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Year 2 > NEURO: Part 8 > Flashcards

NEURO: Part 8 Flashcards

1
Q

What is Uhtoff’s phenomenon

A

A worsening of symptoms due to exposure to higher the n normal temperature - MS

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2
Q

What is Lhermitte’s sign

A

In MS, an electrical sensation that runs down the back when bending the neck - CHARACTERISTIC of MS

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3
Q

What factors increase risks of relapses in MS

A

COLD
Influenza
Gastroenteritis

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4
Q

Biomarkers for MS

A
  1. Oligoclonal bands (found in lumbar puncture - proteins present in the CNS but not the blood)
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5
Q

Signs of Myasthenia Gravis in the eyes

A

MUSCLES OF EYES AFFECTED INITIALLY:

  1. ptosis - levator palpeerde superioris
  2. diplopia - due to weakness of extra ocular muscles
  3. Symptoms worsen when watching television, reading or driving in bright conditions

Isolated symptoms to eye is called ocular myasthenia graves

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6
Q

Signs of Myasthenia Gravis when eating

A
  1. DYSPHAGIA (weakness of oesophageal muscles)
  2. Weakness of muscles of mastication
  3. Velopharyngeal insufficiency (regurgitation of food and liquids into nose than down the throat)
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7
Q

Signs of myasthenia graves when speaking

A
  1. Dysarthria

2. Hypophonia and nasal quality

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8
Q

Signs of myasthenia graves in the fcae

A

Weakness of facial expression muscles: Can’t keep mouth closed, dropping eye lids

THEY LOOK SAD

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9
Q

What is a dangerous red sign of myasthenia graves

A

Muscles that control breathing - dyspnea and limb movement is affected = takes years to occur

Results in myasthenic crisis

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10
Q

What is myasthenic crisis

A

When paralysis of res muscles occur

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11
Q

Pathophysiology of myasthenia graves

A
  1. Antibodies produced against nicotinic cholingeric receptor or muscle-specific kinase
  2. Deposition of complex anti-ACHr IgG and complement at post-synaptic membranes = destruction of receptors
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12
Q

What condition is MG in females associated with

A

THYMIC HYPERPLASIA
RA
SLE
pernicious anaemia

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13
Q

What conditions are associated in males with MG

A

THYMIC ATROPHY?TUMOUR
RA
SLE

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14
Q

What causes transient MG

A

D-PENICILLAMINE TREATMENT

WILSON’S DISEASE

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15
Q

Differential diagnosis of MG

A
  1. MS
  2. Hyperthyroidism
  3. Acute Guillain-Barre syndrome
  4. Lambert-Eaton myasthenic syndrome
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16
Q

What is Lambert-Eaton syndrome

A
  1. Causes defective ACh release at neuromuscular junction but weakness IMPROVES after exercise compared to MG
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17
Q

Physical examination done in MG

A
  1. Ask patient o do repetitive movements (allows us to see ptosis)
  2. Curtain sign : Holds a patient’s eye open which will lead to the other eye closing
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18
Q

FBC in MG

A
  1. autoantibody for AChR (not very sensitive in ocular myasthenia gravis)
  2. If negative, look for MUSK protein antibodies
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19
Q

Diagnostics for MG

A
  1. Electromyography
  2. ICE Test
  3. Edrophonium test
  4. CXR / CT/MRI
  5. Pulmonary function test
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20
Q

What do we look for in EMG for MG

A
  1. Repetitive nerve stimulation as muscle fibres are easily fatigued in MG
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21
Q

What do we look for in the ice test

A
  1. Apply ice for 4-5 mins to eyelids: ACh esterase is inhibited at lower temperatures

Positive if there is greater than 2mm rise in the eye lid after ice is removed

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22
Q

Role of CXR in myasthenia graves

A
  1. Mediastinum widening (thymoma or hyperplasia of thymus)
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23
Q

