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FINALS > NEUROLOGY > Flashcards

NEUROLOGY Flashcards

1
Q

What is MS?

A

chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system (affects the white matter of the brain and spinal cord).
Inflammatory process involving activation of the immune cells against myelin.

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2
Q

What type of hypersensitivity reaction is MS?

A

Type 4 - T cell mediated

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3
Q

When does MS present?

A

Young adults <50 years

Women

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4
Q

Which types of cells provide myelin?

A 
Schwann cells (peripheral nervous system)
Oligodendrocytes (central nervous system)
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5
Q

Which myelin producing cells are mostly affected in MS?

A

Oligodendrocytes

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6
Q

Name 5 causes of MS.

A 
Genetic
EBV
Low vitamin D
Smoking 
Obesity
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7
Q

When might MS symptoms improve?

A

Pregnancy

Postpartum period

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8
Q

How do you describe the frequency of MS symptoms?

A

Disseminated in time and space

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9
Q

Name five different ways that MS can present.

A 
Optic neuritis
Eye movement abnormalities
Focal weakness
Focal sensory symptoms
Ataxia
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10
Q

How long does first-presentation of MS usually last?

A

Symptoms progress over 24 hours

Lasts days-weeks and then improves

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11
Q

What is the most common presentation of MS?

A

Optic neuritis (demyelination of the optic nerve)

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12
Q

Which cranial nerve is commonly affected in MS?

A

CN 6 - abducens

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13
Q

How does a CN6 lesion present?

A

Internuclear ophthalmoplegia

Conjugate lateral gaze disorder

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14
Q

Give some examples of focal weakness in MS.

A

Bell’s palsy
Horner’s syndrome
Limb paralysis
Incontinence

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15
Q

Give some examples of sensory symptoms in MS.

A

Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign - electric shock sensation that travels down the spine when flexing the neck

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16
Q

What is Lhermitte’s sign?

A

Lhermitte’s sign is an electric shock sensation that travels down the spine and into the limbs when flexing the neck. It indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column.

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17
Q

Name two types of ataxia that are seen in MS.

A

Sensory ataxia - loss of proprioceptive sense (results in positive Romberg’s test)
Cerebellar ataxia - suggests cerebellar lesions

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18
Q

Name four types of disease patten in MS.

A

Clinically isolated - may never progress to MS
Relapsing-remitting -
Secondary progressive
Primary progressive

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19
Q

Which is the most common disease patten seen in MS?

A

Relapsing-remitting

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20
Q

What is meant by active or not active MS?

A

Active = new symptoms or lesions are developing

Not active = no new symptoms or lesions are developing

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21
Q

What is meant by worsening or not worsening MS?

A

Worsening = overall disability is worsening over time

Not worsening = there is no worsening of disability over time

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22
Q

Describe the disease pattern seen in secondary progressive MS.

A

Initially relapsing-remitting.

Then progressive worsening of disability over time.

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23
Q

What is primary progressive MS?

A

The disease progressively worsens overtime without relapse or remission.

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24
Q

How does optic neuritis present?

A

Central scotoma
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect

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25
Q

Name 7 causes of optic neuritis.

A 
Sardcoidosis
SLE
Diabetes
Syphilis
Measles
Mumps
Lymes disease
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26
Q

What is Uhthoff’s phenomenon?

A

Symptoms brought on by changes in temperature

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27
Q

What signs might be elicited in a patient with MS?

A

Reduced visual acuity
Weakness
Increased tone
Loss of proprioception

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28
Q

How is MS diagnosed?

A

Clinical picture - symptoms suggesting lesions change location
Other causes for the symptoms must be excluded

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29
Q

How is primary progressive MS diagnosed?

A

Symptoms must be progressive over a period of 1 year.

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30
Q

Which investigations can support the diagnosis?

A

MRI scans - demonstrate lesions

LP - oligoclonal bands

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31
Q

What type of MRI is requested in MS?

A

MRI contrast

FLAIR sequence can help distinguish non-specific white matter lesions.

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32
Q

How many lesions are expected to be seen on MRI investigating for MS?

