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4th year everything > neurology > Flashcards

neurology Flashcards

1
Q

spastic gait

A

Pace shortens and narrow base is maintained

more pronounced in extensor muscles causing stiff and slow walking.

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2
Q

parkinsonian gait

A

posture is stooped and arm swing reduced

gait becomes hesitant with shorter rapid steps which slows down to a shuffle in advanced disease

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3
Q

Describe the presentation of cerebellar ataxia

A

In lateral cerebellar disease - stance becomes broad-based and uncoordinated

In midline (vermis) cerebellar disease - truncal ataxia leads to a tendency to fall backwards or sideways

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4
Q

Outline the effect of gait occurring in sensory ataxia?

A

Loss of proprioception - leading to a broad-based, high-stepping gait

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5
Q

syncope

A

a short duration (usually 20-30s) of loss of consciousness caused by a global reduction in cerebral blood flow

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6
Q

components of motor axis

A

motor cortex
corticospinal tracts
anterior horn cells
spinal nerve roots
peripheral nerves
neuromuscular junctions
muscle fibres

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7
Q

components of pyramidal system

A

corticospinal tract

corticobulbar tract

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8
Q

upper motor neurone lesion features

A

signs on opposite side to lesion

no muscle wasting
spasticity (+/- clonus)
hyperreflexia
extensor plantar response (Babinski signs)

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9
Q

lower motor neurone lesion features

A

signs on same side as the lesion

fasciculations
wasting
hypotonia
hyporeflexia

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10
Q

two patterns of clinical features which occur in an upper motor neurone lesion?

A

hemiparesis and paraparesis

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11
Q

hemiparesis

A

weakness of limbs on one side (usually caused by a lesion within the brain or brainstem e.g. a stroke)

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12
Q

paraparesis

A

weak legs.

indicative of bilateral damage to the corticospinal tracts (most commonly due to lesions below the T1 spinal level

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13
Q

lower motor neurone

A

motor pathway from anterior horn cell or cranial nerve via a peripheral nerve to the motor endplate

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14
Q

most common causes of a lower motor neurone lesion

A

anterior horn cells lesions e.g. motor neurone disease

spinal root lesion e.g. cervical and lumbar disc lesions

peripheral nerve lesions e.g. trauma, compression etc.

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15
Q

most common disease of the neuromuscular junction?

A

Myaesthenia Gravis

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16
Q

elevation of what plasma muscle enzyme indicates muscle disease?

A

creatine kinase

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17
Q

sensory peripheral nerves carry information from the dorsal root ganglion to the brain via three main pathways, what are they?

A

posterior columns

spinothalamic tracts

spinocerebellar tract

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18
Q

sensory modalities transmitted via the posterior columns

A

vibration

two-point discrimination

light touch

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19
Q

sensory modalities transmitted via the spinothalamic tract

A

pain

temperature

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20
Q

route of the posterior column

A

fibres ascend uncrossed to the gracile and cuneate nuclei in the medulla.

axons from the second-order neurones cross the midline to form the medial lemniscus and pass to the thalamus

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21
Q

route of the spinothalamic tract

A

fibres synapse in dorsal horn of the cord, cross the cord at that spinal level and ascend to the thalamus

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22
Q

sensory modalities are transmitted via the spinocerebellar tract?

A

proprioception

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23
Q

route of the spinocerebellar tract

A

does not decussate i.e. innervates the ipsilateral side of the body

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24
Q

The quality and distribution of the symptoms depend on the site of the lesion. Outline the potential sites of nerve lesions and their corresponding characteristics?

A

Peripheral nerve lesions - symptoms in the distribution of the affected nerve

Spinal root lesions - symptoms referred to affected dermatome

Spinal cord lesions - Symptoms are evident below the level of the lesion

Pontine lesions - Loss of all possible sensation on the opposite side of the lesion

Thalamic lesions - A rare cause of complete contralateral sensory loss

Cortical lesions - sensory loss, neglect of one side of the body and subtle disorders of sensation

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25
Q

What root value does the ankle jerk reflex correspond to?

A

S1

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26
Q

What root value does the knee jerk reflex correspond to?

A

L2, 3, 4

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27
Q

What root value does the biceps jerk reflex correspond to?

A

C5

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28
Q

What root value does the supinator jerk reflex correspond to?

A

C6

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29
Q

What root value does the triceps jerk reflex correspond to?

A

C7

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30
Q

What root value does the abdominals reflex correspond to?

A

T8-11

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31
Q

corticobulbar tract

A

component of the pyramidal system.

responsible for transmitting neurones from cerebrum to the cranial nerves.

  • control muscles of the face and neck - facial expression
  • mastication, swallowing
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32
Q

extrapyramidal system

A

component of the motor system which do not travel through the pyramids.

  • complex movements
  • postural control
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33
Q

components of extrapyramidal system

Hint = RPMLT

A

rubrospinal tract

pontine reticulospinal tract

medullary reticulospinal tract

lateral vestibulospinal tract

tectospinal tract

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34
Q

cranial nerve nuclei that are located in midbrain

A

CN 1, 2, 3, 4

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35
Q

cranial nerve nuclei that are located in pons

A

CN 5, 6, 7, 8

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36
Q

cranial nerve nuclei that are located in medulla

A

CN 5, 7, 8, 9, 10, 11, 12

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37
Q

causes of anosmia (first cranial nerve pathology)

A

nasal congestion (most common)

anterior fossa tumours

head injury

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38
Q

what structure do the optic nerves enter the cranial cavity through?

A

optic foramina

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39
Q

Outline the course of the optic nerve

A

Optic nerve transmitted into the cranial cavity

Forms optic chiasm

Continued as the optic tracts

Fibres of the optic tract project to the visual cortex of the occipital lobe through the lateral geniculate body and third cranial nerve nucleus for pupillary light reflex.

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40
Q

Specific visual field losses can indicate a specific pathology. What does the presence of paracentral scotoma indicate?

A

Retinal lesion

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41
Q

Specific visual field losses can indicate a specific pathology. What does the presence of monocular field loss indicate?