Role of MR in myasthenia graves

A

Eliminates lesions of cranial nerves and ocular muscles

Mediastinal widening

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24
Q

How are symptoms of MG controlled

A

ACh esterase inhibitor

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25
Q

Immunosuppression treatment for MG

A
  1. ORAL PREDNISOLONE (increase dose per week)
  2. Bosphosphonates to stop osteoporosis
  3. METHOTREXATE or ORAL AZATHIOPRINE if disease becomes more general
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26
Q

Surgical intervention for MG

A

Thymectomy

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27
Q

When is a thymectomy done

A

If onset is less than 50 years or poorly controlled with AChesterases

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28
Q

How to treat myasthenic crisis

A
  1. PLASMAPHERESIS (antibody removal) and IV immunoglobulin to stop trigger of relapses
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29
Q

Define apraxia

A

Disorder of consciously organised pattern of movement or impaired ability to recall acquired motor skill

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30
Q

How is movement fine-tuned

A
  1. First we think about the idea of movement
  2. Activate upper motor neurones in pre-central gyrus
  3. Impulses travel down LMB and motor units via corticospinal tract
  4. Modulating activity of cerebellum and basal ganglia
  5. Further modification of movement depending on sensory feedback
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31
Q

What type of motor neurone are LMNs

A

Alpha motor neurone

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32
Q

How is muscle tone regulated

A
  1. Stretch receptor sin the muscle are innervated by gamma motor neurones
  2. Muscle stretched -> afferent impulse from muscle spindles -> reflex partial contraction of muscle
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33
Q

What are stretch receptors in the muscle called

A

MUSCLE SPINDLES

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34
Q

Potential sites of damage along motor pathway

A
  1. Motor nuclei of cranial nerves
  2. Motor neurones in spinal cord
  3. Spinal ventral roots
  4. Peripheral nerves
  5. NMJ
  6. Muscle
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35
Q

Physical examination of UMN signs

A
  1. EVERYTHING GOES UP
    Brisk reflexes - tension + jaw reflexes
    Babinski sign
    Limb muscle weakness
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36
Q

What is babinski’s sign

A

Planters are upturned on stimulation

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37
Q

Physical examination of LMN signs

A

EVERYTHING GOES DOWN

  1. Flaccidity
  2. Muscle wasting
  3. Fasciculations (needs weakness to diagnose LMN)
  4. Reflexes absent
38
Q

What is motor neurone disease

A
  1. Cluster of major degenerative diseases characterises by selective loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells
39
Q

What is MND called in other countries

A

ALS

40
Q

In what gender is MND common in

A

Males

41
Q

Age onset of MND

A

60 years

42
Q

How can all eyes of MND be differentiated

A
  1. Is disease sporadic or inherited

2. Involvement of UMN, LN or both

43
Q

What is the Hoffmann’s reflex

A

Loosely hold middle finger and flick fingernail downward allowing middle finger to flick upwards reflexively

(upper limb equivalent to babinski’s sign)

44
Q

What genetic mutation causes MND

A
  1. Mutation in free radical scavenging enzyme superoxide disumtase
45
Q

Pathophysiology of NMD

A

Relentless and unexplained destruction of UMN and anterior horn cells in CNS

46
Q

What distinguishes MND from MS and polyneuropathies

A

NO SENSORY LOSS OR SPHINCTER DISTURBANCES seen

NO EYE MOVEMENTS AFFECTED (MG differentiated)

47
Q

What causes MND

A

Oxygen species which damage lipids, DNA and proteins

48
Q

How do patients with NMD die

A

3 years from res failure due to bulbar palsy and pneumonias

49
Q

What is ALS

A

Death of neurones of voluntary muscles

50
Q

Clinical presentation of ALS

A

UMN and LMN

  1. Weakness and UMN signs (upping planters + LMN wasting in ONE LIMB)
  2. Split hand sign - thumb side of the hand is adrift due to excessive wasting around int but less than hypothenar
  3. Cramps
  4. Brisk reflexes in wasted muscles, extensor plantar response and spasticity
  5. Foot drop and wrist drop
51
Q

