis

- Strep.pneumoniae

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76
Q

Give three causes of meningitis in the elderly.

A
  • Neisseria meningitidis
  • Strep.pneumoniae
  • Listeria
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77
Q

What is the condition called if Neisseria meningitidis is found in the blood culture?

A

Meningococcal septicaemia

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78
Q

Give three viruses that can cause acute meningitis.

A
  • Enterovirus
  • Herpes simplex virus
  • Varicella zoster virus
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79
Q

Give three organisms that can cause chronic meningitis.

A
  • Mycobacterium tuberculosis
  • Syphilis
  • Cryptococcus
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80
Q

Give four ways that infection can spread to the meninges.

A
  • Extracranial infection (nasal, otitis media, sinusitis)
  • Neurosurgical complications
  • Trauma
  • Bloodstream
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81
Q

Describe the pathophysiology of bacterial meningitis.

A
  • Bacteria enter CSF and replicate
  • Blood vessels dilate and allow WBC to enter CSF
  • This causes meningeal inflammation +/- brain swelling
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82
Q

What are the symptoms of meningitis?

A
  • Fever
  • Headache
  • Neck stiffness (meningism)
  • Photophobia
  • Leg pains
  • Cold hands and feet
  • May develop neurological signs
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83
Q

What is the management of meningitis if the patient presents to primary care?

A
  • IM benzylpenicillin

- Send to hospital

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84
Q

Describe the immediate management of suspected meningitis in hospital.

A
  • Assess GCS
  • Blood cultures
  • Broad spectrum antibiotics
  • Steroids (IV dexamethosone)
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85
Q

Why are steroids given in suspected meningitis?

A

They reduce brain swelling and neurological sequelae

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86
Q

What empirical antibiotics should be given in suspected meningitis?

A

Ceftriaxone/Cefotaxime

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87
Q

Describe the reasoning behind the choice of empirical antibiotics in meningitis.

A

Cephalosporins are bactericidal and can cross BBB.

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88
Q

What empirical antibiotics should be given in meningitis if the patient has a penicillin allergy?

A

Chloramphenicol

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89
Q

What empirical antibiotics should be added (and why) for immunocompromised patients with suspected meningitis?

A

Amoxicillin for Listeria

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90
Q

What empirical antibiotics (and why) should be added in suspected meningitis in patients with a recent history of travel?

A

Vancomycin for penicillin resistant Strep pneumoniae

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91
Q

What investigation should be carried out in suspected meningitis, and what further investigations should be carried out on the sample obtained?

A

Lumbar puncture

  • Microscopy
  • Gram stain
  • Culture
  • Protein
  • Glucose
  • Viral PCR
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92
Q

Give three contraindications to lumbar puncture in suspected meningitis.

A
  • Abnormal clotting
  • Petichial rash
  • Raised intracranial pressure
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93
Q

Give three unique clinical features of TB meningitis.

A
  • Weight loss
  • Night sweats
  • Insidious onset
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94
Q

What would you find on performing a lumbar puncture in cryptococcal meningitis?

A

High opening pressure

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95
Q

Describe the differences between the clinical features of bacterial and viral meningitis.

A

BACTERIAL may appear septic with focal neurology and rash.

VIRAL is less severe.

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96
Q

Give a group of patients more likely to get viral meningitis.

A

Small children

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97
Q

Describe the appearance of the CSF in bacterial meningitis.

A

Cloudy

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98
Q

Describe the appearance of the CSF in viral meningitis.

A

Clear

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99
Q

Describe the appearance of the CSF in TB meningitis.

A

Fibrin web

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100
Q

Describe the appearance of the CSF in cryptococcal meningitis.

A

Fibrin web

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101
Q

What cells would be seen on CSF microscopy in bacterial meningitis?

A

Neutrophils

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102
Q

What cells would be seen on CSF microscopy in viral meningitis?

A

Lymphocytes

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103
Q

What cells would be seen on CSF microscopy in TB meningitis?

A

Lymphocytes

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104
Q

What cells would be seen on CSF microscopy in cryptococcal meningitis?

A

Lymphocytes

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105
Q

What stain would be used to see cryptococcus on CSF microscopy?

A

India Ink

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106
Q

Describe the CSF protein levels in meningitis.

A

high

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107
Q

Which type of meningitis will show a normal (instead of low) CSF glucose?

A

Viral

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108
Q

Give six differential diagnoses of meningitis.

A
  • Subarachnoid haemorrhage
  • Migraine
  • Flu/other viral illness
  • Sinusitis
  • Brain abscess
  • Malaria
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109
Q

What is the mortality rate in treated meningitis?

A

5%

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110
Q

What percentage of patients with treated meningitis will have permanent effects?

A

20%

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111
Q

Give five complications of bacterial meningitis.

A
  • Skin scars
  • Amputation
  • Hearing loss
  • Seizures
  • Brain damage
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112
Q

Who should be called in cases of meningitis?

A

Public health

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113
Q

How are close contacts of patients with Neisseria meningitidis treated?

A

Antibiotic prophylaxis of ciprofloxacin or rifampicin

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114
Q

What is encephalitis?

A

Inflammation of the brain

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115
Q

What is the most common cause of encephalitis?

A

Herpes simplex

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116
Q

How does Herpes simplex cause encephalitis?

A

Reactivation in the trigeminal ganglion

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117
Q

Give nine causes of encephalitis.

A
  • Herpes simplex
  • Varicella zoster
  • Measles
  • Mumps
  • Rubella
  • EBV
  • HIV
  • CMV
  • Coxsackie
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118
Q

Is encephalitis usually bacterial or viral?

A

Viral

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119
Q

Give four causes of encephalitis that are associated with travel.

A
  • Japanese encephalitis virus
  • Tick-borne encephalitis
  • Rabies
  • West Nile
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120
Q

Give two non-infective causes of encephalitis.

A
  • Autoimmune

- Paraneoplastic

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121
Q

Describe the clinical presentation of encephalitis.

A
  • Preceding flu-like illness hours to days before
  • Altered GCS (confusion, drowsiness, coma)
  • Fever
  • Seizures
  • Memory loss
  • May have meningism
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122
Q

What investigations should be carried out in encephalitis?

A
  • MRI head +/- EEG
  • Lumbar puncture
  • HIV test
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123
Q

What is the treatment for encephalitis?

A
  • Mostly supportive (neurorehab)

- Aciclovir if HSV or VZV

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124
Q

What is tetanus and what organism is it caused by?

A

Clinical syndrome caused by Clostridium tetani

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125
Q

How is tetanus contracted by humans?

A

Through skin

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126
Q

Where is Clostridium tetani found?

A

Globally in soil

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127
Q

What is the incubation period for Clostridium tetani?

A

8 days

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128
Q

What are the two toxins produced by Clostridium tetani, and what are their effects?

A
  • Tetanolysin (tissue destruction)

- Tetanospasmin (clinical tetanus)

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129
Q

Describe the pathophysiology of tetanus.

A
  • Tetanospasmin toxin travels retrogradely along axons
  • Interferes with neurotransmitter release to increase neurone firing
  • Unopposed muscle contraction and spasm
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130
Q

Give two presentations of generalised tetanus.

A
  • Risus sardonicus (facial muscles)

- Opisthotonos (whole body)

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131
Q

What is it called if tetanus only affects the muscles around the injury?

A

Localised tetanus

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132
Q

Describe the management of tetanus.

A
  • Vaccinate if patient has risk injury
  • Supportive (muscle relaxants, paracetamol, cooling)
  • Immunoglobulin to mop up toxin
  • Metronidazole for residual bacteria
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133
Q

Is rabies a bacterial or viral infection?

A

Viral

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134
Q

Where is rabies found?

A

Saliva of animals (dogs, cats, foxes, bats)

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135
Q

How do humans catch rabies?

A

Inoculation through the skin (eg. Lick, bite, splash)

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136
Q

Where is there high risk of Rabies?

A

Parts of Africa and South East Asia

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137
Q

What is the incubation period for rabies?

A

Can be 2 weeks to years, depending on size and site of inoculation (virus has to get to CNS)

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138
Q

How does rabies affect nerves?

A

Travels retrogradely along them

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139
Q

Describe the presentation of rabies.

A
  • Paraesthesia around bite

- Furious or paralytic presentation once it reaches CNS

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140
Q

Describe the furious reaction to rabies.

A
  • Hydrophobic

- Aerophobic

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141
Q

What is the management for rabies?

A
  • Sedatives (fatal once symptomatic)

- Pre and post exposure prophylaxis (vaccination and immunoglobulin)

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142
Q

Is non-missile or penetrating head trauma more common?

A

Non-missile

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143
Q

Give four types of diffuse head trauma.

A
  • Diffuse axonal injury
  • Diffuse vascular injury
  • Hypoxia-ischaemia
  • Swelling
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144
Q

Give two focal head traumas affecting the scalp.

A
  • Contusions

- Lacerations

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145
Q

Give a focal head trauma involving the skull.

A

Fracture

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146
Q

Give two focal head traumas involving the meninges.

A
  • Infection

- Haemorrhage

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147
Q

Give four focal head traumas involving the brain.

A
  • Contusions
  • Lacerations
  • Haemorrhage
  • Infection
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148
Q

Define contusion.

A

A region of injured tissue/skin in which capillaries have been ruptured (a bruise).

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149
Q

Define laceration.

A

A deep cut or tear in skin or flesh.

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150
Q

Give three possible consequences of skull fracture.

A
  • Haematoma
  • Infection
  • Aerocele
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151
Q

Describe the type of skull fracture associated with pointed objects.

A

Localised fractures that are open or depressed.

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152
Q

Describe the skull fractures that can be caused by flat surfaces.

A

Linear fractures that can extend to skull base.

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153
Q

What can be used to work out the order that skull fractures were sustained?

A

New fracture lines don’t cross pre-existing fracture lines.

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154
Q

Which artery is often torn to form an extradural haematoma?

A

Middle meningeal artery

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155
Q

What other head injury is extradural haematoma usually associated with?

A

Skull fracture

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156
Q

Describe the rate of onset of extradural haematoma.

A

Occurs slowly (hours)

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157
Q

Describe the clinical presentation of an extradural haematoma.

A

Patient usually has a lucid interval before deterioration.

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158
Q

Give three consequences of an extradural haematoma.

A
  • Brain displacement
  • Raised intracranial pressure
  • Herniation
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159
Q

What vessels tear to cause a subdural haematoma?

A

Bridging veins which cross the subdural space.

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160
Q

Describe what causes acute and chronic subdural haematoma.

A
  • SLOW onset in elderly

- QUICK onset in trauma

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161
Q

What type of head trauma commonly causes subdural haematoma?

A

Acceleration/deceleration

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162
Q

Describe the appearance of subdural haematoma.

A

Usually surrounded by a membrane of granulation tissue.

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163
Q

Describe the severity of trauma required to cause a subdural haematoma in the elderly.

A

Can be caused by mild trauma

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164
Q

Give four causes of traumatic subarachnoid haematoma.

A
  • Contusions/lacerations
  • Base of skull fracture
  • Vertebral artery rupture/dissection
  • Intraventricular haemorrhage
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165
Q

What causes deep and superficial cerebral and cerebellar haemorrhage?

A

SUPERFICIAL - Severe contusion

DEEP - acceleration and deceleration (related to diffuse axonal injury)

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166
Q

What type of head injury commonly causes infection?

A

Skull fracture

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167
Q

What is a ‘coup’ contusion?

A

Contusion at the site of impact

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168
Q

What is a ‘contrecoup’ injury?

A

Injury away from the site of impact.

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169
Q

Where do most contrecoup injuries occur and why?

A

Base of the brain due to a more bumpy skull.

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170
Q

Describe how brain contusions change over time.

A
  • Haemorrhagic at first
  • Then become brown/orange and soft
  • Then indented or cavitated after months/years
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171
Q

When does laceration occur in relation to contusion?

A

Laceration occurs when contusion is severe enough to tear Pia Mater.

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172
Q

Give two diffuse brain lesions which take time to develop.

A
  • Swelling

- Hypoxia-ischaemia

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173
Q

Give two diffuse brain lesions which occur immediately on trauma.

A
  • Diffuse axonal injury

- Diffuse vascular injury

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174
Q

What is diffuse axonal injury?

A

Syndrome of widespread axonal damage. Can be caused by a variety of processes.

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175
Q

What head trauma usually causes diffuse traumatic axonal injury?

A

Acceleration and deceleration.

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176
Q

What does traumatic acceleration and deceleration of the head cause?

A

Tearing of long structures (blood vessels and axons)

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177
Q

Describe the prognosis of mild diffuse traumatic axonal injury.

A

Recovery of consciousness +/- long term deficit

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178
Q

Describe the prognosis of severe diffuse traumatic axonal injury.

A

Unconscious from impact and remain unconscious or severe disability.

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179
Q

Describe the histology of diffuse axonal injury.

A

Build up of transported materials due to tear in axon and degeneration of involved fibre tracts.

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180
Q

In what percentage of head injury patients does brain swelling occur?

A

75%

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181
Q

Give two consequences of brain swelling.

A
  • Raised intracranial pressure

- Hypoxic-ischaemic change

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182
Q

Give three mechanisms of brain swelling.

A
  • Congestive brain damage
  • Vasogenic oedema
  • Cytotoxic oedema
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183
Q

Describe congestive brain damage.

A

Vasodilation and increased cerebral blood volume.

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184
Q

Describe how vasogenic oedema causes brain swelling.

A

Extravasation from damaged blood vessels.

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185
Q

Describe how cytotoxic oedema causes brain swelling.

A

Increased water content of neurones and glia.

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186
Q

What is the prognosis for diffuse vascular injury in the brain.

A

Usually results in near immediate death.

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187
Q

Describe the appearance of diffuse vascular injury of the brain.

A

Multiple petechial haemorrhages throughout the brain.

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188
Q

Give two causes of brain herniation.

A
  • Bleeding

- Brain swelling

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189
Q

What is seen on radiology in brain herniation?

A

Midline shift

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190
Q

Give three types of brain herniation.

A
  • Subfalcine herniation of cingulate gyrus
  • Transtentorial herniation of medial temporal lobe
  • Transforaminal herniation of cerebellar tonsil
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191
Q

Give three risk factors for hypoxia-ischaemia of the brain.

A
  • Clinically evident hypoxia
  • Hypotension (<80mmHg for >15mins)
  • Raised intracranial pressure
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192
Q

Give two vulnerable regions where brain hypoxia-ischaemia may occur.

A
  • Susceptible neurones

- Border zones between major cerebral territories

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193
Q

How long after head injury does chronic traumatic encephalopathy occur?

A

Years

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194
Q

Describe the type of head injury that usually causes chronic traumatic encephalopathy.

A

Repetitive mild traumatic brain injury

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195
Q

Describe the initial presentation of chronic traumatic encephalopathy.

A
  • Irritability
  • Impulsivity
  • Aggression
  • Depression
  • Memory loss
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196
Q

Describe the later presentation of chronic traumatic encephalopathy.

A
  • Dementia
  • Gait problems
  • Speech problems
  • Parkinsonism
  • Some have motor neurone disease like symptoms
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197
Q

Give four parts of the brain that are atrophied in chronic traumatic encephalopathy.

A
  • Neocortex
  • Hippocampus
  • Diencephalon
  • Mamillary bodies
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198
Q

Describe the ventricles and septum pellucidum in chronic traumatic encephalopathy.

A
  • Enlarged ventricles

- Fenestrated septum pellucidum

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199
Q

Describe protein/plaque build up in chronic traumatic encephalopathy.

A
  • Tau-positive neurofibrillary and astrocytic tangles

- TDP-43 pathology

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200
Q

Give three regions of the brain where tau-positive neurofibrillary tangles accumulate in chronic traumatic encephalopathy.