A

Optic nerve lesion

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42
Q

Specific visual field losses can indicate a specific pathology. What does the presence of bitemporal hemianopia indicate?

A

Chiasmal lesion

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43
Q

Specific visual field losses can indicate a specific pathology. What does the presence of homonymous hemianopia indicate?

A

Optic tract/radiation/cortex/pole lesion (usually due to posterior cerebral artery infraction)

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44
Q

Specific visual field losses can indicate a specific pathology. A lesion in what lobe(s) of the brain may present as a homonymous quadrantanopia indicate?

A

Temporal/parietal lesion

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45
Q

Name some causes for persistent pupillary dilatation

A

A third cranial nerve palsy
Antimuscarinic eye drops
Myotonic pupil (no pathological indication - no constriction on light or convergence)

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46
Q

Name some causes of persistent pupillary constriction

A
  • Parasympathomimetic eye drops (used in treatment of glaucoma)
  • Horner’s Syndrome
  • Argyll Robinson pupil (abnormality seen in neurosyphilis - absent reaction to light but convergence causes constriction)
  • Opiate addiction
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47
Q

A palsy of the seventh cranial nerve, cerebellar signs and involvement of the fifth, sixth and eighth cranial nerves indicates a lesion at what anatomical position?

A

Cerebellopontine angle (most commonly meningioma or acoustic neuroma)

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48
Q

What is the motor function of the trochlear nerve (CN IV)?

A

Superior oblique muscle

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49
Q

What is the motor function of the abducens nerve (CN VI)?

A

Lateral rectus muscle

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50
Q

What is the motor function of the oculomotor nerve (CN III)?

A

Superior, inferior and medial rectus muscles
Sphincter pupilae
Levator palpebrae superioris

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51
Q

The brainstem, cortex and cerebellum coordinate the third, fourth and sixth cranial nerve to ‘conjugate’ eye movements. What is the clinical presentation of a defect in this coordination (called supranuclear palsy)?

A

Lead to paralysis of conjugate movements of the individual muscles innervated by the third, fourth and sixth cranial nerves

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52
Q

Describe the clinical picture of an infranuclear palsy of the third cranial nerve

A

Unilateral complete ptosis with ‘down and out’ appearance

Total paralysis leads to a dilated, fixed pupil
Partial paralysis paralysed pupil but still reacted to reactive to light

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53
Q

Describe the clinical picture of an infranuclear palsy of the fourth cranial nerve

A

Torsional diplopia (two objects at an angle) when attempting to look down

Head is tilted away from the side of the lesion

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54
Q

Describe the clinical picture of an infranuclear palsy of the sixth cranial nerve

A

The eye cannot be abducted beyond the midline

Eye turns in medially with concurrent diplopia

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55
Q

What is the most common cause of a total and partial third cranial nerve palsy respectively?

A

Total palsy - berry aneurysm of the posterior communicating artery

Partial palsy - diabetes mellitus

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56
Q

What is often the earliest sign of a fifth cranial nerve lesion?

A

Diminution of the corneal reflex

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57
Q

What is the clinical presentation of a total fifth cranial nerve palsy?

A

Unilateral sensory loss on the face, tongue and buccal mucosa with jaw deviation to the side of the lesion

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58
Q

What is the cardinal feature of a supranuclear palsy of the fifth cranial nerve?

A

Brisk jaw jerk reflex

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59
Q

What is trigeminal neuralgia?

A

Severe paroxysms of knife-like pain occur in one or more sensory divisions of the trigeminal nerve brought on by a specific trigger

No objective clinical signs

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60
Q

How is trigeminal neuralgia treated?

A

Anticonvulsant carbamazepine suppresses attacks

Thermocoagulation of the tigeminal ganglion may be necessary

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61
Q

What are the two major branches of the seventh cranial nerve unrelated to facial muscle innervation?

A

Chorda tympani - providing taste to the anterior two third of the tongue

Nerve to the stapedius - dampening effect on sound

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62
Q

What are the potential features of a facial nerve palsy in addition to the paralysis of facial muscles?

A

Hyperacusis (undue sensitivity to sounds)

Loss of taste to the anterior two thirds of the tongue

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63
Q

Outline the features of a lower motor neurone lesion of the facial nerve

A

Ipselateral weakness of the facial muscles
Hyperacusis
Loss of taste of the anterior two thirds of the tongue

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64
Q

What is Bell’s Palsy?

A

Common, acute isolated unilateral facial nerve palsy probably due to a viral herpes simplex infection causing swelling within the petrous part of the temporal bone

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65
Q

How is a lower motor neurone facial palsy managed?

A 
Protect cornea from ulceration
Oral prednisolone (60mg/day for 10 days)

Antivirals used in severe cases

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66
Q

What is the differential diagnosis of paralysed facial muscles?

A

Bell’s Palsy
Ramsey-Hunt Syndrome
Parotid Tumour

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67
Q

What is Ramsey-Hunt Syndrome?

A

Herpes zoster (shingles) of the geniculate ganglion causing facial muscles palsy and herpetic vesicles of the external auditory meatus/soft palate

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68
Q

Outline the features of an upper motor neurone lesion of the facial nerve

A

Weakness of the lower part of the face on the side opposite to the lesion

Wrinkling of the forehead and eye closure are normal

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69
Q

What are the features of an eighth cranial nerve palsy?

A

Cochlear nerve branch - sensorineural deafness and tinnitus

Vestibular nerve branch - vertigo +/- nausea/vomiting

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70
Q

List some causes of eighth nerve palsy

A

Brainstem (tumour, mutiple sclerosis)
Cerebellopontine angle (acoustic neuroma)
Petrous temporal bone (trauma, middle ear infection)

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71
Q

What is nystagmus?

A

Rhythmic oscillation of the eyes

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72
Q

What are the two types of nystagmus?

