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Neurology > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the normal volume of CSF

A

120-150ml at one time

500ml is produced per day so lots of turnover

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2
Q

What does CSF usually contain

A

Should be clear with some protein and glucose

No RBC, neutrophils and only a small number of lymphocytes

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3
Q

What suggests an infection in the CSF

A

Increase in the number of neutrophils or lymphocytes

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4
Q

What causes hydrocephalus

A

Obstruction to flow of CSF - tumour, pus etc
Decreased reabsorption of CSF - post SAH or meningitis
Overproduction of CSF - tumour in the choroid plexus (rare)

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5
Q

What is hydrocephalus

A

Accumulation of excessive CSF within the ventricular system of the brain

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6
Q

what is the difference between communicating and non-communicating hydrocephalus

A

Non-com - obstruction to CSF is within the ventricular system

Com - obstruction to flow is outside of ventricle (e.g. in the subarachnoid space)
- all of the ventricles will dilate

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7
Q

How can hydrocephalus present in very young children

A

If hydrocephalus occurs before the sutures close, then the head enlarges

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8
Q

What is hydrocephalus ex vacuo

A

When the ventricles dilate due to loss of brain parenchyma and there is a compensatory increase in CSF volume
Seen in Alzheimer’s

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9
Q

What can lead to raised ICP

A 
Hydrocephalus - increase in CSF  
Space occupying lesion 
Idiopathic Intracranial Hypertension 
Oedema 
Cerebral venous sinus thrombosis 
Increased venous volume 
Physiological - hypoxia, hypercapnia and pain
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10
Q

What effects does raised ICP have on the brain

A

Intracranial shifts and herniation
Pressure on the cranial nerves and vital brain centres
Impaired blood flow
reduced consciousness

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11
Q

How do you work out cerebral perfusion pressure

A

MAP-ICP

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12
Q

What would a subfalcine herniation cause

A

Results in weakness and/or sensory loss on the opposite side (particularly in legs)

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13
Q

What would a tentorial herniation cause

A

Pupil dilation on that side

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14
Q

What would a cerebellar herniation cause

A

Death = life-threatening as causes brain stem compression

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15
Q

What is a transcalvarial herniation

A

Swollen brain will herniate through any defect in the dura and skull if there is damage (post-trauma)

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16
Q

What are the early clinical signs of raised ICP

A

Papilloedema – pressure on the optic nerve
Pupillary dysfunction and vision changes
N and V – due to pressure on the vomiting centre in the brain
Headache – worse when lying down, due to pressure on the dura
Neck stiffness
Decreased consciousness - drowsy

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17
Q

Where do single brain abscesses tend to come from

A

Local extension - infection in nearby area such as mastoiditis

Direct implantation - due to skull fracture

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18
Q

Where do multiple brain abscesses tend to come from

A

Haematogenous spread - often from lungs (pneumonia) or heart (endocarditis)

Usually occur at boundary between grey & white matter

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19
Q

What lifestyle factor increases risk of brain abscess

A

IV drug use

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20
Q

What effect does a brain abscess have

A

Can cause a mass effect and also leads to oedema

Toxic injury can occur

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21
Q

How does a brain abscess present clinically

A

Fever
Symptoms of raised ICP
May also have symptoms of the underlying cause

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22
Q

How do you diagnose a brain abscess

A

CT or MRI

Can aspirate to determine organism and therefore treatment

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23
Q

How do you treat a brain abscess

A

Weeks of antibiotics

Depends on organism

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24
Q

What is meningitis

A

Inflammation of the meninges and CSF within the subarachnoid space

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25
Q

What would you see on an LP of someone with meningitis

A

Abundant polymorphs

Decreased glucose

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26
Q

What features must you ask about in a neuro history

A 
Date of onset
Nature of main symptom (e.g. weakness)
Associated neurological symptoms
Exacerbating / relieving factors
Evolution
Recurrence
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27
Q

Where can neurological deficits/injury arise from

A

CNS
PNS
NMJ
or the muscle itself

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28
Q

Which area tends to be affected by a CNS issue

A

Often whole limb - larger area

Hemi or paraplegia

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29
Q

Which area tends to be affected by a PNS issue

A

Usually causes distal/peripheral problems
Often localised
Can affect whole limb though

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30
Q

Which area tends to be affected by a NMJ issue

A

Ocular - vision
Bulbar - speech and swallow
Proximal limb

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31
Q

Which area tends to be affected by a muscle issue

A

Proximal muscles

usually symmetrical

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32
Q

How does weakness present in a CNS issue

A

Feeling of heaviness
Due to a combination of numbness and weakness

Pyramidal pattern: arms have weaker extensors and legs the flexors are weaker
Therefore have flexed arms and hyperextended legs

Weakness will be contralateral if brain, below level of lesion if spinal

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33
Q

How does weakness present in a PNS issue

A

Usually positional - e.g. when asleep
Ascending - works its way up from glove and stocking
Affects distal areas - may be some wasting

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34
Q

How does weakness present in a NMJ issue

A

As fatiguable
Weakness gets worse when you’ve used to muscle - worse at the end of the day or on repeated movement
Pattern is variable

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35
Q

How does weakness present in a muscle issue

A 
May have insidious onset 
Muscle wasting
Symmetrical and in proximal  muscles 
May be accompanied by aching (myalgia)
Hard to rise from chair without using arms
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36
Q

Are sensory symptoms seen in CNS issues

A

Yes
If in brain it is hemisensory and contralateral to the lesion
If in spinal cord the issue will be below the level of the lesion
(spinothalamic on contralateral side and dorsal column on ipsilateral)

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37
Q

Are sensory symptoms seen in PNS issues

A

Yes
Pain is often prominent
Typically glove and stocking distribution - peripherals

