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N&SS - Neuro & Stroke > Common Neurological Conditions > Flashcards

Common Neurological Conditions Flashcards

Done: To Do: Epilepsy MS Parkinson's Disease Migraine and Headaches Venous Sinus Thrombosis Temporal Arteritis

1
Q

Define epilepsy.

A

2 or more unprovoked seizures occuring more than 24 hours apart.

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2
Q

What are the 2 main types of seizure?

A

Focal and generalised

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3
Q

How can focal seizures be classified?

A

Simple partial or Complex partial, or secondary generalised seizures.

Further classified by the area of the brain they affect.

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4
Q

Which are the 2 main areas in the brain that patients most commonly get focal seizures in?

A

Temporal and frontal

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5
Q

How common is epilepsy?

A

0.5% prevalence - it is very common!

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6
Q

What are the main types of generalised epilepsy?

A 
Absence
Myoclonic
Atonic
Tonic
Tonic-Clonic
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7
Q

A patient has a seizure. This is the first one they have ever had, and investigation shows no identifiable cause, and no ongoing risk.

How long will the DVLA ask them not to drive for?

A

They must go 6 months without a seizure before they can drive again.

Depending on circumstances, this may be extended to 12 months.

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8
Q

A patient who drives HGVs for a living has a seizure. This is the first one they have ever had, and investigation shows no identifiable cause, and no ongoing risk.

How long will the DVLA ask them not to drive for?

A

They cannot drive an HGV/Class II vehicle until they have been seizure-free for 5 years.

If they take medication for the seizures, they must have gone 5 years seizure free without medication.

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9
Q

A patient has epilepsy that has been well controlled on medication. Their last seizure was 6 months ago.

How long will the DVLA ask them not to drive for?

A

A further 6 months at least, so be seizure free for 12 months total at least.

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10
Q

A patient with epilepsy has some of their medications changed.

The want to know about driving. What can you tell them?

A

They must wait at least 6 months after medication is changed.

Depending on how many seizures they have had, they may need to wait a further 6-12 months after that.

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11
Q

A patient has well controlled epilepsy, and has been on the same medications for years. They continue to get seizures at night time however.

How long will the DVLA ask them not to drive for?

A

They need to have gone 3 years seizure free in the DAY TIME/WHILE AWAKE before they can drive again.

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12
Q

What are the risk factors for epilepsy?

A 
Family Hx
Developmental abnormalities
Trauma/surgery/hypoxic brain injury
Space occupying lesion in skull
Drugs
CNS infection
Metabolic disturbance
Vascular abnormalities
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13
Q

What factors can lower the seizure threshold in some individuals?

A
  • Sleep deprivation
  • Alcohol
  • Drugs
  • Physical/mental exhaustion
  • Particular times in menstrual cycle
  • Flickering lights
  • Infection/metabolic disturbance
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14
Q

A patient presents with recurrent episodes of “funny turns”.

They describe them as starting with their head turning to one side, then one limb jerking on the other side of the body. They remain conscious through these episodes.

What seizure type does this sound like?

A

Simple partial seizure

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15
Q

A patient with simple partial seizures also finds that after each episode, one side of their face “stops working” for an hour.

They are worried about a stroke. What phenomenon is this more likely to be?

A

Todd’s paralysis - weakness of the limbs/face following a simple partial seizure.

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16
Q

A patient with recurrent seizures describes:

  • LoC or unaware of surroundings but may appear conscious still
  • Vertigo
  • Lip smacking
  • Tachycardia

What seizure type does this describe, and what other features might they have?

A

Complex partial seizure.

Deja vu
Jamais vu
Visual or auditory hallucinations
Emotional disturbance
Automatism (impaired consciousness but motor function not impaired so they wander off)
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17
Q

How do secondary generalised seizures occur?

A

Start as a partial seizure then electrical activity spreads to the lower brain areas.

Secondary generalised seizures are usually tonic-clonic.

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18
Q

Describe the pattern of activity of a generalised seizure.

A

Start in the midbrain or brainstem, then spread simultaneously to both cortices.

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19
Q

Which age and demographic groups is epilepsy more common in?

A
  • Onset as children or people over 60.