A

Pendular - no rapid phase (due to longstanding visual impairment)

Jerk - rapid and slow phases (two subtypes: horizontal or vertical)

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73
Q

The lower four cranial nerves lie in the medulla (the “bulb”) are usually affected together. Outline the features of a lower motor neurone type palsy of the bulbar cranial nerves (bulbar palsy)

A

Dysarthria (slow speech)
Dysphagia
Nasal regurgitation
Wasting and fasciculation of the tongue

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74
Q

What are the most common causes of bulbar palsy?

A

Motor neurone disease

Syringobulbia (fluid-filled cavity in the brainstem)

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75
Q

Outline the features of an upper motor neurone type palsy of the bulbar cranial nerves (pseudobulbar palsy)

A

Weakness of the muscles of speech and swallowing with small, spastic tongue (no wasting or fasciculation)

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76
Q

What are the most common causes of pseudobulbar palsy?

A

Motor neurone disease

Multiple sclerosis

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77
Q

What is normal CSF pressure?

A

80-120 mmH2O

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78
Q

What is the purpose of nerve conduction studies?

A

Differentiates between axonal and demyelination neuropathy

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79
Q

What are some known complications of lumbar punctures?

A

Post-procedure headache, infection, herniation (coning)

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80
Q

What are the cardinal investigations of suspected muscle disease? (4)

A 
Serum creatine kinase and aldose
EMG
Muscle biopsy (histology and immunohistochemical staining)
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81
Q

What area of the brain is chiefly responsible for states of arousal?

A

Reticular formation (extending from the brainstem to the thalamus)

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82
Q

What is coma?

A

A state of unconsciousness from which the patient cannot be roused

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83
Q

What is a stuporous state?

A

When a patient is sleepy but can be roused with vigorous stimulation

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84
Q

A patient unresponsive to anything except pain is broadly corresponsive to what GCS level?

A

8

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85
Q

What must coma be differentiated from?

A

Persistent vegetative state
Brain death
Locked-in syndrome

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86
Q

What is a persistent vegetative state?

A

A state of wakefulness in which sleep-wake cycle persists but without detectable awareness

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87
Q

What is the cardinal sign of brain death?

A

Bilaterally fixed and dilated pupils

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88
Q

What are dysconjugate eyes a sign of?

A

Brain stem lesion

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89
Q

Conjugate lateral deviation of the eyes indicates what two potential pathologies?

A

Ipselateral cerebral haemorrhage/infarction

Contralateral pontine lesion

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90
Q

What is brain death?

A

Irreversible loss of the capacity for consciousness, combined with the irreversible loss of the capacity to breathe

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91
Q

What are the three main criteria of the diagnosis of brain death?

A
  1. Irremediable structural brain damage
  2. Absent motor responses to any stimulus
  3. Absent brainstem function (lack of pupillary, corneal, gag, cough, doll’s head or caloric reflexes, lack of spontaneous breathing)
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92
Q

What is the definition of a stroke?

A

Rapid onset of neurological deficit lasting greater than 24-hours, which is the result of a vascular origin.

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93
Q

What is the definition of stroke in evolution?

A

When symptoms and signs are getting worse (usually within 24-hours of onset)

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94
Q

What is the definition of a minor stroke?

A

When the patient recovers without significant neurological deficit, usually within one week

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95
Q

What is the definition of a transient ischaemic attack?

A

Transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction.

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96
Q

Arterial thrombosis causing stroke can arise from what locations?

A

Atheromatous plaques
Cardiac mural thrombi (post-MI)
Left atrium (due to atrial fibrillation)

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97
Q

What is the differential diagnosis of stroke?

A

Intracranial venous thrombosis
Multiple sclerosis
Space-occupying lesion e.g. tumour/abscess

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98
Q

In young adults, 20% of are caused by carotid/vertebral artery dissection. What clinical picture might be suggestive of this pathophysiology?

A

Recent neck pain, trauma or neck manipulation

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99
Q

What are the major risk factors for thromboembolic stroke?

A

Hypertension, diabetes mellitus, cigarette smoking, hyperlipidaemia, obesity, excessive alcohol consumption

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100
Q

What are the differential diagnoses for transient ischaemic attack?

A

Demyelination, tumour

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101
Q

How is the risk of stroke measured following a confirmed TIA?

A

ABCD2 risk

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102
Q

Hemiplegia is often caused by infarction of what area of the brain during a cerebral haemorrhage stroke?

A

Infarction of the internal capsule

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103
Q

What is the internal capsule?

A

Narrow zone of motor and sensory fibres that converges on the brainstem from the cerebral cortex

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104
Q

Brainstem infarction can manifest in a number of different clinical presentations. Name a few. (4)

A

Lateral medullary syndrome
Coma
Locked-in syndrome
Pseudobulbar palsy

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105
Q

What is lateral medullary syndrome?

A

Most common of the brainstem vascular syndromes caused by occlusion of the posteiror inferior cerebellar artery

Presents as sudden vomiting, vertigo, facial numbness, Horner’s syndrome, diminished gag reflex

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106
Q

Coma as a result of stroke is caused by infarction of what site in the brain?

A

Reticular activating syndrome

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107
Q

Upper brainstem stroke causes what pathology?

A

Locked-in syndrome

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108
Q

Lower brainstem stroke causes what pathology?

A

Pseudobulbar palsy

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109
Q

What is multi-infarct dementia?

A

Also called vascular dementia

Multiple small cortical infarcts resulting in generalised intellectual loss with step-wise progression

Clinical picture of dementia, pseudobulbar palsy and Parkinsonian ‘shuffling’ gait

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110
Q

What is the indicated acute treatment of stroke?

A

Aspirin (300mg ASAP)

Thrombolysis (IV tPA) given within 4.5hrs in acute ischaemic stroke

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111
Q

What secondary interventions are put in place following acute stroke?

A

Hypertension management

Carotid endarterectomy (in the case of stenosed carotid artery to prevent recurrence of stroke)

Address other modifiable risk factors including smoking, obesity etc.

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112
Q

What are the major risk factors for intracerebral haemorrhage?