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38
Q

Are sensory symptoms seen in NMJ issues

A

No

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39
Q

Are sensory symptoms seen in muscle issues

A

No

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40
Q

What are the additional features of a CNS pathology

A

Spasms or jerks

May have sphincter involvement

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41
Q

What are the additional features of a PNS pathology

A 
Cramp 
Twitching - e.g. fasciculations 
Distal wasting 
Loss of grip 
Tripping up 
Unsteady when eyes are closed
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42
Q

What are the additional features of a NMJ pathology

A 
Swallowing and speaking difficulty 
May struggle with lots of chewing/talking 
Diplopia and ptosis 
Opthalmoplegia 
Orthopnoea 
Worse later in the day
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43
Q

What are the additional features of a muscle pathology

A

Myalgia - pain
Cramp
May struggle with specific movement - e.g. getting up from a low chair

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44
Q

What physical signs of CNS pathology might you see on inspection

A

Abnormal limb posture
Upper limb fixed flexion
Lower limb hyperextension

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45
Q

What physical signs of PNS pathology might you see on inspection

A

Muscle wasting - distal
Fasciculations
Pes cavus

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46
Q

What physical signs of NMJ pathology might you see on inspection

A

Ptosis

Ophthalmoplegia

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47
Q

What physical signs of muscle pathology might you see on inspection

A

Proximal wasting

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48
Q

How is tone affected in CNS pathology

A

Increased

Spasticity or clonus

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49
Q

How is tone affected in PNS pathology

A

Decreased

Particularly distally

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50
Q

How is tone affected in NMJ pathology

A

Either the same or slightly decreased if very long standing

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51
Q

How is tone affected in muscle pathology

A

Either the same or slightly decreased if very long standing

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52
Q

How are reflexes affected in CNS pathology

A

Increased

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53
Q

How are reflexes affected in PNS pathology

A

Decreased or absent

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54
Q

How are reflexes affected in NMJ pathology

A

Usually the same

May be slightly decreased if very long standing

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55
Q

How are reflexes affected in muscle pathology

A

Either the same or slightly decreased

Reflexes usually retained until pathology is very advanced or long standing

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56
Q

What is the plantar response like in CNS pathology

A

Get an extensor response

Toes splay out and extend

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57
Q

What is the plantar response like in PNS pathology

A

Flexor response - normal

Toes curl down

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58
Q

What is the plantar response like in NMJ pathology

A

Flexor response - normal

Toes curl down

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59
Q

What is the plantar response like in muscle pathology

A

Flexor response - normal

Toes curl down

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60
Q

What is clonus

A

Continued jerking after sharp, fast movement

3 beats is abnormal, 6 is pathological

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61
Q

Pathology in the cervical spinal cord will affect which area of the body

A

The hands and arms

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62
Q

Pathology in the thoracic spinal cord will affect which area of the body

A

The legs

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63
Q

What kind of disease pattern is seen in CNS inflammatory conditions

A

Tend to come and go symptom wise

Relapsing and remitting seen in MS

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64
Q

What kind of disease pattern is seen in CNS vascular conditions

A

Normally a sudden deficit that slowly gets better

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65
Q

What kind of disease pattern is seen in CNS space occupying lesions

A

Gradual increase in the deficit

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66
Q

What kind of disease pattern is seen in disc prolapse

A

Disc prolapse issue can come on and get gradually worse or a sudden event can lead to a more intense deficit that stays at that level

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67
Q

How can you test for a bulbar deficit in NMJ pathology

A

Ask them to count out loud - may decline as goes on

Say tough phrase at the start and end ‘West Register Street

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68
Q

How can you test for a ocular deficit in NMJ pathology

A

Get them to fix their gaze on a set horizontal point and ask if they develop diplopia

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69
Q

How do you test for ptosis

A

Get patient to look up for 30secs and see if their eyes start to droop (ptosis)

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70
Q

Ocular issues in a suspected NMJ problem is suggestive of what

A

Myasthenia Gravis

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71
Q

What causes myasthenia gravis

A

Autoimmune disease where there are antibodies against the acetylcholine receptors on the post-synaptic membrane
Fewer ACh receptors means transmission becomes inefficient and causes weakness
Loss of action potential leads to lack of muscle contraction
Affects the NMJ

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72
Q

Are you unconscious when asleep

A

Technically not

It is a state between conscious and unconscious as you can be awoken when stimulated

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73
Q

What is REM sleep

A

Rapid eye movement
Mostly occurs at the end of the night
EEG will show fast brain activity - similar to being awake
Muscles will be atonic (except diaphragm and eye muscles)

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74
Q

What is Non-REM sleep

A

Occurs at the start of the night
EEG activity is synchronised and rhythmic
Heart rate, BP and cerebral blood flow are reduced
There is partial relaxation of the muscles

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75
Q

What are the differences between dreams in REM and non-REM sleep

A

REM dreams – act out a story that you remember (narrative dreaming)
A non-REM dream you will not remember but may feel a strong emotion upon waking

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76
Q

What is the function of deep sleep (non-REM)

A

This is essential sleep

Allows the cortex to recover after a busy day

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77
Q

What is the function of REM sleep

A

Mainly for early brain development - important for kids
Adults can cope without
Consolidates memory and possibly deletes unnecessary memory

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78
Q

What role does emotion play in sleep

A

Brain has to feel ready to go to sleep

States of anxiety will make it feel like you haven’t slept as the brain isn’t rested

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79
Q

Describe the circadian rhythm

A

This is our ‘body clock’
Has 2 peaks at 4am and 2pm = most tired at these points
Lasts 25 hours
Also controls appetite, hormone secretion, temperature
Varies with age - kids and elderly wake/sleep early whilst teenagers sleep late