- People with a learning disability

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20
Q

Describe a typical absence seizure.

A

Pt unresponsive to stimuli but no LoC.
Stares, may go pale.
Fairly quick recovery.
May have some muscle jerking during the episode.

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21
Q

Describe the EEG pattern of an absence seizure.

A

3Hz spike and wave pattern

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22
Q

Describe a typical myoclonic seizure.

A
  • Convulsions/limb jerking
  • Eye rolling
  • Tachycardia
  • Breathing is erratic/depressed
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23
Q

Describe a typical atonic seizure.

A

May appear to be a faint.
Limb tone suddenly absent, pt drops to the floor.
Often present with nasty facial/head injuries

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24
Q

Describe a typical tonic seizure.

A

Rigidity of muscles, may bite tongue
Incontinence occurs
Epileptic cry
Hypoxia/cyanosis

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25
Q

Describe a typical tonic-clonic seizure.

A

Aura before attack.
Tonic phase first (10s-1 minute) (rigidity, tongue biting, incontinence)
Clonic phase second (seconds-minutes) (limb jerking, eye rolling)

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26
Q

What are the classic post-ictal symptoms?

A

Confusion
Drowsiness
Headaches
May be agitated/aggressive

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27
Q

How is epilepsy diagnosed?

A

Clinically i.e. through history

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28
Q

What tests would we do to rule out organic pathology causing seizures?

A 
ECG
Calcium
Urine dip for diabetes
CT/MRI brain
Bloods - sugar, U&E, LFTs, CK, prolactin
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29
Q

Name a bunch of AEDs.

A 
Levetiracetam
Lamotrigine
Sodium valproate
Carbamazepine
Phenytoin
Pregabalin
Ethosuximide
Phenobarbital
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30
Q

Which AED is used for absence seizures only?

A

Ethosuximide

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31
Q

When is phenobarbital used? Why?

A

Rarely - it causes sedation and tolerance over time.

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32
Q

Which 3 AEDs ork well for most types of epilepsy?

A

Levetiracetam
Lamotrigine
Sodium Valproate

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33
Q

Which drug is generally first line for generalised epilepsy?

A

Sodium valproate

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34
Q

What is the issue with sodium valproate?

A

It is much more teratogenic than other AEDs - 10% of children whos mothers use SV during pregnancy have a defect at birth of some description.

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35
Q

Which drug is first line for focal seizures?

A

Carbamazepine

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36
Q

A patient presents from GP with suspected epilepsy, but from the history you aren’t convinced.

What other causes might there be for these apparent seizures?

A 
Syncope
Arrhythmias
TIA
Migraine
Paroxysmal vertigo
Metabolic disorder
Encephalopathy
Panic attacks
Non-epileptic seizures
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37
Q

When might surger be considered in a pt with epilepsy?

A

If there is a mass lesion in the brain, or epilepsy is uncontrolled with medications.

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38
Q

How common are migraines?

A

They affect 15% of the population.

M:F 1:2

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39
Q

What symptoms are typically associated with migraines?

A

Nausea

Photophobia

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40
Q

How can a migraine and TIA be distinguished from each other?

A

TIA’s are more sudden in onset, and rare to have headache also.

Migraine usually comes on slowly/deficit occurs gradually.

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41
Q

What are some common triggers/risk factors for migraines?

A
  • Times of relaxation
  • Foods - chocolate, cheese, alcohol, caffeine.
  • Travel
  • Exercise
  • Noise/lights
  • Pregnancy, puberty, menstruation/menopause
  • Obesity
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42
Q

A patient presents with awful headaches accompanied by bright lights in her vision, and zig-zag lines. What is this likely to be?

A

Migraine with visual aura

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43
Q

Why do visual aura occur?

A

Reduced blood flow to occipital cortex before an attack

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44
Q

Other than visual, what auras are possible with migraines?

A

Sensory (pins and needles)

Speech (temporary dysarthria)

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45
Q

Do pts with migraines have clinical signs on examination?

A

No

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46
Q

Do pts with migraines always get an aura?

A

No - they can have a migraine without an aura.

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47
Q

What is the management of an acute migraine?