A

Hypertension, excess alcohol consumption, increasing age and smoking

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113
Q

What is the presentation of intracerebral haemorrhage?

A

Sudden loss of consciousness and stroke often accompanied by severe headache

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114
Q

What is a subarachnoid haemorrhage?

A

Refers to spontaneous arterial bleeding into the subarachnoid space

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115
Q

What is the radiological appearance of a subarachnoid haemorrhage?

A

Hyperdense appearance typically around the branching points of arteries of the Circle of Willis

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116
Q

What are the most common aetiologies of subarachnoid haemorrhage?

A

Rupture of saccular ‘berry aneurysms’

Congenital arteriovenous malformation

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117
Q

What are the symptoms of a berry aneurysm before it ruptures?

A

Often asymptomatic before they rupture

Any symptoms are due to mass effect, most commonly a painful third cranial nerve palsy

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118
Q

What are the symptoms of a berry aneurysm when it ruptures?

A

Sudden onset of severe headache (often occipital), accompanied by nausea and vomiting

Potential loss of consciousness and meningeal irritation (neck stiffness and positive Kernig’s sign)

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119
Q

Lumbar punctures must be delayed until at least 12 hours after onset of symptoms in order to confirm diagnosis. Why is this?

A

To allow sufficient time for haemoglobin to degrade into oxyhaemoglobin and bilirubin (detectable for up to two weeks following SAH)

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120
Q

How is subarachnoid haemorrhage immediately managed?

A

Best rest and supportive measures with control of hypertension and IV nimodipine (CCB) to reduced cerebral artery spasm.

Discussion with neurosurgeon for obliteration of aneurysm to prevent re-bleeding

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121
Q

What is a subdural haematoma?

A

Accumulation of blood in the subdural space following a venous bleed.

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122
Q

What is the aetiology of subdural haematoma?

A

Almost always trauma. Latency between trauma and onset of symptoms may be weeks or months

123
Q

What are the main clinical features of a subdural haematoma?

A

Headache, drowsiness and fluctuant confusion

124
Q

What is an extradural haematoma?

A

Bleeding outside of the dura mater most commonly due to temporal bone fracture and subsequent rupture of the underlying middle meningeal artery

125
Q

Clinically how does extradural haematoma present?

A

Head injury with a brief period of unconsciousness followed by a lucid interval of recovery.

Then followed by rapid neurological deterioration if drainage is not immediately carried out.

126
Q

seizure

A

transient occurrence of signs and symptoms due to abnormally excessive or asynchronous neuronal activity within the brain.

127
Q

epilepsy

A

a continuing tendency to have seizures

128
Q

epilepsy classification

A

generalised seizure type

partial seizure type

129
Q

tonic seizures

A

intense body stiffening

130
Q

tonic-clonic seizures (grand mal)

A

sudden onset

rigid tonic phase followed by a convulsion (clonic) phase

eyes remain open; lasts seconds to minutes

may be associated with tongue biting or urinary incontinence

131
Q

what period typically follows a grand mal seizure?

A

post-ictal phase

132
Q

post-ictal phase

A

flaccid unresponsiveness followed by confusion or drowsiness lasting several hours.

headache is common

133
Q

absence seizures (petit mal)

A

disorder of childhood in which the child ceases all activity, stares and pales for a few seconds only.

tendency to develop generalised tonic-clonic seizures in adulthood

134
Q

myotonic seizures

A

isolated muscle jerking

135
Q

akinetic seizures

A

cessation of movement, falling and loss of consciousness

136
Q

partial seizures

A

epileptic activity involving part of the brain only

  1. simple (not affecting consciousness or memory)
  2. complex (affecting awareness and memory)

May become generalised (secondarily generalised)

137
Q

stimuli that may induce seizures in an epileptic patient?

A

flashing lights or a flickering television screen may provoke an attack

138
Q

how is a seizure medically aborted?

A

rectal or IV diazepam or lorazepam

139
Q

repeated seizures with minimal recovery periods between may lead to what medical emergency?

A

status epilepticus

140
Q

status epilepticus

A

continuous seizures for greater than thirty minutes

141
Q

risk to life in status epilepticus

A

death from cardiorespiratory failure

142
Q

What may precipitate status epilepticus?

A

Sudden withdrawal of anti-epileptic drugs, intercurrent illness or alcohol abuse

143
Q

How is status epilepticus managed outside of a hospital setting?

A

Rectal diazepam or buccal midazolam

144
Q

How is status epilepticus managed in a hospital setting?

A

Administer oxygen and obtain IV access

IV lorazepam/rectal diazepam (first line)

If seizures continue - given phenytoin (second line) then phenobarbital (third line)

145
Q

For refractory status epilepticus, what management is required?

A

Intubation, ventilation and anaesthesia in intensive care

146
Q

What is the principle of treatment for epilepsy?

A

Monotherapy is the goal with dose titrated up until seizures are controlled

147
Q

Describe the common syndrome of intoxication of all anti-convulsants

A

Ataxia, nystagmus and dysarthria

148
Q

What is the pathophysiology of idiopathic Parkinson’s disease?

A

Progressive depletion of dopamine-secreting cells in the substantia nigra due to abnormal accumulation of cytoplasmic inclusions called Lewy bodies

149
Q

Outline the clinical features of Parkinson’s disease

A

Combination of rest tremor, rigidity and bradykinesia (slow movements)

Poverty of movement and speech

Postural changes (stoop)

Non-motor features (depression, hallucinations, dementia, insomnia, fatigue, weight loss etc.)

150
Q

How is Parkinson’s disease managed?

A

Levodopa (combined with peripheral decarboxylase inhibitor)

Dopamine agonists

Monoamine oxidase B inhibitors (inhibit dopamine catabolism)

Physiotherapy

151
Q

What is benign essential tremor?

A

Familial (autosomal dominant) tremor of the arms and head. Not usually present at rest and made more obvious when adopting a posture and anxiety.

Improved by alcohol, propranolol and mirtazepine

152
Q

What is chorea?

