Chapter 18: Facial Pain and Neuromuscular Diseases

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1

(...) is an acute weakness or paralysis of the facial nerve without an identifiable cause.

card image

Bell palsy

2

A variety of conditions may increase the risk for developing Bell palsy. What are six?

  1. pregnancy (especially third trimester)
  2. preeclampsia
  3. diabetes
  4. hypertension
  5. obesity
  6. upper respiratory infections
3

Bell palsy is the most common cause of facial paresis and should be considered first. True or false?

False: although Bell palsy is the most common cause of facial paresis or paralysis, it is a diagnosis of exclusion.

4

Bell palsy can occur at any age, but it develops most frequently in (...)-aged adults.

young to middle

5

Infrequently, bilateral involvement is seen in Bell palsey, however, it should alert the clinician to the possibility of other diseases. What is another disease that causes rapid onset of bilateral facial weakness?

Guillain-Barré syndrome

6

Bell palsy is a self-limiting condition, and most patients will recover over (...) months.

3 to 4 months

7

As many as (...) % of patients with Bell palsy will not recover completely.

20 to 30%

8

What is the most consistently effective treatment for Bell palsy?

systemic corticosteroids

9

For treatment of Bell palsy, a (...)-day tapering course of prednisone is often prescribed, beginning at a dosage of (...) mg per day.

  1. 10-day
  2. 60 mg
10

(...) is characterized by facial flushing and sweating along the distribution of the auriculotemporal nerve.

Frey syndrome

11

What is the most widely accepted mechanism of Frey syndrome?

aberrant neuronal regeneration

12

More than 40% of patients with (...) develop clinically evident Frey syndrome as a complication of surgery.

parotidectomies

13

What are the most common presenting signs and symptoms of Frey syndrome? (4)

  1. sweating
  2. flushing
  3. warmth
  4. pain during chewing
14

What test is used to detect sweating in cases where Frey syndrome is suspected?

Minor starch-iodine test

15

To detect sweating, a Minor starch-iodine test may be used. How does this test work?

card image

The sweat mixes with the iodine, allowing to react with the starch and produce a blue color.

16

If treatment of Frey syndrome is desired, intracutaneous injections of (...) can provide long-term relief, although injections may need to be repeated.

botulinum toxin A

17

Pain fibers from the orofacial region travel to the spinal nucleus caudalis of the trigeminal nerve in a process known as (...).

trigeminal convergence

18

(...), the most serious and the most common of the facial neuralgias, is characterized by an extremely severe electric pain limited to one or more branches of the trigeminal nerve.

trigeminal neuralgia

19

Which two divisions of the trigeminal nerve are most often affected in trigeminal neuralgia?

  1. maxillary (V2)
  2. mandibular (V3)

*The ophthalmic division (V1) is affected alone in only 4% of cases.

20

The significance of trigeminal neuralgia is underscored by the fact that it has one of the highest (...) of any disease.

suicide rates

21

(...) trigeminal neuralgia has no definite etiology, although it is thought to be related to compression of the trigeminal nerve by aging blood vessels.

classical

22

(...) trigeminal neuralgia may develop in patients with multiple sclerosis, or due to compression of the nerve by tumors or arteriovenous malformations.

secondary (or symptomatic)

23

Trigeminal neuralgia characteristically affects (...) older than (...) years of age.

  1. women
  2. 50
24

In trigeminal neuralgia, patients may experience spasmodic contractions of the facial muscles during attacks, a feature that lead to the use of the term (...) for this disease.

tic douloureux (i.e. painful jerking)

25

In trigeminal neuralgia, painful episodes typically last no longer than 2 minutes, and are followed by a refractory period. How can this be clinically useful?

It distinguishes trigeminal neuralgia from stimulus-provoked odontogenic pain.