A

Simple analgesia (paracetamol/aspirin/NSAIDs)
Antiemetics
Triptans may be useful for some patients

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48
Q

What can we use for migraine prophylaxis?

A

Propanol

Amytriptiline

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49
Q

When is migraine prophylaxis suggested?

A

If the pt experiences more than 2 episodes of migraine per month.

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50
Q

What can make migraines worse once treatment has been started?

A

Overuse of analgesics

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51
Q

Describe a cluster headache.

A

Severe short-lived headache, usually unilateral around one eye.

Often associated with nasal congestion.

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52
Q

How can we manage cluster headaches?

A 
High dose O2
Triptans
Analgesics
Steroids
Lithium/Verapamil
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53
Q

How do tension headahces typically present?

A

With a band-like headache, no aura

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54
Q

What is the most common cause of Parkinsonism?

A

Idiopathic Parkinson’s disease

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55
Q

What is the classic triad/tetrad of symptoms associated with Parkinson’s disease?

A

Bradykinesia
Rigidity
Tremor
Postural instability

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56
Q

Describe the tremor that Parkinson’s patients tend to have.

A

Pill-rolling, resting tremor.

Frequency 5-7 Hz.

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57
Q

When is the mean age of onset for IPD?

A

45-60 years

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58
Q

Define IPD.

A

Progressive neurodegenerative disease caused by loss of dopaminergic neurones in the substantia nigra.

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59
Q

Is IPD typically symmetrical?

A

Nope, usually asymmetrical.

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60
Q

How can bradykinesia manifest clinically?

A

Short, shuffling steps.
Reduced arm swing.
Difficulty initiating movements.

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61
Q

Decsribe the rigidity that classically accompanies IPD.

A

Lead pipe rigidity (i.e. bending arm is like bending a lead pipe, smooth consistent rigidity)

Cogwheel rigidity in wrists when slowly moved.

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62
Q

What are some other features of IPD, other than the classic triad?

A
  • Mask-like face
  • Flexed posture
  • Micrographia
  • Drooling
  • Psychiatric symptoms
  • Impaired smell
  • Sleep disturbance
  • Postural hypotension
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63
Q

How does drug induced parkinsonism differ in presentation to IPD?

A

Rigidity and rest tremor are uncommon in drug induced parkinsonism.

Drug induced has rapid onset, and bilateral motor symptom onset.

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64
Q

What kind of dementia is associated with IPD?

A

Lewy body dementia

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65
Q

What is parkinsonism?

A

Syndrome clinically similar to IPD, but which have additional features and a known aetiology

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66
Q

What are the causes of parkinsonism?

A
  • Drug induced
  • Progressive supranucelar palsy
  • Multiple systems atrophy
  • Wilson’s disease
  • Toxins
  • Post-encephalitis
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67
Q

Which drugs are associated with parkinsonism?

A
  • Chlorpromazine
  • Prochlorperazine
  • Haloperidol
  • Droperidol
  • Metoclopramide
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68
Q

What toxins can cause parkinsonism?

A

Carbon monoxide

MPTP

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69
Q

What are the steps to managing IPD?

A
  • Exercise and physiotherapy
  • Medications
  • Symptom control
  • Surgery sometimes
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70
Q

Which drug tends to be first line in the management of IPD?

A

Levodopa

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71
Q

What is the problem with levodopa?

A

It requires some functioning neurones to convert it to dopamine, so only works in early stage disease, and may only work for 3-5 years.

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72
Q

Which IPD drug shows the most improvement in movement/motor symptoms?

A

Levodopa

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73
Q

Other than levodopa, what drugs can we use in IPD?

A

MAOIs
Dopamine agonists
COMT inhibitors
Amantadine

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74
Q

What can we give with levodopa? Why do we do this?

A

A decarboxylase inhibitor e.g. carbidopa to prevent peripheral metabolism of levodopa to dopamine.

This maximises the amount of dopamine that reaches the CNS.

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75
Q

What can we do to help motor symptoms associated with drug-induced parkinsonism?

A

Stop the offending drug.

Can also give antimuscarinics (block cholinergic receptors)

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76
Q

What imaging can we do to diagnose IPD?

A

We can’t!

MRI will be normal.
PET scans are only for fancy research purposes at the moment.

