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Geriatrics > Neurology > Flashcards

Neurology Flashcards

1
Q

How do you examine mental status in neuro?

A 
Attention
Language
Memory
Visuospatial function
Neglect
Frontal lobe function
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2
Q

How do you examine cranial nerve II?

A

Visual acuity
Visual fields
Pupils
Funds copy

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3
Q

What nerves are extra ocular movements testing?

A

Cranial nerves III, IV and VI

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4
Q

How do you test the trigeminal nerve?

A

Facial sensation

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5
Q

What nerve supplies facial muscles?

A

Facial, CNVII

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6
Q

How do you test cranial nerves IX, X and XII?

A

Palate and tongue movement

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7
Q

What are the aspects of testing motor function?

A

Bulk (inspection)
Tone
Power

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8
Q

What is the C5 myotome?

A

Shoulder abduction

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9
Q

Describe the myotomes of the upper limb

A 
C5 shoulder abduction
C5,6 elbow flexion
C7 elbow extension
C6,7 wrist extension
C7,8 wrist flexion
C7 finger extension
C8 finger flexion
T1 thumb/finger abduction
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10
Q

Describe the myotomes of the lower limb

A 
L1,2 hip flexion
L5,S1,2 hip extension
L5,S1,2 knee flexion
L3,4 knee extension
L4,5 ankle dorsiflexion
S1,2 ankle plantar flexion
L5 dorsiflexion of great toe
L4,5 ankle inversion
L5,S1 ankle ever soon
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11
Q

Describe the MRC grading of muscle power

A

0 no visible contraction
1 flicker or trace of contraction
2 active movement with gravity eliminated
3 active movement against gravity
4 active movement against some resistance
5 normal power

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12
Q

Describe the innervation of the upper limb reflexes

A

Biceps C5/6
Brachioradialis C5/6
Triceps C7

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13
Q

Describe the innervation of the lower limb reflexes

A

Knee L3/4

Ankle S1/2

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14
Q

What is the babinski reflex?

A

Stroke the lateral sole
Up going plantar reflexes is an UMN sign
I.e. The first movement is up = abnormal

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15
Q

What are the aspects to checking sensation?

A

Pinprick
Temperature
Vibration
Proprioception

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16
Q

How do you test coordination?

A

Finger-to-nose or heel-to-shin

Rhythm of movements - rapid alternating movements

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17
Q

What is Romberg’s test?

A

Steadiness with feet together and eyes closed

Tests for sensory ataxia

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18
Q

What are you looking for in gait in neuro exam?

A

Stance - narrow or wide base
Shuffling gait and decrease arm swing (PD)
Ataxia

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19
Q

What are the distinguishing features of a brain lesion?

A 
Higher cortical functions disrupted I.e. Speech, personality, memory etc
Unilateral signs (contra lateral to affected side)
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20
Q

What are extra pyramidal signs?

A

Akinesia
Rigidity
Tremor

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21
Q

What are the signs of a brainstem problem?

A

Cranial nerve signs / abnormalities

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22
Q

What are the cerebellar signs?

A 
Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Past-pointing
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23
Q

What are the distinguishing features of a spinal cord lesion?

A

Attributable to a level
Bilateral
Bladder/bowel involvement

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24
Q

How does a nerve root lesion present?

A

Dermatomal and myotomal distribution

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25
Q

How does a peripheral nerve lesion present?

A

LMN signs
Glove and stocking sensorineural deficit
Sensory ataxia

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26
Q

Where and what is Broca’s area?

A

Frontal lobe
Motor area for speech
Damage leads to expressive dysphasia

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27
Q

Where are what is Wernicke’s area?

A

Parietal lobe
Sensory input for speech
Receptive dysphasia

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28
Q

What are the symptoms and signs of a frontal lobe lesion?

A

Personality changes
Mono paresis (legs)
Incontinence
Dysphasia (expressive)

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29
Q

What are the signs and symptoms of parietal lobe lesions?

A 
Language difficulties
Hemlineglect
Visuospatial deficit
Leg weakness
Homonomous hemianopia
Dyspraxia
Agnosia
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30
Q

What is the function of the temporal lobe?

A

Auditory

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31
Q

What is the function of the occipital lobe?

A

Visual

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32
Q

What is the function of the cerebellum?

A

Coordination

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33
Q

What are the different parts of the brainstem called?

A

Midbrain
Pons
Medulla oblongata

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34
Q

What are the functions of the meninges?

A

Support and mechanically stabilise the contents of the cranium
Organise/divide cranial cavity into anatomical parts
Membranous envelopes that completely cover the brain

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35
Q

What are the meningeal layers?