A
  • Frontal/temporal cortex
  • Limbic regions
  • Depths of sulci and limbic regions
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201
Q

What is dementia?

A

A syndrome encompassing progressive deficits in several cognitive domains.

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202
Q

What is the most common first presentation of dementia?

A

Memory loss over months/years

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203
Q

Give three symptoms that may develop in later stage dementia.

A
  • Agitation
  • Aggression
  • Apathy
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204
Q

What is the most common cause of dementia?

A

Alzheimer’s dementia

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205
Q

What are the second and third most common causes of dementia?

A 
2nd = Vascular
3rd = Lewy bodies
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206
Q

Briefly describe the pathology of vascular dementia.

A

Cumulative effects of many small strokes.

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207
Q

Give a characteristic history in vascular dementia.

A

Sudden onset and stepwise deterioration.

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208
Q

What is fronto-temporal (Pick’s) dementia?

A

Frontal and temporal atrophy without Alzheimers.

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209
Q

Give twelve less common causes of dementia.

A
  • Hypothyroidism
  • Low B12/folate
  • Thiamine deficiency (alcohol)
  • Syphilis
  • Tumours
  • Subdural haematoma
  • Parkinson’s
  • CNS cysticercosis
  • HIV
  • Hydrocephalus
  • Whipple’s disease
  • Pellagra
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210
Q

Give four features of vascular/mixed dementia.

A
  • Attention difficulties
  • Motor/cognitive slowing
  • Executive problems
  • Visuo-spatial difficulties
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211
Q

Briefly describe the pathology in Dementia with Lewy bodies.

A

Intracytoplasmic Lewy bodies in the neurones.

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212
Q

Give five features of Dementia with Lewy bodies.

A
  • Fluctuating cognition
  • Pronounced disturbances in attention and concentration
  • Working memory and early visuospacial deficits
  • Visual hallucinations
  • Spontaneous Parkinsonism
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213
Q

What is Alzheimer’s disease?

A

A neurodegenerative disease characterised clinically by dementia and histopathologically by neuronal loss in the cerebral cortex in association with numerous amyloid plaques and neurofibrillary tangles.

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214
Q

What is a major component of neurofibrillary tangles?

A

Tau

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215
Q

What is the most common variant of Alzheimer’s dementia?

A

Amnesic

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216
Q

Describe the pattern of degeneration in the amnesic variant of Alzheimer’s dementia.

A

Early degeneration in medial temporal lobe, then spreads to temporal neocortex, frontal and parietal association regions.

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217
Q

Give five things that the temporal lobe is responsible for.

A
  • Hearing
  • Language comprehension
  • Semantic knowledge
  • Memory
  • Emotional/affective behaviour
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218
Q

Give three of the first features in amnesic Alzheimer’s dementia.

A
  • Selective amnesia
  • Semantic impairment
  • Language impairment
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219
Q

What is the second thing to be affected in amnesic Alzheimer’s dementia?

A

Attention (divided, selective, and attention switching)

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220
Q

What deficits appear in late stage amnesic Alzheimer’s dementia?

A
  • Visuospacial
  • Sustained attention
  • Executive functioning
  • Global deficits
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221
Q

Give three areas of the brain which may be affected in visual Alzheimer’s dementia.

A
  • Posterior occipitoparietal
  • Occipitotemporal
  • Primary visual cortex
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222
Q

Give five deficits experienced in visual Alzheimer’s dementia.

A
  • Visual deficits
  • Dyspraxia
  • Dysgraphia
  • Simultanagnosia
  • Eventuall global deficits
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223
Q

What area of the brain is affected in linguistic Alzheimer’s dementia?

A

Lateral temporal regions.

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224
Q

What is the deficit experienced in linguistic Alzheimer’s dementia?

A

Progressive aphasic syndrome.

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225
Q

Give four psychiatric changes which may occur later on in Alzheimer’s dementia.

A
  • Subtle behaviour changes
  • Apathy/disengagement
  • Psychotic symptoms (delusions/hallucinations)
  • Agitation/anxity
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226
Q

Give five behaviour changes which may occur in Alzheimer’s dementia.

A
  • Inattentiveness
  • Mild cognitive dulling
  • Social withdrawal
  • Emotional withdrawal
  • Agitation
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227
Q

Give three criteria in the history/examination of the patient for Alzheimer’s dementia.

A
  • Presence of early and significant memory impairment
  • Gradual and progressive change in memory function over more than 6 months
  • Objective evidence of amnesic syndrome of hippocampal type (based on performance of episodic memory test)
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228
Q

Give three pieces of in vivo evidence for Alzheimer’s dementia.

A
  • Decreased b-amyloid and increased T-tau/P-tau in CSF
  • Increased tracer retention on amyloid PET
  • AD autosomal dominant mutation present
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229
Q

Give three genes which are associated with Alzheimer’s dementia.

A
  • PSEN1
  • PSEN2
  • APP
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230
Q

How is Down’s Syndrome associated with Alzheimer’s dementia?

A

The APP gene which produces amyloid precursor protein is on chromosome 21 so people with Down’s syndrome will have more b-amyloid.

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231
Q

Give seven clinical criteria which can exclude Alzheimer’s dementia.

A
  • Sudden onset
  • Early occurrence of gait disturbances/seizures
  • Major and prevalent behaviour changes
  • Focal neurological features
  • Early extrapyramidal signs
  • Early hallucinations
  • Cognitive fluctuations
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232
Q

Give three specialised diagnostic tests for Alzheimer’s dementia.

A
  • Structural MRI
  • Amyloid imaging (PET)
  • Functional MRI
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233
Q

Give five ‘criteria’ for diagnosing amnesic prodrome (preclinical Alzheimer’s dementia).

A
  • Poor performance on episodic memory tests
  • General cognitive function preserved
  • Activities of daily living intact
  • No evidence of dementia
  • Score >24/30 on MMSE
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234
Q

Give nine lifestyle factors that may help to prevent Alzheimer’s dementia.

A
  • Smoking cessation
  • Healthy BMI
  • Healthy diet
  • Physical activity
  • Low alcohol
  • Socially active
  • Cognitively active
  • Control vascular risk factors
  • Treat mood/anxiety
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235
Q

Give two general categories of medication that can be used in Alzheimer’s dementia.

A
  • Acetlycholineesterase inhibitors

- Anti-glutamate

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236
Q

Give three examples of acetylcholineesterase inhibitors used in Alzheimer’s dementia.

A
  • Donepezil
  • Rivastigmine
  • Galantamine
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237
Q

Give an anti-glutamate medication that can be used in Alzheimer’s dementia.

A

Memantine

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238
Q

Give three differential diagnoses of Alzheimer’s dementia.

A
  • Vascular/mixed dementia
  • Dementia with Lewy bodies
  • Depressive pseudo-dementia
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239
Q

Compare the onset of dementia and depression.

A

DEMENTIA
- Vague, insidious onset

DEPRESSION
- Onset and decline often rapid (may follow trigger)

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240
Q

Compare the patient’s experience of symptoms in dementia and depression.

A

DEMENTIA
- Unaware or attempt to hide problems

DEPRESSION
- Patient complains of memory loss

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241
Q

Compare the patient’s mood in dementia and depression.

A

DEMENTIA
- Mood may be labile

DEPRESSION
- Patient distressed/unhappy

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242
Q

Describe the cognitive performance in dementia and depression.

A

DEMENTIA

  • Cognitive performance consistent
  • Attempts all questions

DEPRESSION

  • Variability in cognitive performance
  • ‘Don’t know’ answers
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243
Q

What is multiple sclerosis?

A

A relapsing and remitting demyelinating disease of the CNS in which episodes of neurological disturbance affect different parts of the CNS at different times.

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244
Q

At what age does MS usually begin?

A

20-40yrs

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245
Q

Describe and explain the geographical distribution of MS.

A

Much less common near equator, perhaps due to more vitamin D.

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246
Q

Is MS more common in white or black people?

A

White

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247
Q

Is MS more common in males or females?

A

Females

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248
Q

When might the potential for developing MS be established?

A

In early life (eg. A childhood virus)

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249
Q

Give nine conditions which may affect a person’s susceptibility for developing MS.

A
  • Race
  • Latitude
  • Age
  • Diet
  • Sanitation
  • Socioeconomic status
  • Multiple gene loci
  • Climate
  • Mutations
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250
Q

Describe the pathophysiology of MS.

A
  • Genetic susceptibility + environmental trigger activate autoreactive T lymphocytes
  • T cells activate B cells to produce autoreactive antibodies
  • Activated macrophages, T cells, antibodies, and complement cause inflammatory attack with demyelination
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251
Q

Describe Uhthoff’s Phenomenon.

A

Heat (eg. Hot shower, exercise) stresses the nerves and causes temporary decline in MS symptoms

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252
Q

Compare the presence of demyelination breakdown products in active and inactive MS.

A

ACTIVE
- Breakdown products present

INACTIVE
- Breakdown products absent

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253
Q

Compare the oligodendrocyte loss in active and inactive MS.

A

ACTIVE
- Variable oligodendrocyte loss

INACTIVE
- Variable oligodendrocyte loss

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254
Q

Compare the cell content of plaques in active and inactive MS.

A

ACTIVE
- Hypercellular plaque edge due to infiltration of tissue with inflammatory cells

INACTIVE
- Hypocellular plaque

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255
Q

Compare the inflammatory infiltrate in active and inactive MS.

A

ACTIVE
- Perivenous inflammatory infiltrate (mainly macrophages and T lymphocytes)

INACTIVE
- Variable inflammatory infiltrate

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256
Q

Compare blood-brain barrier disruption in active and inactive MS.

A

ACTIVE
- Extensive BBB disruption

INACTIVE
- Moderate to minor BBB disruption

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257
Q

Compare the gliosis of plaques in active and inactive MS.

A

ACTIVE
- Older plaques may have central gliosis

INACTIVE
- Plaques gliosed

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258
Q

Are most presentations of MS monosymptomatic or polysymptomatic?

A

Monosymptomatic

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259
Q

Describe the types of symptoms experienced in MS when the cerebral hemispheres are affected.

A

Large variety of symptoms, but also may be silent lesions.

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260
Q

Describe the types of symptoms experienced in MS when the spinal cord is affected.

A
  • Weakness
  • Paraplegia
  • Spasticity
  • Tingling
  • Numbness
  • Lhermitte’s sign
  • Bladder and sexual dysfunction
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261
Q

What is Lhermitte’s sign?

A

Feeling of ‘electric shock’ down spine upon bending head forward.

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262
Q

Describe the types of symptoms experienced in MS when the optic nerve is affected.

A
  • Impaired vision

- Eye pain

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263
Q

Describe the types of symptoms experienced in MS when the medulla and pons are affected.

A
  • Dysarthria
  • Double vision
  • Vertigo
  • Nystagmus
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264
Q

Describe the types of symptoms experienced in MS when the cerebellar white matter is affected.

A
  • Dysarthria
  • Nystagmus
  • Intention tremor
  • Ataxia
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265
Q

What are the typical signs/symptoms of MS?

A
  • Optic neuritis
  • Other cranial nerve symptoms
  • Spasticity
  • Weakness
  • Tremor
  • Ataxia
  • Sensory signs and symptoms (paraesthesiae, numbness)
  • Lhermitte’s sign
  • Nystagmus
  • Double vision
  • Vertigo
  • Bladder/sexual dysfunction
  • Cognitive problems and depression
  • Fatigue
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266
Q

Give five symptoms that are not typical of MS.

A
  • Aphasia
  • Hemianopia
  • Extrapyramidal movement disturbance
  • Severe muscle wasting
  • Muscle fasciculation
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267
Q

Describe relapsing/remitting MS.

A

Clearly defined disease relapses with full recovery or with sequelae and residual deficit upon recovery.
Periods between disease relapses characterised by a lack of disease progression.

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268
Q

Describe primary progressive MS.

A

Disease progression from the onset with occasional plateaus and temporary minor improvements allowed.

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269
Q

Describe secondary progressive MS.

A

Initial relapsing/remitting disease course followed by progression with or without occasional relapses, minor remissions, and plateaus.

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270
Q

Describe progressive/relapsing MS.

A

Progressive disease from onset, with some clear relapses, with or without full recovery, with periods between relapses characterised by continuing progression.

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271
Q

Give two essential diagnostic criteria of MS.

A
  • Two or more CNS lesions disseminated in time or space

- Exclusion of conditions giving a similar clinical picture

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272
Q

Give three tests that may aid in the diagnosis of MS.

A
  • Evoked potentials
  • MRI
  • CSF electrophoresis
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273
Q

How might evoked potentials help to diagnose MS.

A

Speed of conduction may be slower.

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274
Q

What might the MRI scan show in MS?

A

Inflammation

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275
Q

What might be seen on CSF electrophoresis which suggests MS?

A

Thicker IgG band than on plasma electrophoresis, showing inflammation is contained to the CNS.

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276
Q

Give eight factors suggesting that suspected MS may not actually be MS.

A
  • No objective neurological deficits
  • No objective evidence for dissemination of lesions in time or space
  • Strongly positive family history
  • Progressive disease from outset in young patients
  • No eye involvement
  • Localised disease
  • No CSF abnormalities
  • Pain as the predominant symptom
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277
Q

Give seven differential diagnoses of MS.

A
  • Autoimmune (SLE, Sjogrens)
  • Infectious diseases (Lyme, syphilis, AIDS)
  • Adrenomyeloceuropathy
  • Mitochondrial encephalopathy
  • Arnold-Chiari malformation
  • Olivopontocerebellar atrophy
  • Cardiac embolic event
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278
Q

What treatment can be used to shorten relapses in MS?

A

Methyprednisolone

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279
Q

How can interferons (betaferon) help in MS?

A

It decreases relapses and lesion accumulation on MRI.

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280
Q

Give three possible side effects of betaferon.

A
  • Flu symptoms
  • Depression
  • Abortion
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281
Q

Describe two monoclonal antibodies that can be used in MS.

A
  • Alemtuzumab against T lymphocytes

- Natalizumab against receptors allowing immune cells across BBB

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282
Q

Give an immunosuppressive treatment used in MS.

A

Azathioprine

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283
Q

How can spasticity be treated in MS?

A
  • Baclofen
  • Diazepam
  • Dantrolene
  • Tizanidine
  • Peripheral nerve blocks (botox)
  • Surgery
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284
Q

How can tremor be treated in MS?

A
  • Beta blockers
  • Barbiturates
  • Gabapentin
  • Orthotic devices (wristbands with weights)
  • Surgery
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285
Q

How can sexual dysfunction be treated in MS?

A
  • Counselling
  • Intracorporeal injection
  • Penile prosthesis
  • Lubricating gels
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286
Q

What is an epileptic seizure?

A

Paroxysmal event in which changes of behaviour, sensation, or cognitive processes are caused by excessive, hypersynchronous neuronal discharges in the brain.

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287
Q

What is syncope?

A

Paroxysmal event in which changes in behaviour, sensation, and cognitive processes are caused by an insufficient blood or oxygen supply to the brain. This can be related to the heart or low blood pressure.

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288
Q

What is a nonepileptic seizure?

A

Paroxysmal event in which changes in behaviour, sensation, and cognitive function caused by mental processes are associated with psychosocial distress.

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289
Q

Compare the durations of epileptic seizures, syncope, and non-epileptic seizures.

A

EPILEPTIC
30-120secs

SYNCOPE
5-30secs

NON-EPILEPTIC
1-20mins

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290
Q

Describe the ictal symptoms in an epileptic seizure.

A

Positive - feeling something that isn’t there

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291
Q

Describe the ictal symptoms in non-epileptic seizures.