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80
Q

What is suspected to reset the circadian rhythm

A

Light - specifically blue light which is picked up by retinal cells
This is why its harder to wake up in winter when its dark

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81
Q

What are the risks of chronic sleep deprivation

A

Loss of inhibition and sense of danger
Leads to poor judgement and decision making
Can cause irritability, suspiciousness and even visual illusions
Will end up having lapses in concentration and microsleeps

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82
Q

Missing out on which type of sleep will cause sleep deprivation

A

Non-REM (deep) sleep

Can get by without REM

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83
Q

Which area of the brain is most effected by lack of sleep

A

The cortex
It can only rest during sleep
Therefore a lot of the symptoms of sleep deprivation are pre-frontal

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84
Q

How can sleep deprivation kill you

A

No cases of dying just due to lack of sleep but it would probably kill you
Most common cause is RTA - spikes early hours of the morning

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85
Q

How much sleep do we need

A

Around 7-7.5 hours a night minimum

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86
Q

Can you catch up on sleep

A

Nope

Long lie at weekend will not make up for sleep deprivation in the week

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87
Q

What is a REM sleep disorder

A

People will act out dreams (e.g. kick, running)
Will shout out in sleep
Only an issue if it occurs regularly
Seen in Parkinson’s

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88
Q

List some common parasomnias

A 
REM or non-REM 
Sleep walking 
Restless legs 
Sleep terrors 
Sleep paralysis
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89
Q

How does narcolepsy present

A

Daytime sleepiness - may fall asleep during conversations/meals
Cataplexy - sudden loss of muscle tone triggered by strong emotion
If people get very angry or laugh a lot they can suddenly slump to the ground
Hallucinations occurring at sleep onset - hypnagogic

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90
Q

How would you investigate narcolepsy

A

Overnight polysomnography
Multiple sleep latency test - assess how quickly someone falls asleep
narcoleptics will fall asleep almost immediately and go straight into REM sleep
LP will show low CSF hypocretin

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91
Q

What are the complications of narcolepsy

A

Job impairment - struggle to stay awake

Increased risk of death in car accidents - shouldn’t drive if not controlled

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92
Q

How does decorticate rigidity present

A

Upper limb flexed

Lower limb extended and internally rotated

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93
Q

How does decerebrate rigidity present

A

Arms are extended and pronated
Wrists flexed
Plantars flexed

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94
Q

How does a central cord syndrome present

A

Affects the medial corticospinal fibres

Get a cape like loss of sensation

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95
Q

What commonly causes a central cord syndrome

A

Common in the elderly who have cervical injuries or overextension

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96
Q

How does an anterior cord syndrome present

A

DCML is intact but other tracts affected

Bilateral loss of spinothalamic sensation

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97
Q

What commonly causes an anterior cord syndrome

A

Usually due to interruption of blood supply in the anterior artery
Can present as spinal shock

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98
Q

How does brown-sequard syndrome present

A

Ipisilateral loss of motor below the level of the lesion

Loss of sensation on opposite side

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99
Q

What is a common cause of brown-sequard syndrome

A

Penetrating injury to the back or neck

Stab wound is buzzword

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100
Q

Syringomyelia is a type of what cord syndrome

A

Central cord syndrome

Due to increased CSF pressure around the cord

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101
Q

What investigation would give you a definitive diagnosis in suspected brain cancer

A

Biopsy

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102
Q

What investigation would give you a definitive diagnosis in suspected extradural haemorrhage

A

CT scan

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103
Q

What investigation would give you a definitive diagnosis in suspected SAH

A

CT angiography

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104
Q

What are the symptoms of cerebral herniation

A

Cause by raised ICP
Extensor responses - upgoing plantars
Cushing’s triad - hypertension, bradycardia and irregular breathing
Unreactive pupil

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105
Q

What type of herniation is most likely to cause unresponsive pupil

A

Uncal

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106
Q

What type of back pain gets better when walking uphill

A

That caused by lumbar stenosis

The lean forward opens up the canal

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107
Q

What type of back pain gets worse with sitting or turning over

A

Mechanical

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108
Q

How does an anterior circulation stroke present

A

Higher cerebral dysfunction (e.g. dysphasia).
Homonymous visual field defect
Contralateral motor and/or sensory deficit

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109
Q

How does a posterior circulation stroke present

A

Cerebellar dysfunction
Isolated homonymous visual field defect
Cranial nerve dysfunction

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110
Q

How does a lacunar stroke present

A

Purely motor or sensory symptoms

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111
Q

What are sunset eyes a sign of

A

Hydrocephalus

Upward gaze will be impaired

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112
Q

What are the symptoms of normal pressure hydrocephalus

A

Ataxia - shuffling gait like Parkinson’s but no stopping issues
Incontinence
Dementia

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113
Q

Disorders of the pyramidal tracts present with what symptoms

A

Pyramidal weakness

Spasticity

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114
Q

Disorders of the basal ganglia present with what symptoms

A

Can be hyperkinetic: dystonia, tics, myoclonus, chorea

Or Hypokinetic = rigidity, bradykinesia

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115
Q

What is the Babinski reflex

A

When you drag a pointer up the sole of the foot the plantar reflex is increased
Toes splay outward

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116
Q

Describe the pattern of upper motor neuron disease

A

Increased tone - stiffness and spasticity
Minimal muscle wasting
No fasciculations
Clonus present
Brisk reflexes
Extensor plantar reflex - Babinski present
Pyramidal/ corticospinal pattern of weakness (= weak extensors in the arm, weak flexors in the legs)
Central pattern of sensory loss

