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Neuro > Peripheral Pathology > Flashcards

Peripheral Pathology Flashcards

1
Q

Compare and contrast axonal regeneration and segmental regeneration

A

Axon= slow recovery

Segment =rapid recovery

Both= new myelin internodes are shorter and thinner

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2
Q

Compare and contrast axon injury involved in axonal and segmental degeneration

A

Axonal: involves distal axon and its associated myelin sheath with chromatolysis

Segmental: spares axons

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3
Q

compare and contrast the myofibers and nerve conduction presentation in axonal and segmental degeneration

A

Axonal: denervated myofibers become atrophied and there is no nerve conduction

Segmental: Muscle fibers are not affected and nerve conduction is only slowed

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4
Q

Define Neuropraxia and describe it with regards to its features and prognosis

A

Definition: compression injury causing temporary disruption of nerve conduction

Features: whole nerve remains structurally intact

Prognosis: Good chance of complete recovery of nerve function

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5
Q

Define Axonotmesis and describe it with regards to its features and prognosis

A

Definition: axon is damaged, but the perineurium and epineurium remain intact

Features: Chromatolysis and Wallerian Degeneration

Prognosis: good chance of at least partial recovery in a few months

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6
Q

what is chromatolysis?

A

reaction of a neuronal cell body in response to an axonal injury

It reflects an increase in protein synthesis in effort to restore the integrity of the damaged neurons

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7
Q

what does chromatolysis look like

A

swelling of the neuronal cell body

dispersion of Nissl Bodies

Displacement of the nucleus to the periphery

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8
Q

What is Wallerian Degeneration

A

active neuronal degeneration process in response to axonal injury to clear axonal debris and prevent scarring

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9
Q

Describe Wallerian Degeneration

A
  1. Initially retained electrical excitability of axonal membranes distal to the injury for up to 36 hours
  2. progressive degeneration of the distal segment cytoskeleton with dissolution of axonal membrane
  3. Degradation of residual myelin sheath by macrophages and Schwann cells
  4. Proximal stump stays in place, ultimately sprouting regenerative nerve fibers that ideally reinnervate the distal tissues
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10
Q

Define Neurotmesis and describe it with regards to its features and prognosis

A

Definition: complete nerve resection

Features: connective nerve sheath damage

Prognosis: Chance of recovery is poor without surgical repair

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11
Q

What is a traumatic neuroma

A

a painful, but benign nodular thickening resulting from a failure of the regenerating axons to find their distal target

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12
Q

Compare and contrast Wallerian degeneration in CNS and PNS with regards to its cell type, timing and likelihood of regeneration

A
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13
Q

why doesn’t regeneration occur in CNS Wallerian degeneration

A

persistence of myelin debris

secretion of inhibitory factors

dense glial scarring

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14
Q

Why does myelin debris last for so long in CNS Wallerian degeneration

A

macrophages and microglia are slowly recruited due to the BBB

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15
Q

Compare and contrast neurofibromas and schwannomas with respect to:

  • location
  • nerve involvement
  • capsule presence
  • patterns
  • cell types involved
  • risk of malignancy
  • Associations
A
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16
Q

Describe Neurofibromas

A

small nodular tumors of the skin and subQ tissues, arising from small cutaneous nerves

  • has no neurologic deficits
  • can be isolated
  • may cause local pain or bleeding
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17
Q

Describe the different subtypes of neurofibromas

A

Diffuse: large plaque-like elevations of the skin

Plexiform: multiple nodular masses affecting nerve roots, plexuses or large nerves

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18
Q

What causes neurofibromas

A

germline mutations of NF1 on chromosome 17 cause intracellular neurofibromin proteins.

These proteins increase the RAS signalling cascade

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19
Q

Describe the morphology of a neurofibroma

A

heterogenous composition of Schwann cells, admixed with perineural-like cells, fibroblasts and CD34+ spindle cells

20
Q

Complications of neurofibromas

A

Malignant peripheral nerve sheath tumors

21
Q

What are Malignant peripheral nerve sheath tumors and where do you usually find them

A

poorly defined tumor masses that frequently infiltrate along the axis of the parent nerve and invade soft tissues

Usually found on the:

  • chest
  • abdomen
  • pelvis
  • neck
  • limb girdle
22
Q

how are most Malignant peripheral nerve sheath tumors formed

A

from transformation of a plexiform neurofibroma

23
Q

Describe the morphology of Malignant peripheral nerve sheath tumors

A

fasciculated arrangements of spindle cells, commonly seen with mitoses, necrosis and nuclear aplasia

S-100 +

24
Q

Describe a schwannoma with regards to symptoms, location, and appearance

A

symptoms resemble local compression of involved nerves or adjacent structures

Cranial vault: occurs at the cerebellopontine angle, where they are attached to the vestibular branch of CN8

Dura: involves sensory nerves

Extradural: can arise in association with large nerve trunks or soft tissue lesions without an identifiable associated nerve

