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Neurology > Peripheral Neuropathy > Flashcards

Peripheral Neuropathy Flashcards

1
Q

what are the causes of nervous system injury?

A 
hypoxia
trauma
toxic insult
metabolic abnormalities
nutritional deficiencies
infections
abnormalities - intrinsic, ageing
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2
Q

what are the two speeds of neuron damage?

A

rapid necrosis

slow atrophy

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3
Q

acute neuronal injury also is also known as…

A

red neuron

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4
Q

when does acute neuronal injury occur?

A

hypoxia/ischaemia

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5
Q

what are the microscopic features of acute neuronal injury?

A
  • Shrinking and angulation of nuclei
  • Loss of the nucleolus
  • Intensely red cytoplasm
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6
Q

what are the electro toxicity affects in acute neuronal injury?

A

Glutamate and Oxygen free radical formation bringing about CALCIUM influx

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7
Q

what is the consequence of electrotoxicity in acute neuronal injury?

A 
Calcium entry triggers:
•	Protease activation
•	Mitochondrial dysfunction
•	Oxidative stress
•	Apoptosis and Necrosis
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8
Q

what is the axonal reaction in nerve injury?

A

o Increased protein synthesis -> cell body swelling, enlarged nucleolus
o Chromatolysis – margination and loss of Nissl granules
o Degeneration of axon and myelin sheath distal to injury “Wallerian degeneration”

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9
Q

what are the features of simple neuronal atrophy?

A 
o	Shrunken
o	Angulated and lost neurons
o	small dark nuclei
o	lipofuscin pigment
o	reactive gliosis
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10
Q

what are subcellular neuronal alterations?

A

o Alterations to neuronal organelles and cytoskeleton

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11
Q

what are examples of subcellular alterations?

A

neurofibrillary tangles in Alzheimer’s disease
lewy bodies in lewy body dementia and Parkinsons
Viral infections

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12
Q

gliosis affects which type of neuronal cell?

A

astrocytes

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13
Q

what are the features of gliosis?

A

o Astrocyte hyperplasia and hypertrophy – grow in number and size
o Nucleus enlarges, becomes vesicular and the nucleolus is prominent
o Cytoplasmic expansion with extension of ramifying processes

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14
Q

what do old gliotic lesions look like?

A

nuclei become small and dark and lie in a dense net of processes

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15
Q

how do oligodendrocytes respond to damage?

A

limited reaction to injury - Less sensitive than neurones, due to having low anti-oxidant reserves and high intracellular iron

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16
Q

Oligodendrocytes damage is feature of which primary demyelinating diseases?

A

Multiple Sclerosis, Acute disseminated encephalomyelitis, Acute haemorrhagic leukoencephalitis

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17
Q

Oligodendrocytes damage is feature of which secondary demyelinating diseases?

A

Viral - Progressive multifocal leukoencephalopathy (PML)
Metabolic - E.g. central pontine myelinosis
Toxic - CO, organic solvents, cyanide

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18
Q

axonal loss in the CNS is generally….

A

irreversible

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19
Q

ependymal cells are effected in which pathological processes?

A

Infection and tumours

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20
Q

what is the process of microglia response?

A
  • Microglia proliferate
  • Recruited through inflammatory mediators
  • Form aggregates around areas of necrotic and damaged tissues
  • Seen aggregating and phagocytosing cell debris, removing dead and dying cellular material and taking on foamy cytoplasm
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21
Q

what is the role of M2 microglia?

A

anti-inflammatory, phagocytic, more acute

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22
Q

what is the role of M1 microglia?

A

pro-inflammatory, more chronic (important mediators of Alzhemiers and MS)

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23
Q

oedema in neuronal cells occurs due to

A

cytotoxic
ionic
vasogenic
haemorrhage conversion

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24
Q

how to cytotoxic processes lead to cellular oedema?

A

dying cells accumulate water because osmotically active extracellular ions such as Na+ and Cl- move into cells and take water with them

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25
Q

when does cytotoxic oedema occur?

A

intoxication, Reye’s and severe hypothermia

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26
Q

what are the causes of ionic oedema?

A

hyponatraemia and excess water intake e.g. SIADH

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27
Q

ionic oedema of neuron cells is the…

A

first dysfunction of the BBB

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28
Q

what is the process of ionic oedema?

A

o cytotoxic oedema, causes extracellular space to lack Na+

o Na ions cross the blood brain barrier (BBB), causing chloride ion transport = osmotic gradient

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29
Q

when does vasogenic oedema occur?

A

along with deterioration and breakdown in the BBB

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30
Q

what are the causes of vasogenic oedema?

A

trauma, tumours, inflammation and infection and hypertensive encephalopathy

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31
Q

what is the process of vasogenic oedema?

A

Disruption of endothelial tight junctions allows plasma proteins, such as albumin which are osmotic factors, cross into the extracellular space, and water follows

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32
Q

what is haemorrhagic conversion in neuronal injury?