A
  • Ictal crying and speaking
  • Eyes closed
  • Dramatic motor phenomena or prolonged atonia
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292
Q

Describe the recovery in epileptic seizures, syncope, and non-epileptic seizures.

A

EPILEPTIC
- (Normally negative) postictal symptoms

SYNCOPE
- Recovery within 30 secs

NON-EPILEPTIC
- Surprisingly rapid or slow postictal recovery

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293
Q

Describe how one person’s seizures differ in epilepsy.

A

Seizures are normally always the same for that one individual.

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294
Q

Describe the movements experienced in syncope.

A

Can involve jerking, but duration much shorter than tonic-clonic seizures.

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295
Q

Which out of epileptic seizures, syncope, and non-epileptic seizures can occur from sleep?

A

Epileptic seizures

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296
Q

Which of epileptic seizures, syncope, and non-epileptic seizures are situational?

A

Syncope

Non-epileptic seizure

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297
Q

Instead of sleep, where does syncope typically occur from?

A

Sitting or standing

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298
Q

Give six features of a seizure suggestive of epilepsy.

A
  • Tongue biting
  • Head turning
  • Muscle pain
  • Loss of consciousness >5mins
  • Cyanosis
  • Postictal confusion
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299
Q

Give four features of loss of consciousness/seizure suggestive of syncope.

A
  • Prolonged upright position
  • Sweating prior to loss of consciousness
  • Nausea
  • Presyncopal symptoms
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300
Q

Give some features of seizures suggestive of a non-epileptic seizure.

A 
- Pelvic thrusting-
 No ictal injury
- No seizures from sleep
- No incontinence
- No tongue biting
- Pre-ictal anxiety
- Unusually rapid or slow recovery
- Long duration
- Eyes closed
- Mouth closed during tonic-clonic movements
- No cyanosis
- Ictal crying/weeping
- Vocalisation during tonic-clonic phase
- Change in amplitude but no frequency of motor activity
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301
Q

What may cause focal epilepsy?

A

Localised brain abnormality (eg. Scarring from encephalitis or prolonged febrile seizure)

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302
Q

At what age does focal epilepsy typically start?

A

May start at any age

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303
Q

Give three types of seizures which occur in focal epilepsy.

A
  • Simple partial seizure
  • Complex partial seizure
  • Secondary generalised seizure
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304
Q

Describe simple partial seizures.

A

Partial seizures without impairment of consciousness.

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305
Q

Describe complex partial seizures.

A

Partial seizures with impairment of consciousness.

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306
Q

Describe secondary generalised seizures.

A

Starts focally but spreads widely.

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307
Q

Describe the brain abnormality usually associated with generalised epilepsy.

A

No abnormality

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308
Q

At what age does generalised epilepsy usually present?

A

Childhood (<30yrs)

*Can grow out of it

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309
Q

Give four types of generalised seizure.

A
  • Absence seizure
  • Myoclonic seizure
  • Primary generalised tonic-clonic seizure
  • Atonic (akinetic) seizure
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310
Q

Give two examples of epilepsy which feature absence seizures.

A
  • Childhood absence epilepsy

- Juvenile absence epilepsy

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311
Q

Describe absence seizures.

A

Stops taking mid-sentence (<10secs) then resumes.

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312
Q

Give an example of epilepsy which features myoclonic seizures.

A

Juvenile myoclonic epilepsy

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313
Q

Describe myoclonic seizures.

A

Sudden jerking of a limb/face/trunk.

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314
Q

Describe a tonic-clonic seizure.

A
  • Tonic phase (limbs stiffen) followed by clonic phase (limbs jerk)
  • Loss of consciousness
  • Post-ictal confusion and drowsiness
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315
Q

Describe atonic seizures.

A
  • Sudden loss of muscle tone causing a fall

- No loss of consciousness

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316
Q

What proportion of people with epilepsy have normal brain scans?

A

7/10

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317
Q

When can epilepsy be diagnosed after only one seizure?

A

If a scan/EEG is suggestive of a high risk of other seizures.

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318
Q

Give 11 differential diagnoses of epilepsy.

A
  • Postural syncope
  • Dystonia
  • TIA
  • Cardiogenic syncope
  • Migraine
  • Hypoglycaemia
  • Parasomnia
  • Benign paroxysmal positional vertigo
  • Cataplexy
  • Hyperventilation
  • Nonepileptic seizure
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319
Q

Give three potential treatments for focal epilepsy.

A
  • Carbamazepine
  • Lamotrigine
  • Surgery
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320
Q

Give two possible treatments for generalised epilepsy.

A
  • Valporate

- Lamotrigine

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321
Q

How many different drugs are usually used to treat epilepsy?

A

Monotherapy is usually used but combination therapy can be tried.

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322
Q

What percentage of patients become seizure-free with anti-epileptic drugs?

A

70%

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323
Q

Give seven different mechanisms how anti-epileptic drugs can act.

A
  • Block voltage gated Na channels
  • Increase K channels
  • Blocks Ca channels
  • Blocks neurotransmitter release
  • Targets GABA receptor
  • Inhibits GABA degradation
  • Inhibits GABA transport out of synapse
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324
Q

What are the common side effects of anti-epileptic drugs (valproate)?

A

VALPROATE

  • Appetite increase/weight gain
  • Liver failure
  • Pancreatitis
  • Reversible hair loss (grows back curly
  • Oedema
  • Ataxia
  • Teratogenicity, tremor, thrombocytopenia
  • Encephalopathy
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325
Q

Give four potential treatments for refractory epilepsy.

A
  • Resective surgery
  • Hemispherectomy
  • Tractotomy
  • Electrostimulation (vagus nerve stimulation)
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326
Q

Give some non-epileptic causes of seizures.

A
  • Trauma
  • Stroke
  • Haemorrhage
  • Raised intracranial pressure
  • Alcohol/benzodiazepine withdrawal
  • Hypoxia
  • Hyper/hyponatraemia
  • Hypocalcaemia
  • Hyper/hypoglycaemia
  • Uraemia
  • Liver disease
  • Infection
  • High temperature
  • Drugs
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327
Q

What is Todd’s palsy?

A

Transient paralysis after a frontal lobe seizure.

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328
Q

What are automatisms?

A

Complex motor phenomena with impaired awareness and no recollection.
Occur in temporal lobe seizures.

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329
Q

What is the embryological derivation of somatic motor and sensory nerves?

A

Somites

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330
Q

What is the embryological derivation of branchial motor nerves?

A

Pharyngeal arches

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331
Q

What spinal levels supply the autonomic nerve supply to the heart?

A

T1-T4

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332
Q

How many cervical spinal nerves are there?

A

8

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333
Q

Give two consequences of a trapped nerve.

A
  • Numbness

- Pain

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334
Q

At which vertebral level does the spinal cord end?

A

L1

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335
Q

How is the needle for an epidural different from a lumbar puncture needle?

A

Epidural needle is blunt so that it doesn’t penetrate the dura.

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336
Q

Which arteries branch to give the vertebral arteries?

A

Right and left subclavian arteries

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337
Q

Give three structures that the vertebral arteries give branches to as they ascend.

A
  • Neck muscles
  • Spinal meninges
  • Spinal cord
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338
Q

Describe the course of the vertebral arteries.

A
  • Enter foramina transversarium at C6

- Ascend and enter foramen magnum anterolateral to medulla

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339
Q

Give three branches of the vertebral arteries before they join together.

A
  • Anterior spinal artery
  • Small medullary perforators
  • Posterior inferior cerebellar artery
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340
Q

What artery is formed from the two vertebral arteries?

A

Basilar artery

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341
Q

Give four branches of the basilar artery.

A
  • Perforating branches to brainstem
  • Posterior cerebral artery
  • Superior cerebellar artery
  • Anterior inferior cerebellar artery
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342
Q

Describe the course of the posterior cerebral artery.

A
  • Partially encircles midbrain

- Supplies cortical territories

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343
Q

Give four structures that the posterior cerebral artery supplies as it encirles the midbrain.

A
  • Thalamus
  • Geniculate bodies
  • Cerebral peduncles
  • Tectum
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344
Q

What cortical territories does the posterior cerebral artery supply?

A
  • Inferior temporal lobe
  • Posterior 1/3 of interhemispheric surface
  • Visual cortex and occipital lobe
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345
Q

At what vertebral level do the common carotid arteries bifurcate?

A

C3-C4

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346
Q

Name the four divisions of the internal carotid artery.

A
  • Cervical
  • Petrous
  • Cavernous
  • Supraclinoid
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347
Q

Describe the path of the cervical internal carotid arteries.

A

Ascend anterior and medial to internal jugular vein.

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348
Q

Describe the path of the petrous internal carotid arteries.

A

Penetrates temporal bone and runs horizontally (anteromedially) in carotid canal.

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349
Q

Describe the path of the cavernous internal carotid arteries.

A

Enter cavernous sinus, then pierces dura at the level of the anterior clinoid process.

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350
Q

Give three structures that are supplied by small branches of the cavernous internal carotid artery.

A
  • Dura
  • CN III-VI
  • Posterior pituitary
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351
Q

Give three small branches of the supraclinoid internal carotid artery.

A
  • Ophthalmic artery
  • Superior hypophyseal artery
  • Anterior choroidal artery
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352
Q

Give four structures supplied by the superior hypophyseal artery.

A
  • Pituitary gland
  • Stalk
  • Hypothalamus
  • Optic chiasm
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353
Q

Give five structures supplied by the anterior choroidal artery.

A
  • Choroid plexus
  • Optic tract
  • Cerebral peduncle
  • Internal capsule
  • Medial temporal lobe
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354
Q

Give the three big branches of the internal carotid artery.

A
  • Anterior cerebral artery
  • Middle cerebral artery
  • Posterior communicating artery
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355
Q

Describe the course of A1 of the anterior cerebral artery.

A

Runs medially to connect with the contralateral ACA via anterior communicating artery.

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356
Q

Describe the course of A2 of the anterior cerebral artery.

A

Runs in interhemispheric fissure to genu of corpus callosum and 2 cortical branches.

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357
Q

What does A3 of the anterior cerebral artery consist of?

A

Cortical branches

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358
Q

Describe the course of M1 of the middle cerebral artery.

A

Runs laterally to limen insulae.

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359
Q

What branches does M1 of the middle cerebral artery give off?

A

Lateral lenticulostriate arteries.

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360
Q

Give three structures supplied by the lateral lenticulostriate arteries.

A
  • Lentiform nucleus
  • Caudate nucleus
  • Internal capsule
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361
Q

Describe the path of M2 of the middle cerebral artery.

A

Runs in insular cistern

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362
Q

Describe the path of M3 of the middle cerebral artery.

A

Emerges onto brain surface

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363
Q

What does M4 of the middle cerebral artery consist of?

A

Vessels on the brain surface.

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364
Q

What is the normal role of Tau in neurones?

A

It forms part of the cytoskeleton.

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365
Q

Describe how beta amyloid plaques are formed in Alzheimer’s disease.

A

Amyloid precursor protein is usually broken down by alpha and gamma secretase and waste products are soluble.
If alpha secretase is replaced by beta secretase the breakdown product is no longer soluble.

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366
Q

How are Lewy Bodies formed in Lewy Body dementia?

A

Misfolding of alpha synuclein protein.

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367
Q

Describe the compensatory response for a small increase in brain volume.

A
  • Reduction in CSF volume

- Little/no increase in pressure

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368
Q

Describe the brain’s response to a large increase in volume.

A
  • Pressure increases exponentially

- Ventricle outflow may become obstructed, leading to even bigger increase in pressure

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369
Q

Describe a herniation (duret) haemorrhage.

A
  • Pontine arteries torn when the brain is pushed
  • Haemorrhages seen in medulla/pons
  • Usually fatal
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370
Q

Give three consequences of tonsillar herniation.

A
  • Ataxia
  • VI nerve palsy
  • Upgoing plantar responses
  • Compression of cardiorespiratory centre
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371
Q

Give four consequences of lateral tentorial (uncal) herniation.

A
  • Oculomotor/parasympathetic nerve palsies
  • Posterior cerebral artery infarction (homonymous hemianopia)
  • Haemorrhage into midbrain or cardiorespiratory centre
  • Motor weakness due to pressure on cerebral peduncles
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372
Q

What may be seen in a subfalcine (cingulate) hernia?

A

Ischaemic stroke of anterior cerebral artery.

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373
Q

Give three anatomical effects of mass lesions of the brain.

A
  • Local deformity and shift of structures
  • Decreased volume of CSF
  • Pressure gradients lead to internal herniation
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374
Q

Give six signs of raised intracranial pressure.

A
  • Decreased conciousness
  • Focal neurological signs
  • Papilloedema
  • Increased blood pressure*
  • Irregular breathing*
  • Bradycardia*
  • Cushing’s triad
375
Q

How is raised intracranial pressure diagnosed?

A
  • CT/MRI for mass lesions

- As a last resort can measure opening pressure on lumbar puncture (However this is usually contraindicated)

376
Q

What should be normal intracranial pressure be?

A

15mmHg

377
Q

Give five possible treatments for raised intracranial pressure.

A
  • Treat underlying cause
  • External ventricular drain
  • Decompressive craniotomy
  • Osmotic therapy (mannitol)
  • If intubated, hyperventilate to decrease CO2 (this causes cerebral vasoconstriction)
378
Q

What does the external carotid artery supply?

A
  • Skull
  • Meninges
  • Everything outside skull
379
Q

What causes lateral medullary syndrome?

A

Embolus in the anterior inferior cerebellar artery or posterior inferior cerebellar artery.

380
Q

Give four structures that become ischaemic in lateral medullary syndrome.

A
  • CN VII
  • CN VIII
  • CN IX
  • Middle cerebellar peduncle
381
Q

Why are the lenticulostriate arteries prone to rupture?

A

They have a thin adventitia.

382
Q

Does a haemorrhagic stroke usually kill grey or white matter, and what is the prognosis for recovery?

A

Usually kills white matter so there can be substantial recovery.

383
Q

Does an embolic stroke usually kill white or grey matter and what is the prognosis for recovery?

A

Usually kills grey matter (cell bodies).

No recovery.

384
Q

Where are the meningeal vessels found?

A

Extradural space

385
Q

In which layer of the meninges is the Circle of Willis found?

A

Subarachnoid space

386
Q

Which blood vessels are found deep to the pia mater?

A

There are no vessels deep to the pia.

387
Q

Which sensations pass through the thalamus?

A

All of them apart from olfaction.

388
Q

What usually causes an extradural haemorrhage?

A

Skull fracture

389
Q

Describe the pathology of an extradural haemorrhage.

A

Tearing of the middle meningeal artery causes blood to accumulate between bone and dura.

390
Q

Describe the presentation of an extradural haemorrhage.

A
  • Lucid interval (may be few hours to days) before deteriorating consciousness
  • Headache
  • Vomiting
  • Confusion
  • Seizures
  • May be hemiparesis, brisk reflexes, upgoing plantar
391
Q

Describe the appearance of an extradural haemorrhage on imaging.

A

Rounded convex shape

392
Q

What is the management and prognosis for an extradural haemorrhage?

A

Good prognosis if transferred to neurology early.

393
Q

Give four groups of people in who subdural haemorrhage is more common.

A
  • Alcoholics
  • Dementia
  • Elderly
  • Children
394
Q

Describe the pathology of a subdural haemorrhage.

A
  • Bleeding from bridging veins (low pressure, soon stops)
  • Days/weeks later haematoma starts to autolyse
  • Massive increase in oncotic and osmotic pressure sucks water into haematoma
  • Gradual rise in ICP over many weeks
395
Q

Describe the symptoms of a subdural haemorrhage.