A

One lesion per decade = normal

>1 lesions per decade = increased likelihood of MS

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33
Q

What investigation can be done to test nerve function in MS?

A

Evoked potential studies

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34
Q

What are the aims of MS treatment?

A

Induce remission - DMARDs

Treat relapses - methylprednisolone

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35
Q

How are relapses of MS treated?

A

Methylprednisolone 500mg for 5 days

1g IV for 3-5 days if oral treatment fails/relapse is severe

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36
Q

How are symptoms managed in MS?

A

Exercise - maintain activity and strength
Neuropathic pain - amitriptyline/gabapentin
Depression - SSRIs
Urge incontinence - oxybutynin
Spasticity - baclofen, gabapentin

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37
Q

Which medication is used to treat fatigue in MS?

A

Amantadine

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38
Q

What is the management of optic neuritis?

A

Urgent referral to ophthalmology
Steroids
2-6 weeks recovery
50% of patients will develop MS in the next 15 years

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39
Q

What is GBS?

A

Acute paralytic polyneuropathy
Causes demyelination of the peripheral nervous system
Usually triggered by an infection

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40
Q

Which infections are associated with GBS?

A

Campylobacter jejuni
Cytomegalovirus
EBV

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41
Q

What is the pathophysiology of GBS?

A

Molecular mimicry: B cells target antibodies on the pathogen, which are similar to antigens on the myelin sheath of motor neurons.

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42
Q

How does GBS present?

A

Ascending symmetrical weakness
Reduced reflexes
Peripheral loss of sensation or neuropathic pain
May progress to facial nerves and cause facial weakness

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43
Q

When do patients present with GBS?

A

4 weeks after preceding infection

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44
Q

How long is the recovery period for GBS?

A

Months - years

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44
Q

How long is the recovery period for GBS?

A

Months - years

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45
Q

How is GBS diagnosed?

A

Clinically: Brighton criteria

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46
Q

Which investigations support the diagnosis of GBS?

A

Nerve conduction studies

Lumbar puncture

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47
Q

What might be seen on a LP in GBS?

A

Raised protein, normal cell count

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48
Q

What is the management of GBS?

A

IV IG
Plasma exchange
Supportive care
VTE prophylaxis

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49
Q

What is the leading cause of death in GBS?

A

PE

Respiratory failure

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50
Q

What is the prognosis in GBS?

A

80% fully recover
15% left with some neurological disability
5% will die

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51
Q

Name some differentials for degenerative myelopathy.

A 
Compressive myelopathy (cancer, trauma)
Peripheral neuropathy (diabetes)
Infectious myelitis
Anterior spinal artery occlusion = sensory, motor
Posterior spinal artery occlusion = proprioception, vibration
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52
Q

How do patients present with myelopathy?

A

Neck pain
Loss of motor function (digital dexterity)
Loss of sensory function
Loss of autonomic function (urinary or faecal incontinence and/or impotence)
Hoffman’s sign

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53
Q

What is Hoffman’s sign?

A

Hoffman’s sign: is a reflex test to assess for cervical myelopathy. It is performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick.

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54
Q

What investigation is needed for myelopathy?

A

MRI cervical spine

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55
Q

What is the management of myelopathy?

A

Spinal decompression surgery: laminectomy

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56
Q

What is a seizure?

A

Transient episodes of abnormal electrical activity in the brain.

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57
Q

Name 6 different types of seizure.

A 
Tonic-clonic
Focal seizures
Absence
Atonic
Myoclonic
Infantile spasms
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58
Q

Where do focal seizures typically start?

A

Temporal lobes

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59
Q

Name 5 differentials for epileptic seizures.

A 
Syncope:
- Vaso-vagal
- Cardiac
- Orthostatic
Non-epileptic seizures:
- Psychogenic
- Hypoglycaemic
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60
Q

When do generalised seizures usually present?

A

< 30 years

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61
Q

How do clonic-tonic seizures present?