Clinical presentation of progressive muscular atrophy

A

LMN ONLY:

  1. Weakness
  2. Muscle wasting
  3. Fasciculations in one limb that spread to other spinal segment s
  4. Affects distal muscle groups before proximal
52
Q

Clinical presentation of progressive bulbar palsy

A

LMN ONLY:

  1. CN 9,10,11,12 affected initially
  2. Dysarthria, dysphagia, nasal regurgitation of fluids and choking
  3. LMN lesions affecting tongue and talking/swallowing muscles
  4. Flaccid, fasciculation tongue
  5. Jaw jerk absent
  6. Speech quiet, horse or nasal
53
Q

Clinical presentation of primary lateral sclerosis

A

UMN ONLY:

  1. Loss of Betz cells in motor cortex
  2. Main UMN signs in legs
  3. Causes pseudo bulbar palsy
54
Q

Complications of MND

A
  1. FORNTOTEMPORAL DEMENTIA
55
Q

What patients will have MND

A 
Over 40
Stumbling spastic gait 
Foot drop 
Proximal myopathy
Weak grip (door handles don't turn)
Hair-washing is hard (poor shoulder abduction)
Aspiration pneumonia
56
Q

Differential diagnosis of MND

A
  1. MS
  2. MG
  3. Diabetic amyotrophy
  4. Guillain-Barre syndrome
  5. Spinal cord tumours
57
Q

How is MND diagnosed

A
  1. LMN + UMN in 3 regions - definite
  2. LMN + UMN in 2 regions - probable
  3. LMN + UMN in 1 region + EMG shows acute denervation in more than 2 limbs
  4. LMN + UMN signs in 1 legion
  5. MRI of CNS: exclude structural causes
  6. Lumbar puncture (exclude inflammatory causes
  7. NCS + EMG: Denervation of muscles due to degeneration of LMN confirmed by EMG
58
Q

Treatment of MND

A
  1. Antiglutamatergic drugs
  2. ORAL AMITRYPTYLINE for muscles of mastication
  3. Dysphagia (Nasogastric tube)
  4. Spasms: ORAL BACLOFEN
  5. Ventilation for res failure
  6. DICLOFENAC
  7. Speech, language therapists and physic
59
Q

Define Guillain-Barre syndrome

A

Acute inflammatory demyelinating ascending polyneuropathy affecting PNS Schwann cells following upper res infection or GI infection

60
Q

What gender is affected din GBS

A

MALES

61
Q

Peka age for GBS

A

15-35 and 50-75

62
Q

What microbes cause GNS

A
  1. Campylobacter jejune
  2. Cytomegalovirus
  3. Mycoplasma
  4. Zoster
  5. HIV
  6. EBV
63
Q

What does Campylobacter jejune do

A

Causes diarrhoea

64
Q

Pathophysiology of Guillain-Barre syndrome

A

—— Shwann cell attack—-
Immune attack on nerve cells of PNS
2. T cells and macrophages damage myeline sheets
3, Activation of complements
—–Axon attack—-
IgG antibodies and complement against cell membrane covering axon without lymphocyte involvement

65
Q

How do microbes cause GNS

A

Share same antigens are Schwann cells leading to autoantibody mediated nerve cell damage formation

66
Q

Diagnosis of Guillain-Barre syndrome

A
  1. Lumbar puncture: Elevated protein (greater than 0.55g/L levels and fewer than 10 WBC/mm^3
  2. NCS and EMG may show delayed nerve conduction of electrical impulses (not seen until after 2 weeks)
  3. Spirometry to monitor FVC if there is res involvement
67
Q

Differential diagnosis of GBS

A
  1. Hypokalaemia
  2. Stroke
  3. Brianstem compression
  4. Encephalitis
  5. Spinal cord compression
  6. Poliomyelitis
  7. Vasculitis
  8. MG
68
Q