A
  • Fluctuating level of consciousness
  • Insidious physical or intellectual slowing
  • Sleepiness
  • Headache
  • Personality change
  • Unsteadiness
396
Q

Give three signs of a subdural haemorrhage.

A
  • Raised intracranial pressure
  • Seizures
  • Focal neurological symptoms (often appear late)
397
Q

Give two signs on imaging of a subdural haemorrhage.

A
  • Midline shift

- Crescent shape over one hemisphere

398
Q

Give three management points for a subdural haemorrhage.

A
  • Irrigation/evacuation
  • Craniotomy
  • Address causes of haemorrhage
399
Q

What is the usual cause of a subarachnoid haemorrhage?

A

Berry aneurysms

400
Q

Describe the pathology of a subarachnoid haemorrhage.

A

Rupture of arteries forming the circle of Willis

401
Q

Describe the symptoms of a subarachnoid haemorrhage.

A
  • Sudden (usually occipital) ‘thunderclap’ headache
  • Photophobia
  • Vomiting
  • Collapse
  • Seizures
  • Coma
  • May have experienced sentinel headache earlier due to small leak from offending vessel
402
Q

Give four signs of a subarachnoid haemorrhage.

A
  • Neck stiffness
  • Kernig’s sign
  • Retinal/subhyaloid/vitreous bleeds (Terson’s syndrome)
  • Focal neurology
403
Q

How is a subarachnoid haemorrhage diagnosed?

A
  • CT detects >90% in first 48hrs

- If CT-ve and no contraindications, do lumbar puncture

404
Q

Describe the CSF in subarachnoid haemorrhage.

A

Bloody early on but then turns yellow due to breakdown products.

405
Q

Describe the midline shift seen on imaging in subarachnoid haemorrhage.

A

No midline shift because bleeding spreads round both sides of the brain at the same time.

406
Q

Describe the management of a subarachnoid haemorrhage.

A
  • Refer to neurosurgery
  • Observation
  • Maintain cerebral perfusion (hydrate)
  • Nimodipine (Ca channel blocker to reduce vasospasm)
  • Endovascular coiling
407
Q

What is the prognosis in subarachnoid haemorrhage?

A
  • 1/3 die instantly from tonsillar herniation
  • 1/3 become unconscious with high risk of mortality or permanent neurological deficit
  • 1/3 have good outcome (if no rebleeding)
408
Q

Give seven disorders of motor neurones.

A
  • Motor neurone disease
  • Hereditary spastic paraplegia
  • Spinal muscular atrophy
  • Kennedy’s disease
  • Post-polio syndrome
  • Motor neuropathies
  • Hyperactivity disorders of motor neurones (eg. Stiff person syndrome)
409
Q

Define paresis.

A

Impaired ability to move a body part at will (weakness).

410
Q

Define paralysis.

A

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

411
Q

Define ataxia.

A

Willed movements are clumsy, ill-directioned, or uncontrolled (incoordination).

412
Q

Define ‘involuntary movements’.

A

Spontaneous movement of a body part, independently of will.

413
Q

Define apraxia.

A

Disorder of consciously organised patterns of movement or impaired ability to recall acquired motor skills.
Can’t put a series of movements together.

414
Q

What does a motor unit consist of?

A

Lower motor neurone + the supplied muscle fibres.

415
Q

Which motor neurones innervate muscle spindles?

A

Y motor neurones

416
Q

What are four neural inputs to the final common motor pathway?

A
  • Reflex arc
  • Corticospinal/pyramidal pathway
  • Extrapyramidal/basal ganglia system
  • Cerebellum
417
Q

Give the six ‘stations’ in the brain that the corticospinal tracts pass through.

A
  • Motor cortex
  • Corona radiata
  • Internal capsule
  • Cerebral peduncle in midbrain
  • Pyramidal bundles in pons
  • Pyramid in medulla
418
Q

Give the clinical features of an upper motor neurone lesion.

A
  • Increased muscle tone (spasticity)
  • Brisk tendon reflexes
  • Extensor plantar responses
  • Upper limb extensors weaker than flexors
  • Lower limb flexors weaker than extensors
  • Fine skillful movements most severely impaired
  • Emotional lability may be present
  • Pyramidal drift
419
Q

What is pyramidal drift?

A

When a patient with an UMN lesion puts arms out (supinated), one arm (contralateral) will pronate and drop.

420
Q

Describe two features of an UMN lesion which suggests it may arise from the cortex.

A
  • Contralateral weakness

- Dispersion over wide area

421
Q

Describe how an internal capsule lesion is likely to present.

A

Complete contralateral hemiparesis.

422
Q

Give three features suggestive of a brainstem Motor neurone lesion.

A
  • Often bilateral weakness (involvement of both corticospinal tracts)
  • Involvement of cranial nerve nuclei
  • Bulbar involvement often present
423
Q

Which side would the weakness be on in a spinal cord motor neurone lesion?

A

Often bilateral lesions

424
Q

What clinical feature suggests a cervical spinal cord motor neurone lesion?

A

Tetraparesis

425
Q

What clinical feature suggests a spinal cord motor neurone lesion below the cervical region?

A

Paraparesis

426
Q

Give five causes (And examples) of upper motor neurone lesions.

A
  • Vascular (stroke)
  • Inflammatory (MS)
  • Compression/degeneration (tumour)
  • Infiltration of corticospinal tract (tumour)
  • Neurodegenerative disease of UMN +/- LMN (MND)
427
Q

Give three tests (and what they look for) that can be used to assess UMN lesions.

A
  • Neuroimaging (MRI)
  • Blood tests (metabolic disease)
  • CSF (oligoclonal bands)
428
Q

Give the features of a lower motor neurone disorder.

A
  • Normal/reduced muscle tone (flaccid)
  • Muscle wasting
  • Fasciculation
  • Reflexes depressed/absent
429
Q

Give six examples of diseases which can cause a lower motor neurone lesion in the Brainstem/spinal cord.

A
  • Motor neurone disease
  • Spinal muscular atrophy
  • Poliomyelitis
  • Syringomyelia/syringobulbia
  • Spinal cord/brainstem compression
  • Vascular disease
430
Q

Give four causes of LMN lesions in the spinal roots.

A
  • Prolapsed intervertebral disk
  • Cervical/lumbar spondylosis
  • Tumours
  • Malignant infiltration
431
Q

Give two causes of peripheral nerve LMN lesions.

A
  • Axonal degeneration

- Demyelinating

432
Q

Give three examples of LMN diseases affecting the neuromuscular junction.

A
  • Myaesthenia gravis
  • Lambert Eaton myasthenic syndrome
  • Congenital diseases
433
Q

Give two features Of the pattern of disease that can help distinguish between a LMN and a muscle disease.

A
  • Nerve affects distal muscles first and reflexes are lost

- Muscle affects proximal limb and trunk muscles, and reflexes are preserved until late

434
Q

Give four investigations (and what they’re looking for) to help assess LMN disorders.

A
  • Neurophysiology nerve conduction studies/EMG
  • Neuroimaging (MRI)
  • Blood tests (muscle enzymes, autoantibodies)
  • Lumbar puncture
435
Q

What percentage of malignant childhood tumours do brain tumours account for?

A

20%

436
Q

Where are the majority of adult brain tumours found?

A

Supratentorial

437
Q

Where are the majority of childhood brain tumours found?

A

Posterior fossa

438
Q

Give two groups of people who are more likely to get CNS lymphoma.

A
  • Elderly

- Immunosuppressed

439
Q

Give a group of patients in who germ cell tumours are more common.

A

Children

440
Q

What percentage of brain tumours are malignant?

A

55%

441
Q

Where are brain tumours likely to spread?

A

They NEVER spread outside the CNS

442
Q

Give three potential risk factors for developing a brain tumour.

A
  • Ionising radiation (especially in childhood)
  • Family history (sometimes)
  • Immunosuppression (CNS lymphoma)
443
Q

Give six groups of brain tumours according to the WHO classification.

A
  • Neuroepithelial tumours (gliomas)
  • Cranial and spinal nerve tumours
  • Meningeal tumours
  • Lymphomas
  • Germ cell tumours
  • Metastatic tumours
444
Q

Which cells form gliomas?

A

Neurones or glial cells

445
Q

Which is the largest group of brain tumours?

A

Neuroepithalial tumours (gliomas)

446
Q

Give seven types of gliomas.

Which is the most common?

A
  • Astrocytic (most common)
  • Oligodendroglial
  • Ependymal
  • Neuronal and neuro-glial
  • Pineal
  • Embryonal
  • Choroid plexus
447
Q

Give four general clinical manifestations of a brain tumour.

A
  • Loss of function (focal neurological symptoms)
  • Non-focal neurological symptoms
  • Seizures
  • Headache
448
Q

What is the ‘most predictive’ symptom of a brain tumour?

A

Seizures

449
Q

Give four examples of focal neurological symptoms that may occur with a brain tumour.

A
  • Weakness
  • Sensory loss
  • Visual/speech disturbance
  • Ataxia
450
Q

Describe the rate of onset of focal neurological symptoms associated with a brain tumour.

A

Usually come on over a few weeks or days

451
Q

Give three examples of non-focal neurological symptoms that can occur in a brain tumour.

A
  • Personality/behaviour change
  • Memory disturbance
  • Confusion
452
Q

Why do people with brain tumours get headaches?

A

From raised intracranial pressure

453
Q

Describe the features of the headache associated with raised intracranial pressures/brain tumours.

A
  • Woken by headache
  • Worse in morning and when lying down
  • Associated with nausea and vomiting
  • Exacerbated by coughing/sneezing
  • Associated with drowsiness
454
Q

Give two signs of a brain tumour.

A
  • Papilloedema

- Focal neurological deficit

455
Q

Give four focal neurological deficit signs that can occur in association with brain tumours.

A
  • Hemiparesis
  • Hemisensory loss
  • Visual field defect
  • Dysphasia
456
Q

Give four red flags for brain tumours.

A
  • Headache (+ features of raised ICP/focal neurology)
  • New onset focal seizure
  • Rapidly progressing focal neurology
  • Past history of other cancer
457
Q

How do low grade brain tumours typically present?

A

Seizures, but can be incidental finding.

458
Q

How does the brain adapt in low grade brain tumours?

A

Because the tumour is slow growing the brain can move out of the way so important structures aren’t affected.

459
Q

How do high grade brain tumours typically present?

A
  • Rapidly progressive neurological deficit

- Symptoms of raised ICP

460
Q

What investigations should be carried out to diagnose a brain tumour?

A
  • Contrast CT/MRI (MRI is better)

- Brain biopsy

461
Q

How will the brain scan appear in a high grade brain tumour?

A
  • Lots of oedema

- Lights up with contrast dye

462
Q

What is the five year survival in brain tumours?

A

19%

463
Q

Describe the treatment for high grade gliomas.

A
  • Steroids reduce oedema
  • Surgery (resection, relief of raised ICP)
  • Radiotherapy (mainstay)
  • Chemotherapy
464
Q

Give two chemotherapy options for brain cancer.

A
  • Temozolamide

- PCV

465
Q

Describe the treatment options for low grade gliomas.

A
  • Surgery (resection)

- Radiotherapy + chemotherapy

466
Q

How does radiotherapy affect the prognosis of low grade gliomas?

A

Delays disease progression but doesn’t improve survival.

467
Q

What age do astrocytic tumours usually occur in?

A

Adults

468
Q

Name a WHO grade I astrocytic tumour.

A

Pilocytic astrocytoma

469
Q

Name a WHO grade II astrocytic tumour.

A

Diffuse astrocytoma

470
Q

Name a WHO grade III astrocytic tumour.

A

Anaplastic astrocytoma

471
Q

Name a WHO grade IV astrocytic tumour.

A

Glioblastoma

472
Q

Who is more likely to get a primary (de novo) glioblastoma.

A

Older people

473
Q

Describe a secondary glioblastoma.

A

Progresses from a lower grade astrocytoma.

474
Q

Describe the behaviour of diffuse astrocytomas.

A
  • Infiltrate diffusely

- Undergo progressive anaplasia (progress from low to high grade)

475
Q

Describe the isocitrate dehydrogenase status in grade II/III and glioblastoma de novo astrocytomas.

A
  • Grade II/III = isocitrate dehydrogenase 1 mutation

- Glioblastoma de novo = wild type IDH1

476
Q

Describe the prognosis for a pilocytic astrocytoma.

A

Good

477
Q

Describe the histological criteria for a diffuse astrocytoma.

A

Nuclear atypia

478
Q

Describe the prognosis for a diffuse astrocytoma.

A

> 5yrs

479
Q

Describe the histological criteria for an anaplastic astrocytoma.

A
  • Nuclear atypia

- Mitoses

480
Q

Describe the prognosis for an anaplastic astrocytoma.

A

2-5yrs

481
Q

Describe the histological criteria for a glioblastoma.

A
  • Nuclear atypia
  • Mitoses
  • Necrosis + vascular proliferation
482
Q

Describe the prognosis for a glioblastoma.

A

<1yr

483
Q

What is MGMT?

A

An enzyme which repairs DNA damage.

484
Q

Describe how the MGMT methylation status in astrocytomas affect the prognosis and treatment.

A

If MGMT is methylated there is a good response to chemotherapy.

485
Q

Who do pilocytic astrocytomas usually occur in?

A

Children

486
Q

Will pilocytic astrocytomas usually progress to glioblastomas?

A

No - they are their own entity

487
Q

Where do pilocytic astrocytomas usually occur?

A

Posterior fossa

488
Q

Describe the appearance of a pilocytic astrocytoma.

A

Often cystic

489
Q

What are rosenthal fibres, and what do they indicate when seen in a brain tumour?

A

Protein aggregated often seen in grade I lesions, therefore indicating a good prognosis.

490
Q

At what age are oligodendrogliomas most common?

A

4th/5th decade

491
Q

Describe the common clinical presentation of oligodendrogliomas.

A

May have seizures

492
Q

What WHO grade are oligodendrogliomas?

A

WHO grade II

493
Q

Describe the appearance of the anaplastic variant of oligodendrogliomas.

A

They have mitotic figures and microvascular proliferation.

494
Q

What feature on a scan can help to diagnose oligodendrogliomas?

A

Calcification

495
Q

Give two molecular criteria for an oligodendroglioma to be diagnosed.

A
  • Mutation in isocitrate dehydrogenase 1

- 1p19q co-deletion

496
Q

At what age do medulloblastomas occur?

A

Childhood

497
Q

Describe the appearance of a medulloblastoma.

A
  • Primitive ‘small blue cell’ tumour
  • Densely cellular
  • Embryonal tumour
498
Q

Where do medulloblastomas occur?

A

Cerebellum

499
Q

Describe the prognosis/treatment for medulloblastomas.

A
  • Highly malignant but may respond to excision/radiotherapy/chemotherapy
  • Potentially curable
500
Q

What is the issue with treating medulloblastomas with chemo/radiotherapy?

A

The brain is still developing.

501
Q

What is the risk of the medulloblastoma if the tumour is desmoplastic (connective tissue is present)?

A

Lower risk

502
Q

What is the risk of a medulloblastoma if the tumour is large cell anaplastic?

A

Higher risk

503
Q

Give two mutations that give a better prognosis in medulloblastomas.

A
  • WNT

- SHH

504
Q

How is a WNT mutation identified in a medulloblastoma?

A

Presence of nuclear b-catenin protein

505
Q

Describe the activity of meningioma.

A

Dural based and push into brain.

506
Q

What grade are most meningiomas?

A 
Grade I
(There are more aggressive variants (Grade II/III))
507
Q

Describe the appearance of brain metastases on a scan.