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117
Q

Describe the pattern of lower motor neuron disease

A 
Muscle wasting - early atrophy
Fasciculations
Decreased power 
Decreased tone - flaccid
Decreased or absent reflexes 
No clonus
Flexor plantar reflex - normal (no Babinski)
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118
Q

Describe the neurological pattern of functional disorders

A

No wasting
Normal tone and reflexes
Erratic changes in muscle power - e.g. able to walk but power on the couch is much lower
Migrating and fluctuating sensory patterns

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119
Q

What causes upper motor neuron lesions

A

Strokes
Space occupying lesions
Spinal cord problems

120
Q

What causes lower motor neuron lesions

A

Motor neuron disease
Spinal muscular atrophy
Peripheral nerve issues - diabetes, toxic or metabolic insult
Nerve compression - carpal tunnel etc

121
Q

What causes neuromuscular junction disorders

A

Myasthenia gravis - ACh receptor antibodies

Lambert-Easton paraneoplastic syndrome - interferes with calcium channels

122
Q

What nerve roots are responsible for the ankle jerk reflex

A

S1 and S2

123
Q

What nerve roots are responsible for the knee reflex

A

L3 and L4

124
Q

What nerve roots are responsible for the biceps reflex

A

C5 and C6

125
Q

What nerve roots are responsible for the triceps reflex

A

C7 and C8

126
Q

What does a glove and stocking distribution of sensory loss suggest

A

Length dependant neuropathy

Can range from mild to severe

127
Q

What does a sensory level distribution of sensory loss suggest

A

Spinal cord lesion

128
Q

What does loss of temp/pain sensation but preserved light touch suggest

A

Hemicord damage

129
Q

What does the cerebellar gait look like

A

Broad based
Unsteady
Cannot walk heel to toe (tightrope) - very unsteady

130
Q

What is dysdiadochokinesis

A

Clumsy when attempting fast, alternating movements

131
Q

What are signs of cerebellar disorders

A 
Dysdiadochokinesis 
Ataxia - cerebellar gait 
Nystagmus 
Intention tremor 
Speech issue - dysarthria 
Hypotonia
132
Q

List the key extra-pyramidal symptoms seen in Parkinsonism

A 
Bradykinesia 
Rigidity 
Resting tremor 
Impaired gait and posture - stooped and small steps 
Impaired postural reflexes 
Reduced arm swing 
Hypophonia - slow speech
133
Q

Are motor symptoms in Parkinson’s disease symmetrical

A

Nope
They are asymmetrical in Parkinson’s
Symmetry suggests drug induced or atypical parkinsonism

134
Q

What are the symptoms of large motor fibre damage

A

weakness, unsteadiness and muscle wasting
Reduced power
Absent reflexes

135
Q

What are the symptoms of large motor fibre damage

A

Numbness, paraesthesia, unsteadiness
Reduced vibration sensation
Absent reflexes

136
Q

What is a high stepping gait suggestive of

A

Peroneal nerve palsy - causes a foot drop
Often due to an L5 issue - e.g. prolapse
They have to lift their feet up high due to foot drop
Front of shoe may be scuffed

137
Q

What is mononeuritis multiplex

A

Neurological issue affecting one side of the body
Can be due to an underlying inflammatory disorder
Lose function quickly
Patchy sensory loss
Can present with wrist or foot drop

138
Q

What is a radiculopathy

A

When the nerve root is damaged

Can be due to a disc prolapse or inflammation

139
Q

What is a plexopathy

A

Affects a nerve plexus
Traction injuries common cause (especially in kids)
Causes a lot of pain

140
Q

What is the most common cause of peripheral nerve demyelination?

A

Guillain-Barre syndrome

141
Q

How can nerves be damaged (underlying process)

A

Axonal loss
Demyelination
Trauma

142
Q

How does demyelination present on nerve conduction studies

A

Slow conduction

Amplitude is preserved

143
Q

How does axonal loss present on nerve conduction studies

A

Loss of amplitude

Can also determine severity

144
Q

What can cause demyelinating neuropathy

A

Acute - Guillain-Barre syndrome

Chronic - CIDP or hereditary sensory motor neuropathy

145
Q

How does Guillain-Barre Syndrome present

A

Progressive paraplegia over days up to 4 weeks.
Will quickly go ‘off legs’ and lose reflexes
Associated sensory symptoms proceed weakness - tingling or numbness
Peripheral glove and stocking pattern mainly
Severe pain is common
Can lead to breathing difficulty

146
Q

Describe how Guillain-Barre syndrome progresses

A

Usually preceeded by some form of infection - e.g. food poisoning
Progressive symptoms over days to weeks
Peak symptoms are usually 10-14 days of onset
Sensory symptoms usually precede weakness
Can lead to breathing problems and death

147
Q

How can Guillain-Barre syndrome cause death

A

Through cardiac arrhythmia as the autonomic nerves also become demyelinated
The breathing problems can kill if not dealt with - muscle weakness affects the respiratory muscles too
DONT miss this presentation

148
Q

How do you treat Guillian-Barre syndrome

A

Immunoglobulin infusion
or
Plasma exchange

Mechanical ventilation if breathing affected

149
Q

How do hereditary neuropathies present

A

Pure motor, sensory, sensorimotor, small fibre and autonomic variants
May get orthopaedic complications - HMSN type 1
Can be axonal loss or demyelinating
Hundreds of possible mutations
Genetic testing is available for the most common types

150
Q

What can cause axonal neuropathies

A 
Idiopathic - age related 
Vasculitic - RA or ANCA 
Paraneoplastic 
Infections - HIV, syphilis, HB/C
Drugs and toxins  - alcohol included 
Metabolic - diabetes, b12, porphyria
151
Q

Which neuropathies can affect the autonomic nerves

A

Acute - GBS or porphyria

Chronic - Diabetes, amyloidosis or hereditary

152
Q

How do you treat axonal neuropathies

A

Treat underlying cause

Symptomatic - physio, orthotics, pain relief

153
Q

How do you treat neuropathies caused by vasculitis conditions

A

Pulsed IV methylprednisolone + cyclophosphamide

154
Q

What is Lambert Eaton Myasthenic Syndrome

A

Condition where there are antibodies to presynaptic calcium channels which cause less vesicle release
Associated with small cell carcinoma
May present like myasthenia but need to look for underlying cancer

155
Q

How do you treat Lambert Eaton Myasthenic Syndrome

A

3- 4 diaminopyridine.

