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Year 2 > NeURO: Part 7 > Flashcards

NeURO: Part 7 Flashcards

1
Q

Where does the cord end

A

L1/L2 (conus medullar is)

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2
Q

Where do we take lumbar puncture

A

L4

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3
Q

What is the Cauda Equina

A

Lumbar and sacral nerve roots

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4
Q

Define paraplegia

A

Paralysis of BOTH LEGS ALWAYS caused by spinal cord lesion

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5
Q

Define Hemiplegia

A

Paralysis of ONE SIDE of body caused by lesion of th brain

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6
Q

What side of the body do upper motor neurones effect

A

CONTRALATERAL to lesion

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7
Q

Where is a lesion in upper motor neurone located

A

ABOVE anterior horn cell (spinal cord, brainstem and motor cortex)

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8
Q

Signs of upper motor neurones

A
  1. SPASTICITY (increased muscle tone)
  2. Weakness
  3. Hyperreflexia
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9
Q

What is Spasticity

A

INCREASED Muscle tone where the faster you move, the greater the resistance

CLASP-KNIFE manner

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10
Q

Why is there weakness in upper motor neurone

A

Flexors are generally weaker than extensors in legs

Extensors are weaker than flexors in arms

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11
Q

In relation to the site of lesion, where are lower motor neurone signs seen (which part of th body)

A

IPSILATERAL to lesion

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12
Q

Where is lesion found in lower motor neurone disease

A

ANTERIOR horn cell or distal to anterior horn (plexus, peripheral nerve)

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13
Q

Signs of lower motor neurone disease

A
  1. DECREASED muscle tone
  2. WASTING (atrophy) + FASCICULATIONS
  3. Weakness that corresponds to muscles supplied by involved cord segment, nerve root, part of plexus or peripheral nerve
  4. HYPOREFLEXIA
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14
Q

What are FASCICULATIONS

A

Spontaneous involuntary twitching

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15
Q

What symptoms suggest a root problem in lower motor neurone disease

A
  1. Back pain + sciatica
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16
Q

What is sciatica

A

Pain radiating from the back to down th buttocks

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17
Q

What causes sciatica

A

Manual lifting (anything that causes lower back pain)

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18
Q

What suggests cord disease in lower motor neurone

A

Weakness of biceps with absence of biceps reflex

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19
Q

What suggests cord disease in upper motor neurone

A

Weakness of legs suggests lesion is below that level

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20
Q

Define spondylolisthesis

A
  1. Slippage of one vertebra over the one below
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21
Q

What nerve root is compressed in spondylolisthesis

A

Nevre root comes out ABOVE the disc and so root affected is the one BELOW disc herniation (L4/5 herniation leads to L5 root compression)

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22
Q

What is Olisthesis

A

Spondylolisthesis that shows displacement in any direction

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23
Q

What is anterolisthesis

A

Displacement anteriorly

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24
Q

What vertebra is affected in anterolisthesis

A

L5

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25
Q

What causes spondylolisthesis

A
  1. Degenerative anterolisthesis due to ligamentum flavour weakness and facet arthritis
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26
Q

What is the ligamentous flavour

A

Connect the laminae of adjacent vertebrae

Elasticity to preserve upright posture after flexion

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27
Q

Define spondylosis

A

Degenerative disc disease due to ANY disease

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28
Q

What causes spondylosis

A

YEARS of abnormal constant pressure (sports, repetitive trauma or poor posture) causing body to form new bone to distribute weight (pressure is being applied to vertebrae and discs between them)

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29
Q

What is a myotome

A

Group of muscles that is innervated by a single spinal nerve

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30
Q

What myotome is innervated by C5

A

Shoulder abduction/bicep jerk

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31
Q

What myotome is innervated by C6

A

Elbow flexion/supinator jerk

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32
Q

What myotome is innervated by C7

A

Elbow extension/triceps jerk

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33
Q

What myotome is innervated by L3/4

A

Knee extension/knee jerk

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34
Q

What myotome is innervated by L5

A

Ankle dorsiflexion

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35
Q

What myotome is innervated by S1

A

Ankle plantar flexion/ankle jerk

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36
Q

Define myelopathy

A

Compression of spinal cord resulting in upper neurone signs and symptoms dependant on where the compression is