A
  • Tend to be rounded

- Likely to be multiple tumours, but solitary tumours can also be mets

508
Q

Give five cancers that are likely to spread to the brain.

A
  • Lung
  • Breast
  • Melanoma
  • GI tract
  • Kidney
509
Q

Name three ‘movement disorders’.

A
  • Parkinson’s disease
  • Essential tremor
  • Dystonia
510
Q

Give two movement disorders that are due to ‘hardware problems’ (AKA cell death) in the basal ganglia.

A
  • Parkinson’s disease

- Huntington’s disease

511
Q

Give two diseases that are due to ‘software problems’ (AKA no cell death) in the basal ganglia.

A
  • Dystonia

- Tourette

512
Q

What percentage of people over 65 years will have Parkinson’s disease?

A

3%

513
Q

What causes Parkinson’s disease?

A

Genetic and environmental factors.

514
Q

Describe the pathology of Parkinson’s disease.

A
  • Loss of dopaminergic neurones in the substantia nigra

- Presence of intracytoplasmic Lewy bodies in substantia nigra

515
Q

What methods cause cell loss in Parkinson’s disease?

A
  • Mitochondrial dysfunction

- Oxidative stress

516
Q

Give the three cardinal features of Parkinson’s disease/Parkinsonism.

A
  • Bradykinesia/Akinesia
  • Resting tremor
  • Rigidity
517
Q

Describe the symptoms/signs of Parkinson’s disease.

A
  • Shuffling
  • Stooped gait
  • Drag (usually one) leg while walking
  • Problems with intricate movements
  • Writing smaller
  • Resting tremor (may be unilateral)
  • Stiffness (increased tone)
  • Pain (not usually a major presenting feature)
  • Problems with turning in bed
  • Decreasing amplitude/accuracy of repetitive movements (much better at beginning, gradual worsening)
518
Q

Describe the symmetry/asymmetry of symptoms in Parkinson’s disease.

A

Symptoms always start (or are much worse) on one side.

519
Q

Give four features that are more suggestive of pressure hydrocephalus and should not be present in Parkinson’s disease (at least at the start).

A
  • Incontinence
  • Dementia
  • Symmetry
  • Early falls
520
Q

Describe how a diagnosis of Parkinson’s disease is made.

A
  • Usually clinical

- Can do DaTSCAN

521
Q

What would a DaTSCAN show in Parkinson’s disease?

A

Reduced dopamine supply to the striatum.

522
Q

What is the aim of treatment in Parkinson’s disease?

A

Compensate for loss of dopamine (treat symptoms)

523
Q

Give two lifestyle treatments that may help Parkinson’s disease.

A
  • Maintain healthy weight

- Exercise as much as possible

524
Q

Give four groups of medications that can be used to treat Parkinson’s disease.

A
  • L-dopa
  • Dopamine agonists
  • Catachol-O-Methyl-Transferase (COMT) inhibitors
  • Monoamine oxidase (MAO) inhibitors
525
Q

Which is the most powerful drug class used in Parkinson’s disease?

A

L-dopa

526
Q

What is the first line drug treatment for Parkinson’s disease in younger patients?

A

Dopamine agonists

527
Q

Give three possible side effects of dopamine agonists.

A
  • Tiredness
  • Gambling
  • Hypersexuality
528
Q

Give seven examples of dopamine agonists.

A
  • Ropinirole
  • Pramipexole
  • Rotigotine
  • Bromocriptine
  • Pergolide
  • Cabergoline
  • Amantadine
529
Q

Give two examples of COMT inhibitors used in Parkinson’s disease.

A
  • Entacapone

- Tolcapone

530
Q

Which class of Parkinson’s drugs has the best neuroprotective effect?

A

MOA inhibitors

531
Q

What is the downside of using MAO inhibitors to treat Parkinson’s disease?

A

They aren’t that powerful

532
Q

Give two examples of MAO inhibitors used to treat Parkinson’s disease.

A
  • Rasagiline

- Selegiline

533
Q

Why aren’t anticholinergics used to treat Parkinson’s disease?

A

They have side effects

534
Q

Give three side effects of anti-cholinergic drugs.

A
  • Cognition
  • Confusion
  • Systemic
535
Q

When should treatment for Parkinson’s disease be started?

A

Doesn’t have to be straight away - discuss with patient.

536
Q

Give four drug complications of long-lasting Parkinson’s disease.

A
  • Wearing off (drug doesn’t work as long)
  • On-dyskinesias (when drugs work)
  • Off-dyskinesias (when drugs don’t work)
  • Freezing (unpredictable loss of mobility)
537
Q

Give five complications that may develop in Parkinson’s disease

A
  • Depression
  • Psychotic problems (phobias, anxiety disorder, hallucinations)
  • Dementia
  • Autonomic problems (constipation, increased urinary frequency)
  • Anosmia
538
Q

Describe the prognosis in Parkinson’s disease.

A

Disease is slowly progressive

539
Q

Describe the clinical features of essential tremor.

A
  • Postural and intention tremor
  • Gradual worsening
  • No increased tone or problems with fine finger movements
540
Q

Give four potential treatments for essential tremor.

A
  • Beta blocker
  • Primidone
  • Gabapentin
  • Clonazepam
541
Q

What is generalised dystonia?

A

Syndrome of sustained muscle contraction, frequently causing twisting and repetitive movements as well as abnormal posture.

542
Q

Describe the typical history/onset of generalised dystonia.

A
  • Often positive family history

- Typical onset in childhood

543
Q

What is motor neurone disease?

A

A group of neurodegenerative diseases characterised by the selective loss of motor neurones in the motor cortex, cranial nerve nuclei, and anterior horn cells.

544
Q

Are upper or lower motor neurones affected in motor neurone disease?

A

Both

545
Q

Is motor neurone disease more common in men or women?

A

Slightly more common in men

546
Q

At what age do most cases of motor neurone disease present?

A

50-70yrs

547
Q

What are most cases of motor neurone disease caused by?

A

Idiopathic

548
Q

Give three genes that may be implicated in some cases of motor neurone disease.

A
  • SOD1
  • TDP-43
  • FUS
549
Q

Give a macroscopic change that may occur in motor neurone disease.

A

Atrophic anterior roots of spinal cord.

550
Q

What microscopic change may be seen in motor neurone disease?

A

Selective loss of motor neurones in the motor cortex and anterior horns of the spinal cord.

551
Q

Give the four clinical patterns of motor neurone disease.

A
  • Amyotrophic lateral sclerosis
  • Progressive bulbar palsy
  • Progressive muscular atrophy
  • Primary lateral sclerosis
552
Q

Describe the pathology of amyotrophic lateral sclerosis.

A

Loss of motor neurones in the motor cortex and anterior horn of spinal cord.

553
Q

Describe the pattern of signs/symptoms in ALS.

A

UMN and LMN signs

554
Q

Describe split hand sign (and when it may occur).

A

Thumb side of hand seems cast adrift owing to excessive wasting around it (much less hypothenar wasting).
Seen in ALS.

555
Q

What is the most common clinical pattern of MND?

A

ALS

556
Q

Describe the pathology of progressive bulbar palsy.

A

MND only affecting cranial nerves IX-XII

557
Q

Describe the clinical presentation of progressive bulbar palsy.

A

LMN signs in tongue and muscles of talking/swallowing.

558
Q

Describe the pathology in corticobulbar palsy.

A

UMN lesion of muscles of swallowing and talking due to bilateral lesions above mid pons.

559
Q

Is bulbar or corticobulbar palsy more common?

A

Corticobulbar palsy

560
Q

Give four signs/symptoms of corticobulbar palsy.

A
  • Slow tongue movements
  • Slow deliberate speech
  • Increased jaw jerk
  • Increased pharyngeal/palatal reflexes
561
Q

Describe the pathology in progressive muscular atrophy.

A

MND with lesions in the anterior horn cells only.

562
Q

Describe the UMN signs in progressive muscular atrophy.

A

Absent

563
Q

Which muscle groups are affected first in progressive muscular atrophy.

A

Distal muscle groups

564
Q

Compare the prognosis for progressive muscular atrophy with ALS.

A

Better prognosis for progressive muscular atrophy.

565
Q

Describe the pathology in primary lateral sclerosis.

A

Loss of Betz cells in the motor cortex.

566
Q

Describe the pattern of signs/symptoms in primary lateral sclerosis.

A

Mainly UMN signs

567
Q

Give three signs of primary lateral sclerosis.

A
  • Marked spastic leg weakness
  • Pseudobulbar palsy
  • No cognitive decline
568
Q

Describe the signs of MND in the limb muscles.

A
  • Weakness
  • Wasting
  • Fasciculation
  • Spasticity
569
Q

Describe the symmetry/asymmetry of signs in MND.

A

Asymmetric

570
Q

Give five signs of MND affecting the face.

A

Difficulty:

  • Swallowing
  • Chewing
  • Speaking
  • Coughing
  • Breathing
571
Q

Do cognitive changes occur in MND?

A

Potentially

572
Q

Give a feature that can distinguish MND from MS/polyneuropathies.

A

No sensory loss/sphincter disturbance.

573
Q

Give a feature that can distinguish MND from Myaesthenia gravis.

A

MND never affects eye movements.

574
Q

What test is carried out to diagnose MND?

A

There is no diagnostic test

575
Q

Why can a brain/cord MRI be helpful when diagnosing MND?

A

To exclude structural causes

576
Q

Why can a lumbar puncture be useful when diagnosing MND?

A

To exclude inflammatory causes

577
Q

Why can neurophysiology tests be useful when diagnosing MND?

A

They can detect subclinical denervation.

578
Q

What is the diagnostic criteria for definite MND?

A

Lower + upper motor neurone signs in 3 regions

579
Q

What is the diagnostic criteria for probably MND?

A

Lower + upper motor neurone signs in 2 regions

580
Q

What is the diagnostic criteria for probable (+ lab support) MND?

A

Lower and upper motor neurone signs in 1 region with EMG showing acute denervation in 2 or more limbs

OR

Upper motor neurone signs in one or more regions with EMG showing acute denervation in 2 or more limbs

581
Q

What is the diagnostic criteria for possible MND?

A

Lower + upper motor neurone signs in 1 region.

582
Q

What is the diagnostic criteria for suspected MND?

A

Upper or lower motor neurone signs only - in 1 or more regions.

583
Q

Give an antiglutaminergic drug that can help to treat MND.

A

Riluzole

584
Q

How can antiglutaminergic drugs help MND?

A

Prolong life by about 3 months

585
Q

Give 6 side effects of anti-glutaminergic drugs.

A
  • Raised LFTs
  • Vomiting
  • Fast pulse
  • Somnolence
  • Headache
  • Vertigo
586
Q

Give two possible treatments for drooling in MND.

A
  • Propantheline

- Amitiptyline

587
Q

Give three possible treatments for dysphagia in MND.

A
  • Blend food
  • NG tube
  • Percutaneous catheter gastrostomy
588
Q

Give a treatment for joint pains/distress in MND.

A

Analgesia

589
Q

Give a treatment for respiratory failure in MND.

A

Non-invasive ventilation

590
Q

How long do people with MND usually survive?

A

2-4yrs

591
Q

What is the most common cause of death in MND?

A

Aspiration pneumonia

592
Q

What is Huntington’s disease?

A

An inherited neurodegenerative disorder caused by a mutation of the HTT gene.

593
Q

At what age does Huntington’s disease present?

A

Most present between 35-45yrs but can occur at any age.

594
Q

Is Huntington’s disease more common in men or women?

A

Equal

595
Q

Describe the inheritance pattern in Huntington’s disease.

A

Autosomal dominant

596
Q

Describe the genetic element of Huntington’s disease.

A
  • HTT contains a sequence of CAG trinucleotide repeats
  • Usually <36 repeats
  • Mutant HTT has >36 repeats
597
Q

Describe how Huntington’s disease changes with increasing number of trinucleotide repeats.

A
  • Fuller penetrance

- Younger age of onset

598
Q

Describe how the number of trinucleotide repeats changes between generations in Huntington’s disease.

A

Tends to get larger (anticipation)

599
Q

What protein does HTT code for?

A

Huntingtin

600
Q

In which cells is Huntingtin expressed?

A

All cells, but more in brain and testis.

601
Q

How does mutated Huntingtin cause Huntington’s disease?

A

Mutated Huntingtin thought to be cytotoxic to certain cell types, most notably neurones in the caudate nucleus and putamen.

602
Q

Give the three cardinal features of Huntington’s disease.

A
  • Chorea
  • Dementia
  • Psychiatric problems
603
Q

Describe the presentation (and how this changes over time) of Huntington’s disease.

A
  • Irritability
  • Depression
  • Incoordination
  • Chorea
  • Over time, there is motor, neuropsychiatric, and cognitive decline
  • Will eventually develop dementia
604
Q

What is chorea?

A

Uncontrolled, random jerky movements

605
Q

Give three psychiatric problems experienced in Huntington’s disease.

A
  • Personality change
  • Depression
  • Psychosis
606
Q

Give four signs of Huntington’s disease.

A
  • Abnormal eye movements (problems initiating saccades, broken pursuit)
  • Chorea
  • Ataxia (problems with heel to toe walking)
  • Often have a touch of Parkinsonism
607
Q

Give two macroscopic features found in Huntington’s disease.

A
  • Atrophy of caudate nucleus and putamen

- Cortical atrophy may be present

608
Q

Give two microscopic features that may appear in Huntington’s disease.

A
  • Marked neuronal loss from caudate nucleus

- Surviving neurones contain abundant amounts of Huntingtin protein

609
Q

How is chorea treated in Huntington’s disease?

A

Neuroleptic (sulpiride)

610
Q

How is depression treated in Huntington’s disease?

A

Selective serotonin reuptake inhibitor (seroxate)

611
Q

How is psychosis treated in Huntington’s disease?

A

Neuroleptic (haloperidol)

612
Q

How is aggression treated in Huntington’s disease?

A

Risperidone

613
Q

What is the average survival time from the onset of symptoms in Huntington’s disease?

A

20yrs

614
Q

Give two common causes of death in Huntington’s disease.

A
  • Pneumonia

- Cardiac failure

615
Q

Why does cardiac failure occur in Huntington’s disease?

A

Abnormal Huntingtin expressed in cardiac muscle

616
Q

What are neuroleptic drugs?

A

Antipsychotics which depress nerve functioning.

617
Q

Give seven causes of spinal cord compression.

Which is the most common?

A
  • Secondary malignancy in spine (most common)
  • Infection (epidural abscess)
  • Cervical disk prolapse
  • Haematoma (Warfarin)
  • Intrinsic cord tumour
  • Atlanto-axial subluxation
  • Myeloma
618
Q

Describe the symptoms of spinal cord compression.

A
  • Weak legs
  • Spinal or root pain
  • Arm weakness
  • Bladder and anal sphincter involvement
619
Q

Compare the arm and leg weakness in spinal cord compression.

A

Arm weakness is usually less severe than leg weakness

620
Q

What does arm weakness indicate in spinal cord compression?

A

Cervical lesion

621
Q

At what stage of spinal cord compression is there bladder and anal sphincter involvement?

A

Late

622
Q

How does bladder and anal sphincter involvement manifest in spinal cord compression?

A
  • Hesitancy
  • Frequency
  • Painless retention
623
Q

Describe the leg weakness in spinal cord compression.

A

Spastic and hyperreflexic

624
Q

Describe the clinical examination findings above the level of the lesion in spinal cord compression.

A

Normal

625
Q

Describe the clinical examination findings of spinal cord compression at the level of the lesion.

A

Lower motor neurone signs

626
Q

Describe the clinical examination findings of spinal cord compression below the level of the lesion.