A

Continuous flow of jerky, quasi-purposive movements interfering with voluntary movements but absent during sleep

153
Q

What is Huntington’s Disease?

A

Autosomal dominant (full penetrance) relentlessly progressive course with chorea, personality change preceding dementia and death

154
Q

What is the pathophysiology of Huntingdon’s Disease?

A

CAG repeats in the Huntingdon’s disease gene on chromosome 4 leads to the production of mutant huntingtin protein leading to a depletion of GABA and acetylcholine in the basal ganglia

155
Q

What is hemiballismus?

A

Violent swinging of one side of the body usually caused by infarction or haemorrhage in the contralateral subthalamic nucleus

156
Q

What is myoclonus?

A

Sudden, involuntary jerking of a single muscle or group of muscles. Most commonly benign essential myoclonus which is a sudden body jerk just before falling asleep.

157
Q

What is multiple sclerosis

A

A chronic debilitating autoimmune disorder of the CNS in which multiple plaques of demyelination occur disseminated in time and space.

158
Q

Multiple sclerosis has a predilection for distinct CNS sites; name five.

A
  1. Optic nerves
  2. Periventricular white matter
  3. Brainstem
  4. Cerebellum
  5. Cervical spinal cord
159
Q

The clinical features of multiple sclerosis depend on the site of demyelination. Outline the clinical presentation of optic neuropathy caused by multiple sclerosis

A

Blurred vision and unilateral eye pain

Inflammation at the optic head causes pallor and disc swelling (optic neuritis)

Retrobulbar (proximal to the fundus) neuritis may occur in which case fundus examination is normal

160
Q

The clinical features of multiple sclerosis depend on the site of demyelination. Outline the clinical presentation of brainstem demyelination caused by multiple sclerosis

A

Diplopia, vertigo, dysphagia, dysarthria, facial muscle weakness

161
Q

The clinical features of multiple sclerosis depend on the site of demyelination. Outline the clinical presentation of spinal cord lesions caused by multiple sclerosis

A

Numbness/paraesthesia are common in MS and reflect involvement of the spinothalamic tract and posterior column lesions.

162
Q

There are four main clinical patterns of multiple sclerosis; what are they?

A
  1. Relapsing-remitting MS (85-90%)
  2. Secondary progressive MS
  3. Primary progressive MS (10-15%)
  4. Relapsing-progressive MS (<5%)
163
Q

Describe the relapsing-remitting variant of multiple sclerosis

A

Symptoms occur in attacks with onset over days which then recover over a period of weeks. Disability is accumulated over time due to suboptimal recovery of relapses.

164
Q

Describe the secondary progressive variant of multiple sclerosis

A

Late-stage of relapsing-remitting MS with a progressive disability over years.

165
Q

Describe the primary progressive variant of multiple sclerosis

A

Characterised by progressive worsening disability with no evidence of relapsing or remitting.

166
Q

What is the differential diagnosis of multiple sclerosis?

A

Early MS, without the diagnostic necessity of time, may be difficult to distinguish from other inflammatory conditions including:

  • SLE
  • Sarcoidosis
  • Mass or vascular lesion
167
Q

What investigations are indicated for the diagnosis and monitoring of multiple sclerosis?

A

MRI of brain and spinal cord
Electrophysiological tests
CSF examination (usually unnecessary - useful for exclusion of other pathology)

168
Q

Outline some of the treatment options for multiple sclerosis

6

A
  1. Short courses of steroids - reduces severity of relapses
  2. Subcutaneous beta-interferon - reduces relapse rate
  3. Glatiramer acetate - similar effect to interferon
  4. Natalizumab - monoclonal antibody (second line option)
  5. Newer agents e.g. fingolimod - reduce relase rate significantly
  6. Physiotherapy nand occupational therpay
169
Q

What is Kernig’s sign?

A

Inability to allow full extension of the knee when the hip if flexed to 90 degrees

170
Q

Outline the clinical picture of infective meningitis

A

Headache, neck stiffness and fever develop over minutes to hours

Photophobia, vomiting and papilloedema

171
Q

List three major complications of infective meningitis

A

Venous sinus thrombosis
Severe cerebral oedema
Cerebral abscess

172
Q

How may a major complication present with ongoing meningitis?

A

Progressive drowsiness
Lateralising signs
Cranial nerve lesions

173
Q

What is the cardinal sign of meningococcal septicaemia?

A

Non-blanching, petechial or purpuric rash (with shock)

174
Q

Outline the course of viral meningitis

A

Usually benign and self-limiting condition lasting about 4-10 days with no serious sequelae

175
Q

Outline the presentation of chronic meningitis

A

Long history of vague symptoms including headache, lassitude, anorexia, vomiting etc.

176
Q

List some potential diagnosis of meningitis

A

Subarachnoid haemorrhage
Migraine
Viral encephaliits
Cerebral malaria (can mimic meningitis)

177
Q

Give four examples of bacteria which can cause meningitis

A

Neisseria meningitidis
Streptococcus pneumoniae
Staphylococcus aureus
Listeria monocytogenes

178
Q

Give four examples of viruses which can cause meningitis

A

Enterovirus (ECHO, Coxsackie)
Poliomyelitis
Mumps
HIV

179
Q

Give two examples of fungi which can cause meningitis

A

Cryptococcus neoformans

Candida albicans

180
Q

It is important to immunise close contacts of those diagnosed with meningococcal meningitis (i.e. close family). What prophylaxis is used?

A

Oral rifampicin/ciprofloxacin to erradicate nasal carriage of causative organism

181
Q

How is tuberculous meningitis diagnosed?

A

Auramine stain

182
Q

How is cryptococcal meningitis diagnosed?

A

India ink stain

183
Q

What investigation should not be performed if meningococcal sepsis is suspected?

A

Lumbar puncture (due to risk of cerebellar coning)

184
Q

How is acute suspected bacterial meningitis treated?

A

Immediate third-generation cephalosporin (e.g. ceftriaxone) and amoxicillin (covering Listeria) and dexamethasone

Specific antibiotics following results of Gram staining, culture and sensitivities

185
Q

What is encephalitis?