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77
Q

Thinking about the non-motor symptoms of IPD, what can we do to help patients with IPD?

A
  • Physiotherapy
  • Pain relief (neuropathic pain)
  • Laxatives
  • Social support & OT
  • SALT assessment
  • Psychological support (counselling, antidepressants)
  • Manage acute conditions e.g. UTI promptly
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78
Q

Define motor neurone disease.

A

A common condition caused by degeneration of motor neurones in the motor cortex and spinal cord.

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79
Q

Does motor neurone disease affect UMNs or LMNs?

A

Both!

80
Q

What is never caused by motor neurone disease?

A

Sensory problems

81
Q

What are the different types of motor neurone disease?

A
  • Amyotrophic lateral sclerosis
  • Progressive bulbar palsy
  • Progressive muscular atrophy
  • Spinal muscular atrophy
82
Q

What are the most convincing cause of MND?

A

Genetic predisposition

83
Q

When MND is inherited, what inheritance pattern does it follow?

A

Autosommal dominant

84
Q

With what symptoms do 70% of MND patients present?

A
  • Muscle weakness and wasting, usually at extremities
  • Cramps

There is not usually any pain

85
Q

O/E of a patient with distal muscle weakness and wasting, what signs might indicate MND?

A

UMN and LMN signs:
Brisk reflexes
Fasciculations

No sensory loss or sphincter problems.

86
Q

Who does MND tend to affect?

A

Slightly more males, usually middle aged onset.

87
Q

A 55 year old man presents to you with dysphagia and dysarthria, as well as muscle wasting in his distal legs, and hands.

What does the dysphagia suggest? What pattern of dysphagia would support this?

A

Bulbar or pseudobulbar MND.

Progressive pattern would support this.

88
Q

How can we distinguish MND from myasthenia gravis?

A

MND never affects eye movements

89
Q

When are spastic paraparesis and loss of muscle tone seen together?

A

In motor neurone disease!

Upper limbs tend to be weak in extension, lower in flexion.

90
Q

How is MND diagnosed?

A

Clinically, sometimes supported by investigations

91
Q

Which investigations can be used to support a diagnosis of MND?

A

EMG

Nerve conduction studies

92
Q

What investigations should be done with suspected MND to rule out other differentials?

A

MRI (foramen magnum/SC compression)
TFTs (hyperthyroid)
Ca (calcium/parathyroid issues)
Bloods for CK for muscle breakdown

93
Q

Why do thyroid and parathyroid issues need to be ruled out when suspecting MND?

A

Hyperthyroidism and hyperparathyroidism can both cause muscle wasting and hyperreflexia.

94
Q

Other than MND, what conditions exhibit both upper and lower MN signs?

A

Cervical spondylitis

Spinal tumours

95
Q

What is the prognosis for MND?

A

Poor - survival is usually less than 3 years.

96
Q

Which teams should be involved in the care of a pt with MND?

A
  • Specialist nurse
  • Physio
  • OT
  • Orthotics
  • SALT
  • Dietician
  • Respiratory and Gastro teams

Palliative care later on

97
Q

How can we manage MND pharmacologically?

A

With:

  • Riluzole (Na channel blocker)
  • Baclofen
  • Amitriptyline/propantheline
98
Q

What does riluzole do in the management of MND?

A

Increase survival by 3-5 months

Delays need for supportive intervention e.g. gastrostomy, ventilatory support

Prolongs muscle strength

99
Q

What does baclofen do in the management of MND?

A

Help reduce spasticity as a GABA agonist

100
Q

What symptom can amitriptyline/propantheline help with in MND?

A

Drooling

101
Q

What is multiple sclerosis?

A

A chronic autoimmune disorder characterised by CNS demyelination.

102
Q

Tell me about the epidemiology of MS.

A

M:F 1:3
Most commonly presents between ages 20-40
More common at higher latitudes

103
Q

What is the pathophysiology underlying MS?

A

Autoimmune destruction of oligodendrocites -> axonal loss mediated by antibodies to myelin. Macrophages express a different protein that allows them to cross the BBB.

Active sites of inflammation (plaques) can form anywhere in the CNS.