A

Dura mater (periosteal + meningeal layers)
Arachnoid mater
Pia mater

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36
Q

What is in the subarachnoid space?

A

CSF

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37
Q

What are the functions of CSF?

A

Bathes the brain
Cushions against mechanical agitation
Reservoir for metabolic substrates for the brain
Dissolves and carries away products of metabolism

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38
Q

What is the difference between the meninges of the brain and spinal cord?

A

Dura mater is a single layer in the spinal cord

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39
Q

At what level is an LP done and why?

A

L3/4 in adults

Spinal cord terminates at L2

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40
Q

Where is the thalamus?

A

Wrapped around the 3rd ventricle

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41
Q

What is the function of the hypothalamus?

A

Regulates visceral functions eg temperature, endocrine, feeding/drinking, emotional states and sexual behaviour

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42
Q

What is the function of the cerebellum?

A

Integration, regulation and coordination of motor processes

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43
Q

What forms the brainstem?

A

Midbrain, medulla oblongata and pons

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44
Q

What is the function of the medulla oblongata?

A

Controls autonomic function

Eg respiration, cardiac centre + baroreceptors, vomiting, coughing, sneezing and swallowing centres

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45
Q

Where do the cranial nerves originate?

A

3&4 midbrain
5,6,7,8 pons
9,10,11,12 medulla

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46
Q

What is the cauda equina?

A

Group of nerve roots running in the lumbar cistern

Extend beyond the termination of the cord at L2 level, to reach the remaining vertebral foramina

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47
Q

Where does the spinal cord terminate in adults?

A

L2

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48
Q

How does cauda equina present?

A

Bladder, bowel and sexual dysfunction
Sensory changes in saddle and perianal areas
Back pain
Sensory changes or weakness in lower limbs
Reduction or loss of reflexes in lower limbs

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49
Q

What are the common causes of cauda equina syndrome?

A

Large central IV disc at L4/5 or L5/S1 level

Tumours, trauma, spinal stenosis, inflammatory disease

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50
Q

Which tract is responsible for fine touch and Proprioception?

A

Dorsal column

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51
Q

Where does the dorsal column decussate?

A

Medulla (brainstem)

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52
Q

What tract is responsible for pain and temperature sensation?

A

Lateral spinothalamic

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53
Q

Where does the lateral spinothalamic tract decussate?

A

Spinal cord (ie straight away)

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54
Q

Which column is responsible for crude touch and pressure sensation?

A

Anterior spinothalamic

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55
Q

What is the clinical significance of the decussation of the lateral spinothalamic tract?

A

It decussates straight away in the spinal cord, meaning a lesion always causes CONTRAlateral signs - for pain and temperature

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56
Q

What are pyramidal tracts?

A

Originating in cerebral cortex

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57
Q

What are extra-pyramidal tracts?

A

Don’t originate in the cerebral cortex

Eg originating in brainstem eg tectospinal, rubrospinal

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58
Q

Name 2 descending tracts of the pyramidal system

A

Lateral corticospinal

Ventral corticospinal

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59
Q

What is amyotrophic lateral sclerosis?

A

Progressive degenerative disease in which corticospinal tracts and central horn cells degenerate
Results in weakness and loss of control to muscles

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60
Q

What is Brown-Sequard syndrome?

A

Lateral hemisection of the cord

Causes loss of sensation and motor function

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61
Q

How does Brown-Sequard syndrome present?

A

Spastic paralysis of ipsilateral side
Loss of fine touch and proprioception ipsilaterally
Loss of pain, temp and pressure sensation to CONTRAlateral side due to damage to spinothalamic tract

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62
Q

What is the classic cause of Brown-Sequard syndrome?

A

Stab wound to back

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63
Q

What is anterior spinal artery syndrome?

A

Caused by ischaemia of the spinal artery

Affects corticospinal tracts and results in motor paralysis

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64
Q

What is syringomyelia?

A

Development of cyst/cavity around the central canal
Grows and spreads out over time
Typically affects spinothalamic tract as this decussates just anterior to the central canal
Reduced temp and pain sensation at level of lesion
Can affect motor as it extends

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65
Q

Name the bones of the skull

A 
Frontal
Parietal
Occipital
Ethmoid
Sphenoid
Temporal
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66
Q

What are the cranial fossae?

A

Anterior, middle and posterior

Accommodate and support the brain

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67
Q

Name the meninges

A

Dura mater
Arachnoid mater
Pia mater

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68
Q

What are the falx cerebri and tent oriel cerebelli?

A

Thick infoldings of the meninges

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69
Q

What are the CSF spaces in the brain?

A

Sulci
Fissures
Basal cisterns
Ventricles

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70
Q

What are the calcified structures within ventricles?