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37
Q

What s the most common cause of acute compression

A

Vertebral body neoplasms

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38
Q

What causes vertebral body neoplasms

A

Secondary malignancy from lung, breast, prostate, myeloma and lymphoma

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39
Q

What happens to the disc in pathology

A

Herniation and prolapse

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40
Q

What happens in disc herniation

A

Centre of disc (nucleus pulpous) moves out through annulus (outer part of disc) = pressure on nerve root and pain

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41
Q

What happens in disc prolapse

A

Nucleus pulposus moves and presses against annulus but doesn’t escape outside annulus

Causes bulge in disc which pressures on nerve root = pain but less than herniation

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42
Q

What is an epidural abscess

A

Collection of puss in epidural space which presses on nerve root causing paralysis

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43
Q

What else can cause spinal cord compression

A

HAEMATOMA (warfarin)

TUMOUR

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44
Q

Clinical presentation of myelopathy

A
  1. Spinal or root pain precedes leg weakness and sensory loss
  2. Progressive weakness of legs CONTRALATERAL
  3. Signs of UMN: CONTRALATERAL spasticity and hyperreflexia
  4. Bladder sphincter involvement: hesitancy, frequency and painless retention
  5. SENSORY LOSS below level of lesion
  6. LMN signs AT level and UMN below level
45
Q

Extra Clinical presentation seen in cervica cord lesion

A

ARM WEAKNESS

46
Q

Clinical presentation in Sciatica

A

S1 NERVE ROOT COMPRESSOIN:

Sensory loss/pain in back of thigh/leg/lateral aspectt of little toe

47
Q

Clinical presenttaion in L5 nerve root compression

A

Sensory loss/pain in lateral thigh/leg and medial side of big toe

48
Q

Differential diagnosis of Myelopathy

A
  1. Transverse myelitis
  2. MS
  3. Cord vasculitis
  4. Trauma
  5. Dissecting aneurysm
49
Q

How is myelopathy diagnosed

A

DO NOT DELAY IMAGING AT ANY COST

  1. MRI - gold standard
  2. BIOPSY/ SURGICAL EXPLORATION
  3. FBC
  4. CXR
50
Q

Why should Imaging (MRI) be done straight away

A

Irreversible paraplegia may occur if cord is not decompressed

51
Q

Role of MRI in myelopathy

A

Identifies cause and site of compression

52
Q

Role of biopsy in myelopathy

A

Nature of mass

53
Q

What would I be looking for in FBC

A
  1. ESr
  2. B12
  3. U+E
  4. Syphylis
  5. LFT
  6. PSA
54
Q

Role f CXR in myelopathy

A

Malignancy or TB

55
Q

Treatment of malignancy causing myelopathy

A

IV DEXAMETHASONE and radiotehrapy/chemotherapy

56
Q

Role of IV DEXAMETHASONE

A

Reduces inflammation/oedema around malignancy and improves outcome

57
Q

How is epidural abscess treated

A

Surgically decompressed and antibiotics given

58
Q

Treatment of myelopathy when cord herniation or prolapse is present

A
  1. EPIDURAL steroid injection for leg pain
  2. LAMINECTOMY (removal of lamina tissue between discs to relief pressure and symptoms
  3. MICRODISECTOMY (removal of herniated tissue from disc
59
Q

