PNS diseases Flashcards

1
Q

What are Negative manifestation?

A

Negative Manifestations

Partial or complete loss of normal function→Less of something

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2
Q

What are positive manifestations?

A

Positive Manifestations

Excess of normal function→More of something

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3
Q

What are the negative manifestations of PNS diseases?

A
Negative Manifestations
• Paresis or paralysis
Paresis: Partial or incomplete paralysis
Paralysis: Loss of voluntary muscle movement
• Hyporeflexia or areflexia Hyporeflexia: Reduced deep tendon
reflexes
Areflexia: Absence of these reflexes
• Anhidrosis
Absence of sweating

Numbness
Partial or complete loss of sensations

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4
Q

What are the positive manifestations?

A
Positive Manifestations
• Fasciculations
Involuntary contractions or twitching of
groups (fascicles) of muscle fibers
• Paresthesia
Subjective report of abnormal sensations, such as tingling, or what is colloquially described as “pins and needles”
• Pain
Such as brief attacks of severe, sharp, shooting facial pain in trigeminal neuralgia
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5
Q

Describe assessment of patients with PNS disease

A

Things to consider in the assessment of the patient with signs and symptoms of a peripheral nervous system disease:
• Onset and progression Acute versus chronic
• Parts of the nervous system affected Sensory, motor or sensorimotor (both), autonomic
• Number of nerves affected Mononeuropathy: single nerve Polyneuropathy: multiple nerves
• Histopathology
Small fibers versus large fibers, myelinated versus unmyelinated

-electrophysiological consequences
Demyelination, axonal damage, and nerve conduction studies

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6
Q

What are patch clamp recordings?

A
  • Patch Clamp Recordings
  • Primarily used in research labs
  • Measure electrical current running through small membrane patches of neurons and the ion channels located within these patches
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7
Q

What are intracellular recordings?

A
  • Intracellular Recordings
  • Primarily used in research labs
  • Measure changes of the electrical potential (resting potential, graded potential, action potential) of a single neuron
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8
Q

What are extracellular recordings?

A

Extracellular recordings
Frequently used in clinical medicine

  • Examples are electroencephalogram (EEG) and nerve conduction studies (NCS)
  • Measure electrical potential changes of several cells surrounding the recording electrodes
  • Signals from individual cells overlap, and the recording shows the sum of the electrical activity of all of these cells
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9
Q

What causes Carpel tunnel syndrome?

A
  • Occurs due to reduction in tunnel size, such as swelling of tendon sheaths or swelling of soft tissue due to edema.
  • Occurs spontaneously often in middle- aged women, during pregnancy and with hypothyroidism.
  • Pain and/or tingling sensation in the cutaneous distribution of the thumb, index and middle fingers.
  • Difficulty in handling small objects, due to muscle weakness of thenar eminence
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10
Q

What happens after Wallerian Degeneration?

A

Regeneration begins after Wallerian degeneration is complete. Schwann cells play a major role in promoting axonal regeneration.

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11
Q

Describe axonal sprouting after axonal injury/regeneration

A

Axonal sprouting may occur. The sprouts may use the myelin debris as guiding tubes for regrowth.

In some instances, cells may survive the axonal injury, but sprouting axons make navigational errors, re-growing to the wrong targets, yielding aberrant motor output during attempts at volitional movement (e.g., blinking instead of smiling,
salivating instead of sweating).

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12
Q

Describe axonal regrowth

A

Nerve growth factor (released from Schwann Cells), laminins and adhesion molecules promote regrowth. The probability of successful regrowth is higher when the site of injury is closer to the original target

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13
Q

When does remyelination occur?

A

After regrowth of axons

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14
Q

Describe the reinnervation of the muscle

A

Reinnervation of the Muscle depends on Basal Lamina
• Basal lamina intact – axon reinnervates muscle at same point

  • Basal lamina lost – No reinnervation
  • Critical components of the basal lamina are laminins and agrin.
  • Laminin 11 – expressed at synaptic junction, prevents Schwann Cell invasion
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15
Q

Describe regeneration in the CNS after axonal injury

A

When axons in the central nervous system are cut or badly crushed, they rarely regenerate over a significant length because:
• Oligodendrocytes do neither release nerve growth factor, nor do they guide regenerating axonal sprouts.
• Astrocytes multiply in regions of trauma and form glial scar tissue, which acts as a mechanical barrier to sprouting axons. This process is called gliosis.
• There is an inhibitory chemical messenger released within the central nervous system that opposes axonal regeneration in the adult

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16
Q

What is Guillain-Barre syndrome?