A

Choroid plexus

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71
Q

What is the difference between white and grey matter on CT and why?

A

White matter is darker
It has a high content of myelinated (fatty) axons
So it has a lower density

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72
Q

What are the important grey matter structures in the brain?

A

Cerebral cortex
Insula
Basal ganglia
Thalamus

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73
Q

What is the insula?

A

Inner surface of the cortex

Found deep in the Sylvian fissure

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74
Q

What are the internal capsules?

A

White matter tracts which connect with the corona radiata, white matter of cerebral hemispheres and the brainstem

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75
Q

What is the corpus callosum?

A

White matter tract located in the midline

Arches over lateral ventricles

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76
Q

How can malignant lesions spread between hemispheres?

A

Via the corpus callosum

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77
Q

What is found in the posterior cranial fossa?

A

Cerebellum and brainstem

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78
Q

Which artery supplies the largest area of cortex?

A

Middle cerebral artery

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79
Q

What calcified structures are found within the brain?

A

Choroid plexus
Pineal gland
Basal ganglia
Falx cerebri

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80
Q

How can you differentiate between cranial sutures and fractures?

A

Along the edge of the lesion, if the bone is corticated this means it is a suture
Fractures are also straighter than suture lines

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81
Q

What is hydrocephalus?

A

Increased production or decreased absorption of CSF

Can result in massive enlargement of ventricles

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82
Q

What changes do you see on CT in Alzheimer’s disease?

A

Temporal lobes reduced in volume

Enlargement of temporal horns of lateral ventricles

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83
Q

What is the likely diagnosis with generalised reduction in CSF space volume?

A

Cerebral oedema

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84
Q

What is small vessel disease on CT?

A

Generalised low density (darkening) of cerebral white matter
Represents chronic ischaemia
Associated with vascular risk factors

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85
Q

What are lacunae infarcts?

A

Area of brain cell death due to a focal ischaemia event

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86
Q

What are the signs of acute stroke on CT?

A

Subtle low density
Hyper dense artery sign - thromboembolic material within a cerebral artery
Insular ribbon sign - loss of clarity in the insular ribbon

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87
Q

What are the different types of extra-axial haemorrhage?

A

Extra dural, su dural and subarachnoid

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88
Q

Where does the blood commonly originate from in an epidural haematoma?

A

An intracranial artery, most commonly middle meningeal

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89
Q

What does an extra dural haematoma look like on CT?

A

Lens-shaped collection

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90
Q

What is the underlying pathology of a sub dural haematoma?

A

Fragile cerebral VEINS
Increased risk in elderly and anticoagulated
May result from minor trauma, or no trauma at all

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91
Q

What does a sub dural haematoma look like on CT?

A

Crescent-shaped collection (ie all along one side of the brain)

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92
Q

What are subarachnoid haematomas commonly caused by?

A

Trauma

Spontaneous bleeding from an intracranial aneurysm

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93
Q

What does a subarachnoid haemorrhage look like on CT?

A

Blood in ventricles or Sulci, fissures

Small foramina connect the subarachnoid space with the CSF spaces

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94
Q

What is the difference between intra- and extra-axial lesions?

A

Intra axial are within the brain

Extra axial are outside the brain

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95
Q

What are the most common intraaxial lesions?

A

Neoplastic and malignant
Single - more likely to be primary
Multiple - more likely to be metastatic

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96
Q

What are the most common extra axial lesions seen on head CT?

A

Meningiomas

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97
Q

What are Meningiomas?

A

Benign tumours arising from meninges and remaining in contact with them
Can grow very large and surrounded by an area of cerebral oedema

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98
Q

What is mass effect in the cranium?

A

Intracranial volume can’t change
Any space-occupying intracranial lesion may increase the intracranial pressure and displace the soft tissues of the brain

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99
Q

What pathological process affects mass effect?

A

Cerebral oedema - worsens mass effect

In infarcts, mass effect comes solely from cerebral oedema

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100
Q

What happens in extreme cases of mass effect?

A

Coning - extrusion of the posterior fossa structures through the for amen magnum

101
Q

What is herniation?

A

Tentorial - structures pass through the incisura tentoria (gap at top of tent normally occupied by brainstem and basal cisterns)

102
Q

What is meningism?

A

Acute severe headache
Felt over most of head
Accompanied by neck stiffness

103
Q

What are the causes of meningism?

A

Meningitis
Encephalitis
Subarachnoid haemorrhage

104
Q

How do you manage a patient presenting with meningism?

A

Admit urgently for CT head

If CT negative, do LP to look for signs of infection or blood products in CSF

105
Q

What are the features of meningitis?