156
Q

Which part of the nerve pathway is affected in myasthenia gravis

A

It is a post-synaptic disorder

157
Q

Name 2 pre-synaptic NMJ disorders

A

Botulinum toxicity

Lambert Eaton Myasthenic Syndrome (LEMS)

158
Q

How does myasthenia gravis present

A

Muscle weakness and FATIGUE - worse at end of day
Weakness is extraocular (ptosis), facial and bulbar
Limb weakness is typically proximal
Can have rapid onset respiratory issues
Bilateral facial weakness makes it hard to smile

159
Q

How is the thymus related to myasthenia gravis

A

75% of patients will have either thymus hyperplasia or a thymoma
Therefore always get a CT chest to look for thymoma if MG is suspected

160
Q

Who gets myasthenia gravis

A

2 peaks - Females in 3rd decade and Males in 6/7th decade
Slightly more common in women
Lots of patients will have another autoimmune condition

161
Q

How do you treat myasthenia gravis

A

Acetylcholinesterase inhibitor – pyridostigmine (prevents ACh breakdown)

Steroids or steroid sparing agents - slow intro to avoid side effects

Intravenous immunoglobulin - given IV short term

Thymectomy

162
Q

What drug should you avoid in people with myasthenia

A

Gentamicin

Precipitates myasthenia crisis in many people – go into respiratory failure

163
Q

What are fasciculations

A

Visible, fast, fine , spontaneous twitch
May be seen in normal muscle after stress, caffeine or in fatigue

Occurs in denervated muscles - has become hyper excitable
Usually a sign of disease in the motor neurone

164
Q

What is myotonia

A

Failure of muscle relaxation after use
Will look very stiff
e.g. they will shake your hand but be unable to let go as muscle wont relax

165
Q

What causes myotonia

A

An issue with the chloride channels

Usually hereditary

166
Q

Give examples of some immune mediated muscle disorders

A

Polymyositis - symmetrical and progressive proximal weakness
Dermatomyositis - similar but with skin lesions

167
Q

How do you grade muscle power

A

0 – no movement at all
1 - flicker of movement when attempting to contract muscle
2 – some muscle movement if gravity removed but none against gravity
3 - movement against gravity but not against resistance
4 – movement against resistance but not full strength
5 – normal strength

168
Q

What is myotonic dystrophy

A

Commonest muscular dystrophy
Autosomal dominant - inherited muscle disorder
Multisystem involvement
Myotonia, weakness, cataracts, ptosis, frontal balding, cardiac defects
Trinucleotide repeat disorder with anticipation

169
Q

Why must you screen family members if someone presents with myotonic dystrophy

A

Some other members may only have the heart defects which need to be found before they cause a real issue

170
Q

Which common drug class is a major cause of myopathy

A

Statins

lots get myalgia and some get myopathy

171
Q

What is rhabdomyolysis and how does it present

A

Breakdown or dissolution of skeletal muscle
Triad of myalgia, muscle weakness and myoglobinuria
Complications of acute renal failure and DIC

172
Q

What can cause rhabdomyolysis

A

Damage to skeletal muscle causes leakage of large quantities of toxic intracellular contents into plasma.

This can occur due to crush injuries, toxins, post-convulsions or after extreme exercise - marathons

173
Q

Is chronic pain considered a disease

A

Yes it is officially recognised

This hopes to improve coordination and management

174
Q

What is the definition of pain

A

An unpleasant sensory and emotional experience, associated with actual tissue damage, or described in terms of such damage

175
Q

How is pain received

A

Painful stimulus is recognised
A-delta and C fibres carry it from receptor to spinal cord
This is then sent up to the thalamus which passes them on to the somatosensory cortex
This is the sensory path

The emotional response is cause by the impulse also being sent to the amygdala and hypothalamus
This brings it to attention

176
Q

What is peripheral sensitisation

A

Change that occurs in the nervous system after tissue injury
There is a reduction in the threshold of peripheral afferent nociceptors

177
Q

What is central sensitisation

A

Change that occurs in the nervous system after tissue injury
There is increased excitability of spinal neurons
Rewiring in the spinal cord and changes in the brain
May be that more pain signals are able to be received

178
Q

What are the signs of chronic regional pain syndrome

A 
Allodynia - pain caused by a non-painful stimulus 
Hyperalgesia - increased pain response 
Swelling 
Hair and nail changes 
Osteopenia
179
Q

What is allodynia

A

Pain caused by a non-painful stimulus such as being touched by cotton wool

180
Q

What is nociceptive pain

A

Pain from injury relayed through a normal nervous system

181
Q

What is neuropathic pain

A

Pain generated within the nervous system

182
Q

How does neuropathic pain present

A

Burning, shooting, tingling and increased sensitivity

Allodynia and hyperalgesia

183
Q

What can cause neuropathic pain

A

Shingles or post-herpetic neuralgia
Surgery
Trauma
Diabetic neuropathy

184
Q

What medication can be used to treat neuropathic pain

A 
Tricyclic antidepressants - amitriptyline (most common)
Anticonvulsant - gabapentin
Opioids 
NMDA antagonists - ketamine 
Na channel blockers such as lignocaine
Capsaicin 
GABA agonists
185
Q