What is the Cauda Equine syndrome

A
  1. Where nerve bundles in caudal equine are damaged
60
Q

Most common cause of Cauda Equina syndrome

A

Lumbar disc herniation at L4/5 or L5/S1

ALSO:
Tumours
Trauma
Infection 
Spondylolisthesis
Post-op haematoma
61
Q

Pathophysiology of cauda equina syndrome

A
  1. Nerve root compression distal to termination of spinal cord at L1/2

Usually large central disc herniations at L4/5 and L5/S1 levels

62
Q

What roots are compressed in cauda equina syndrome

A

S1-S5

63
Q

Clinical Presentation of Cauda Equina syndrome

A
  1. Leg Weakness is FLACCID and AREFLEXIC (LMN) not spastic and hyperreflexic
  2. Sciatic pain, numbness and tingling from lower back to legs and lateral small toe
  3. Bilateral sciatica
  4. Saddle anaesthesia
  5. Bladder/BOwel dysfunction
  6. Erectile dysfunction
  7. Variable leg weakness that is FLACCID + AREFLEXIC
64
Q

Differential Diagnosis of Cauda Equina Syndrome

A
  1. Conus medullar is syndrome
  2. Vertebral fracture
  3. Peripheral neuropathy
  4. Mechanical back pain
65
Q

Diagnostics of Cauda Equina syndrome

A
  1. MRI (to find lesion)
  2. Knee flexion (L5-S1)
  3. Ankle planter flexion test (S1-S2)
  4. Straight leg raising (L5,S1)
  5. Femoral stretch test (L4 root problem)
66
Q

Treatment of Cauda Equina Syndrome

A
  1. REFER to neurosurgeon ASAP to relieve pressure or risk irreversible paralysis
  2. Microdiscectomy (removal of part of the disc)
  3. Epidural steroid injection
  4. Surgical spine fixation
  5. Spinal fusion
67
Q

Complications of microdiscectomy

A

Tears dura

68
Q

Why is surgical spine fixation done

A

If vertebra slips

69
Q

Role of spinal fusion

A

Reduce pain from motion and nerve root inflammation

70
Q

Define MS

A

Chronic autoimmune, T-cell mediated inflammatory disorder of CNS in which there are multiple plaques of demyelination within the brian and spinal cord, occurring sporadically over years

71
Q

What cells are attacked in MS

A

Oligodendrocytes NOT Schwann Cells of PNS

72
Q

What gender is effected by MS

A

FEMALES

73
Q

Age presentation of MS

A

20-40

74
Q

Risk factors for MS

A
  1. Exposure to EBV in childhood
  2. Low levels of sunlight or Vit D (less lesions are seen on MRi in established MS)
  3. Female
  4. WHite
75
Q

Pathophysiology of MS

A
  1. Autoimmune mediated demyelination at multiple CNS sites to oligodendrocyte cells
  2. T cell activate B cells to produce auto-antibodies against myelin
  3. T cells cross BBB causing a cascade of destruction to neuronal cells in the brain
  4. Myelin tries to regenerate but new myelin is less efficient and is temperature dependant when exposed to high heat conduction decreases
  5. Repeated demyelination causes axonal loss and incomplete recovery between attacks
76
Q

Where are plaques of demyelination found

A 
perivenular 
Optic nerves
Ventricles of brian
Corpus callous
Brainstem and cerebellar connections
Cervical cord (corticospinal tract and dorsal columns)
77
Q

Why are Schwann cells unaffected in MS

A

Different antigens to oligodendrocytes

78
Q

What causes relapse + remitting MS

A

Poor demyelination healing after an attack

79
Q

Why is movement and sensation impaired in MS

A

Many areas of the neurone develop scar tissue which slows conduction signals

80
Q

What is relapse and remitting MS

A

Periods of good health and remission followed by sudden symptoms

Accumulate disability over time if they do not fully recover after relapses

81
Q

What follows on from relapsing and remitting MS

A

Secondary progressive MS

82
Q

What is secondary progressive mS

A

Worsening of symptoms with very few remissions

83
Q

What is primary progressive MS

A

Gradually worsening disability without relapses or remissions

Presents later and fewer inflammatory changes on MRi

84
Q

Clinical presentation of MS

A
  1. 20-40
  2. Initially mono symptomatic
  3. Worsens with heat/excercise
  4. Unilateral optic neuritis (pain in one eye on movement and reduced central vision)
  5. Numbness and tingling of limbs
  6. Leg weakness
  7. Brainstem demyelination symptoms
  8. Cerebellar symptoms (ataxia)
  9. Trigeminal neuralgia
  10. Constipation
  11. Spasticity and weakness
  12. Intention tremors
  13. Bladder dysfunction
  14. Sexual dysfunction
  15. Cognitive decline
  16. Amnesia
85
Q