A 
Fever
Photophobia
Stiff neck
Purpuric rash
Coma
106
Q

What are the features of venous sinus thrombosis?

A

Subacute or sudden headache

Papilloedema

107
Q

How does sinusitis present?

A

Dull constant ache over frontal or maxillary sinuses
Post-nasal drip
Pain worse on bending over

108
Q

How does acute glaucoma present?

A

Constant aching pain around 1 eye
Radiates to forehead
Reduced vision & visual haloes, nausea and vomiting
Eye looks red and congested, cornea cloudy
Dilated non-responsive pupil

109
Q

How do you manage acute glaucoma?

A

Seek expert help immediately

If delay >1hr start acetazolamide 500mg IV over few mins

110
Q

What are the common causes of recurrent attacks of headache?

A

Migraine
Cluster headache
Trigeminal neuralgia
Recurrent meningitis

111
Q

What are the features of cluster headaches?

A

Rapid onset excruciating pain around 1 eye
Eye may become watery and bloodshot, lid swelling, lacrimation, facial flushing
Pain always UNIlateral
Lasts 15-60mins, 1-2x per day, often nocturnal

112
Q

How do you treat cluster headaches?

A

100% O2 for 15mins

Sumitriptan subcut 6mg at onset

113
Q

What are the features of trigeminal neuralgia?

A

Intense, stabbing pain lasting seconds in trigeminal nerve distribution
Unilateral
Face screws up with pain

114
Q

What are common triggers for trigeminal neuralgia?

A 
Washing affected area
Shaving
Eating
Talking
Dental procedures
115
Q

Give some secondary causes of trigeminal neuralgia

A

Compression of trigeminal root eg tumour
Chronic meningeal inflammation
MS
Zoster

116
Q

What drugs are used to treat TN?

A

Carbamazepine
Lamotrigine
Phenytoin
Gabapentin

117
Q

How does Giant Cell Arteritis present?

A

Subacute headache
Tender, thickened, pulseless temporal arteries
Jaw claudication

118
Q

What investigation is required in suspected GCA?

A

ESR (>40mm/HR)

119
Q

How do you treat GCA?

A

Prednisolone

120
Q

What are the features of tension headache?

A

Bilateral
Non-pulsatile
Scalp muscle tenderness

121
Q

What are the features of raised ICP?

A 
Worse on waking / lying down / bending forward / coughing
Vomiting
Papilloedema
Seizures
False localising signs
122
Q

What is medication overuse headache?

A

Episodic headaches becoming chronic daily headache

Especially with mixed analgesics (paracetamol + codeine/opiates)

123
Q

What are the classic symptoms of migraine?

A

Visual or other aura for 15-30mins

Followed within 1 hour by unilateral throbbing headache

124
Q

What are the other presentations of migraine?

A

Isolated aura with no headache
Episodic headaches without aura - often premenstrual
Allodynia - all stimuli produce pain eg brushing hair

125
Q

What is a migraine prodrome?

A

Precedes headache by hours or days

Yawning, cravings, mood or sleep changes

126
Q

What is aura?

A

Precedes migraine headache by minutes
May continue during it
Visual, somatosensory, motor, speech

127
Q

What are the criteria for diagnosing migraine (if no aura)?

A 
5 or more headaches lasting 4-72hrs, nausea or photophobia
\+ 2 of...
Unilateral
Pulsating
Impairs or worsened by routine activity
128
Q

What are the common triggers of migraine?

A 
CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult
Exercise
129
Q

What are the differential diagnoses for migraine?

A 
Cluster or tension headache
Cervical spondylosis
Hypertension
Intracranial pathology
Sinusitis or otitis media
TIAs can mimic aura
130
Q

What are the principles of migraine treatment?

A

Analgesia
Abortive eg triptans
Prevention eg propanolol, amitriptyline

131
Q

What medications are used in acute migraine?

A

NSAIDs eg aspirin
Triptans (5HT agonists) eg sumatriptan
Ergotamine 1mg PO as headache starts

132
Q

What are the medications used to prevent migraines?

A

Propanolol
Amitriptyline
Topiramate

133
Q

What are the non-pharmacological measures to treat migraine?

A

Warm or cold packs to head
Rebreathing into paper bag
Spinal manipulation

134
Q

What is the relationship between migraine and the pill?

A

Slight increased risk of stroke if on the pill and have migraine with aura
Women should stop the pill immediately if they develop migraine with aura, and use alternative or low-dose pill

135
Q

Define stroke

A

Syndrome of rapidly developing symptoms or signs of focal loss of CNS function
Symptoms last more than 24hrs or result in death

136
Q

What are the vascular mechanisms causing stroke?