What can cause chronic pain in cancer survivors

A 
Post surgical pain
Chemotherapy induced painful peripheral neuropathies
Chronic graft vs host disease
Radiation induced pain syndromes
Hormonal therapy and arthralgias
186
Q

Does the NICU increase risk of chronic pain

A

YES
If we keep injuring the nervous system (through procedures etc) then they are more likely to have chronic pain
The nervous system develops differently than a term baby

187
Q

Is chronic pain genetic

A

Some twin studies suggest a genetic influence but very complex

188
Q

Which type of ion channels have an effect on pain reception

A

Voltage gated sodium channels
Many channelopathies that lead to pain disorders
Can cause people to be unable to express pain or leads to extreme pathological pain

189
Q

What type of amputation leads to more chance of chronic pain

A

If there is prolonged damage to the limb and a delay to amputation there is more chance of chronic pain

190
Q

Describe sensory remapping

A

Common after amputation
Sometimes sensation can be remapped so that areas of the brain responsible for sensation the hand (for example) will redirect and instead when stimulated they feel it in another area (as well as the phantom area)

191
Q

What is the risk with prescribing opioids for chronic pain

A

Addiction and potential for overdose

Commonly only used for malignancy pain

192
Q

Give examples of degenerative diseases of the cerebral cortex

A

Alzheimer’s
Pick Disease
CJD

193
Q

Give examples of degenerative diseases of the basal ganglia and brain stem

A

Parkinson Disease
Progressive Supranuclear Palsy
Huntington Disease

194
Q

Give examples of degenerative diseases of the motor neuron disease

A

Motor Neuron disease

195
Q

Which cancers are most likely to metastasise to the brain

A

Breast, bronchus, kidney, melanoma, colon

196
Q

What can lead to central herniation through the foramen magnum

A

SOL

Haemorrhage

197
Q

What is the most common posterior fossa tumour in children

A

Medulloblastoma

Can lead to hydrocephalus by compressing the ventricular system and causing CSF to build up

198
Q

What cellular processes occur after brain tissue is damaged

A

Macrophages come in and clear up the dead cells (this leads to liquefaction)
After this all that is left is a space

199
Q

What takes up the majority of the space in the skull

A

The brain - 80%

CSF and blood make up the rest

200
Q

Describe the Monroe-Kellie principle

A

There are 3 intracranial components (brain, blood and CSF) if one of them increases in volume or you add a 4th (tumour, abscess) then the ICP must rise

201
Q

What can cause a physiological rise in ICP

A

Coughing
Bending forward
Straining

202
Q

Can ICP ever be negative

A

Yes

Seen in new-borns, sedated patients or when standing vertically

203
Q

What is the immediate compensation for raised ICP

A

CSF is pushed out of the foramen magnum into the spinal canal
Sinuses can become squeezed to reduce blood volume

204
Q

How do you calculate the cerebral perfusion pressure

A

MAP-ICP

205
Q

What will obstruction to CSF flow lead to

A

Hydrocephalus

206
Q

What cerebral perfusion pressure will lead to a loss of consciousness

A

Below 20

Patient will become comatose

207
Q

What is the effect of high CO2 in the blood

A

CO2 is a potent dilator – high CO2 in blood will cause vasodilation

208
Q

What can affect the blood flow to the brain

A

pressure changes, metabolic changes, stretch response or CO2 levels
Cerebral flow is autoregulated

209
Q

What is chiari syndrome

A

Cerebellar tonsils protrude into the foramen magnum and block CSF flow
Leads to obstructive hydrocephalus

210
Q

What type of brain tumour can produce CSF

A

Choroid plexus papilloma

Usually only seen in children

211
Q

What is the normal ICP in adults

A

7-15mmHg

212
Q

What are the late clinical signs of raised ICP

A 
Coma 
Fixed, dilated pupils 
Can have hemiplegia 
Bradycardia (Cushing’s triad) 
Hyperthermia 
Increased urinary output (BP trying to compensate)
213
Q

How do you manage raised ICP or hydrocephalus

A

Maintain CPP and prevent ischaemia
Maintain head in the midline to facilitate blood flow
Loosen jewellery, collars etc
Set the head of the bed to 30-45 degrees
Avoid anything that could lead them to raise ICP – coughing, gagging etc
Decrease environmental stimuli
Treat the hyperthermia
Maintain the fluid balance and normalise electrolytes Keep CO2 at normal level

214
Q

What medications can be used in the treatment of raised ICP

A 
Use diuretics (mannitol, furosemide etc) 
Anti-epileptics 
Barbiturate coma (reduces brain function to a minimum)
215
Q

What surgery can be used in the treatment of raised ICP

A

Surgical decompression - remove part of the skull to allow pressure to escape
Remove any mass lesions and drain abscesses
CSF shunts - from ventricles to peritoneal space

216
Q

What is the risk of craniotomy

A

Leads to disfigurement and the cranioplasty to repair carries a large risk

217
Q

What can cause communicating hydrocephalus

A

Meningitis
Trauma
SAH

218
Q

What can cause non-communicating hydrocephalus

A

Colloid cyst
Tumours
Chiari syndrome

219
Q

What are the physical signs of hydrocephalus

A

Sunset eyes – unable to look up due to midbrain pressure
Broad, flat face is a sign in kids
Enlarged head in very young children

220
Q

How does normal pressure hydrocephalus present

A

Abnormal gait - wide based and shuffling
Urinary incontinence
Dementia - mild
Called Hakim’s triad