A

Loss of consciousness
Tonic (muscle tensing)
Clinic (muscle jerking)

Typically the tonic phase comes before the clonic phase
There may be associated tongue biting, incontinence, groaing and irregular breathing

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62
Q

What is a post-ictal period? What symptoms are experienced?

A

Confusion, drowsy, irritable or depressed

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63
Q

How can focal seizures present?

A

Temporal - deja-vu, lip-smacking, auditary hallucinations
Parietal - sensory changes
Occipital - visual
Frontal - jacksonian march

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64
Q

What are simple and complex focal seizures?

A 
Simple = with consciousness
Complex = without consciousness
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65
Q

How do absence seizures present?

A

Blank, staring into space
Typically present in children
Last 10-20 seconds

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66
Q

How do atonic seizures present?

A

‘Drop attacks’
< 3 minutes
May be indicative of Lennox-Gastaut syndrome

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67
Q

How do myoclonic seizures present?

A

Sudden brief muscle contractions
Remains conscious
Typically in juvenile myoclonic epilepsy

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68
Q

What is West syndrome?

A

Infantile spasms
Starts around 6 months of age
Clusters of full body spasms
Poor prognosis (1/3 die by age of 25)

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69
Q

What investigations can help support a diagnosis of epilepsy?

A

EEG

MRI - structural pathology

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70
Q

What investigations can help exclude other causes of seizures?

A

ECG

Bloods - FBC, BMs, serum prolactin (true seizure)

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71
Q

Which patients require imaging following a seizure?

A

Over 25 and new onset

Focal

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72
Q

What is the aim of treatment for epilepsy?

A

To be seizure free on the minimum dose of anti-epileptic dose

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73
Q

What is the management for a first-time unprovoked seizure?

A

No treatment needed

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74
Q

What is the management for a second unprovoked seizure (tonic-clonic)?

A

Anti-convulsive monotherapy: sodium valproate (1st line)

Second line: lamotrigine or carbamazepine

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75
Q

What is the management of focal seizures?

A

First-line: carbamazepine or lamotrigine

Second-line: sodium valproate or levetiracetam

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76
Q

What is the management of absence seizures?

A

Typically stop in adulthood

First-line: sodium valproate or ethosuximide

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77
Q

What is the management of atonic seizures?

A

First-line: sodium valproate

Second-line: lamotrigine

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78
Q

What is the management of myoclonic seizures?

A

First-line: sodium valproate

Second-line: lamotrigine, levetiracetam or topiramate

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79
Q

What is the management of infantile spasms?

A

Prednisolone

Vigabatrin

80
Q

What is the mechanism of action of sodium valproate?

A

Increasing GABA activity

81
Q

What are the side effects of sodium valproate?

A

Teratogenic - advise about contraception
Liver damage
Hair loss
Tremor

82
Q

What is the mechanism of action of carbamazepine?

A

Sodium channel blocker

83
Q

What are the side effects of carbamazepine?

A

Hyponatraemia
Agranulocytosis
Aplastic anaemia

84
Q

What is cubital tunnel syndrome?

A

Compression of the ulnar nerve causing paraesthesia in the 4th and 5th fingers

85
Q

What is the first-line treatment for restless leg syndrome?

A

Ropinirole

86
Q

Which type of dementia is associated with MND?

A

frontotemporal dementia

87
Q

What is the treatment for Bell’s palsy?

A

PO Prednisolone within 72 hours
Artificial tears

No improvement within 3 weeks = urgent referral to ENT

88
Q

Give some causes of Parkinsonism

A
  • Parkinson’s disease
  • drug-induced e.g. antipsychotics, metoclopramide*
  • progressive supranuclear palsy
  • multiple system atrophy
  • Wilson’s disease
  • post-encephalitis
  • dementia pugilistica (secondary to chronic head trauma e.g. boxing)
  • toxins: carbon monoxide, MPTP
89
Q

What is first-line treatment for a low pressure headache following LP?

A

Caffeine & fluids

90
Q

What is seen on EEG in absence seizures?

A

EEG: bilateral, symmetrical 3Hz spike and wave pattern

91
Q

Give two causes of bitemporal hemianopia

A

upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour

lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

92
Q

What are the 5 MRC grades?