A

Upper motor neurone signs

627
Q

What is the definitive imaging modality to evaluate spinal cord compression?

A

MRI

628
Q

How is the nature of a mass causing a spinal cord compression investigated?

A

Biopsy or surgical exploration

629
Q

Give eight blood investigations that should be carried out in spinal cord compression.

A
  • FBC
  • ESR
  • B12
  • Syphilis
  • U and E
  • LFT
  • PSA
  • Serum electrophoresis
630
Q

Give another image/scan that must be carried out in spinal cord compression and explain why.

A

CXR to look for lung malignancy/TB

631
Q

What treatment should be carried out for cord compression caused by a malignancy, while considering more specific chemo/radiotherapy?

A

Dexamethosone

632
Q

Give a method of relieving spinal cord compression.

A

Decompressive laminectomy

633
Q

How should epidural abscesses be treated in spinal cord compression?

A

Surgical decompression and antibiotics

634
Q

Give eight differential diagnoses of spinal cord compression.

A
  • Transverse myelitis
  • MS
  • Carcinomatous meningitis
  • Cord vasculitis
  • Spinal artery thrombosis
  • Trauma
  • Dissecting aneurysm
  • Guillain-Barre
635
Q

Give five causes of unilateral foot drop.

A
  • Diabetes mellitus
  • Common peroneal nerve palsy
  • Stroke
  • Prolapsed disk
  • MS
636
Q

Give three causes of weak legs with no sensory loss.

A
  • Motor neurone disease
  • Polio
  • Parasagittal meningioma
637
Q

Give ten causes of chronic spastic paraparesis.

A
  • MS
  • Cord tumour
  • Cord metastases
  • Motor neurone disease
  • Syringomyelia
  • Subacute combined degeneration of the spinal cord
  • Hereditary spastic paraparesis
  • Taboparesis
  • Histiocytosis X
  • Parasites (Schistosomiasis)
638
Q

Give two causes of chronic flaccid paraparesis.

A
  • Peripheral neuropathy

- Myopathy

639
Q

Give three causes of absent knee jerks and extensor plantars.

A
  • Combined cervical and lumbar disk disease
  • Conus medullaris lesions
  • MAST (MND, ataxia, Subacute combined degeneration, Taboparesis)
640
Q

Describe the leg weakness in cauda equina and conus medullaris lesions.

A

Flaccid and areflexic

641
Q

Give the signs/symptoms of a conus medullaris lesion.

A
  • Mixed UMN/LMN leg weakness
  • Early urinary retention and constipation
  • Back pain
  • Sacral sensory disturbance
  • Erectile dysfunction
642
Q

Describe the signs/symptoms of cauda equina lesions.

A
  • Back pain
  • Radicular pain down legs
  • Asymmetrical, atrophic, areflexic paralysis of the legs
  • Sensory loss in a root distribution
  • Decreased sphincter tone
643
Q

Give four things to address when taking care of a paralysed patient.

A
  • Turn to avoid pressure sores
  • Anticoagulant, compression stockings, movement to avoid DVT
  • Bladder care (eg. Catheter)
  • Bowel evacuation may be needed
644
Q

What is myasthenia gravis?

A

An organ-specific autoimmune disease caused by the production of autoantibodies directed against the nicotinic acetylcholine receptor (nAChR) at the neuromuscular junction.

645
Q

At what age is myasthenia gravis more common in women?

A

<50yrs

646
Q

At what age is myasthenia gravis more common in males?

A

> 50yrs

647
Q

What percentage of patients with myasthenia gravis have a thymus abnormality?

A

75%

648
Q

What percentage of patients with myasthenia gravis have a thymoma?

A

5-10%

649
Q

Describe the pathology of myasthenia gravis.

A

Autoantibodies binding to the nAChR limit depolarisation at the motor end plate and therefore impair muscle contraction.

650
Q

What are the symptoms of myasthenia gravis?

A

Increasing muscular fatigue

651
Q

What muscles are affected in myasthenia gravis (in order of appearance of symptoms)?

A
  • Extraocular
  • Bulbar
  • Face
  • Neck
  • Limb girdle
  • Trunk
652
Q

What are the signs of myasthenia gravis?

A
  • Ptosis
  • Diplopia (complex ophthalmoplegia)
  • Myasthenic snarl on smiling
  • Dysarthria
  • Head drop
  • Limb fatigability
  • Peek sign
  • Voice fading
  • Normal tendon reflexes
  • Ice pack test (ptosis improves after application of ice pack)
  • Cogan’s lid twitch
653
Q

Give thirteen conditions/things that can worsen weakness in myasthenia gravis.

A
  • Pregnancy
  • Hypokalaemia
  • Infection
  • Over-treatment
  • Change of climate
  • Emotion
  • Exercise
  • Gentamicin
  • Opiates
  • Tetracycline
  • Quinine
  • Procainamide
  • Beta blockers
654
Q

Give three investigations that should be carried out in myasthenia gravis.

A
  • Antibodies
  • Neurophysiology
  • Imaging
655
Q

If the antibody test for AChR antibody is negative in myasthenia gravis, what other antibody should be looked for?

A

Anti-MuSK

656
Q

What does MuSK stand for?

A

Muscle specific tyrosine kinase

657
Q

What are MuSK and LRP4?

A

Proteins which support the acetylcholine receptor complex.

Can have antibodies against these in myasthenia gravis.

658
Q

What would be seen in neurophysiology tests in myasthenia gravis?

A

Decremental muscle response to repetitive electrical nerve stimulation.

659
Q

What imaging should be carried out in myasthenia gravis?

A

CT of thymus

660
Q

What age does ocular myasthenia gravis affect?

A

Any age

661
Q

Is ocular myasthenia gravis more common in males or females?

A

Males

662
Q

Describe the prognosis in ocular myasthenia gravis.

A

Most progress to generalised MG within a year.

663
Q

What percentage of patients with ocular myasthenia gravis have anti-AChR antibody?

A

50%

664
Q

How do most people with late-onset myasthenia gravis present?

A

Ocular MG

665
Q

Describe the prognosis in late-onset myasthenia gravis.

A

Becomes generalised after 2-3yrs

666
Q

Describe the thymus in Anti-MuSK myasthenia gravis.

A

Normal

667
Q

Describe the tongue, cheek, and orbit muscles in Anti-MuSK myasthenia gravis.

A

Fatty change occurs

668
Q

Describe the onset of anti-MuSK myasthenia gravis.

A
  • 36% have ocular onset

- 26% have oculo-bulbar onset

669
Q

What is congenital myasthenic syndrome?

A

Mutations in ColQ, DOK7, or CHRNE which produce a myasthenia gravis-like picture.

670
Q

What can be used to control symptoms in myasthenia gravis?

A

Acetylcholineesterase inhibitor (pyridostigmine)

671
Q

Give seven side effects of pyridostigmine.

A
  • Increased salivation
  • Lacrimation
  • Sweats
  • Vomiting
  • Miosis (excessive pupil constriction)
  • Diarrhoea
  • Colic
672
Q

How can relapses of myasthenia gravis be treated?

A

Prednisolone

673
Q

Give a steroid sparing agent used to treat myasthenia gravis.

A

Azathioprine

674
Q

Give a type of surgery which can be used to treat myasthenia gravis, and when it would be used.

A

Thymectomy

- Consider if onset <50yrs and not easily controlled by acetylcholineesterase inhibitors, and they are sero-positive

675
Q

How is Anti-MuSK myasthenia gravis treated?

A
  • Poor response to pyridostigmine

- Better response to rituximab

676
Q

Give five lifestyle changes/factors to help myasthenia gravis.

A
  • Avoid exacerbating drugs
  • Follow up in clinic
  • Exercise is safe
  • Encourage normal pregnancy
  • Avoid live vaccines
677
Q

Describe the prognosis in myasthenia gravis.

A

Relapsing, but not progressive symptoms.

678
Q

What is a myasthenic crisis?

A

Weakness of respiratory muscles during a relapse.

679
Q

How is a myasthenic crisis treated?

A

Plasmapheresis or IV Ig

680
Q

Give four differential diagnoses of myasthenia gravis.

A
  • Poliomyelitis
  • SLE
  • Takayasu’s arteritis
  • Botulism
681
Q

What is complex ophthalmoplegia?

A

Eye movements are reduced in all direction, and patient has double vision.

682
Q

Give six differential diagnoses for complex ophthalmoplegia.

A
  • Myasthenia gravis
  • Graves disease
  • Botulism toxin
  • Miller Fisher (variant of Guillan Barre)
  • Mitochondrial chronic progressive external ophthalmoplegia (CPEO)
  • Brainstem stroke
683
Q

Describe partial ptosis.

A

Eyelid drooping but still above the pupil.

684
Q

Describe complete ptosis.

A

Eyelid covers the pupil.

685
Q

Describe the criteria for exophthalmos.

A

Bottom eyelid below inferior limbus.

686
Q

Describe the criteria for lid retraction.

A

Top eyelid above superior limbus.

687
Q

Describe how muscle strength changes in Lambert-Eaton Myasthenic Syndrome.

A

Movements become stronger.

688
Q

Describe the presentation of Lambert-Eaton Myasthenic Syndrome.

A
  • Dry eyes and mouth
  • Limb weakness
  • Erectile dysfunction
689
Q

Describe the pathology in Lambert-Eaton Myasthenic Syndrome.

A

Usually associated with antibodies to voltage gated calcium channels in the presynaptic terminal.

690
Q

Give two causes (and their frequencies) of Lambert-Eaton Myasthenic Syndrome.

A
  • Autoimmune (50%)

- Paraneoplastic (50%)

691
Q

What cancer usually causes Lambert-Eaton Myasthenic Syndrome?

A

Small cell lung carcinoma

692
Q

What investigation can diagnose Lambert-Eaton Myasthenic Syndrome?

A

Incremental potential on repetitive stimulation of EMG.

693
Q

How is Lambert-Eaton Myasthenic Syndrome treated?

A
  • 3,4-diaminopyridine

- Immunosuppression

694
Q

What is the difference between dysarthria and dysphasia?

A

DYSARTHRIA
- Problem with speech and pronunciation (not language)

DYSPHASIA
- Problem with understanding and producing language

695
Q

What is the main role of the cerebellum?

A

Control the timing and pattern (coordination) of motor activation during movement.

696
Q

Give six causes of progressive ataxias (in order of prevalence).

A
  • Familial/genetic
  • Gluten ataxia (coeliac disease)
  • Idiopathic
  • Alcohol
  • Degenerative (multi-system atrophy)
  • Paraneoplastic
697
Q

What is the most common familial/genetic ataxia?

A

Friedreich’s ataxia

698
Q

Give three features of ataxia which may suggest it is paraneoplastic.

A
  • Rapid onset
  • Fast progression
  • Associated with oscillopsia
699
Q

What is the most likely cause of sporadic idiopathic ataxia?

A

Autoimmune

700
Q

Give three features of sporadic idiopathic ataxia which lead to the conclusion that it is likely to be autoimmune.

A
  • 47% have other autoimmune conditions
  • 71% have HLA DQ2
  • 60% have anti-cerebellar antibodies
701
Q

Give an autoantibody which has been linked to cerebellar ataxia.
Name another autoimmune disease in which this antibody has been implicated.

A

Anti-GAD

Also appears in T1DM.

702
Q

Describe the macroscopic changes to the cerebellum in autoimmune ataxia.

A

Swells at first and then becomes atrophic.

703
Q

Describe the symptoms of cerebellar ataxia.

A
  • Slurring/staccato speech
  • Swallowing difficulties
  • Oscillopsia
  • Clumsiness
  • Intention tremor
  • Unsteadiness when walking
  • Falls
  • Cognitive abnormalities
704
Q

Describe oscillopsia.

A
  • Patient experiences blurred vision, and objects in the visual field appear to oscillate
  • Other people see involuntary eye movement of both eyes in random directions
705
Q

Describe the signs of cerebellar ataxia.

A
  • Dysarthria
  • Nystagmus
  • Limb ataxia
  • Intention tremor
  • Truncal ataxia
  • Gait ataxia
  • Oscillopsia
706
Q

What is it called when damage to the cerebellum leads to cognitive abnormalities?

A

Cerebellar cognitive affective syndrome

707
Q

Give four cognitive processes that can be abnormal in cerebellar cognitive affective syndrome.

A
  • Sequencing
  • Language
  • Executive function
  • Visuospatial abilities
708
Q

Give the four classifications of ataxia.

A
  • Congenital
  • Diseases where ataxia is one of the many features
  • Familial ataxia (divided into autosomal dominant and recessive)
  • Sporadic (acquired) ataxias

*Ataxias due to structural damage is not included in the classification

709
Q

What investigation should be carried out in people with ataxia and why?

A

MRI scan to exclude structural problems.

710
Q

What spinal roots form the median nerve?

A

C6-T1

711
Q

Give the signs of a median nerve lesion at the wrist.

A
  • Weakness of abductor pollicis brevis

- Sensory loss over radial 3.5 fingers and palm

712
Q

Give a sign of a median nerve lesion of the anterior interosseous nerve.

A

Weakness of flexion of distal phalanx of thumb and index finger.

713
Q

Give the causes of carpel tunnel syndrome.

A

MEDIAN TRAPS

  • Myxoedema
  • Enforced flexion (eg. Colles’ splint)
  • Diabetic neuropathy
  • Idiopathic
  • Acromegaly
  • Neoplasms
  • Tumours
  • Rheumatoid arthritis
  • Amyloidosis
  • Pregnancy/pre-menstrual oedema
  • Sarcoidosis
714
Q

Give three treatment options for carpel tunnel syndrome.

A
  • Splinting
  • Local steroid injection
  • Decompression surgery
715
Q

Give a sign of a brachial plexus lesion.

A

Pain/paraesthesiae and weakness in affected arm in a variable distribution.

716
Q

Give six causes of a brachial plexus lesion.

A
  • Trauma
  • Radiotherapy (breast carcinoma)
  • Heavy rucksack
  • Cervical rib
  • Thoracic outlet compression
  • Neuralgic amyotrophy
717
Q

What spinal roots make up the ulnar nerve?

A

C7-T1

718
Q

What is the most common cause of an ulnar nerve lesion.

A

Elbow trauma

719
Q

What are the signs of an ulnar nerve lesion?

A
  • Weakness/wasting of medial wrist flexors, interossei, and medial lumbricals (claw hand)
  • Hypothenar eminence wasting
  • Sensory loss over medial 1.5 fingers and ulnar aide of hand
  • Weak flexion of 4th and 5th DIPJ
720
Q

Give three treatment options for an ulnar nerve lesion.

A
  • Rest and avoid elbow pressure
  • Soft elbow splinting
  • Surgery
721
Q

What spinal roots make up the radial nerve?

A

C5-T1

722
Q

What is the most common cause of a radial nerve lesion?

A

Compression against the humerus

723
Q

What are the signs of a radial nerve lesion?

A
  • Test for wrist and finger drop with elbow flexed and arm pronated
  • Variable sensory loss (anatomical snuff box reliably affected)
724
Q

Give four muscles or groups of muscles involved with a radial nerve lesion.

A

BEST

  • Brachioradialis
  • Extensors
  • Supinator
  • Triceps
725
Q

What spinal roots make up the lateral cutaneous nerve of the thigh?

A

L2-L3

726
Q

Give a sign of a lesion of the lateral cutaneous nerve of the thigh.

A

Meralgia paraesthetica is anterolateral burning thigh pain from entrapment under the inguinal ligament.

727
Q

What spinal roots supply the phrenic nerve?

A

C3-C5

728
Q

Give two signs of a phrenic nerve lesion.

A
  • Orthopnoea

- Raised hemidiaphragm on CXR

729
Q

Give 13 causes of a phrenic nerve lesion.