221
Q

Who gets normal pressure hydrocephalus

A

The elderly

Its idiopathic

222
Q

How does normal pressure hydrocephalus appear on scans

A

Large sylvian fissure
Enlarged ventricles
Crowned brain (a lot of brain up at the top of the skull – pushed up by pressure)
Angle between the lateral ventricles is 90’ or less

223
Q

How do you treat normal pressure hydrocephalus

A

VP shunt, medium or low-pressure valve

224
Q

Who gets idiopathic intracranial hypertension

A

Usually young and common in women of child-bearing age
Some will develop it in pregnancy and get better after birth
Mainly in western civilisations
Usually overweight - biggest risk factor

225
Q

What are the symptoms of idiopathic intracranial hypertension

A 
Debilitating headaches
Double vision and blurriness
Reduced visual acuity 
Tinnitus (often pulsatile)
Radicular pain (affects arms)
Papilloedema
Unsteadiness
226
Q

What is the main complications of idiopathic intracranial hypertension

A

Permanent visual loss

Seen in 25% of patients

227
Q

How does the CT scan appear in idiopathic intracranial hypertension

A

CT will be normal

These patients never have enlarged ventricles

228
Q

What causes idiopathic intracranial hypertension

A

Exact cause is unknown

May be due to CSF imbalance, hormones (oestrogen) or venous pressure

229
Q

What investigations are done for idiopathic intracranial hypertension

A

LP
CT/MRI head
CTV - venogram
Fundoscopy

230
Q

How can you treat idiopathic intracranial hypertension

A

Reduce pressure with LP and drainage
Weight loss
Carbonic anhydrase inhibitors - acetazolamide, topiramate
Diuretics
CSF diversion - shunt
Interventional radiology - venous stents
ONSF (optic nerve sheath fenestration)

231
Q

What is mechanical pain

A

Pain on movement

232
Q

If a problem presents acutely what are the likely causes

A

Trauma

Vascular

233
Q

If a problem presents over days or weeks what are the likely causes

A

Infection

234
Q

If a problem presents over weeks to months what are the likely causes

A

Tumour

Degenerative disease

235
Q

What is cervical myelopathy

A

Compression of the upper MN
Leads to hyperreflexia and hypertonia
Will have a spastic gait and positive Hoffman’s test

236
Q

Which type of haemorrhage has a lucid interval

A

Extradural

237
Q

What is pronator drift

A

Get the patient to hold their arms out with their eyes closed
If one side is weaker it will slowly drop
Seen in upper MN conditions

238
Q

What are the signs of cerebellar pathology

A 
Dyskinokinesia 
Ataxia 
Nystagmus 
Intention tremor 
Staccato speech 
Hypotonia
239
Q

Spastic gait can be seen in which conditions

A

Cervical myelopathy - unilateral

Cerebral palsy

240
Q

Which gait is seen in cerebral palsy

A

Spastic

Scissoring - legs are so stiff that they almost end up crossing them when swinging forward

241
Q

Those who have had a stroke can present with which type of gait

A

Flexed arm - flexors stronger
Stiff and straightened leg - extensors stronger
Will swing leg round in a circular motion to stop foot scraping

242
Q

How are reflexes affected by UMN lesions and LMN lesions

A

UMN - hyperreflexia

LMN - hyporeflexia

243
Q

How can timescale help you diagnose the underlying cause of a neuro issue

A

Acute - infection or vascular
Days/weeks - infection
Weeks/months - tumour or degenerative

244
Q

Night pain is a red flag for which cause of back pain

A

Cancer

Focal tenderness may be elicited over the site of mets

245
Q

Night sweats are a red flag for which cause of back pain

A

TB

246
Q

A trendelenberg gait is seen in which conditon

A

In someone which weak hip abductors

e.g. osteoarthritis

247
Q

How does cervical myelopathy present

A

Spastic gait
Increased tone in hands - struggle with fine motor skills
Clumsiness - dropping things a lot
Legs jump at night - hyperreflexia
Poor balance if they shut eyes - loss of proprioception

248
Q

How does lumbar claudication present

A

Commonly in the elderly - degenerative
Bilateral tingling, numbness, heaviness and occasionally pain
Decreased walking distance
Improves on leaning forward - e.g. when walking uphill or leaning on shopping trolley

249
Q

Why does lumbar claudication improve on leaning forward

A

It is in part caused by a thickened ligamentum flavum which narrows the spinal canal
When you lean forward this ligament changes shape and gets thinner - opening canal and improving symptoms

250
Q

What makes the headache caused by raised ICP worse

A

Worse on waking, lying down, bending forward, coughing, vomiting

251
Q

What initial test would you do in clinic if you suspect raised ICP

A

Fundoscopy to exclude papilloedema

252
Q

List general red flags for neurology

A

Focal neurology
Change in behaviour
New onset seizure

253
Q

How does cauda equina present

A

Saddle paresthesia
Genital numbness
Erectile dysfunction
Painless urinary retention with urinary incontinence.

254
Q

How does functional weakness present

A

Variable power with normal bulk, tone & reflexes
May have collapsing weakness - before you put any pressure on them their limb collapses back down
Power may vary depending on how distracted the patient is - i.e. normal on the ‘trick’ tests such as Hoovers

255
Q

Acute unilateral weakness is usually due to what

A

Stroke

256
Q

What conditions can cause acute generalised weakness

A

Guillain-Barre syndrome,
Myasthenia
Myopathy
Cord pathology.