A 
Grade 0 = no movement
Grade 1 = flicker of movement
Grade 2 = movement when gravity is removed 
Grade 3 = movement against gravity
Grade 4 = movement against resistance 
Grade 5 = full power
93
Q

What triad of symptoms is seen in CJD?

A

Rapidly progressive dementia
Myoclonus
Rigidity

94
Q

What is the gold standard test for diagnosing a venous sinus thrombosis?

A

MR venogram

95
Q

Where do brain metastases most commonly spread from?

96
Q

Which anti epileptic drug is most associated with weight gain?

A

Sodium valproate

97
Q

Which scale is used to assess disability following a stroke?

A

Barthel index

98
Q

What are the characteristic features of CJD?

A

Rapidly progressive dementia

Myoclonus

99
Q

Which spinal tract is affected by Syringomyelia?

A

SPinoThalamic - pain & temperature

Syringomyelia = Superman - “cape-like” distribution of loss in shoulders and upper limbs

100
Q

What is Parkinson’s?

A

Progressive neurodegeneration of dopaminergic neurones in the basal ganglia
Results in movement disorders

101
Q

Where in the brain is dopamine produced?

A

Substantia nigra

102
Q

Give 7 causes of Parkinsonism.

A 
Parkinson's disease
Parkinson's plus conditions (4)
Drug-induced parkinsonism
Toxins - CO/MPTP
Wilson's
Post-encephalitis
Dementia pugilistica
103
Q

What is dementia pugilistica?

A

A form of chronic traumatic encephalopathy

104
Q

How does bradykinesia present in Parkinson’s disease?

A

• Shuffling gait
• Micrographia (handwriting gets smaller)
• Difficulty initiating movement
- Hypomimia (reduced facial expression)

105
Q

What is the triad of symptoms seen in Parkinson’s? Name some other symptoms outside of the triad.

A

Bradykinesia
Rigidity
Tremor

Depression, postural instability, anosmia, insomnia, cognitive impairment

106
Q

Describe the features of a tremor seen in Parkinsons.

A

Unilateral
4-6hz
Resting (improves with intentional movement)
Pill-rolling

107
Q

What are the key differences between essential tremor and Parkinson’s tremor?

A 
Parkinson's:
• Asymmetric/unilateral
• 4-6hz
• Resting
• Not improved by alcohol
Essential:
• Bilateral
• 5-8hz
• Intention
- Improved by alcohol
108
Q

How can you differentiate between essential tremor and Parkinson’s tremor?

A

Clinical features

SPECT if uncertainty

109
Q

Give another name for a SPECT? What is it used for?

A

DaTScan - also used to diagnose LBD

110
Q

Name 4 Parkinson’s plus syndromes.

A
  1. Multiple system atrophy
  2. Lewy-body dementia
  3. Progressive supranuclear palsy
  4. Corticobasal degeneration
111
Q

What are the features of multiple system atrophy?

A

Parkinsonism
Autonomic dysfunction = ED, loss of bladder control, postural hypotension
Cerebellar dysfunction = ataxia

112
Q

What are the features of LBD?

A

Parkinsonism
Dementia
Visual hallucinations/delusions
Fluctuating consciousness

113
Q

What are the features of progressive supranuclear palsy?

A

Vertical diplopia
Poor response to L-dopa
Cognitive impairment

114
Q

How is Parkinson’s diagnosed?

A

Clinically

UK Parkinson’s Disease Society Brain Bank Criteria

115
Q

What is the first-line management for Parkinson’s disease?

A

Movement affecting life = levodopa

Movement not affecting life = dopamine agonist

116
Q

What is levodopa?

A

Dopamine precursor
Often combined with peripheral carboxylase inhibitor to prevent breakdown before reaching the brain = co-benyldopa, co-carledopa
Loses effect overtime - 2 years

117
Q

Give two examples of peripheral carboxylase inhibitors.

A

Carbidopa

Benserazide

118
Q

What is the second-line treatment of Parkinson’s disease?