A

Infarction - embolisation or thrombotic

Haemorrhage

137
Q

In what conditions can cardiac emboli arise and cause stroke?

A

AF
Endocarditis
MI

138
Q

What are the modifiable risk factors for stroke?

A 
Hypertension
Smoking
Diabetes
Heart disease - valvular, ischaemia, AF
PVD
Past TIA
Carotid bruit
Hyperlipidaemia
Excess alcohol
139
Q

What are the different types of stroke according to the Oxford classification?

A

TACS
PACS
LACS
POCS

140
Q

What artery is involved in TACS?

A

Middle or anterior cerebral

141
Q

What is the commonest cause of TACS?

A

Cardiac emboli (AF)

142
Q

What are the signs of TACS?

A

Higher cortical dysfunction
Hemiparesis or hemisensory
Homonymous hemianopia

143
Q

What artery is affected in PACS?

A

Middle or anterior cerebral

144
Q

What is the commonest cause of PACS?

A

Carotid disease

145
Q

What is the difference between TACS and PACS?

A

PACS has better prognosis

PACS only has 2 out of 3 signs, or higher cortical dysfunction alone

146
Q

What is the cause of a lacunar stroke?

A

Thrombus in situ

147
Q

What are the signs of LACS?

A

Only motor or only sensory

Arm, face and leg

148
Q

What are the signs of POCS?

A

1 of:
A. Cerebellar or brainstem syndromes
B. LOC
C. Isolated homonymous hemianopia

149
Q

What is the prognosis of posterior cerebral stroke?

A

Many don’t survive, but if they do then prognosis is good

150
Q

What is the ROSIER score?

A 
Score greater than 0 raises suspicion of stroke. 1 pt each:
Face
Arm
Leg weakness
Speech disturbance
Visual field defect
Minus 1 for: seizure, LOC or syncope
151
Q

What is the acute management of suspected stroke?

A 
Airway
Pulse, BP, ECG
Blood glucose: aim for 4-11
Urgent CT if thrombolysis considered or high-risk of bleed or signs of raised ICP
Thrombolysis: if onset within 4-5hr
NBM if ?dysphagia
Aspirin 300mg AFTER haemorrhage excluded
152
Q

What is used for thrombolysis?

A

IV alteplase

153
Q

What are the contraindications to thrombolysis?

A 
Major infarct or haemorrhage on CT
Past CNS bleed
Severe liver disease
Seizures at presentation
Anticoagulants or INR>1.7
Platelets <100
BP >220/130
154
Q

What is the NIHSS?

A

National institute of health stroke scale
Used to assess deficits on admission then again at review
Higher score means more severe stroke

155
Q

What are the differential diagnoses for stroke?

A 
SAH
Subdural haemorrhage
Venous infarcts
Malignancy
Abscesses
Hemiplegic migraine
Functional hemiparesis
156
Q

What are the factors involved in primary prevention of stroke?

A

Treat hypertension, diabetes, Hyperlipidaemia, cardiac disease
Exercise
Smoking cessation
Folate supplements
Anticoagulation for AF, prosthetic valves

157
Q

How do you decide if someone with AF should be anticoagulated?

A

CHADSVASc

158
Q

What is secondary prevention for stroke?

A

Prevent further strokes…
Control risk factors
Antiplatelets after stroke - clopidogrel (as long as no haemorrhage)
Anticoagulation if stroke from AF - warfarin from 2 weeks after stroke

159
Q

What investigations are done in stroke patients and why?

A 
BP, HbA1c, lipid profile
24hr ECG ?AF
CXR
Echo ?mural thrombus
Carotid Doppler USS (>70% stenosis is significant)
160
Q

What is the mortality for strokes in the UK?

A

20% at 1 month

161
Q

What are the complications of stroke?

A 
Aspiration pneumonia
Broncho-pneumonia
Pressure sores
Subluxation (flaccid paralysis) or contractures (spastic)
Constipation
Vascular dementia
Depression
162
Q

What 4 areas can you quickly assess for cognitive functions?

A

Perceptual function: point to a part of body
Spatial ability: copying matchstick patterns
Apraxia: copy a clock face
Agnosia: picking out and naming easy objects

163
Q

How are TIAs followed up?

A

Aspirin 300mg for 14 days
Clinic appt within 24hrs if high-risk; 7days if low
No driving for 1 month
Return immediately if they have more symptoms

164
Q

How do you calculate risk of imminent stroke following TIA?

A 
ABCD2 score...
Age >60
BP >140/90
Speech disturbance (1) unilateral weakness (2)
Duration of TIA 10-59mins (1) >60mins (2)
Diabetes
1-3=Low
4-5=Mod
6-7=High
165
Q

What is myasthenia gravis?