25
Q

What causes schwannomas

A

germline mutations of NF2 on chromosome 22, causes loss of function mutations to merlin protein. In its absence, cells hyperproliferate in response to uninhibited growth factors like EGFR

26
Q

Describe spinal muscular atrophy with respect to clinical features, subtyping, and prognosis

A

symptoms: muscle weakness, hypotonia, bulbar symptoms, preserved sensations, Preserved eye movement and continence

Type 1: non-sitters

Type 2: sitters

Type 3: Walkers

Prognosis improves with later onset

27
Q

what causes spinal muscular atrophy

A

Autosomal recessive inherited mutation of SMN1 gene on chromosome 5q causes apoptosis of LMN in late stages of fetal development and postnatal period

28
Q

Diagnostics of spinal atrophy

A

normal or mildly elevated Creatine kinase

spontaneous large-amplitude, low frequency electrical activity with rarified interface pattern

29
Q

Morphology of spinal muscular atrophy

A

atrophy to groups of motor units interspersed with normal or hypertrophies motors skills

30
Q

what causes carpal tunnel syndrome and what contributes to it

A

cause: compression of the median nerve causes impaired blood flow and altered vascular structuring, leading to edema, hypoxia and axonal degeneration

Contributions:

prior wrist trauma

manual work

pregnancy

hypothyroidism

DM

Rheumatoid arthritis

dialysis associated amyloidosis

31
Q

clinical presentation of carpal tunnel syndrome

A

sensory impairment and motor weakness in medial nerve distribution

thenar atrophy and motor weakness during thumb abduction and opposition

weakened pinch grip

wrist flexion and tapping over the flexor surface exacerbate symptoms

32
Q

presentation of Guillain Barre

A

ascending flaccid paralysis about 1-4 weeks post infection

33
Q

Pathology of Guillan Barre

A

autoantibodies against gangliosides or other known antigens of Schwann cells cause immune-mediated segmental demyelination and axonal degeneration

34
Q

Describe diagnostics seen in Guillain Barre

A

elevated proteins, but normal cells in CSF

reduced nerve conduction velocity due to demyelination eith increased F wave frequency

35
Q

common pathogens in association with Guillain Barre

A

C. jejuni

EBV

CMV

HIV

Influenza

Mycoplasm

36
Q

How do you differentiate from Guillain Barre and Chronic Inflammatory Demyelinating Polyradiculopathy

A

Chronic Inflammatory Demyelinating Polyradiculopathy’s symptoms last for at least 2 months with subacute or chronic course relapses and remissions

Pertaining to morphology: Chronic Inflammatory Demyelinating Polyradiculopathy displays onion bulb changes on biopsy

37
Q

What does Charcot-Marie Tooth Disease Look like

A

calf muscle atrophy (stork legs)

symmetric distal sensorimotor polyneuropathy

claw foot

intrinsic hand musculature may become involved after several years

38
Q

What causes Charcot-Marie Tooth Disease

A

mutations of peripheral myelin protein PMP22 causes unstable myelin, which causes decreased impulse conduction velocity

39
Q

Describe the morphology of Charcot-Marie Tooth Disease

A

segmental demyelination and remyelination with onion bulb formations

40
Q

Associations of Charcot-Marie Tooth Disease

A

sleep apnea

41
Q

features of Leprosy polyneuropathy

A

segmental demyelination, remyelination

loss of myelinated and demyelinated axons

42
Q

Describe the pathogenesis of Diptheria polyneuropathy and discuss its features

A

Pathogenesis: Diptheria toxin inhibits protein synthesis by deactivation of EF-2 and ADP ribosylation, leading to nerve demyelination

Features: prominent bulbar and respiratory dysfunction

43
Q

describe the pathogenesis of VZV polyneuropathy and discuss its features

A

Pathogenesis: reactivation of latent virus within neurons of the sensory ganglia

Features: shingles

44
Q

What is the most common cause of peripheral neuropathy and how does it occur

A

Diabetes Mellitus

  1. hyperglycemia causes glycalation of proteins, lipids and amino acids
  2. Glycation causes activation of inflammatory signaling through AGE receptors
  3. Inflammatory signaling causes Endoneural arteriole hyalinization
  4. Arterial hyalinization causes polyneuropathy
45
Q

Metabolic factors that cause polyneuropathy

A

uremia

Vitamin B1 deficiency

Vitamin B6 deficiency

Vitamin B12 deficiency

Vitamin E deficiency

Chronic liver disease

Chronic respiratory disease

46
Q

Per powerpoint, the following malignancies are associated with which neuropathies?

Lung apex neoplasms

Malignant pelvic neoplasms

meningeal carcinomatosis

small cell lung cancer

A

Lung apex neoplasms= brachial plexopathy

Malignant pelvic neoplasms= obturator palsy

meningeal carcinomatosis causes cauda equina syndrome, yielding lower extremity polyradiculopathy

small cell lung cancer= sensorimotor neuropathy

Neuro (13 decks)

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