A

If symptoms persist after L-dope/dopamine agonist:

Combination: [L-dopa + peripheral carboxylase inhibitor] AND [MOA-inhibitor, dopamine agonist, COMT inhibitor]

119
Q

What is the purpose of using COMT inhibitors and MAO-inhibitors in Parkinson’s disease? Give examples

A

Extends the effective duration of levodopa by preventing breakdown

Entacapone = COMT inhibitor
Selegiline, rasagiline = MOA-inhibitor

120
Q

What is the purpose of using dopamine agonists in Parkinson’s disease? Give an example.

A

Delay the need for leva-dopa

Cabergoline
Bromocriptine
Pergolide

121
Q

Why should Parkinson’s medication not be stopped?

A

Can cause neuromalignant syndrome

If patient cannot tolerate oral medication or has vomiting/diarrhoea = use transdermal patch

122
Q

What are impulse control disorders?

A

Disinhibited behavioural change caused by dopamine-agonists e.g. gambling

123
Q

What drug can be used to treat daytime sleepiness in Parkinson’s disease?

124
Q

What drug can be used to treat hypersalivation in Parkinson’s?

A

Glycopyronium bromide

125
Q

What is neuroleptic induced Parkinsonism?

A

Parkinsonism caused by anti-psychotics

126
Q

How is orthostatic hypotension treated in Parkinson’s?

A

Medication review
Lifestyle - ^fluids, ^salt
Fludrocortisone

127
Q

Which Parkinson’s medications might cause pulmonary fibrosis?

A

Dopamine agonists

128
Q

What is myasthenia gravis?

A

autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest

129
Q

Which conditions are associated with MG?

A

Pernicious anaemia
RA
SLE

130
Q

When does MG present?

A

Women < 40 years

Men > 60 years

131
Q

Which antibodies are seen in MG?

A
  1. ACh receptor antibodies (85%)
  2. MuSK - Muscle-specific tyrosine kinase antibodies
  3. LDR4 - Low-density lipoprotein receptor-related protein 4
132
Q

What is the pathophysiology of MG?

A

Autoantibodies act on NMJ to prevent the effective contraction of muscles:
1. Anti-Ach receptor = block and damage receptor cells, activate complement system
Anti-MuSK and Anti-LDR4 = prevent rebuilding/organisation of Ach receptors

133
Q

Which drugs are likely to exacerbate MG?

A 
Penicillamine
Quinidine, procainamide
Beta-blockers
Lithium
Phenytoin
Antibiotics: gentamicin, macrolides, quinolones, tetracyclines
134
Q

What is the hallmark feature of MG?

A

Fatiguability

135
Q

Which muscle groups are most affected in MG?

A

Proximal muscles

Muscles of the head and neck

136
Q

What symptoms are seen in MG?

A

Proximal muscles - difficulty getting up

Muscles of the head and neck - diplopia, ptosis, facial droop, dysphagia, dysarthria

137
Q

How can you elicit fatiguability during examination in MG?

A

Blink

Should abduction

138
Q

What signs might you see on examination in MG?

A

Thymectomy scar
Ptosis
Facial droop

139
Q

Which investigations should be done in MG?

A
  1. Single fibre electromyography
  2. Bloods:
    - antibody tests: anti-Ach, anti-MuSK, anti-LDR4
    - CK = normal
  3. CXR - thymoma
  4. Tensilon test (edrophonium test) - not commonly used due to arrythmia risk
140
Q

How can you distinguish MG from statin induced myopathy?

A

CK = normal

141
Q

What is the Tensilon test?

A

Give neostigmine and measure response - positive if improvement of symptoms

142
Q

Why should you order an CXR for patients with newly diagnosed myasthenia gravis?

143
Q

What is the 1st line treatment for MG? What is second line?

A
  1. Pyrostigmine

2. Immunosuppressants - prednisolone, then azathioprine

144
Q

What can be used if there is poor response to immunosuppression?

A

Monoclonal antibodies

145
Q

Which monoclonal antibodies are used in MG?