A

o occurs when endothelial integrity is completely lost and blood can enter the extracellular space

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33
Q

what are the symptoms of peripheral neuropathy of large fibre motor nerves?

A

Weakness, Unsteadiness, wasting

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34
Q

what are the symptoms of peripheral neuropathy of large fibre sensory nerves?

A

Numbness
Paraesthesia
Unsteadiness

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35
Q

what are the symptoms of peripheral neuropathy of small fibre nerves?

A

Pain

Dysesthesia

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36
Q

what are the symptoms of peripheral neuropathy of autonomic nerves?

A

Dizziness (postural hypotension)
Impotence
Nausea and vomiting (gastroparesis)

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37
Q

how is power affected in peripheral neuropathy of large fibre motor nerves?

A

Reduced

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38
Q

how is power affected in peripheral neuropathy of large fibre sensory nerves?

A

Normal

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39
Q

how is power affected in peripheral neuropathy of small fibre nerves?

A

Normal

40
Q

how is power affected in peripheral neuropathy of autonomic nerves?

A

Normal

41
Q

how is sensation affected in peripheral neuropathy of large fibre motor nerves?

A

Normal

42
Q

how is sensation affected in peripheral neuropathy of large fibre sensory nerves?

A

Vibration and JPS reduced

43
Q

how is sensation affected in peripheral neuropathy of small fibre nerves?

A

Pin prick and temperature reduced

44
Q

how is sensation affected in peripheral neuropathy of autonomic nerves?

A

Normal

45
Q

how are reflexes affected in peripheral neuropathy of large fibre motor nerves?

A

Absent

46
Q

how are reflexes affected in peripheral neuropathy of large fibre sensory nerves?

A

Absent

47
Q

how are reflexes affected in peripheral neuropathy of small fibre nerves?

A

Present

48
Q

how are reflexes affected in peripheral neuropathy of autonomic nerves?

A

Present

49
Q

what are the patterns of loss in length dependent peripheral neuropathy?

A
  • Glove and stocking
  • Mild
  • Moderate
  • Severe
50
Q

what are the different types of nerve damage based on location?

A

Radiculopathy
Plexopathy
Peripheral Neuropathy

51
Q

what are the different types of peripheral neuropathy?

A 
Mononeuropathy
Mononeuritis Multiplex
(length dependent) peripheral neuropathy
52
Q

what is mononeuropathy?

A

neuropathy affecting a single nerve

53
Q

what are the causes of mononeuropathy?

A

physical compression

direct injury to a nerve, ischemia, or inflammation

54
Q

what is mononeuritis multiplex?

A

is simultaneous or sequential involvement of individual noncontiguous nerve trunks, either partially or completely, evolving over days to years

55
Q

what is the pattern of involvement?

A

initally asymmetric but becomes more symmetrical

56
Q

what are the clinical features of mononeuritis multiplex?

A

pain

muscle weakness and loss of reflexes

57
Q

what are the causes of mononeuritis multiplex?

A

diabetes mellitus polyarteritis nodosa, granulomatosis with polyangiitis and eosinophilic granulomatosis with polyangiitis, rheumatoid arthritis, systemic lupus erythematosus (SLE), leprosy, lyme disease, Parvovirus B19, HIV, sarcoidosis, cryoglobulinemia,

58
Q

what is radiculopathy?

A

mechanical compression of a nerve root, usually at the exit foramen or lateral recess

59
Q

what are the causes of radiculopathy?

A

o degenerative disc disease, OA, facet joint degeneration/hypertrophy, ligamentous hypertrophy, spondylolisthesis
o rarer causes – radiation, DM, neoplastic disease, meningeal based disease

60
Q

what are the clinical features of radiculopathy?

A

motor or sensory deficits, pain, weakness, numbness in distribution of nerve root

61
Q

where does radiculopathy most commonly occur?

A

cervical spine C6-C8

62
Q

what are the clinical features of plexopathy?

A

pain, loss of motor control and sensory deficits in regions supplied

63
Q

what is plexopathy?

A

disorder affecting network of nerves, blood vessels or lymph vessels of the brachial or lumbosacral plexus

64
Q

what are the causes of plexopathy?

A

o Primary – trauma

o Secondary – co morbid vascular disease, infection, idiopathic

65
Q

what is autonomic neuropathy?

A

group of symptoms that occur when there is damage to the nerves that manage every day body functions

66
Q

what are the causes of autonomic neuopathies?

A

o Chronic – diabetes, amyloidosis, hereditary
o Acute – GBS, porphyria
o Other – alcohol abuse, Guillain Barre, HIV/AIDs, MS< Parkinson, Spinal cord injury

67
Q

what are the two ways in which nerves are damaged?