Signs of brainstem demyelination

A
  1. Diplopia
  2. Vertigo
  3. Facial numbness
  4. Dysarthria/ dysphagia
  5. Loss of proprioception
86
Q

Differential diagnosis of MS

A
  1. Hereditary spastic paraplegia
  2. Cerebral variant of SLE
  3. Sarcoidosis
  4. HIV
87
Q

How is MS diagnosed

A
  1. Requires TWO or more attacks in different parts of the CMS (2 lesions at different points in time)
  2. Exclude differentials with FBC
  3. MRI scan of brian and spinal cord - GOLD
  4. Lumbar puncture
  5. Electrophysiology
88
Q

Role of MRI scan in MS

A
  1. Shows periventricular lesions
  2. Discrete white matter abnormalities
  3. Scattered plaques
89
Q

Role of lumbar puncture in MS

A
  1. CSF examination shows oligoclonal IgG bands

2. CSF cell count raised

90
Q

Role of Electrophysiology

A

Delayed nerve conduction suggests demyelination

91
Q

Primary treatment of MS

A

1, Encourage stress-free life (reduces lesions)

2. Poor diet and sun exposure = vit D

92
Q

Treatment of ACUTE relapses of mS

A
  1. IV METHYLPREDNISOLONE (shorten relapse)
  • —–FREQUENT relapses)
    2. SC INTERFERON 1B or 1A to reduce relapses by 30% in Relapse + remitting MS
    3. Monoclonal antibodies
93
Q

What monoclonal antibodies are given in frequent relapsing and remitting MS

A
  1. IV ALETUZUMAB
  2. IV NATALIZUMAB
  3. DIMETHYL FUMARATE
94
Q

Role of iV ALETUZUMAB

A

CD52 monoclonal antibody that targets T cells

95
Q

Role of IV NATALIZUMAB

A

Acts against VLA-4 receptors that allow immune cells to cross the BBB (reduces number of immune cells that can enter the CNS)

96
Q

Symptomatic treatment of MS spasticity

A
  1. Physiotherapy
  2. BACLOFEN
  3. TIZANIDINE
  4. BOTOX INJECTIONS
  5. DOXAZOSIN (for incontinence)
  6. Stem cell transplant
97
Q

What is Baclofen

A

GABA analogue that reduces Ca@+ influx

98
Q

What is Tizanidine

A

Alpha 2 agonist

99
Q

What is Botox injection

A

Reduces ACh in neuromuscular junction = less spasticity

100
Q

Cons of botox

A

Only lasts 2-12 weeks

101
Q

How is urinary incontinence treated in MS

A
  1. Intermittent self-catheterisation

2. DOXASOSIN (anti-cholinergic alpha blocker

102
Q

What causes death in MS

A

Aspiration pneumonia

103
Q

Define myasthenia Gravis

A

Autoimmune disease against AChR in neuromuscular junction

104
Q

What gender is affected in Myasthenia Gravis

A

FEMALES than males

105
Q

Peak incidence of MG in females

A

30

106
Q

Peak incidence of MG in males

A

60

107
Q

What diseases are associated with MG for females

A

pernicious anaemia
SLE
Rheumatoid arthritis
THYMIC HYPERPLASIA

108
Q

What disease is associated with MG in men

A

THYMIC ATROPHY
THYMIC CTUMOUR
rheumatoid arthritis
SLE

109
Q

What causes transient MG

A

D-PENICILLAMINE treatment

Wilson’s disease

Year 2 (155 decks)

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