A

Rituximab - B cells

Eculizumab (not NICE approved) - complement

146
Q

What is a myasthenic crisis? What can cause it?

A

Acute worsening of symptoms –> resp failure

Triggered by infection

147
Q

How do you manage a myasthenic crisis?

A
  1. A–>E (include bedside FVC)
  2. BiPAP –> intubation
  3. IVIG
148
Q

What is motor neurone disease?

A

Cluster if degenerative diseases due to axonal degeneration of neurones in the motor cortex, CN nuclei and anterior horn cells.

149
Q

What is the pattern of motor function seen in MND?

A

Mixed upper and lower motor neurone (if only one, polyneuropathy).

150
Q

Which differential is considered more likely if there is sensory disturbance in suspected MND?

151
Q

Which differential is considered more likely if there is eye involvement in suspected MND?

152
Q

What is the prevalence of MND?

153
Q

What percentage of MND cases are considered to be familial? What is the most common gene that causes MND?

A

10%

SOD1 - CX21

154
Q

What are the different classifications of MND? Which is most common?

A

Amyotrophic lateral sclerosis - 50%
Progressive muscular atrophy
Progressive bulbar palsy
Primary lateral sclerosis

155
Q

What are the features of ALS?

A

LMN signs in the arms, UMN signs in the legs

SOD1 (CX21)

156
Q

What are the features of primary lateral sclerosis?

A

UMN signs only
Loss of Betz cells in the motor cortex
Pseudobulbar palsy

157
Q

What are the features of progressive muscular atrophy?

A

LMN signs only (anterior horn cell lesions) - affects distal before proximal
Better prognosis

158
Q

What are the features of progressive bulbar palsy?

A

Palsy of the tongue, muscles of chewing/swallowing

159
Q

How is MND diagnosed?

A

Clinically - need to rule out other causes.

160
Q

Which investigations should be ordered? What are the expected results?

A

MRI spine (rule out structural cause e.g. myelopathy)
LP (rule out inflammatory cause)
Nerve conduction studies - normal

161
Q

What can be seen on electromyography in MND?

A

Reduced number of action potentials with increased amplitude

162
Q

What is the management of MND?

A

Riluzole - can slow progression and extend survival by a few months
NIV can be used to assist breathing at night
End of life care planning - advanced directives

163
Q

What is the most common cause of death from MND?

A

Respiratory failure

Pneumonia

164
Q

What is the mechanism of action of riluzole?

A

Prevents the stimulation of glutamate receptors

165
Q

What causes polio?

A

RNA virus - affects anterior horn cells

166
Q

What other symptoms might be seen during a polio infection?

A

Sore throat
Myalgia
Fever

167
Q

What is the most common cause of death due to polio?

A

Respiratory failure - muscle paralysis

168
Q

Is there any sensory involvement in polio?

168
Q

Is there any sensory involvement in polio?

169
Q

What is the pattern of motor function seen in polio?

A

Asymmetric LMN paralysis

170
Q

Where does the spinal cord end?

A

Between L1 and L2

171
Q

What is the blood supply to the spinal cord?

A

3 longitudinal blood vessels:
• 2 posterior - supplies dorsal 1/3
• 1 anterior - supplies anterior 2/3

Longitudinal veins drain into extradural plexus.

172
Q

Name two tracts that contain upper motor neurons.

A 
Corticospinal = cortex --> spine (voluntary movement of skeletal muscle)
Corticobulbar = cortex --> brainstem (voluntary movement of head/neck)
173
Q

Where do UMNs of the corticospinal tract synapse with LMNs?

A

Anterior grey horn of spinal cord

174
Q

Where do UMNs of the corticobulbar tract synapse with LMNs?

A

Cranial nerve nuclei:

  • CN V = muscles of mastication
  • CN VII = muscles of facial expression
  • Nucleus ambiguous = CNIX, CNX & CNXI = swallowing, speech, uvula
  • CNXII = muscles of the tongue
175
Q

What is bulbar palsy?

A

LMN lesions affecting cranial nerves

176
Q

What is pseudobulbar palsy?