A

Inflammation fo the brain parenchyma

186
Q

How does encephalitis differ from meningitis?

A

Unlike meningitis, there is usually cerebral dysfunction with altered mental status, motor and sensory deficits

187
Q

What are the clinical features of acute viral encephalitis?

A

Mild, self-limiting illness with fever, headache and drowsiness

Severe disease is rare but can cause seizures and coma

188
Q

In the case of suspected HSV or VZV encephalitis, what is the treatment?

A

IV aciclovir (10mg/kg every 8 hrs for 14-21 days)

189
Q

Cerebral abscess follows infection spread from parameningeal infective focuses or from a distal site e.g. bloodstream. Give examples of parameningeal infective focuses.

A

Paranasal air sinuses
Middle ear
Skull fracture

190
Q

Outline the clinical features of a cerebral abscess

A

Headache, focal neurological signs, seizures

Potential raised intracranial pressure

191
Q

What investigation is contraindicated in the case of suspected cerebral abscess?

A

Lumbar puncture (due to risk of cerebellar coning)

192
Q

How is cerebral abscess treated?

A

IV antibiotics and sometimes surgical decompression

193
Q

How doe spinal epidural abscess present?

A

Back pain and fever accompanied by paresis/root lesions

194
Q

What four clinical syndromes may arise from untreated neurosyphilis?

A
  1. Asymptomatic neurosyphilis
  2. Meningovascular syphilis
  3. General paralysis of the insane
  4. Tabes dorsalis
195
Q

How is neurosyphilis treated? What is the outcome of the treatment

A

Benzylpenicillin 1g IM daily for 10 day

May arrest but not reverse any neurological damage

196
Q

Outline the presentation and treatment of Creutzfeldt-Jakob disease

A

Pathologically spongiform change in the brain due to infective prion causing progressive dementia and death (incurable)

197
Q

The HIV virus is not directly neuroinvasive or neurovirulent but can cause meningitis in a variety of ways. How?

A

HIV seroconversion
AIDS-demnetia complex
Progressive multifocal leukoencephalopathy (PML)

198
Q

What is progressive multifocal leukoencephalopathy?

A

A fatal demyelinating disease of the central nervous system (CNS), caused by the lytic infection of oligodendrocytes by a human polyomavirus, JC virus (JCV)

199
Q

How is progressive multifocal leukoencephalopathy related to HIV?

A

Patients become susceptible to JCV infection at very low CD4 counts, as in HIV infection

200
Q

What are the clinical features of a cerebral tumour?

3

A

Progressive focal neurological deficits
Raised intracranial pressure
Focal/generalised epilepsy

201
Q

List three of the most common primary malignant brain tumours

A

Glioma
Embryonal tumours (e.g. medulloblastoma)
Lymphoma

202
Q

List two of the most common primary benign brain tumours

A

Meningioma

Neurofibroma

203
Q

What primary cancers commonly metastasise to the brain?

A

Bronchus, breast, prostate

204
Q

What neurological defects may arise from frontal lobe tumours?

A

Personality change, aparthy, intellectual deterioration

Frontal speech area (Broca’s area) - expressive dysphasia

Motor cortex (pre-central gyrus) - hemiparesis

205
Q

What neurological defects may arise from parietal lobe tumours?

A

Homonymous field defect
Cortical sensory loss
Hemiparesis
Seizures

206
Q

What are the cardinal signs/symptoms of raised intracranial pressure?

A

Headache (changes with posture, worse on coughing, sneezing, bending or straining)
Vomiting
Papilloedema

207
Q

As tumours grow, there may be compression of the brainstem causing what symptoms?

A

Drowsiness respiratory depression, bradycardia, coma and death

208
Q

What are the potential differential diagnoses of brain tumour?

A 
Other masses (cerebral abscess, tuberculoma, subdural/intracranial haematoma)
Stroke
Benign idiopathic intracranial hypertension
209
Q

What is benign idiopathic intracranial hypertension?

A

Benign condition common in young obese women presenting with headache and papilloedema causing raised intracranial pressure

210
Q

What is hydrocephalus?

A

Excessive amounts of CSF within the cranium

211
Q

Where is CSF produced in the brain?

A

In the cerebral ventricles

212
Q

What are the two potential mechanisms behind the cause of hydrocephalus?

A
  1. Increased production of CSF (rare)

2. Blockage to outflow

213
Q

What is a congenital cause of hydrocephalus?

A

Arnold-Chiari malformation

214
Q

What is Arnold-Chiari malformation?

A

Cerebellar tonsils descend into the cervical canal - blocking drainage of CSF

215
Q

List some causes of adult hydrocephalus

A

Posterior fossa/brainstem tumours
Subarachnoid haemorrhage/head injury/trauma
Third ventricle colloid cyst (intermittent hydrocephalus)
Normal-pressure hydrocephalus

216
Q

What is normal pressure hydrocephalus?

A

Dilation of the cerebral ventricles without signs of raised ICP.

217
Q

How does normal pressure hydrocephalus present?

A

Common in the elderly

Dementia, urinary incontinence and ataxia

218
Q

How is hydrocephalus treated?

A

Surgical insertion of a shunt to allow drainage of CSF (ventriculoperitoneal/ventriculoatrial)

219
Q

What are the key features of a headache history?

12

A 
Location, severity and character 
Associated symptoms e.g. nausea, photophobia, fever
Presence of autonomic symptoms e.g. ptosis or tearing
Triggers - the effect of posture? 
Is the headache episodic or part of a pattern?
Duration 
Analgesic use
Family history 
Red flag symptoms 
Sudden onset?
Features of raised ICP?
Jaw claudications/scalp tenderness?
220
Q

What is a tension headache? What is the cause?

A

Very common bilateral headache

Neurovascular irritation and referred tenderness to scalp

221
Q

What does a tension headache feel like?

A

Feeling of pressure/tightness all around the scalp

No associated symptoms common in migraine such as aura or photophobia

222
Q

How is tension headache treated?