104
Q

Where do plaques most commonly form in MS?

A

At the:

  • optic nerves
  • perventricular lesion
  • brainstem
  • cerebellar connections
105
Q

How do most cases of multiple sclerosis progress?

A

In a relapsing-remitting fashion

106
Q

A 30 year old man presents with blurred vision, muscle weakness, and fatigue. He also experiences parasthesia in his left arm.

What would you expect to see on fundoscopy of this patient?

A

Optic disc swelling

107
Q

What cerebellar sign is commonly exhibited in MS?

A

Ataxia

108
Q

How long do acute attacks of MS typically last?

A

1-2 months

109
Q

What are the common features of multiple sclerosis?

A 
Optic neuropathy
Optic disc swelling
Worse on hot day/after exercise
UMN signs
Relative afferent pupillary defect
Lethargy
Gait disturbance
Sensory symptoms
Muscle weakness
Ataxia
Tremor
Urinary incontinence
Sexual dysfunction
110
Q

A 35 year old woman presents to neurology with gait disturbance, pins and needles down her right leg, and visual disturbance.

What investigations do we need to do, considering the top differential?

A

MS:

MRI (85% have plaques)
VEP (visual evoked potentials, for optic nerve lesion)
Oligoclonal bands in CSF (LP)

111
Q

How is MS diagnosed?

A
  1. At least one attack + multiple plaques on MRI

Or

  1. Single attack/progressive MS + multiple plaques on MRI + additional evidence
112
Q

How do we treat MS?

A

We can’t cure it, but we can induce remssion in acute relapses, prevent relapses, and manage symptoms.

Nothing really alters long term outcomes.

113
Q

What can we do for an acute relapse of MS?

A

Give a short course of high dose steroids (5 days)

114
Q

What is the problem with using steroids for acute relapses of MS?

A

They should not be used more than twice a year.

They also don’t alter long term outcomes.

115
Q

What drug can we use to reduce the symptoms of MS, and how does it work?

A

Baclofen - GABA receptor antagonist

116
Q

Other than baclofen, what can we give for MS relapse prevention?

A

B-interferon
Glatiramer acetate
Natalizumab

Mitoxantrone (experimental)

117
Q

What holistic elements of care do MS patients need?

A
  • Practical changes to living conditions
  • Counselling
  • Mx of infections esp. UTIs
  • OT/PT
  • Prevent pressure sores
  • Sativea (cannabis extract for symptom relief)
118
Q

How should fatigue be managed in MS patients?

A

Exclude all other causes e.g. anaemia, thyroid dysfunction, depression.

Mindfullness, CBT

Maximise management of MS.

Ensure good enough support networks.

119
Q

Define dementia.

A

A syndrome characterised by chronic progressive cognitive impairment, significant enough to impact on a pts ADLs, existing for at least 6 months. No altered level of consciousness.

120
Q

What is the most common cause of dementia?

A

Alzheimer’s disease

121
Q

Other than alzheimer’s, what are the other causes of dementia?

A

Vascular dementia/multi-infarct
Lewy body dementia
Frontal lobe dementia

122
Q

In terms of memory impairment, what kind of memory is most affected in dementia?

A

Generally short term memory is impaired, but long term memory is preserved.

123
Q

An older gentleman comes to you with low mood, memory loss, and problems with speech that have been progressing.

Other than dementia, what is an important differential here?

A

Depression - can manifest in similar ways to dementia, or may co-exist.

124
Q

What are some of the cognitive functions impaired in dementia?

A 
Memory
Attention
Concentration
Language processing
Speech
Thinking
Judgement
125
Q

What % of people over 85 are affected by dementia?

A

25%

20% at 80, 15% at 75, 10% at 70, 5% at 65

126
Q

What is the average time from diagnosis of dementia to death?

A

10 years

127
Q

Which medical conditions are associated with dementia?

A

Huntington’s
MS
HIV
Down’s syndrome

128
Q

Define Alzheimer’s disease

A

A form of dementia characterised by insidious onset of symptoms, associated with the formation of amyloid plaques, neurofibrillary tangles, and brain atrophy.

129
Q

What are some of the features of late stage dementia?