26

Specific and strict criteria must be met for an accurate diagnosis of trigeminal neuralgia. What are they? (6)

  1. onset of a pain is abrupt, often initiated by a light touch to a specific and trigger point
  2. each “spasm” is less than 2 minutes
  3. a “refractory period” follows each attack
  4. pain is be limited to the known distribution of one or more branches of the trigeminal nerve
  5. responsiveness to carbamazepine
  6. spontaneous remissions occur
27

The initial treatment for trigeminal neuralgia is pharmacological, with the anticonvulsant (...) being the first drug of choice.

carbamazepine

28

If medical management of trigeminal neuralgia fails, surgical treatment may be considered. Although this is associated with risks, (...)% of patients will be pain free 10 years or longer after surgery.

65 to 73%

29

After surgery for trigeminal neuralgia, up to 8% of patients develop distorted sensations of the facial skin called (...) or a combination of anesthesia and spontaneous pain called (...).

  1. facial dysesthesia
  2. anesthesia dolorosa
30

(...) is similar to trigeminal neuralgia except the pain is centered on the tonsil and the ear.

glossopharyngeal neuralgia

31

As with trigeminal neuralgia, two subtypes of glossopharyngeal neuralgia are recognized. What are they?

  1. classical
  2. symptomatic (secondary)
32

Like trigeminal neuralgia, glossopharyngeal neuralgia is often associated with multiple sclerosis. True or false?

False: it is uncommon for glossopharyngeal neuralgia to be associated with multiple sclerosis.

33

Glossopharyngeal neuralgia usually occurs in (...)-aged adults. There is no sex predilection.

middle to older

34

In glossopharyngeal neuralgia, paroxysmal pain may be felt in the ear due to (...).

tympanic plexus neuralgia

35

Because the pain of glossopharyngeal neuralgia is related to jaw movement, it may be confused with (...).

temporomandibular joint dysfunction (TMD)

36

In glossopharyngeal neuralgia, syncope, hypotension, seizures, bradycardia, or cardiac arrest may occur in up to 10% of patients due to (...)

vagoglossopharyngeal neuralgia

37

For most patients with classical glossopharyngeal neuralgia, the first line of therapy is (...) drugs.

anticonvulsant (e.g. carbamazepine)

38

For individuals with vagoglossopharyngeal neuralgia, (...) can be used to prevent the cardiac phenomena.

atropine

39

(...) is an immune-mediated vasculitis that affects medium and large arteries, leading to occlusion and ischemia.

Giant cell arteritis

40

Because the (...) artery is the most commonly affected site in giant cell arteritis, the condition also is known as (...).

  1. superficial temporal
  2. temporal arteritis
41

A higher frequency of giant cell arteritis in patients who express certain human leukocyte antigen (HLA) types. Which HLA type is associated with this condition?

HLA-DR4

42

(...) are more often affected by giant cell arteritis, and patients are rarely younger than (...) years.

  1. women
  2. 50 years
43

A highly characteristic feature of giant cell arteritis is (...), which is described as cramping pain of the masseter and temporalis muscles that increases with usage (chewing or talking) but is relieved by rest.

jaw claudication

44

The most significant complication of giant cell arteritis in the head and neck region is (...) due to vascu­litis of the posterior ciliary artery and ischemic neuropathy.

vision loss

45

Many patients with giant cell arteriti develop (...), which is characterized by aching pain and morning stiffness in the neck, shoulders, and pelvic girdle.

polymyalgia rheumatica

46

The diagnosis of giant cell arteritis usually is confirmed by biopsy of the (...).

temporal artery

47

Giant cell arteritis is characterized by chronic inflammation of the tunica (...) and tunica (...).

  1. intima
  2. media
48

Giant cell arteritis typically responds well to high-dose (...).

systemic corticosteroids

49

(...) is a confounding pain condition that is generally considered neuropathic in nature with both peripheral and central components.

burning mouth disorder (BMD)

50

Because (...) and (...) frequently accompany the onset of burning sensation, BMD was previously referred to as (...), although the use of this term is debated

  1. dysgeusia (altered taste)
  2. xerostomia
  3. burning mouth syndrome
51

BMD is a burning sensation of the oral mucosa. What site is most commonly affected?

tongue

52

Burning sensation of the tongue is called (...), whereas that of other mucosal surfaces is referred to as (...).