A 
Autoimmune
Antibodies against nACh receptors
Causes depletion of post-synaptic sites
Interferes with neuromuscular transmission
Fluctuating weakness of skeletal muscles
166
Q

What muscle groups are commonly involved in myasthenia gravis?

A

Extra ocular
Bulbar: dysphagia, dysphonia, dysarthria
Limbs
Respiratory

167
Q

What is the characteristic symptom of myasthenia gravis?

A

Fatiguability of skeletal muscle during activity
Fluctuating, painless weakness
Muscles strong in morning and progressively weaker with activity

168
Q

What are the effects on extra ocular muscles in MG?

A

Ptosis - often worse 60-90seconds sustained upgaze. Gradual ptosis with compensatory frontalis contraction. Resting (closing eyes) causes muscle power to return
Pupils are UNaffected
Facial mobility may be impaired

169
Q

What factors can precipitate myasthenia gravis?

A 
Emotional stress
Pregnancy
Menses
Thyroid dysfunction
Trauma
Hypokalaemia
Drugs eg beta-blockers, CCBs, ACEi
Surgery
170
Q

What are the complications of myasthenia gravis?

A

Respiratory failure, aspiration or infection
Myasthenic crisis
Cholinergic crisis

171
Q

What is myasthenic crisis?

A 
Severe exacerbation, can be dramatic...
Facial muscles slack, expressionless
Slack jaw
Unable to support head
Limp body
Gag reflex lots - risk of aspiration
172
Q

What is cholinergic crisis?

A 
Miosis + SSLUDGE
Salivation
Sweating
Lacrimation
Urinary incontinence
Diarrhoea
GI upset
Emesis
173
Q

What causes cholinergic crisis?

A

Excess cholinesterase inhibitors
Excessive ACh stimulation of striated muscle at nicotinic junctions produces flaccid paralysis, clinically hard to distinguish from weakness due to MG

174
Q

How do you diagnose myasthenia gravis?

A

AChR antibodies
Tensilon test: IV anticholinesterase (tensilon) - improves muscle contractility
Caution in asthma, MI and bradycardia (cardiac monitoring and have atropine ready)
EMG may show muscle fatigue

175
Q

How do you diagnose cholinergic crisis?

A

Tensilon test - IV anticholinesterase agent, makes weakness worse
NB in diagnostic tensilon test for MG, improvement is seen

176
Q

How do you manage acute myasthenia gravis?

A

Beside spirometry: monitor FBC

Falling FVC may require ICU for ventilation

177
Q

What are the drugs used to treat myasthenia gravis?

A

Anticholinesterase inhibitors e.g. Neostigmine
Steroids: decrease immune response
Azathioprine

178
Q

What is Lambert-Eaton syndrome?

A

Destruction of pre synaptic calcium channels to prevent neurotransmitter release
Gives a lot of autonomic symptoms due to similarity between channels
NB no autonomic problems in myasthenia gravis

179
Q

What is Guillain-Barré syndrome?

A

Ascending polyneuropathy

180
Q

What is the commonest form of GBS?

A

Post-infectious polyneuropathy
Causes ascending polyneuropathic paralysis
Acute, rapidly progressing and potentially life-threatening

181
Q

What is the Miller Fisher variant of GBS?

A

Sensory ataxia
Arreflexia
Ophthalmoplegia

182
Q

What are the required features for GBS diagnosis?

A

Progressive weakness in both arms and legs

Arreflexia

183
Q

When does GBS commonly occur?

A

1-3 weeks after URTI or GI infection

184
Q

What are the complications of GBS?

A 
Autonomic dysfunction:
Cardiac arrhythmias
Postural hypotension
Hypertension
Urinary retention
Ileus
Resp failure: bedside spirometry!
185
Q

How do you manage Guillain-Barré syndrome?

A 
Close observation (weakness is progressive)
Bedside spirometry
Ventilatory support
ECG
Nutritional support 
VTE prophylaxis
Catheter
Laxatives
Pain control
186
Q

What is the prognosis for Guillain-Barré syndrome?

A

25% require ventilation
70% have complete recovery at 1yr
25-30% have some residual deficit

187
Q

How do polyneuropathies present?

A

Distribution usually symmetrical and widespread

Often distal weakness and sensory loss (glove and stocking)

188
Q

What conditions cause mainly motor polyneuropathy?

A

Gillian-barre syndrome
Lead poisoning
Charcot-Marie-Tooth syndrome

189
Q

What conditions cause mostly sensory polyneuropathy?