A
  • Severe and pervasive memory features/cognitive symptoms
  • Marked behavioural changes, both positive and negative
  • Severe disability - assistance required almost constantly
  • No insight
130
Q

Define frontotemporal dementia

A

Chronic progressive neurodegenerative syndrome characterised by change in personality and social conduct, with usually preserved memory and visuospatial skills. Due to frontotemporal lobe degeneration.

131
Q

Define vascular dementia

A

Syndrome of cognitive decline caused by multiple acute ischaemic events that progresses in a step-wise manner.

132
Q

Define Lewy body dementia

A

Syndrome of cognitive decline characterised by the presence of Lewy bodies in the brainstem and neocortical areas.

133
Q

What is considered when distinguishing between types of dementia?

A 
Course
Onset
Initial symptoms
Mood and behavioural changes
Other symptoms
Neurological features
Structural brain imaging
134
Q

Can pts get mixed type of dementia? Eg?

A

Yes

Eg Alzheimer’s with vascular dementia

135
Q

What is an important part of the history to get in a pt with suspected dementia?

A

Collateral Hx (alongside pts own account)

136
Q

What is the aim of treatment for dementia?

A

Reduce rate of disease progression and prevent/manage complications/comorbidities in a timely manner.

137
Q

What are the elements of care for dementia patients?

A
  • Reduce disease progression
  • Manage risk factors
  • Social support
  • Promote independance
138
Q

How can we reduce disease progression for a patient with Alzheimer’s disease?

A

Use of anticholinesterase drugs - delay cognitive decline by ~3-6 months in about 40% of patients.

139
Q

Name some anticholinesterase drugs.

A

Donepezil
Galantamine
Rivastigmine

140
Q

What are the side effects of anticholinesterase drugs?

A 
Anorexia
Nausea
Vomiting
Diarrhoea
Abdo pain
Insomnia
Confusion
Agitation
Headache
141
Q

Other than anticholinesterase drugs, what can we use pharmacologically for Alzheimer’s?

A

NMDA receptor antagonists e.g. memantine

Antipsychotics for anxiety and sleep disorders

142
Q

How can we prevent vascular dementia?

A

Reduce vascular risk factors - aspirin/warfarin therapy, control BP, and control cholesterol.

143
Q

What is essential in primary care in a suspected dementia case?

A

Bloods and full screening for a reversible cause e.g. hypothyroid, metabolic distrubance, infection, depression.

144
Q

What is essential in secondary care in a suspected dementia case?

A

Structural imaging to rule out reversible conditions, and to guide prognosis and Mx based on aetiology

145
Q

What is a polyneuropathy?

A

Damage or disease affecting peripheral nerves in roughly the same areas on both sides of the body.

146
Q

How are polyneuropathies classified?

A

According to which part of the nerve cell is affected; distal axonopathy, myelinopathy, and neuronopathy.

147
Q

Give some examples of distal axonopathies/causes.

A 
Diabetic neuropathy
Kidney failure
Connective tissue disease
Deficiency (malnutrition, alcohol)
Chemical (toxins/drugs e.g. chemotherapy)
148
Q

Why are the feet often the first affected part of the body with polyneuropathies?

A

They are the most distal, and therefore have the longest axons, so blood supply is more likel to be compromised.

149
Q

What is the acronym we can use to remember causes of peripheral neuropathies? What does it stand for?

A 
DAVID:
Diabetes
Alcoholism
Vitamin B12 deficiency
Infective or Inherited
Drugs
150
Q

Give some examples of myelinopathies.

A

Guillain-Barré syndrome (acute or chronic inflammatory demyelinating polyneuropathy)

151
Q

Give some examples of neuronopathies/causes.

A

MND
Sensory neuropathies
Toxins/chemotherapy
Autonomic dysfunction

152
Q

Can regeneration occur in peripheral neuropathies?

A

It can, but it is limited.

Can be via remyelination, or rarely axonal regrowth

153
Q

Which drugs can cause peripheral neuropathy?

A

Antimicrobials - Isoniazid, ethambutol, nitrofurantoin, metronidazole.
Chemotherapy esp. vinca alkaloids/cisplatin.
Amiodarone

154
Q

Tell me about Guillian-Barré syndrome.