  1. glossopyrosis
  2. stomatopyrosis
53

Various local and systemic factors have been postulated to cause BMD. What are four local factors associated with this condition?

  1. xerostomia
  2. tongue thrust habit
  3. mouth breathing
  4. candidiasis
54

Various local and systemic factors have been postulated to cause BMD. What are systemic local factors associated with this condition?

  1. vitamin B deficiency
  2. diabetes mellitus
  3. hypothyroidism
  4. AIDS
55

BMD is one of the most common non-dental orofacial pains encountered in the clinical practice. True or false?

True: it affects 0.7% to 15% of adults to some degree (12.2% of postmenopausal women).

56

(...) are more likely be affected by BMD, and the syndrome is rare before the age of (...) years

  1. women
  2. 30 years (40 for men)
57

Evidence suggests that (...) should be a first line therapy in patients with BMD, and may provide greater benefit when combined with the antioxidant (...).

  1. clonazepam
  2. alpha lipoic acid (ALA)
58

(...) is defined as a persistent abnormal taste.

dysgeusia

59

Dysgeusia is less common than deficiencies in smell called (...), or deficiencies in taste called (...).

  1. hyposmia (anosmia)
  2. hypogeusia (ageusia)
60

Ischemia and infarction of the brainstem can lead to (...), which is ageusia of the ipsilateral half of the tongue.

hemiageusia

61

Why might persons with severe dry mouth suffer from both hypogeusia and dysgeusia?

Because the perception of a particular taste depends on its concentration in a liquid environment.

62

The clinician must be careful to distinguish dysgeusia disorders from parosmia, because (...)% of “flavor” information is derived from smell.

75%

63

Patients with dysgeusia may describe the new taste as metallic, foul, or rancid; the latter two are more likely to be associated with (...) than dysgeusia.

parosmia

64

Dysgeusia may require a stimulus, such as certain foods or liquids. If no stimulus is required, then the dysgeusia is classified as a (...).

phantom taste

65

Fortunately, (...)% of dysgeusia patients experience spontaneous resolution after 10 months.

66% (two-thirds)

66

(...) is a common degenerative and destructive alteration of the joints.

osteoarthritis

67

Osteoarthritis usually involves multiple joints, typically the large (...) joints.

weight-bearing

68

(...) is a late sign of osteoarthritis and is, therefore, associated with more pronounced damage.

crepitation

69

In osteoarthritis, the muscles of mastication frequently exhibit tenderness because of the constant strain of (...).

“muscle guarding”

70

Radiographically, joints affected by osteoarthritis demonstrate mild changes early in the course of the disease. What changes are seen as the disease progresses? (6)

  1. erosion of the cortical outline
  2. narrowing of the joint space
  3. flattening of the articular surface
  4. exostoses
  5. subchondral cysts
  6. ossicles
71

A (...) is a large degenerative space beneath the articular cartilage of a joint affected by osteoarthritis.

subchondral cyst

72

The inflamed synovial membrane in osteoarthritis, sometimes forms metaplastic bone granules called (...) or hyaline cartilage granules called (...).

  1. ossicles
  2. chondral bodies
73

The treatment of osteoarthritis is usually palliative and primarily consists of (...) drugs for the symptoms.

nonsteroidal antiinflammatory drugs (NSAIDs)

74

(...) is a chronic, autoimmune disorder characterized by nonsuppurative inflammatory destruction of synovium and subsequent destruction of the affected joints.

rheumatoid arthritis (RA)

75

he human leukocyte antigen (HLA) locus (...) has long been identified as the most significant genetic association for the development of RA.