A

UMN affecting corticobulbar tract

177
Q

Give 3 causes of UMN lesions.

A
  1. Stroke
  2. De-myelination: MS, Freidrich’s ataxia, B12
  3. MND
178
Q

Give 4 causes of LMN lesions.

A
  1. Anterior horn cell damage: polio, SMA
  2. Cauda equine (cord compression)
  3. DM neuropathy
  4. MND
179
Q

What signs are seen in UMN lesions?

A 
Mass: decrease (15%)
Strength: spastic paralysis
Tone: increased
Fasciculations: absent
Babinski: positive
Pronator drift: positive
Hoffman's sign: positive
180
Q

What signs are seen in LMN lesions?

A 
Mass: decrease (80%)
Strength: flaccid paralysis
Tone: decreased
Fasciculations: present
Babinski: absent
Pronator drift: absent
Hoffman's sign: absent
181
Q

What are the two broad types of spinal cord injury?

A

Incomplete

Complete

182
Q

Name 5 types of incomplete spinal cord injury.

A 
Anterior horn lesion
Central cord syndrome
Posterior cord syndrome
Anterior cord syndrome
Brown-sequard
183
Q

What signs/symptoms are seen in anterior horn injury?

A

LMN at the level of injury

184
Q

What causes anterior horn injury?

A

Polio
SMA (spinal muscular atrophy)
MND

185
Q

What signs/symptoms are seen in central cord syndrome?

A

Anterior horn lesion = LMN @ level of injury
Lateral corticospinal tract lesion = UMN below level of injury (upper limbs>lower limbs)
Spinothalamic decussation lesion = loss of pain, temp, crude touch below level of injury - cape sign

186
Q

What is cape sign?

A

Loss of pain, temperature and crude touch sensation in shoulders and upper limbs
Often seen in central cord syndrome due to lesion in spinothalamic tracts
Common cause is syringomyelia

187
Q

Give two causes of central cord syndrome.

A
  1. Hyperextension injury (RTA or minor (OA))

2. Syringomyelia

188
Q

What symptoms are seen in posterior cord syndrome?

A
  1. Demyelination:
    - MS
    - B12
    - Freidrich’s ataxia
189
Q

What symptoms/signs are seen in anterior cord syndrome?

A
  1. Corticospinal tract = UMN below level of injury
  2. Anterior horn cells = LMN @ level of injury
  3. Spinothalamic tract = loss of pain & temperature & crude touch below level of injury

Only thing that stays intact = DCML = fine touch, vibration, proprioception

190
Q

What can cause anterior cord syndrome?

A

Thrombus

Hyperflexion injury

191
Q

What signs/symptoms are seen in Brown-Sequard syndrome?

A

DCML = IPSILATERAL loss of vibration & proprioception below injury
Corticospinal tract = IPSILATERAL UMN signs below injury
Anterior horn cells = IPSILATERAL LMN @ level of injury
Spinothalamic tract = CONTRALATERAL loss of pain, temperature and crude touch below injury

192
Q

Give two causes of Brown-Sequard syndrome.

A

Trauma

Tumour

193
Q

What are the signs/symptoms of a complete spinal cord injury?

A
  1. Paralysis (cervical = quadriplegia; thoracic = paraplegia): flaccid –> spastic overtime
  2. Complete loss of sensation below lesion
  3. Autonomic dysfunction:
    - Faecal/urine incontinence (test using bulbocavernosus reflex)
    - If above T6 –> sympathetic dysfunction –> bradycardia & hypotension
194
Q

What might be seen in spinal cord injury above T6?

A

Neurogenic shock (bradycardia & hypotension) due to loss of sympathetic nerve supply to the heart and great vessels

195
Q

What is the most common cause of complete spinal cord injury?

196
Q

What are the key differences in symptoms of lesions above and below L1/L2?

A

Above spinal cord = UMN signs

Below spinal cord = no UMN signs

197
Q

What is the management for a symptomatic chronic subdural haematoma?

A

burr hole craniotomy

FINALS (26 decks)

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