A

Acute inflammatory demyelinating polyneuropathy, occuring typically several weeks after a viral infection.

155
Q

How can Guillian-Barré syndrome be differentiated from other peripheral neuropathies?

A

Proximal muscles are more affected in GBS.

Trunk, respiratory, and cranial nerves can also be affected.

156
Q

How is Guillian-Barré syndrome investigated, and what do the results show?

A

LP -> increased protein in CSF with normal WCC.

Nerve condction studies -> nerve conduction slow.

157
Q

What is the pathophysiology of Guillian-Barré syndrome?

A

Viral infection -> autoimmune antibodies against peripheral nerves -> myelin damage -> reduced or blocked transmission.

158
Q

How do we manage GBS?

A

ABCDE -> intubation if respiratory muscles involved.

DON’T GIVE STEROIDS.

IV Ig may help.

Usually recover without specific treatment.

159
Q

What is cervical spondylosis?

A

Non-specific degenerative process causing stenosis of the spinal canal and/or nerve roots in the cervical spine.

160
Q

Where is cervical spondylosis most common?

A

C5/C6 or C6/C7

161
Q

How does cervical spondylosis present?

A

Very common - often presents as neck pain

162
Q

What are the pathological features behind cervical spondylosis?

A
  • Degenerate disc
  • Osteophytes
  • Hypertrophy of ligaments
  • Congenitally narrow canal
163
Q

What are the 2 main causes of pain in cervical spondylosis?

A

Mechanical/MSK neck pain

Radiculopathy

164
Q

What are the clinical features of cervical sponylosis -> radiculopathy?

A

Referred pain in the arm due to nerve root irritation
Sensory symptoms first -> myotomal radicular pain
Weakness and abnormal reflexes

165
Q

What are the red flags we should be aware of with cervical sponylosis?

What might they be signs of?

A 
Fever/chills
Weight loss
Relentless nocturnal pain
History of cancer
Immunosuppression

Infection or a tumour

166
Q

What investigation is good for suspected cervical spondylosis?

A

MRI :D

167
Q

How should cervical spondylosis be managed?

A

Conservative - Hard or soft collar.
Medical - NSAIDs, epidural injections of steroids.
Surgical - decompression

168
Q

When is surgery indicated in cervical spondylosis?

A

With uncontrollable pain, severe weakness, or failure of other measures after 12 weeks

169
Q

A 30yo man presents to his GP with a sudden onset facial drooping and weakness of his facial muscles on the right hand side. The forehead is also affected.

What do you suspect?

A

Bell’s palsy (idiopathic facial nerve paralysis)

170
Q

What does forehead sparing/affected tell us abiut facial nerve palsy?

A

If the forehead is affected, it is a LMN facial nerve palsy.

171
Q

Aside from facial muscle weakness/paralysis, what symptoms do pts with Bell’s palsy experience?

A

Post-auricular pain
Altered taste
Dry eyes
Hyperacusis

172
Q

A 30yo man presents to his GP with a sudden onset facial drooping and weakness of his facial muscles on the right hand side. The forehead is also affected.

What is this, and how should it be managed?

A

Bell’s palsy

Prednisolone for 10 days if started within 72 hours of onset of symptoms

Eye care

173
Q

What eye care can we do for pts with Bell’s palsy?

A

Artificial tears and eye lubricants

174
Q

When should a pt with Bell’s palsy be referred for specialist assessment?

A

Refer to ophthalmology if the pt can’t close their eye fully.

175
Q

Why is the forehead spared with an UMN lesion in facial nerve palsy?

A

Due to bilateral innervation of the forehead

176
Q

Which comorbidities confer worse prognosis for a pt with Bell’s palsy?

A

Age over 60
Pregnancy
Diabetes
Hypertension

177
Q

What is the biggest differential to rule out with possible Bell’s palsy?

A

Stroke! Especially in older patients.

178
Q

How can we remember the causes of carpal tunnel syndrome?

A

MEDIAN TRAP

Myoxoedema
Edema
Diabetes
Idiopathic
Acromegaly
Neoplasm
Trauma
Rheumatoid arthritis
Amyloidosis
Pregnancy
179
Q

What is the pathophysiology of carpal tunnel syndrome?