DRβ1

76

In contrast to osteoarthritis, RA begins as an attack against the periarticular structures, such as the synovial membrane, causing (...).

synovitis

77

In RA, a reactive macrophage-laden fibroblastic proliferation from the synovium called a (...) creeps onto the joint surface.

pannus

78

RA affects (...) three times more frequently and is diagnosed at (...) years of age.

  1. women
  2. 35 to 45 years (25 to 35 in men)
79

For many patients with RA, only one or two joints become involved; in others, the disease rapidly progresses to debilitating (...), affecting many joints.

polyarthralgia

80

Typically, the signs and symptoms of RA become more severe over time and may lead to (...), fibrous or bony fusion of opposing articular surfaces.

ankylosis

81

The (...) is the joint most often affected by osteoarthritis and least often affected by RA.

hip joint

82

20% of patients with RA have firm, partially movable, nontender (...) beneath the skin near the affected joint, considered pathognomonic for the disease.

rheumatoid nodules

83

The TMJ is clinically affected to some degree in more than (...)% of persons with RA.

40%

84

(...) have been identified as specific serological markers of RA.

anti-citrullinated protein antibodies (ACPAs)

85

80% of patients with RA exhibit significant elevations of (...), an autoantibody thought to be directed toward an altered host IgG antibody that is no longer recognized by the body as “self.”

rheumatoid factor (RF)

86

(...) can be detected in about 50% of the patients with RA, although it is not diagnostically specific because it also may be associated with other autoimmune diseases.

antinuclear antibodies (ANAs)

87

During active phases of the disease, 90% of patients have an elevated (...); although not highly specific for RA, this test can be used to monitor the clinical course of the disease.

erythrocyte sedimentation rate (ESR)

88

Advances cases of RA may show protrusions of the synovial membrane that undergo necrosis, producing small whitish villi fragments composed of cellular debris, fibrin, and collagen called (...).

rice bodies

89

(...) have been shown to be effective in providing symptomatic relief for patients with RA.

systemic glucocorticoids

90

A number of agents appear to have the capacity to modify the course of RA, and are referred to as (...).

disease-modifying antirheumatic drugs

91

(...), a folic acid antagonist, is the most frequently used first-line agent of the disease-modifying antirheumatic drugs.

methotrexate

92

(...) are broadly defined as a group of musculoskeletal and neuromuscular conditions that involve the temporomandibular joints (TMJs), the masticatory muscles, and all associated tissues.

temporomandibular disorders (TMDs)

93

Pain in the (...) area is the most frequent clinical presentation for TMDs.

preauricular

94

The classification of TMDs remains a challenge due to limited understanding of their etiology. What are the two broad classifications of TMDs?

card image
  1. muscular
  2. arthrogenic
95

TMDs are seen primarily in (...)-aged (...), but they may affect any age and both sexes.

  1. young to middle
  2. women
96

The pain of TMDs may present as a number of symptoms. What are four?

  1. cephalalgia (headache)
  2. tinnitus (ringing in the ears)
  3. otalgia (earach)
  4. odontalgia (toothache)
97

Muscle splinting can lead to involuntary CNS-induced muscular contractions called (...), or inflammation of the the muscle fibers called (...).

  1. myospasms
  2. myositis
98

(...) pain is common in TMD, characterized by taut bands within the muscle that elicit local or referred pain on palpation and may be a source of constant deep pain.

trigger point

99

Derangements of the condyle and meniscus complex are more often associated with joint dysfunction, called (...) than with joint pain, called (...).

  1. arthropathy
  2. arthralgia
100

As many TMDs are transient and self-limiting, reversible and conservative therapies are encouraged. What are four conservative therapies?

  1. rest or immobilization
  2. application of cold or heat
  3. occlusal splints or adjustments
  4. physical therapy
101

Various medications have been used for TMD with some success. What are five types of drugs used to manage TMD?

  1. NSAIDs
  2. acetaminophen
  3. muscle relaxants
  4. benzodiazepine
  5. glucocorticoids