A

Diabetes
Renal failure
Leprosy

190
Q

What are the features of autonomic polyneuropathy?

A 
Postural hypotension
Erectile dysfunction
Reduced sweating
Constipation and nocturnal diarrhoea
Urinary retention
Horner's syndrome
191
Q

What are the causes of autonomic polyneuropathy?

A 
Diabetes
Guillain-Barre
Sjögren's syndrome
HIV
Leprosy
SLE
192
Q

What is the treatment of choice for neuropathic pain?

A

Amitriptyline 10-25mg at night

Or gabapentin/pregabalin

193
Q

What is cervical spondylosis?

A

Degeneration of the annulus fibrosus of cervical intervertebral discs
Causes narrowing of the spinal canal
Most people have no nerve impairment, but it can cause compression of the cord and nerve roots

194
Q

What are the features of cervical spondylosis?

A

Neck stiffness
Limited painful neck movement
Neck flexion may produce tingling down the spine

195
Q

What is radiculopathy and what are the features?

A

Root compression
Pain / electrical sensations in arms or fingers at level of compression
Dull reflexes
LMN weakness and eventual muscle wasting of affected root
UMN signs below level of affected root

196
Q

What is the management of cervical spondylosis?

A

Firm neck collar restricts to relieve pain

Surgical root decompression: laminectomy or laminoplasty

197
Q

What are the diagnostic criteria for neurofibromatosis type 1?

A 
6 or more cafe au lait patches
2 or more neurofibromas
Freckling in axillary or inguinal regions
Optic glioma
Lisch nodules - hamartomas on iris
1st degree relative with NF1
198
Q

How does neurofibromatosis type 2 differ from type 1?

A

Bilateral vestibular schwannomas (acoustic neuroma)

199
Q

What is motor neuron disease?

A

Selective loss of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells
Upper and lower motor neurones affected

200
Q

What are the important negatives in motor neurone disease?

A

No sensory loss or sphincter disturbance

201
Q

What are the 4 clinical patterns of MND?

A
  1. ALS (50%)
  2. Progressive bulbar palsy
  3. Progressive muscular atrophy
  4. Primary lateral sclerosis
202
Q

What are the common presenting features of MND?

A 
>40y
Stumbling spastic gait
Foot drop
Proximal myopathy
Weak grip
Weak shoulder abduction
Aspiration pneumonia
203
Q

What are the UMN signs seen in MND?

A

Spasticity
Brisk reflexes
Up going plantars

204
Q

What are the LMN signs seen in MND?

A

Wasting

Fasciculation

205
Q

What are the bulbar signs in MND?

A

Speech or swallowing affected

206
Q

What makes MND diagnosis definite?

A

Lower and upper motor neuron signs in 3 regions

207
Q

What is the treatment for MND?

A 
Antiglutamatergic drugs
Drooling: amitriptyline
Dysphagia: blend food, NG or PEG
Analgesia
NIV at home for resp failure
208
Q

What part of the nervous system does MS affect?

A

White matter of brain and spinal cord and optic nerves

209
Q

What is the pathophysiology of MS?

A

Inflammatory demyelination of CNS tracts
Causes reduction in conduction velocity, as well as distortion and loss of information
Changes not uniformly distributed, foci of inflammation and demyelination = plaques

210
Q

What is gliosis?

A

Plaques evolve with time and ultimately result in CNS equivalent of scarring

211
Q

What is the epidemiology of MS?

A

Females 3:1
Usually presents age 20 - 40
UK prevalence 1 in 1000

212
Q

What are the most common presentations of MS?

A

Visual disturbance
Limb weakness
Sensory disturbance

213
Q

What is optic neuritis?

A

Inflammatory demyelination of one optic nerve
Pain around one eye, especially on movement
Rapid decline in central vision (central scotoma)
RAPD
Pink, swollen optic disc

214
Q

What are the sensory features of MS?

A

Dysaesthesia
Pins and needles
Decreased vibration sense
Trigeminal neuralgia

215
Q

What are the motor features of MS?

A

Spastic weakness

Myelitis

216
Q

What is the progression of MS?

A

Symptoms worsen over days/weeks, reach plateau then resolve partially or completely
Relapses
Remissions are incomplete with time, so disability accumulates

217
Q

What are poor prognostic signs in MS?

A

Older male
Motor signs at onset
Many relapses early on
Axonal loss

218
Q

How is MS diagnosed?

A

Clinically
MRI is sensitive but not specific for plaque detection
Lesions disseminated in time and space, with no other causes - further evidence needed after 1st episode
CSF: oligoclonal bands of IgG on electrophoresis suggest CNS inflammation

219
Q

What is the treatment for MS?