A

Compression of the median nerve as it passes through the carpal tunnel under the flexor retinaculum

180
Q

What are the symptoms of carpal tunnel syndrome?

A

Pain and parasthesia in lateral 3 fingers

Parasthesia extends to lateral half of 4th finger also

181
Q

When are carpal tunnel syndrome symptoms typically worse?

A

At night or when holding objects like a telephone, newspaper, or steering wheel

182
Q

A 30 year old pregnant woman presents with pain in both her hands.

She reports parasethesia in the lateral aspect of her hand on palmar surface, and discomfort extending up the arm into her shoulder.

Considering the likely diagnosis, what might we see on examination?

A

Sensory impairment in first 3 fingertips
Wasting of the thenar eminences
Weak thumb abduction
Tinel’s and

182
Q

A 30 year old pregnant woman presents with pain in both her hands.

She reports parasethesia in the lateral aspect of her hand on palmar surface, and discomfort extending up the arm into her shoulder.

Considering the likely diagnosis, what might we see on examination?

A

Sensory impairment in first 3 fingertips
Wasting of the thenar eminences
Weak thumb abduction
Tinel’s and Phalen’s sign positive

Flick sign will very often be positive

183
Q

What is Tinel’s sign, and how is it elicited?

A

Tapping the distal wrist causes parasthesia in the median nerve distribution.

184
Q

What is Phalen’s sign, and how is it elicited?

A

Ask pt to flex the wrist to 90 degrees and hold it there for 60 seconds -> parasthesia.

Fairly specific test for carpal tunnel syndrome.

185
Q

What is the flick sign associated with carpal tunnel syndrome and what does it tell us?

A

The patient makes a flicking movement with their wrist to alleviate symptoms.it is both very specific and sensitive for carpal tunnel syndrome.

186
Q

A patient presents with parasthesia in the median nerve distribution, which is worse at night. He has no neck or arm pain.

Considering the diagnosis, what investigations would it be sensible to do, and why?

A

T4 for hypothyroidism
Glucose/HbA1c for diabetes
FBC and CRP forinflammatory or invective causes.

188
Q

A patient presents with parasthesia and pain in the distribution of the median nerve. You suspect carpal tunnel.

What differentials might you want to rule out, and how would you do that?

A

C6 or C7 radiculopathy - usually bilateral, with neck pain, and symptoms on dorsal aspect of the hand. Not worse at night.

Thoracic outlet syndrome - have concurrent C8 and T1 dermatome sensory disturbance.

Thalamic infarcts - symptoms are constant, associated with perioral parasthesia.

189
Q

What measures can we use to treat carpal tunnel syndrome?

A

Splinting the wrist for short term symptoms relief.

Intracarpal corticosteroid injection.

Oral prednisolone may have short term benefit.

Surgical release of carpal tunnel.

190
Q

Which management option for carpal tunnel syndrome has the best efficacy?

A

Surgery - 80-90% of patients improve.

191
Q

Tell me about the ulnar nerve.

A

Arises from C8 T1 nerve roots.

Passes through lower trunk, and medial cord of brachial plexus.

Runs behind the medial epicondyle of distal humerus.

Most common site of injury is at the elbow.

192
Q

Where does the ulnar nerve supply?

A

Motor - intrinsic muscles of hand, flexor carpi ulnaris, and medial half of flexor digitorum profundus.

Sensory - medial one and a half fingers and palmar area, on anterior and posterior surfaces.

193
Q

What is ulnar nerve palsy also known as?

A

Cubital tunnel syndrome

194
Q

What are the clinical features of ulnar neuropathy?

A

Parasthesia and/or numbness in the medial 1.5 fingers.

Initially intermittent, later constant.

May have pain around the elbow.

195
Q

Which muscles waste in ulnar neuropathy?

A

First dorsal interosseus
Hypothenar eminence
Forearm muscles

196
Q

O/E of a pt with ulnar neuropathy, what motor abnormality will be seen?

A

Ulnar claw - on extension of the fingers of the hand, the 4th and 5th fingers remain flexed due to denervation of the lumbricals.

N&SS - Neuro & Stroke (10 decks)

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