A

Explanation and reassurance

Analgesic withdrawal (to avoid overuse headache)

Tricyclic antidepressants in frequently recurrent cases

223
Q

Migraine is a very common, debilitating headache disorder characterised into three types. Name them

A
  1. Migraine with aura (classic migraine)
  2. Migraine without aura (common migraine)
  3. Migraine variants (unilateral motor or sensory symptoms often mistaken as a stroke)
224
Q

What is the typical presentation of migraine?

A

Unilateral, throbbing associated with nausea, vomiting, photophobia

225
Q

What cause visual auras?

A

Related to depression of visual cortex/retinal function and may preceed a migraine by minutes or hours

226
Q

What are some of the potential symptoms of aura?

A 
Scotoma
Unilateral blindness 
Flashes 
Aphasia
Numbness
227
Q

Give a few differential diagnoses of migraine

3

A

Meningitis
Subarachnoid haemorrhage
TIAs/stroke

228
Q

How are mild migraines treated in the acute setting?

A

Simple analgesics and high-dose soluble aspirin/NSAIDs

Antiemetic if nauseous (e.g. metoclopramide)

229
Q

How are moderate/severe migraines treated in the acute setting?

A

Triptans (e.g. sumatriptan)

230
Q

What prophylaxis may be prescribed to prevent migraines?

A

Anticonvulsants e.g. valproate
beta-blockers - propranolol
Amytriptyline

231
Q

What are trigeminal autonomic cephalgias?

A

Headaches characterised by unilateral trigeminal distribution of pain with ipsilateral autonomic features e.g. tearing

232
Q

Name the types of trigeminal autonomic cephalgias

A

Cluster headache
Paroxysmal hemicrania
Hemicrania continua
SUNCT syndrome

233
Q

What are cluster headaches?

A

Rapid onset, short-lived unilateral headaches with clustering of multiple attacks over a period of a few months before a period of remission

234
Q

Describe the clinical presentation of cluster headaches

A

Pain often begins around the eyes and only lasts 1-2 hours

Autonomic features include tearing, rhinorrhoea and Horner’s sydnrome

235
Q

What vertebral levels does the spinal cord extend from and to?

236
Q

What structure continues from the spinal cord at L1?

A

Cauda equina

237
Q

Paraplegias is almost always caused by a lesion in what anatomical location?

A

Spinal cord

238
Q

Hemiparesis is almost always caused by a lesion in what anatomical location?

239
Q

Outline the presentation of spinal cord compression

A

Progressive weakness of the legs with upper motor neurone pattern

240
Q

What are the two patterns of onset for spinal cord compression?

A

Acute (hours to days)

Chronic (weeks to months)

241
Q

At what level are sensory symptoms felt in spinal cord compression?

A

Sensation diminishing one/two spinal levels below the level of the lesion

242
Q

What symptoms are felt in the later stages of spinal cord compression?

A

Painless urinary retention and constipation

243
Q

What is the most common cause of acute spinal cord compression?

A

Vertebral tumour (metastasis from brain, breast, lung etc.)

244
Q

What is a frequent infective cause of spinal compression in some parts of the world?

A

Tuberculosis

245
Q

Chronic compression of the spinal cord due to cervical spondylotic myelopathy is the most common cause of what disability in the elderly?

A

Spastic paraparesis

246
Q

What is the differential diagnosis of spinal cord compression?

A

Intrinsic lesions of the spinal cord:

Transverse myelitis (inflammation due to viral infection)
Anterior spinal artery occlusion
Multiple sclerosis

247
Q

What is cauda equina syndrome?

A

Spinal damage at the L1 level or below

248
Q

Cauda equina syndrome can present acutely or chronically. What are the typical symptoms?

A

Back pain, weakness and numbness of the legs

Reduced reflexes

Saddle paraesthesia

Loss of sphincter control

Reduced desire to void urine progressing to painless urinary retention

249
Q

What is Freidrich’s ataxia?

A

An autosomal recessive disorder is the most common hereditary spinocerebellar degeneration causing ataxia, dysarthria and nystagmus

250
Q

What is motor neurone disease?

A

Destruction of motor neurones and anterior horn cells

251
Q

What is the prognosis of motor neurone disease?

A

Most patients die within three years from respiratory failure as a result of bulbar palsy and pneumonia

252
Q

Motor neurone disease comprises of a mixture of four clinical patterns. What are they?

A
  1. Progressive muscular atrophy
  2. Amyotrophic lateral sclerosis
  3. Progressive bulbar and pseudobulbar palsy
  4. Primary lateral sclerosis
253
Q

What are the features of progressive muscular atrophy?

A

Muscle wasting and fasciculations

254
Q

What are the features of amyotrophic lateral sclerosis?

A

Progressive spastic tetra/paraparesis with lower motor neurone signs e.g. fasciculations

255
Q

What are the features of progressive bulbar/pseudobulbar palsy?

A

Dysarthria, dysphagia with wasting and fasciculation of the tongue

256
Q

What are the features of primary lateral sclerosis?

A

Progressive tetraparesis

257
Q

What are the differential diagnoses of the motor neurone disease?

A

Cervical spine lesion (distinguished by the presence of sensory symptoms)

Idiopathic multifocal motor neuropathy

258
Q

What is the medical treatment for motor neurone disease?

A

Riluzole (slows progression slightly)

259
Q

What is dementia?

A

A clinical syndrome with multiple causes defined by a progressive acquired loss of higher mental function of sufficient severity to cause significant disability

260
Q

What are the four different clinical entities of dementia?

A

Alzheimers disease (most common)
Vascular (multi-infarct) dementia
Dementia with Lewy bodies
Frontotemproal dementia

261
Q

What is the presentation of Alzheimer’s disease?

A

Insidious onset with slow disintegration fo personality and intellect.

Decline in language and visuospatial skills are common

262
Q

How is Alzheimer’s disease treated?

A

Acetylcholinesterase inhibitors (donezepril, rivastigmine and galantaime)

Memantine (NMDA receptor antagonist)

263
Q

What is the typical pattern of progression of vascular dementia?

