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BMS150 Midterm 2 > Neurology - Compressive and Demyelinating Illnesses of the CNS > Flashcards

Neurology - Compressive and Demyelinating Illnesses of the CNS Flashcards

1
Q

CNS damage from demyelinating disease

A

Damage to oligodendrocytes or their processes that myelinate axons

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2
Q

PNS damage from demyelinating disease

A

Damage to Schwann cells
1. genetic = impair ability to compact or produce myelin sheath
2. autoimmune

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3
Q

Immune mediated disease directed against CNS resulting in the loss of myelin and eventual loss of axons

A

Multiple Sclerosis

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4
Q

Most common demyelinating illness

A

Multiple Sclerosis

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5
Q

MS Epidemiology

A

3x more frequent in women; peak incidence 20-40 yo.

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6
Q

Candidate genes for MS

A
  • HLA-II gene (responsible for antigen presentation)
  • IL-2, IL-7, IL-17
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7
Q

Risk of first degree relative having MS

A

15x increase

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8
Q

Risk of identical twin having MS

A

150x increase

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9
Q

Possible non-genetic risk factors for MS

A
  • Link to viral infection
  • Reduced sun exposure and vitamin D
  • Hx of other autoimmune disease
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9
Q

T/F: MS progresses straight to a chronic inflammatory picture with no preceding acute inflammation

A

True

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9
Q

Two phases of MS

A

1st - Active plaques: presence of typical leukocytes found during chronic inflammation

2nd - Inactive plaques: loss of axons, minimal inflammatory leukocytes, gliosis

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10
Q

T/F: Plaques are more prominent in areas rich in grey matter

A

False - they’re found in white matter rich areas

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11
Q

Helper T-cells initiate an immune response against what in MS?

A

Myelin basic protein - helps compact layers of myelin sheath

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12
Q

Major leukocytes involves in MS phase 1?

A
  • Th cells (Th1 and Th17)
  • B-cells
  • Macrophages
  • Cytotoxic T-cells
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13
Q

Areas that lymphocytes seem to reside “permanently” as MS flares continue? Where are they?

A

Lymphocytic follicles - prominent around meninges and blood vessels

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14
Q

MS plaques without prominent inflammation? With prominent inflammation?

A

Without = inactive (phase 2)
With = active (phase 1)

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15
Q

Axons tend to degenerate because…?

A

loss of myelin and oligodendrocytes => destabilization of action potentials => neuronal cell death

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16
Q

Most common initial Sx of MS (3)

A
  • Paresthesia in 1+ extremities, trunk, or one side of face
  • Weakness or clumsiness of a leg or hand
  • Visual disturbances
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17
Q

Cognitive Sx of MS (3)

A
  • Fatigue
  • Depression
  • Slowed cognition and memory effects
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18
Q

What is L’hermitte’s phenomenon?

A

Sensation of an electrical shock running down back and along the limbs

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19
Q

Motor Sx of MS (5)

A
  • Bilateral, spastic weakness (lower extremities)
  • Increased DTRs
  • Charcot triad = dysarthria, nystagmus, tremor
  • Facial twitching
  • Slurred speech
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20
Q

Neurological Sx of MS (5)

A
  • Dizziness
  • Bladder dysfunciton
  • Constipation
  • ED in men/genital anesthesia in women
  • Urinary/fecal incontinence (severe cases)
21
Q

MS diagnosis criteria (3)

A
  • Clinical diagnosis via MacDonald’s criteria
  • Characteristic lesions on brain and spinal MRI
  • Presence of certain types of Ab’s in the CSF
22
Q

Most common progression of MS

A

Relapsing-remitting

23
Q

(defn.) functional disturbance and/or pathological change in the PNS

A

Neuropathy

24
Q

(defn.) pain in the distribution of a particular nerve, usually in the absence of objective signs

A

Neuralgia

25
Q

(defn.) inflammation of a nerve

A

Neuritis

26
Q

(defn.) pain along a dermatome, implying that the problem as at the level of the nerve root

A

Radiculopathy

27
Q

(defn.) neuropathy of the entire plexus

A

Plexopathy

28
Q

Polyneuropathy often presents as:

A
  • Symmetrical distal weakness and sensory loss
  • Hyporeflexia
29
Q

What is multiple neuropathy?

A

Involves more than 1 nerve but not in a symmetrical fashion

30
Q

What are some causes of multiple neuropathy?

A

Toxins, diabetes, AIDS, chronic inflammatory disease

31
Q

Most common inherited neurologic disorder?

A

Charcot-Marie-Tooth Disease (a.k.a. Hereditary Motor and Sensory Neuropathy)

32
Q

HMSN inheritance pattern?

A

Autosomal dominant inheritance - variable penetrance (not same severity in everyone)

33
Q

Demyelination of peripheral nerves due to abnormal myelin production, damage to nerves, and thickened, palpable myelin sheaths

A

CMT1 pathophysiology

34
Q

Axonal death and degeneration without a primary defect in myelin

A

CMT2 pathophysiology (less frequent)

35
Q

CMTD Clinical Presentation (3)

A
  • Slowly progressive distal symmetric muscle weakness and atrophy (champagne bottle legs)
  • Proprioception and touch mainly affected
  • Nerves can become enlarged and palpable
36
Q

Most common cause of acute flaccid paralysis?

A

Guillain-Barre Syndrome (GBS)

37
Q

When does GBS typically occur?

A

Following an infection (with flu-like sx) - infection may be CMV, EBV, mycoplasma pneumoniae, or prior vaccination

38
Q

Cells that aid in destruction in GBS?

A
  • T-cells = recognize and cause segmental demyelination
  • Macrophages
  • Antibodies
39
Q

In GBS, when myelin is destroyed, destruction is accompanied by ________.

A

Inflammation

40
Q

Are axons (often) left intact in GBS?

A

Yes, even though Schwann cells are destroyed

41
Q

What happens after 2-3 weeks of demyelination with GBS?

A

Schwann cells begin to proliferate => inflammation subsides => re-myelination begins

42
Q

Clinical features of GBS (3)

A
  • Acute, rapid, progressive inflammatory polyradiculopathy
  • predominantly MOTOR Sx
  • Ascending Sx (Legs up)
43
Q

Severe GBS can progress to loss of what funciton?

A

Function of the cervical spinal cord

44
Q

Treatment of GBS (3)

A
  • Protect airway/ventilation
  • Plasmapheresis
  • IV immunoglobulins
45
Q

What can/does compression of a nerve in the PNS lead to?

A
  • Pain
  • Reduction or loss of function (motor (sometimes also autonomic) and sensory)
46
Q

Direct mechanical damage to the nerve leads to…?

A

Loss of axonal function (crush injury)

47
Q

Compression of the vessels in the perineurium (ischemia) leads to…?

A

decreased blood flow and reduced function in the nerve

48
Q

What is impingement of a nerve?

A

Inability to “glide” along its course => explains Sx dependant on position

49
Q

Most common cause of unilateral facial paralysis?

A

Bell’s Palsy

50
Q

Bell’s Palsy is thought to be compression of the facial nerve from inflammation/edema caused by what?

A

Herpes virus

51
Q

Compression of CN7 in occurs in what narrow compartment of the temporal bone?

A

Petrous portion

52
Q

Clinical Features of Bell’s Palsy (6)

A
  • Acute onset (48 hr) of unilateral facial paralysis
  • Posterior auricular pain, earache
  • Decreased tearing
  • Hyperacusis (reduced sound tolerance)
  • Taste disturbances
  • Poor eyelid closure on affected side

BMS150 Midterm 2 (14 decks)

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