A
  • Lung cancer
  • Myeloma
  • Thymoma
  • Cervical spondylosis/trauma
  • Thoracic surgery
  • Muscular dystrophy
  • Phrenic nucleus lesion (eg. MS)
  • C3-C5 zoster
  • HIV
  • Lyme disease
  • TB
  • Paraneoplastic syndromes
  • Big left atrium
730
Q

What spinal roots make up the sciatic nerve?

A

L4-S3

731
Q

Give two causes of a sciatic nerve lesion.

A
  • Pelvic tumours

- Pelvic/femur fractures

732
Q

What are the symptoms of a sciatic nerve lesion?

A
  • Lesions affect hamstrings and all muscles below the knee
  • Foot drop
  • Loss of sensation below knee (laterally)
733
Q

What spinal roots make up the tibial nerve?

A

L4-S3

734
Q

What are the signs of a tibial nerve lesion?

A
  • Inability to stand on tiptoe (plantar flexion)
  • Can’t invert foot
  • Can’t flex toes
  • Sensory loss over sole
735
Q

What spinal roots make up the common peroneal nerve?

A

L4-S1

736
Q

Where is the most common place that a common peroneal nerve lesion occurs?

A

It gets damaged as it winds around the fibular head.

737
Q

Give two causes of a common peroneal nerve lesion.

A
  • Trauma

- Sitting cross-legged

738
Q

What are the signs of a common peroneal nerve lesion?

A
  • Foot drop
  • Weak ankle dorsiflexion/eversion
  • Sensory loss over dorsum of foot
739
Q

What is meant by a ‘functional symptom’?

A

Abnormality with the function of the body, with the structure still in tact.
Nothing will be found on examination or investigation.

740
Q

What is meant by an ‘organic symptom’?

A

Structural abnormality with the body that can be detected on examination or investigations.

741
Q

What is meant by ‘somatisation’?

A

The manifestation of psychological distress by the presentation of physical symptoms.

742
Q

What is meant by ‘dissociation’?

A

Dissociating immediate reality into alternative reality by disconnecting from thoughts and feelings.

743
Q

Give eight things that should be examined in a mental state examination.

A
  • Appearance
  • Behaviour
  • Speech
  • Mood
  • Thoughts
  • Perception
  • Cognition
  • Insight
744
Q

What is one set of functions/symptoms that the MMSE doesn’t test for?

A

Frontal lobe functions

745
Q

How does ECT work?

A

Induces seizure into the patient.

746
Q

When is ECT used?

A

For severely depressed patients.

747
Q

Give an advantage and a disadvantage of ECT.

A

ADVANTAGE
- Works fast

DISADVANTAGE
- Can affect episodic memory

748
Q

How do most antipsychotic medications (eg. Haloperidol) work?

A

Block D2 (dopamine) receptor

749
Q

What is depression caused by in Parkinson’s disease?

A

Serotonin, noradrenaline, and dopamine depletion

750
Q

What causes psychosis when treating Parkinson’s disease?

A

Excess dopamine

751
Q

The depletion of which neurotransmitter causes memory impairment in Alzheimer’s disease?

A

Acetylcholine

752
Q

Describe the typical pattern of symptoms if a lesion is in the cerebral hemisphere.

A

Unilateral

753
Q

Describe the typical pattern of symptoms if a lesion is in the spinal cord.

A

Bilateral spastic paraparesis

754
Q

Describe the typical pattern of symptoms if a lesion is in the cerebellum.

A

Coordination problems

755
Q

Describe the typical pattern of symptoms if a lesion is in the brainstem.

A

Unpredictable and symptoms that don’t seem to follow a logical pattern.

756
Q

Describe the typical pattern of symptoms if a lesion is in the peripheral nerves.

A

Symmetrical glove and stocking LMN distribution.

757
Q

Is flashing lights a positive or negative symptom?

A

Positive

758
Q

Give two conditions that may cause patients to see flashing lights.

A
  • Migraine

- Seizures

759
Q

Is visual loss a positive or negative symptom?

A

Negative

760
Q

What condition would result from a lesion of the right optic nerve?

A

Right monocular blindness

761
Q

What condition would result from a lesion of the optic chiasm?

A

Bitemporal hemianopia

762
Q

What condition would result from a lesion of the right optic tract?

A

Left homonymous hemianopia

763
Q

What condition would result from a lesion of the right Meyer’s loop?

A

Left homonymous superior quadrantanopia

764
Q

What condition would result from a lesion of the right baum’s loop?

A

Left homonymous inferior quadrantanopia

765
Q

What condition would result from a lesion of the right primary visual field?

A

Left homonymous hemianopia with macular sparing

766
Q

What is a ‘100%’ sensitive sign of a III cranial nerve palsy due to a space occupying lesion?

A

Pupil involvement

767
Q

Why isn’t pupil involvement in a III cranial nerve palsy specific for a space occupying lesion?

A

It can also occur with a ‘medical’ III nerve palsy (eg. Diabetes).

768
Q

Give the three aspects of Horner’s syndrome.

A
  • Anhydrosis
  • Miosis (small pupil)
  • Ptosis
769
Q

What is Horner’s syndrome caused by?

A

Damage to the sympathetic nerve supply of the face

770
Q

What signs are seen on the ipsilateral side in lateral medullary syndrome?

A
  • Horner’s syndrome
  • Limb ataxia
  • Loss of facial sensation of pain and temperature
  • Reduced corneal reflex
  • Dysarthria
  • Dysphagia
771
Q

What signs are seen on the contralateral side in lateral medullary syndrome?

A

Loss of pain and temperature sensation

772
Q

What symptoms will be seen at the level of the lesion in Brown Sequard Syndrome?

A

Ipsilateral loss of pain and temperature

773
Q

Give three types of primary headache.

A
  • Migraine
  • Cluster
  • Tension type
774
Q

Give five causes of secondary headache.

A
  • Meningitis
  • Subarachnoid haemorrhage
  • Giant cell arteritis
  • Idiopathic intracranial hypertension
  • Medication overuse headache
775
Q

Give a ‘miscellaneous’ type of headache.

A

Trigeminal neuralgia

776
Q

Give four features of the history of headaches which suggest a secondary headache.

A
  • Age >50yrs
  • History of HIV/cancer/trauma/risk factors for cerebral venous sinus thrombosis
  • Changing personality or cognitive dysfunction
  • Vomiting without any other obvious cause
777
Q

Give seven features of the headaches themselves which suggest a secondary cause.

A
  • Jaw claudication/visual disturbance
  • Severe eye pain
  • Changing in frequency, characteristics, or associated symptoms
  • Postural
  • Sudden onset/thunderclap
  • Exacerbated by exercise or valsalva (eg. Coughing, laughing, straining)
  • Focal neurological symptoms
778
Q

Give four features on examination that may suggest a secondary cause for a headache.

A
  • Fever
  • Altered conciousness
  • Neck stiffness
  • Other abnormal neurological examination
779
Q

Give six indications for immediate referral for a headache.

A
  • Thunderclap headache
  • Seizure and new headache
  • Suspected meningitis
  • Suspected encephalitis
  • Red eye
  • Headache + new focal neurology (including papilloedema)
780
Q

Give six red flags for a brain tumour when a patient presents with a headache.

A
  • New headache with a history of cancer
  • Cluster headache
  • Seizure
  • Significantly altered conciousness, memory, confusion, coordination
  • Papilloedema
  • Other abnormal neurological exam or symptom
781
Q

Give four treatment approaches to treating headaches.

A
  • Lifestyle modification and trigger management
  • Pharmacological treatment
  • Psychological and behavioural treatments
  • Surgical treatments
782
Q

Give two pharmacological abortive treatments of a migraine.

A
  • Combination therapy with oral triptan + NSAID/paracetamol

- Anti-emetic

783
Q

What two medications are usually used to prevent migraine.

A
  • Topimarate

- Propranolol

784
Q

Give two alternative treatments for prevention of migraines.

A
  • Acupuncture

- Amitriptyline

785
Q

Give a lifestyle ‘supplement’ that may help to prevent migraines.

A

Riboflavin

786
Q

Give a ‘last resort’ treatment for prevention of migraines if there has been failure to respond to at least three prior pharmacological treatments.

A

Botulinum toxin type A

787
Q

Give four pharmacological treatments for trigeminal neuralgia.

A
  • Carbamazepine
  • Lamotrigine
  • Phenytoin
  • Gabapentin
788
Q

Give two treatments for acute attacks of cluster headaches.

A
  • 100% oxygen for about 15 minutes via non-rebreathable mask (not in COPD)
  • Sumatripan
789
Q

Give five treatments for preventing cluster headaches.

A
  • Suboccipital steroid injections
  • Intranasal civamide
  • Verapamil
  • Lithium
  • Melatonin
790
Q

How many attacks does someone have to have to be diagnosed with a migraine without aura?

A

5 attacks

791
Q

How long does a migraine last?

A

4-72 hours

792
Q

2 of the following 4 features should be present to diagnose a migraine…

A
  • Unilateral
  • Pulsing
  • Moderate/severe
  • Aggravation by routine physical activity
793
Q

During a migraine headache, at least one of the following 2 features should occur…

A
  • Nausea and/or vomiting

- Photophobia and phonophobia

794
Q

How many attacks must the patient have had to be diagnosed with a migraine with aura?

A

2

795
Q

Describe the motor weakness experienced in a migraine aura.

A

No motor weakness

796
Q

Describe two types of migraine aura symptoms.

A
  • Fully reversible visual symptoms including positive features and/or negative features
  • Fully reversible dysphasic speech disturbance
797
Q

In a migraine aura, are the visual symptoms the same or different in each eye?

A

Homonymous (same in each eye)

798
Q

In a migraine aura, are the sensory symptoms unilateral or bilateral?

A

Unilateral

799
Q

Describe the timing of symptoms of a migraine aura.

A
  • At least one aura symptom develops gradually over >5mins and/or different aura symptoms occur in succession over >5mins
  • Each symptom lasts >5mins and <60mins
800
Q

When does the headache occur in a migraine with aura?

A

During aura or follows within 60mins

801
Q

Give nine possible triggers for migraines.

A

CHOCOLATE

  • Chocolate
  • Hangovers
  • Orgasms
  • Cheese
  • Oral contraceptives
  • Lie-ins
  • Alcohol
  • Tumult
  • Exercise
802
Q

Give three ‘types’ of tension type headache.

A
  • Infrequent
  • Frequent
  • Chronic
803
Q

How many and how often do infrequent tension type headaches occur?

A

> 10 attacks occurring <1day/month

804
Q

How long does a tension type headache last?

A

30 minutes to 7 days

805
Q

A tension type headache has 2 of the following characteristics…

A
  • Bilateral
  • Pressing/tightening (not pulsating) quality
  • Mild/moderate intensity
  • Not aggravated by routine physical activity
806
Q

Does nausea/vomiting occur in tension type headaches?

A

No

807
Q

Does photo/phonophobia occur in tension type headaches?

A

No more than one should occur

808
Q

How common are cluster headaches?

A

Not very common

809
Q

How many attacks must someone have to be diagnosed with cluster headaches.

A

5

810
Q

Describe the severity of pain in cluster headaches.

A

Severe or very severe

811
Q

Where is the pain felt in cluster headaches?

A

Unilateral orbital, supraorbital, and/or temporal pain

812
Q

How long do cluster headaches last if left untreated?

A

5-180minutes

813
Q

Give another feature that occurs with cluster headaches.

A

Ipsilateral cranial autonomic features and/or a sense of restlessness or agitation.

814
Q

Describe the frequency of attacks in cluster headaches.

A

1 every other day to 8 per day

815
Q

Describe episodic cluster headaches.

A

> 2 cluster periods lasting 7 days to 1 year separated by pain free periods lasting >1 month.

816
Q

Describe chronic cluster headaches.

A

Attacks occur for more than 1 year without remission or with remission lasting <1month.

817
Q

How many attacks does a patient need to have to be diagnosed with trigeminal neuralgia?

A

3

818
Q

Is the pain unilateral or bilateral in trigeminal neuralgia?

A

Unilateral

819
Q

Describe where the pain occurs in trigeminal neuralgia.

A

One or more distributions of the trigeminal nerve, with no radiation beyond the trigeminal distribution.

820
Q

The pain felt in trigeminal neuralgia has at least 3 of the following 4 characteristics….

A
  • Reoccurring in paroxysmal attacks from a fraction of a second to 2 minutes
  • Severe intensity
  • Electric shock like, shooting, stabbing, or sharp
  • Precipitated by innoculous stimuli to the affected side of the face
821
Q

How long does the pain last in trigeminal neuralgia?

A

Fraction of a second to 2 minutes

822
Q

Describe chronic daily headaches.

A

Headache on >15days per month

823
Q

Give six primary causes of chronic daily headaches.

A
  • Chronic migraine
  • Chronic tension type headache
  • Chronic cluster headache
  • Chronic paroxysmal hemicranias
  • Hemicrania continua
  • New daily persistent headache
824
Q

Give five secondary causes of chronic daily headache.

A
  • Medication overuse headache
  • Chronic post-traumatic headache
  • Raised intracranial pressure
  • Low CSF pressure headache
  • Chronic meningitis
825
Q

How often is a medication overuse headache present?

A

> 15days/month

826
Q

Give four medications likely to cause a medication overuse headache.

A
  • Ergotamine
  • Triptans
  • Opioids
  • Common analgesic medications
827
Q

How are medication overuse headaches treated?

A

Stopping analgesics

828
Q

Give four aetiologies (and examples) of an olfactory nerve lesion.

A
  • Trauma (ethmoid bone fracture)
  • Neurodegenerative disease (Alzheimer’s)
  • Congenital (Kallmann syndrome)
  • Space occupying lesion
829
Q

What are the clinical features of an olfactory nerve lesion?

A

Anosmia

830
Q

Give six aetiologies (and examples) of an optic nerve lesion.

A
  • Ischaemic optic neuropathy
  • Inflammation (MS)
  • Trauma
  • Tumours
  • Impaired nutrition (B12 deficiency)
  • Drugs
831
Q

Give two clinical features of an optic nerve lesion.

A
  • Impaired vision

- Loss of pupillary light reflex

832
Q

Give two aetiologies of an oculomotor nerve lesion.

A
  • Ischaemic

- Compression

833
Q

Give four clinical features of an oculomotor nerve lesion.

A
  • Eye looks down and out
  • Ptosis
  • Horizontal diplopia
  • Fixed dilated pupil (usually happens in compressive trauma)
834
Q

Give three aetiologies of a trochlear nerve lesion.

A
  • Microvascular damage
  • Trauma
  • Cavernous sinus thrombosis
835
Q

Give three clinical features of a trochlear nerve lesion.

A
  • Extorsion of eye
  • Diplopia (especially when looking down)
  • Mild esotropia (eyes turn in)
836
Q

Give five aetiologies of a trigeminal nerve lesion.

A
  • Tumour
  • Vascular compression
  • Oral surgery
  • Inflammation
  • Cavernous sinus thrombosis
837
Q

Give two clinical features of a V1 trigeminal nerve lesion.

A
  • Absent corneal reflex

- Anaesthesia of forehead

838
Q

Give a clinical feature of a V2 trigeminal nerve lesion.

A
  • Anaesthesia of midface
839
Q

Give two clinical features of a V3 trigeminal nerve lesion.

A
  • Anaesthesia of chin, lower lip, and anterior 2/3 of tongue

- Muscles of mastication paralysed

840
Q

Give a clinical feature of a lesion to the tensor tympani branch of the trigeminal nerve.

A

Hearing impairment

841
Q

Give two general features of a trigeminal nerve lesion.