A
  • Axonal loss

* Peripheral nerve demyelination

68
Q

what are the causes of axonal loss?

A 
o	Idiopathic (age related)
o	Vasculitis* 
o	Paraneoplastic
o	Infections 
o	Drugs/Toxins 
o	Metabolic
69
Q

what are the vasculitis causes of axonal loss?

A

ANCA +ve, Rhematoid arthritis/Sjrogens syndrome (ANA/ENA +ve)

70
Q

what are the paraneoplastic causes of axonal loss?

A

Myeloma, Antibody mediated (eg breast cancer/SCLC Anti hu/yo)

71
Q

what are the infective causes of axonal loss?

A

HIV, Syphilis, Lyme*, Hepatis B/C (cryoglobulin mediated)

72
Q

what are the drug/toxin causes of axonal loss?

A

Alcohol, Amiodarone, Phenytoin, Chemotherapy (cisplatin/vincristine)

73
Q

what are the metabolic causes of axonal loss?

A

Diabetes, B12/folate deficiencies (other), Hypothyroidism, Chronic uremia, Porphyria

74
Q

what is the conduction speed in axonal neuropathies?

A

near normal

75
Q

what are the clinical symptoms of axonal neuropathies?

A

Movements of muscles effected

76
Q

what are the clinical symptoms in demyelinating neuropathy?

A

Both sensory and motor nerves

77
Q

what is the conduction speed in demyelinating neuropathy?

A

much slower

78
Q

what are the acute causes of demyelinating neuropathy?

A

Guillaine Barre syndrome or AIDP

79
Q

what are the chronic causes of demyelinating neuropathy?

A
  • CIDP (chronic inflammatory demyelinating polyradiculopathy).
  • Hereditary sensory motor neuropathy
80
Q

what is the the treatment of axonal neuropathy?

A
  • Treat cause (ie clear hepatitis C)

* Symptomatic treatment – physiotherapy, orthotics, neuropathic pain relief.

81
Q

what is the the treatment of vasculitic axonal neuropathy?

A

• Pulsed IV methylprednisolone + cyclophosphamide

82
Q

what is the management of demyelinating neuropathy?

A
  • IVIg (pooled immunoglobulin from donors)
  • Steroids
  • Azathioprine, mycophenalate, cyclophosphamide
83
Q

what type of neuropathy is GBS?

A

acute inflammatory demyelinating polyneuropathy

84
Q

what is the pathophysiology of GBS?

A

• antibody and cell mediated reactions to peripheral nerve myelin are involved

85
Q

which antibodies are involved in GBS?

A

antibodies to gangliosides – pure sensory GD1b, severe GD1a/GD1b or GD1b/GT1b
Also myelin glycoproteins

86
Q

what is the immune process in GBS?

A
  • perivascular infiltration with lymphocytes occurs within peripheral nerve and roots
  • lymphocytes and macrophages release cytokines which damage Schwann cell/myelin
87
Q

what is the disease progression in GBS?

A

• segmental demyelination results with secondary axonal damage if the process is severe

88
Q

what are the causes of GBS?

A 
infection
immunisations
antitoxins
trauma
surgery
malignant disease and immunodeficiency
89
Q

which infections are implicated in GBS?

A

o viral – cytomegalovirus Epstein Barr, varicella zoster, hep B, hep C, mumps
o bacterial – campylobacter jejuni, mycoplasma

90
Q

what are the main clinical symptoms of GBS?

A

begins in lower extremities and ascends bilaterally
1. Weakness
2. Ataxia
3. Bilateral paraesthesia Progressing to Paralysis
Causes problem with - respiration, talking, swallowing, bowel and bladder funciton

91
Q

what is the onset of GBS?

A

progresses over hours to days

92
Q

severe GBS can lead to what involvement?

A

respiratory and bulbar involvement, also autonomic

93
Q

what investigations are used in GBS diagnosis?

A
  • nerve conduction studies
  • LP
  • LFTs
  • spirometry
  • antiganglioside antibody
94
Q

what additional investigations are used in GBS diagnosis?

A

serology, stool culture, HIV antibodies, spinal MRI, Borrelia burgdorferi serology, CSF meningococcal polymerase chain reaction (PCR), CSF cytology, CSF angiotensin-converting enzyme (ACE), chest x-ray, CSF VDRL, CSF West Nile PCR

95
Q

what is the management of GBS?

A

Plasma exchange
Supportive treatment
if without IgA Deficiency or renal failure: IV Immunoglobulin

96
Q

what supportive management is used in GBS?

A

o pulse and BP monitoring
o DVT prophylaxis – heparin and support stockings
o intubation and ventilation
o pain in acute phase: gabapentin or carbamazepine
o Long term pain: Tricyclic antidepressants, tramadol, gabapentin, carbamazepine, or mexiletine
o rehabilitation
o hypotension – fluid boluses

Neurology (18 decks)

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