A

Stepwise deterioration

264
Q

How is dementia with Lewy bodies characterised clinically?

A

Fluctuating cognition and Parkinsonism

265
Q

What is the most prominent feature of frontotemporal dementia?

A

Early personality changes

266
Q

What treatment must be avoided in dementia with Lewy bodies?

A

Neuroleptics

267
Q

What is a mononeuropathy?

A

A process affecting a single nerve

268
Q

What is mononeuritis multiplex?

A

A process affecting several or multiple nerves

269
Q

What is carpal tunnel syndrome?

A

A mononeuropathy of the median nerve due to compression under the flexor retinaculum.

270
Q

What are the clinical features of carpal tunnel syndrome?

A

Pain and paraesthesia in the affected hand, typically worse at night

271
Q

How is carpal tunnel syndrome?

A

Nocturnal splints or local injections of steroids

Surgical decompression is definitive treatment (flexor retinaculum fasciotomy)

272
Q

What is polyneuropathy?

A

Acute or chronic diffuse disease process involving motor, sensory and autonomic nerves.

273
Q

What are the common potential sensory symptoms in polyneuropathy?

A

Numbness, tingling, pain in extremities, unsteadiness

274
Q

What are the common potential motor symptoms in polyneuropathy?

A

Muscular weakness

275
Q

What are the common potential autonomic symptoms in polyneuropathy?

A

Postural hypotension, urinary retention, erectile dysfunction, diarrhoea/constipation, diminished sweating, impaired pupillary response, arrhythmias

276
Q

What are some common causes of mono neuritis multiplex?

A

Diabetes mellitus, malignancy, sarcoidosis

277
Q

What is Guillain-Barre Syndrome?

A

Post-infective acute neuropathy causing inflammatory demyelination

278
Q

What are the clinical features of Guillain-Barre Syndrome?

A

Progressive onset of distal limb weakness/numbness (usually symmetrical) that reaches its nadir in approx. 4 weeks

279
Q

What are the clinical features of Guillain-Barre Syndrome?

A

Sensory symptoms - paraesthesia

Motor symptoms - progressive onset of distal limb weakness/numbness (usually symmetrical)

Autonomic symptoms - postural hypotension, cardiac arrhythmias, ileus and bladder atony

280
Q

What is Miller Fisher Syndrome?

A

A rare variant of Guillain-Barre Syndrome that affects cranial nerves to the eyes causing ophthalmoplegia and ataxia

281
Q

How is Guillain-Barre Syndrome?

A

Diagnosis is made clinically and can be confirmed after a number of weeks with nerve conduction studies

282
Q

What is the differential diagnosis of Guillain-Barre Syndrome?

A

Other causes of neuromuscular paralysis:

Hypokalaemia, polymyositis, myasthenia gravis

283
Q

Outline the management of Guillain-Barre Syndrome?

A

Vital capacity monitored 4-hourly to recognise deteriorating respiratory failure

Intravenous immunoglobulin (+/- plasma exchange)

Supportive treatment (heparin, physiotherapy, NG/PEG tube)

284
Q

What is the most common cause of thiamin (vitamin B1) deficiency?

A

Chronic alcohol dependency

285
Q

What pathology arises from pyridoxine (vitamin B6) deficiency?

A

Sensory neuropathy

286
Q

What pathology arises from vitamin B12 deficiency?

A

Syndrome of subacute combined degeneration of the cord causing distal sensory loss

287
Q

How does the presentation of muscular disease differ from the weakness caused by neuropathy?

A

In muscular disease reflexes and sensation are normal

288
Q

What is myasthenia gravis?

A

An autoimmune disorder of the neuromuscular junction transmission characterised by weakness and fatiguability of ocular, bulbar and proximal limb muscle

289
Q

What is the pathophysiology of myasthenia gravis?

A

Autoantibodies to acetylcholine receptors causing receptor loss

290
Q

What is the presentation fo myasthenia gravis?

A

Fatigue muscle on sustained or repeated activity that improves after rest.

Ocular muscles are the first to be involved causing ptosis
Difficulty talking, swallowing and breathing follows

291
Q

How is myasthenia gravis treated?

A

Anticholinesterases
Immunosuppression
Plasmapheresis and intravenous immunoglobulin
Thymectomy

292
Q

What are the muscular dystrophies?

A

Inherited group of progressive myopathic disorders

293
Q

What is the inheritance patterns of both Duchenne’s and Becker’s muscular dystrophies?

A

X-linked recessive

294
Q

What is the presentation of Duchenne’s muscular dystrophy?

A

Present in early adulthood with weakness in proximal muscles and grossly elevated creatine kinase (100-200x normal limit)

295
Q

What is the presentation of Becker’s muscular dystrophy?

A

Present later in life with a milder degree of clinical involvement than Duchenne’s muscular dystrophy

296
Q

What is myotonia?

A

Delayed muscle relaxation after contraction

297
Q

What are the two most common myotonia disorders?

A

Dystrophia myotonica and myotonia congenita

298
Q

What is dystrophia myotonica?

A

Autosomal dominant condition causing progressive distal muscle weakness, myotonia, facial muscles weakness and ptosis

299
Q

What is myotonia congenita?

A

Autosome dominant condition causing myotonia exacerbated by rest and cold

Becomes evident in childhood

300
Q

What is delirium?

A

Acute or subacute condition in which impairment of consciousness accompanied by changes in personality and mood

Severity can vary and often fluctuates

301
Q

How is delirium managed/treated?

4

A

Investigation and treatment of the underlying condition

Withdrawing all possible drugs responsible (TCAs, opiates and benzodiazepines etc.)

Rehydration

Adequate pain relief/sedation

302
Q

What are the most commonly prescribed hypnotics?

A

Benzodiazepines

303
Q

What are the four most common side effects of a neuroleptic such as haloperidol?

A

Drowsiness, hypotension, tachycardia and convulsions

4th year everything (43 decks)

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