A

Incidence – 2:100,000
• XY > XX

  • Rapidly ascending motor and sensory loss, starting approximately 2-3 weeks after a viral respiratory or gastrointestinal illness. Thought to be autoimmune (‘molecular mimicry’).
  • Functional loss is due to demyelination of axons caused by nerve inflammation and is revealed as slowing or block of nerve conduction (NCV/EMG tests).
  • High protein content (100 – 300 mg/dl) in CSF.

• Treatment (if needed) – plasma exchange,
immunoglobulin, ventilatory support.

• Patients may make a good recovery following remyelination of axons, often without treatment

17
Q

What is Laprosy-Hansen’s Disease?

A

Most common treatable neuropathy worldwide
• Caused by bacterium Mycobacterium leprae

• Easily transferred by contact with infected
individual

  • Accesses the body via skin lesions and multiplies on axons and in interstitial fluid
  • Causes compression and ischemia of axons and tissue
  • Profound sensory losses, particularly of pain and temperature
  • Antibiotic treatment is successful
18
Q

How does lead poisoning lead to chronic peripheral neuropathy?

A
  • Due to exposure to lead from contaminated air, water, soil, food, and consumer products
  • Motor deficiencies, but no sensory loss

• Focal weakness of extensor muscles of
fingers, wrist and arms

  • Bilateral arm weakness and wasting in chronic situations
  • Motor neuropathy in adults but encephalopathy in infants (<6 years)
19
Q

How does alcoholic peripheral neuropathy lead to chronic peripheral neuropathy?

A

Due to consumption of >80 -100g alcohol/day associated to alcoholism >10 years
• Malnutrition leads to Vitamin B1 (thiamine) deficiency
• Motor and sensory losses are symmetric
• Sensory neuropathy arises firsts, with a distal to proximal pattern of development
• Motor neuropathy arises second, typically starting in the lower leg

20
Q

How does diabetic peripheral neuropathy lead to chronic peripheral neuropathy ?

A
  • Poorly controlled type I and II diabetes eventually lead to polyneuropathy.
  • Functional problems include sensory (usually symmetric), motor (usually asymmetric) and autonomic neuropathy.
  • Sensory symptoms usually begin in distal parts of both legs, with a “stocking distribution”, later developing into a “stocking and glove distribution”.
  • The sensory endings and axons of small unmyelinated dorsal root ganglion cells are most vulnerable to hyperglycemia, causing loss of pain and temperature sensations.
  • The problem may originate in failure of the cell body to supply its distant parts with nutrients and essential proteins for its cytoskeleton.
21
Q

What are the characteristics of Ia, Ib fibers?

A

A-alpha

Large dia,eter

Myelinated

100 meters per second comduction velocity

Proprioceptor afferents, alpha motor neurons (lower motor neurons)

22
Q

What are the characteristics of II fibers

A

A-beta - medium fibers, myelinated, 50 meters per second conduction velocity ex. Touch sfferents

A-gamma - small diameter, myelinated, 50 meters per second, ex. - gamma motor neurons

23
Q

What are the characteristics of III fibers?

A

A-delta- small diameter, myelinated, 30 m/s conduction velocity- pain (first pain), afferents

B- small diameter, myelinated, 30 m/s, visceral afferents and efferents

24
Q

What are the characteristics of IV fibers?

A

C fibers- small diameters, not myelinated, 0.5 m/s

Pain (secind pain) afferents

25
Q

What is the impact of demyelination lesion in conduction velocity?

A

Significant reduction

26
Q

What is the impact of mild axonal damage lesion. on conduction velocity?

A

Minimal or no damage

27
Q

What is the impact of severe axonal damage lesion on the impact of conduction velocity?

A

Absence of nerve conductuon

28
Q

What is the impact of compression lesion on the impact of comduction velocoty?

A

Reduction at the site of compression

29
Q

What is the impact of NMJ lesion on conduction velocity?

A

No chane

30
Q

What is the impact of muscle. Lesion on conduction velocity?

A

No change