Clinical presentation of GBS

A
  1. 1-3 weeks post infection sees BILATERAL ASCENDING MUSCLE WEAKNESS = paralysis
  2. PROXIMAL MUSCLES more affected (trunk, res and cranial nerve 7)
  3. Pain
  4. Paraesthesias
  5. Reflexes lost
  6. Systemic symptoms: Sweating, Raised BP , arrhythmias
69
Q

How is GBS treated

A
  1. VENTILATE if FVC < 1.5L/80%
  2. IV IG for 5 days to reduce paralysis
  3. Plasma exchange
  4. LOW MOLECULAR WEIGHT HEPARIN + compression stockings to reduce risk of venous thrombosis
70
Q

When is IV IMMUNOGLOBULIN contraindicated

A

IgA deficiency patients

71
Q

6 ways we can get nerve malfunctions

A
  1. DEMYELINATION
  2. AXONAL DEGENERATION
  3. COMPRESSION
  4. INFARCTION
  5. INFILTRATION
  6. WALERIEN DEGENERATION
72
Q

What happens to conduction velocity in axonal degeneration

A

Normal because axonal continuity is maintained in surviving fibres

73
Q

Name a condition that causes compression of nerve

A

CARPAL TUNNEL SYNDROME

74
Q

How does infarction lead to nerve malfunction

A
  1. Micro-infarction of vast nervous occurs in diabetes and arthritis such as polyarteritis nods and eosinophilic granulomatosis and polyangitis
75
Q

How doe infiltration cause nerve damage

A
  1. Inflammatory cells in leprosy and granulomas
76
Q

What is wallerian degeneration

A

When nerve fibre is cut or crash, distal part of axon separated from cell body degenerates

77
Q

Define neuropathy

A

Pathological process affecting peripheral nerve or nerves

78
Q

Define mononeuropathy

A

Process affecting single nerve

79
Q

Define mononeuritis multiplex

A

Several individual nerves affected

80
Q

What causes mononeuropathies

A

Lesions of individual peripheral or cranial nerves (trauma, entrapment)

81
Q

What is mono neuritis multiplex

A

When 2 or more peripheral nerves are affected when causes are systemic

82
Q

What conditions can cause mono neuritis multiplex

A
  1. WARDS PLC

W - Wegener’s grnaulomatosis

  1. AIDS/AMYLOID
  2. RA
  3. Diabetes mellitus
  4. Sarcoidosis
  5. POlyarteritis nodosa
  6. Leprosy
  7. Carcinoma
83
Q

Most common mononeuropathy

A

Carpal tunnel syndrome

84
Q

What conditions are associated with carpal tunnel d=syndrome

A
  1. Hypothyroidism
  2. Diabetes mellitus
  3. Pregnancy
  4. Amyloidosis
  5. Obesity
  6. RA
  7. Acromegaly
85
Q

Clinical presentation of carpal tunnel syndrome

A
  1. Ahcing pain in hand and arm AT NIGHT makes patient wake up
  2. Paraesthesiae in thumb, index, middle and 1/2 ring fingers and palm (median nerve distribution)
  3. Relieved by dangling hand over edge of bed
  4. Sensory loss and weakness of ABUDCTOR POLICES BREVIS and wasting of thenar eminence (muscles at base of thumb)
  5. Light touch, 2-point discrimination and wearing impaired
86
Q

Differential diagnosis of CTS

A
  1. Peiprheral neurooathy
  2. MND
  3. MS
87
Q

Diagnosis of Carpal tunnel syndrome

A
  1. EMG (shows slowing of conduction velocity in median nerve, confirms lesion site and severity)
  2. PHALEN’s test (patient can only maximally flex wrist for 1 minute)
  3. TINEL’s test (tapping never on wrist causes tingling)
88
Q

How is Capral tunnel treated

A
  1. Wrist splint at night
  2. Steroid injetcion
  3. Decompresison surgery (carpal tunnel ligament cut to reduce pressure)
89
Q

What are MuSK proteins

A

Receptor tyrosine kinase

90
Q

What are MuSK proteins needed for

A

Formation and maintenance of the NMJ

Year 2 (155 decks)

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