257
Q

What is the pyramidal pattern of power changes

A

weak extensors in the arm, flexors in the leg

258
Q

Glove and stocking sensory loss is common in which condition

A

Peripheral neuropathy

Starts in toes and works up to knees before hands become involved

259
Q

What is a resting tremor

A

A tremor which is no worse with action

Seen in Parkinsons

260
Q

What is a pill-rolling tremor

A

A subtype of resting tremor seen in the index and thumb only
Looks like they are rolling something in their fingers
Seen in Parkinson’s

261
Q

What is a postural tremor

A

Tremor most obvious in outstretched hands

Comes on with certain positions

262
Q

What can cause a postural tremor

A

May be physiological
Increases with anxiety, hyperthyroidism and medication eg
thyroxin, lithium and sympathomimetics

263
Q

What is an intention tremor

A

Tremor which is worse during movement, especially when moving towards a target when past-pointing may occur

264
Q

Intention tremors are seen in which conditions

A

It is typically
associated with cerebella disorders, although severe forms occur with
ischaemia or demyelination of the red nucleus.

265
Q

What are the most common causes of peripheral neuropathy

A

Diabetes
Alcohol - nutrition and toxicity
Idiopathic - generally age related

266
Q

Are peripheral neuropathies typically asymmetrical or symmetrical

A

Symmetrical

267
Q

What is the difference between occular and generalised myasthenia

A

Ocular myasthenia is purely eye involvement

Generalised will include limbs, neck, bulbar symptoms

268
Q

How do you diagnose myasthenia gravis

A

Antibody testing
Electrophysiology test
Always get a CT chest - look for thymoma

269
Q

How do essential tremors present

A

Postural
Generally symmetrical
No change in tone
Often have family history

270
Q

How does a cerebellar tremor present

A

Action/intention tremor
Can be symmetrical or asymmetrical depending on pathology
May have reduced tone

271
Q

How might eyes be affected in cerebellar pathology

A

Nystagmus

Eyes may also goes past the point and have to come back - kinda like an intention tremor

272
Q

How can you test for fatiguable muscle weakness

A

Shoulder abduction before and after repetitive movement (flap arm 20x then test again)

273
Q

How do extra-pyramidal tremors present

A

Resting tremor
Can be brought out by distracting the patient, may come with cog-wheeling
Asymmetrical
Will have rigidity

274
Q

What features in a history make a swallowing problem more likely to be neurological

A

Dysphagia to liquids then solids

275
Q

Do steroids have a role in the treatment of Guillian-Barre syndrome

A

No

Unlike many neurological disorders, there is no evidence for steroids in GBS

276
Q

How do you diagnose Guillian-Barre syndrome

A

Neurophysiology
- Generally a demyelinating picture (decreased conduction velocity but normal amplitude of AP)

Lumbar puncture

  • high protein with no cells
  • excludes infective mimics

Antiganglioside antibodies
- Seen in 60% of cases

277
Q

Those presenting with functional disroders may complain of which symptoms

A

Migrating and fluctuating sensory patterns

Motor symptoms - lack of control over limbs, heavy limbs, collapsing limbs

Memory problems are usually exaggerated - persistent and more pronounced
Often lots of fluctuation - some days very distressed and cant remember anything, other days are fine

Often have balance issues - not vertigo or lightheadeness, mainly internal feeling

278
Q

What is a conversion disorder

A

When a psychological trauma in past is not dealt with and presents as a neurological deficit
Now considered to be different to FND

279
Q

How do you manage a functional disorder

A
  • Explaining a functional disorder to patients can be usuful - e.g. Hardware vs software issue
    Don’t go overboard as it is very confusing

May scan them to look for any underlying issue - usually normal

Neuropsychology can help with cognitive symptoms

280
Q

How can Hoover’s test be used to find a functional disorder

A

If you ask them to push their ‘weak’ leg into the bed they will often lack power
However, then tell them you are testing the other side and ask them to lift the ‘unaffected’ leg up
In order to do they you unconsciously press down with the other leg - therefore you know the nerves are intact and power is in fact normal

281
Q

What is a benign essential tremor

A

A sporadic and slower subtype of resting tremor

Typically maximal in the upper limbs, head, jaw and tongue

282
Q

When might an upper motor neurone issue present with flaccidity

A

When associated with spinal shock

Initial flaccidity

283
Q

List general causes of somatosensory disturbance

A

Pathology affecting peripheral nerves, nerve roots, or the CNS sensory
pathways from the spinal cord to the cerebral cortex.

Physiological stimuli affecting a normal nervous system, such as hyperventilation, transient pressure on a nerve, transient ischaemia
or drug treatment

Transient dysfunction of sensory cortex in epilepsy and in migraine

Psychiatric or psychological illnesses

284
Q

What is parasthesiae

A

A burning or prickling sensation

Pins and needles

285
Q

What is hyperpathia

A

Where the pain threshold of one area is much lower

Painful stimuli are much more painful than usual

286
Q

How does functional weakness present

A

Variable power with normal bulk, tone & reflexes

287
Q

Acute unilateral weakness is typically caused by which pathology

A

Stroke

288
Q

What is polyradiculopathy

A

Diffuse disease of the nerves causing generalised weakness

289
Q

List UMN causes of weakness in all 4 limbs

A

Cervical cord lesion
Brainstem lesions
Bilateral cerebral lesions
MND - affects both UMN and LMN

290
Q

List LMN causes of weakness in all 4 limbs

A

Polyradiculopathy
Peripheral neruopathy
MND - affects both UMN and LMN

291
Q

List UMN causes of weakness in both legs

A

spinal cord lesion

292
Q

List LMN causes of weakness in both legs

A

cauda equina lesion

293
Q

List UMN causes of weakness in one leg

A

lesion above highest level

294
Q

List LMN causes of weakness in one leg

A

single nerve = monotherapy

single root = radiculopathy

295
Q

List causes of patchy weakness

A

multiple CNS lesions
polyradiculopathy
multiple single nerves
mononeuritis multiplex

Neurology (18 decks)

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