A
  • Jaw deviates to affected side

- Trigeminal neuralgia

842
Q

Give five aetiologies of an abducens nerve lesion.

A
  • Tumour
  • Trauma
  • Pseudotumour cerebri (benign intracranial hypertension)
  • Cavernous sinus thrombosis
  • Duane syndrome (congenital palsy of abducens nerve)
843
Q

Give two clinical features of an abducens nerve lesion.

A
  • Horizontal diplopia

- Esotropia (medial deviation of eyes)

844
Q

Give nine aetiologies of facial nerve lesions.

A
  • Trauma
  • Infection (Herpes, Lyme)
  • Tumours
  • Pregnancy
  • Diabetes
  • Guillan Barre
  • Sarcoidosis
  • Amyloidosis
  • Stroke
845
Q

Give a clinical feature of a central facial nerve lesion.

A

Contralateral mouth drooping

846
Q

Give three clinical features of a peripheral facial nerve lesion.

A
  • Ipsilateral inability to frown
  • Ipsilateral inability to close eyelids
  • Ipsilateral mouth drooping
847
Q

Give two general clinical features of a facial nerve lesion.

A
  • Taste disorders

- Dry mouth/eyes

848
Q

Give three aetiologies of a vestibulocochlear nerve lesion.

A
  • Bacterial meningitis
  • Lyme disease
  • Tumour
849
Q

Give four clinical features of a vestibulocochlear nerve lesion.

A
  • Sensorineural hearing loss
  • Vertigo
  • Horizontal nystagmus
  • Motion sickness
850
Q

What is the usual cause of a glossopharyngeal nerve lesion?

A

Often unknown (may be associated with compression by a blood vessel)

851
Q

Give six clinical features of a glossopharyngeal nerve lesion.

A
  • Loss of gag reflex
  • Loss of carotid sinus reflex
  • Flaccid paralysis of soft palate
  • Sensory loss over soft palate
  • Mild dysphagia
  • Throat/ear pain (glossopharyngeal neuralgia)
852
Q

Give five aetiologies of a vagus nerve lesion.

A
  • Trauma
  • Diabetes
  • Inflammation
  • Aortic aneurysms
  • Tumours
853
Q

Give six clinical features of a vagus nerve lesion.

A
  • Loss of gag reflex
  • Flaccid paralysis of soft palate
  • Epiglottic paralysis (aspiration)
  • Dysphagia
  • Vocal cord paralysis
  • Gastroparesis (poor gastric emptying)
854
Q

Give an aetiology of an accessory nerve lesion.

A
  • Surgery in lateral cervical region
855
Q

Give two clinical features of an accessory nerve lesion.

A
  • Paresis of sternocleidomastoid

- Paresis of trapezius

856
Q

Give two aetiologies of a hypoglossal nerve lesion.

A
  • Tumours

- Trauma

857
Q

Give two clinical features of a hypoglossal nerve lesion.

A
  • Atrophy and fasciculation of tongue

- Tongue deviates to side of lesion when protruded

858
Q

Give another name for Bell’s Palsy.

A

Idiopathic facial nerve lesion

859
Q

Give two risk factors for Bell’s Palsy.

A
  • Pregnancy

- Diabetes

860
Q

Give a form of treatment which may speed up recovery in Bell’s Palsy.

A

Steroids (Prednisolone)

861
Q

What is a stroke?

A

A clinical syndrome, caused by cerebral infarction or haemorrhage, typified by rapidly developing signs of focal and global disturbance of cerebral function lasting more than 24hrs or leading to death.

862
Q

Give four pathological causes of stroke.

A
  • Small vessel occlusion/cerebral microangiopathy or thrombosis in situ
  • Cardiac emboli
  • Atherothromboembolism
  • CNS bleeds
863
Q

Give three causes of cardiac Emboli which may cause a stroke.

A
  • Atrial fibrillation
  • Endocarditis
  • MI
864
Q

Give five potential causes of CNS bleeds.

A
  • Hypertension
  • Trauma
  • Aneurysm rupture
  • Anticoagulation
  • Thrombolysis
865
Q

Give two types of CNS bleeds which can cause a stroke.

A
  • Intracerebral haemorrhage

- Subarachnoid haemorrhage

866
Q

Give many risk factors for a stroke.

A
  • Hypertension
  • Smoking
  • Diabetes mellitus
  • Heart disease (valvular, ischaemic, atrial fibrillation)
  • Peripheral vascular disease
  • Past TIA
  • Increased packed cell volume
  • Carotid bruit
  • Oral contraceptive pill
  • Hyperlipidaemia
  • Alcohol overuse
  • Increased clotting
  • Increased homocysteine
  • Syphilis
867
Q

Give many differential diagnoses of a stroke.

A
  • Head injury
  • Hypo/hyperglycaemia
  • Subdural haemorrhage
  • Intracranial tumours
  • Hemiplegic migraine
  • Epilepsy (Todd’s palsy)
  • CNS lymphoma
  • Pneumocephalus (air entry via otitis or mastoid air cells)
  • Wernicke’s encephalopathy
  • Drug overdose
  • Hepatic encephalopathy
  • Mitochondrial cytopathies
  • Herpes encephalitis
  • HIV, HTLV-1, toxoplasmosis
  • Abscesses (eg. Typhoid)
  • Mycotic aneurysm
  • Coccidiodes immitis
  • Acanthamoeba/naegleria
868
Q

Describe the rate of onset of stroke symptoms.

A
  • Sudden onset

- May have further progression over hours (rarely days)

869
Q

Give six signs/symptoms of anterior cerebral artery stroke.

A
  • Leg weakness
  • Sensory disturbance in legs
  • Gait apraxia (truncal ataxia)
  • Incontinence
  • Drowsiness
  • Akinetic mutism (decrease in spontaneous speech, stuporus state)
870
Q

Give six clinical features of a middle cerebral artery stroke.

A
  • Contralateral arm and leg weakness
  • Contralateral sensory loss
  • Hemianopia
  • Aphasia
  • Dysphasia
  • Facial droop
871
Q

Give six clinical features of a posterior cerebral artery stroke.

A
  • Contralateral homonymous hemianopia
  • Cortical blindness with bilateral involvement of occipital lobe branches
  • Visual agnosia (can’t interpret visual information, but can see)
  • Prospagnosia (inability to recognise faces)
  • Dyslexia, anomic aphasia, colour naming, and discrimination problems
  • Unilateral headaches
872
Q

Give five clinical features of posterior circulation strokes.

A
  • Motor deficits (hemiparesis, tetraparesis, facial paresis)
  • Dysarthria and speech impairment
  • Vertigo, nausea, vomiting
  • Visual disturbances
  • Altered conciousness
873
Q

Give three clinical features of brainstem infarcts.

A
  • Quadriplegia
  • Disturbances of gaze and vision
  • Locked-in syndrome
874
Q

Give four structures that may be affected in lacunar infarcts.

A
  • Basal ganglia
  • Internal capsule
  • Thalamus
  • Pons
875
Q

Give the five potential syndromes resulting from lacunar infarcts.

A
  • Ataxic hemiparesis
  • Pure motor
  • Pure sensory
  • Sensorimotor
  • Dysarthria/clumsy hand
876
Q

Give three (unreliable) signs which may suggest a haemorrhagic stroke.

A
  • Meningism
  • Severe headache
  • Coma within hours
877
Q

Give four signs which may suggest an ischaemic stroke.

A
  • Carotid bruit
  • Atrial fibrillation
  • Past TIA
  • Ischaemic heart disease
878
Q

Why should pulse/BP/ECG be carried out in a stroke?

A

Rule out atrial fibrillation

879
Q

When should hypertension be treated if someone is having a stroke?

A

Treating high blood pressure may cause harm.

880
Q

What blood glucose should be aimed for in a patient having a stroke?

A

4-11mmol/L

881
Q

Give four indications for an urgent CT/MRI in a stroke patient.

A
  • Thrombolysis considered
  • Cerebellar stroke
  • Unusual presentation
  • High risk of haemorrhage
882
Q

Stroke patients should be imaged ideally within what time frame?

A

24hrs

883
Q

Which type of imaging is most sensitive for an acute infarct in a stroke?

A

Diffusion-weighted MRI

884
Q

What type of imaging best rules out a primary haemorrhage in a stroke patient?

A

CT

885
Q

When can thrombolysis be given for a stroke?

A

Up to 4.5 hours post onset of symptoms

886
Q

Describe what is used as thrombolysis treatment in a stroke.

A

Recombinant tissue plasminogen activator (Alteplase)

887
Q

Give eight contraindications to thrombolysis in a stroke patient.

A
  • Recent surgery
  • Recent arterial puncture
  • History of active malignancy
  • Evidence of brain aneurysms
  • Patient on anticoagulation
  • Severe liver disease
  • Acute pancreatitis
  • Clotting disorder
888
Q

When should a stroke patient be on ‘nil by mouth’?

A

If swallowing attempts might lead to choking

889
Q

When can antiplatelet agents be used to treat a stroke?

A

Only once haemorrhagic stroke is excluded

890
Q

What antiplatelet agent is given in a stroke?

A

Aspirin

891
Q

What is the mortality after a first stroke by day 56?

A

12%

892
Q

In what percentage of patients does a full recovery occur after a stroke?

A

Less than 40%

893
Q

Give six complications of a stroke.

A
  • Aspiration pneumonia
  • Pressure sores
  • Contractures
  • Constipation
  • Depression
  • Stress in spouse
894
Q

Give eight general methods of primary prevention for a stroke.

A
  • Platelet treatments
  • Lower cholesterol
  • Treat atrial fibrillation
  • Lower blood pressure
  • Smoking cessation
  • Control diabetes
  • Folate supplements may help
  • Lifelong anticoagulation if rheumatic or prosthetic heart valves
895
Q

Give three antiplatelet agents that can help to prevent stroke.

A
  • Aspirin
  • Dipyridamole
  • Clopidogrel
896
Q

Give two treatments that can help to prevent stroke in atrial fibrillation.

A
  • Warfarin

- DOACs

897
Q

What antiplatelet agent is commonly used for secondary prevention of a stroke?

A

Clopidogrel

898
Q

Describe anticoagulation treatment regimes after a stroke.

A
  • Start warfarin two weeks after stroke
  • Use antiplatelet therapy until anticoagulated
  • If already anticoagulated, replace with antiplatelet for one week
899
Q

Give three things to look out for which may indicate hypertension in a stroke assessment.

A
  • Retinopathy
  • Nephropathy
  • Cardiomegaly on CXR
900
Q

Give three investigations which may be carried out to assess cardiac sources of emboli in a stroke.

A
  • 24hr ECG to look for atrial fibrillation
  • CXR might show enlarged left atrium
  • Echocardiogram may show thrombus or valvular lesions
901
Q

How would carotid artery stenosis be assess in a stroke?

A

Carotid doppler ultrasound +/- CT/MRI angiography

902
Q

What is a transient ischaemic attack?

A

Sudden onset of focal CNS phenomena due to temporary occlusion of part of the cerebral circulation, usually by emboli, lasting <24hrs.

903
Q

What percentage of first strokes are preceded by a TIA?

A

15%

904
Q

As well as strokes, give another condition that TIAs are a warning sign for.

A

Myocardial infarction

905
Q

Compare the signs of a TIA and a stroke.

A

Features of a TIA mimic those of a stroke in the same arterial territory.

906
Q

Do global events (syncope, dizziness) usually occur in a TIA?

A

No

907
Q

Give a feature of TIAs which suggests critical intracranial stenosis.

A

Multiple highly stereotyped attacks

908
Q

In a TIA, what might the patient experience if there is an embolus in the retinal artery?

A

Amaurosis fugax

909
Q

Give five signs that point to specific causes of a TIA.

A
  • Carotid bruit
  • Hypertension
  • Heart murmur from valve disease
  • Atrial fibrillation
  • Fundoscopy may show retinal artery emboli
910
Q

Give four causes of a TIA.

A
  • Atherothromboembolism
  • Cardioembolism
  • Hyperviscosity
  • Vasculitis (rare)
911
Q

Give five differential diagnoses of a TIA.

A
  • Hypoglycaemia
  • Migraine aura
  • Focal epilepsy
  • Hyperventilation
  • Retinal bleeds
912
Q

Give six rare differential diagnoses of a TIA.

A
  • Malignant hypertension
  • MS
  • Intracranial tumours
  • Peripheral neuropathy
  • Phaeochromocytoma
  • Somatization
913
Q

Give six investigations to carry out in a TIA.

A
  • Bloods
  • CXR
  • ECG
  • Carotid doppler +/- angiography
  • CT or diffusion-weighted MRI
  • Echocardiogram
914
Q

Give four general approaches to management of a TIA.

A
  • Control cardiovascular risk factors
  • Antiplatelet drugs
  • Warfarin
  • Carotid endarterectomy
915
Q

Give four ways to control cardiovascular risk factors after a TIA.

A
  • Lower blood pressure
  • Control hyperlipidaemia
  • Control diabetes
  • Smoking cessation
916
Q

Give three antiplatelet drugs that might be started after a TIA.

A
  • Clopidogrel
  • Aspirin
  • Dipyidamole
917
Q

When is warfarin given after a TIA.

A

If it was caused by cardiac emboli

918
Q

What is an endarterectomy?

A

Surgery to remove an atheromatous plaque

919
Q

When is a carotid enderterectomy carried out in a TIA?

A

If >70% stenosis at origin of internal carotid artery and operative risk is good.

920
Q

What system is used to determine whether urgent referral is required after a TIA?

A

ABCD2

921
Q

Give the elements of ABCD2.

A
  • Age >60yrs (1)
  • Blood pressure >140/90 (1)
  • Clinical features (unilateral weakness (2), speech disturbance without weakness (1))
  • Duration of symptoms (>1hr (2), 10-59mins (1))
  • Diabetes (1)
922
Q

A score of _______ on ABCD2 is strongly predictive that the patient will have a stroke.

A

6+

923
Q

A score of ______ on ABCD2 indicates that the patient should be seen by a specialist in 24 hrs.

A

4+

924
Q

All patients with a suspected TIA should be seen by a specialist within ____________.

A

7 days

925
Q

How long should the patient avoid driving after a TIA?

A

1 month

926
Q

When should the DVLA be informed about TIAs.

A

Multiple attacks in a short period, or residual deficit

927
Q

What is the risk of a stroke within 90 days if a patient is treated for a TIA within 72hrs?

A

2%

928
Q

What is the risk of a stroke within 90 days is a TIA is treated within 3 weeks?

A

10%

929
Q

What is the combined risk of a stroke and MI per year after a TIA?

A

9%

930
Q

Compare the rate of onset in delirium and dementia.

A

DELIRIUM
- Acute (hours to days)

DEMENTIA
- Insidious (months to years)

931
Q

Compare the course of the condition in delirium and dementia.

A

DELIRIUM
- Fluctuating

DEMENTIA
- Progressive

932
Q

Compare the duration of delirium and dementia.

A

DELIRIUM
- Hours to weeks

DEMENTIA
- Months to years

933
Q

Compare the consciousness levels in delirium and dementia.

A

DELIRIUM
- Altered

DEMENTIA
- Normal unless severe

934
Q

Use the pneumonic to give the signs/symptoms of multiple sclerosis.

A

DEMYELINATION

  • Diplopia
  • Eye movements painful (optic neuritis)
  • Motor weakness
  • nYstagmus
  • Elevated temperature worsens symptoms (Uhthoff’s phenomenon)
  • Lhermitte’s sign
  • Intention tremor
  • Neuropathic pain
  • Ataxia
  • Talking slurred
  • Impotence
  • Overactive bladder
  • Numbness

Phase2a (12 decks)

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