A

Steroids: methylprednisolone shortens acute relapse
Interferons
Monoclonal antibodies e.g. Alemtuzumab / Natalizumab

220
Q

What drugs are used to treat spasticity?

A

Baclofen
Diazepam
Dantrolene

221
Q

What is cervical spondylosis?

A

Degeneration of the annulus fibrosus of cervical intervertebral discs
Causes narrowing of the spinal canal
Most people have no nerve impairment, but it can cause compression of the cord and nerve roots

222
Q

What are the features of cervical spondylosis?

A

Neck stiffness
Limited painful neck movement
Neck flexion may produce tingling down the spine

223
Q

What is radiculopathy and what are the features?

A

Root compression
Pain / electrical sensations in arms or fingers at level of compression
Dull reflexes
LMN weakness and eventual muscle wasting of affected root
UMN signs below level of affected root

224
Q

What is the management of cervical spondylosis?

A

Firm neck collar restricts to relieve pain

Surgical root decompression: laminectomy or laminoplasty

225
Q

What are the diagnostic criteria for neurofibromatosis type 1?

A 
6 or more cafe au lait patches
2 or more neurofibromas
Freckling in axillary or inguinal regions
Optic glioma
Lisch nodules - hamartomas on iris
1st degree relative with NF1
226
Q

How does neurofibromatosis type 2 differ from type 1?

A

Bilateral vestibular schwannomas (acoustic neuroma)

227
Q

What is motor neuron disease?

A

Selective loss of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells
Upper and lower motor neurones affected

228
Q

What are the important negatives in motor neurone disease?

A

No sensory loss or sphincter disturbance

229
Q

What are the 4 clinical patterns of MND?

A
  1. ALS (50%)
  2. Progressive bulbar palsy
  3. Progressive muscular atrophy
  4. Primary lateral sclerosis
230
Q

What are the common presenting features of MND?

A 
>40y
Stumbling spastic gait
Foot drop
Proximal myopathy
Weak grip
Weak shoulder abduction
Aspiration pneumonia
231
Q

What are the UMN signs seen in MND?

A

Spasticity
Brisk reflexes
Up going plantars

232
Q

What are the LMN signs seen in MND?

A

Wasting

Fasciculation

233
Q

What are the bulbar signs in MND?

A

Speech or swallowing affected

234
Q

What makes MND diagnosis definite?

A

Lower and upper motor neuron signs in 3 regions

235
Q

What is the treatment for MND?

A 
Antiglutamatergic drugs
Drooling: amitriptyline
Dysphagia: blend food, NG or PEG
Analgesia
NIV at home for resp failure
236
Q

What part of the nervous system does MS affect?

A

White matter of brain and spinal cord and optic nerves

237
Q

What is the pathophysiology of MS?

A

Inflammatory demyelination of CNS tracts
Causes reduction in conduction velocity, as well as distortion and loss of information
Changes not uniformly distributed, foci of inflammation and demyelination = plaques

238
Q

What is gliosis?

A

Plaques evolve with time and ultimately result in CNS equivalent of scarring

239
Q

What is the epidemiology of MS?

A

Females 3:1
Usually presents age 20 - 40
UK prevalence 1 in 1000

240
Q

What are the most common presentations of MS?

A

Visual disturbance
Limb weakness
Sensory disturbance

241
Q

What is optic neuritis?

A

Inflammatory demyelination of one optic nerve
Pain around one eye, especially on movement
Rapid decline in central vision (central scotoma)
RAPD
Pink, swollen optic disc

242
Q

What are the sensory features of MS?

A

Dysaesthesia
Pins and needles
Decreased vibration sense
Trigeminal neuralgia

243
Q

What are the motor features of MS?

A

Spastic weakness

Myelitis

244
Q

What is the progression of MS?

A

Symptoms worsen over days/weeks, reach plateau then resolve partially or completely
Relapses
Remissions are incomplete with time, so disability accumulates

245
Q

What are poor prognostic signs in MS?

A

Older male
Motor signs at onset
Many relapses early on
Axonal loss

246
Q

How is MS diagnosed?

A

Clinically
MRI is sensitive but not specific for plaque detection
Lesions disseminated in time and space, with no other causes - further evidence needed after 1st episode
CSF: oligoclonal bands of IgG on electrophoresis suggest CNS inflammation

247
Q

What is the treatment for MS?

A

Steroids: methylprednisolone shortens acute relapse
Interferons
Monoclonal antibodies e.g. Alemtuzumab / Natalizumab

248
Q

What drugs are used to treat spasticity?

A

Baclofen
Diazepam
Dantrolene

Geriatrics (17 decks)

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