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CLIN MED EXAM 2 > Pathologies related to the head and neck > Flashcards

Pathologies related to the head and neck Flashcards

MS, CVA ,PosteriorCirculationCompromise ,Dizziness,CervicalMyelopathy ,Meningitis, BrainTumors, Horner'sSyndrome, ThyroidDisorders

1
Q

What is multiple sclerosis?

A

A chronic and progressive neurodegenerative disorder of the CNS

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2
Q

What population is multiple sclerosis greatest in?

A

White, biological females between 20 and 50 years of age

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3
Q

How does someone get multiple sclerosis?

A

primarily by a:
- virus leading to an auto-immune response
- presence of another auto-immune condition
- genetic link

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4
Q

What increases the risk of multiple sclerosis?

A

low vitamin D, smoking, and obesity

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5
Q

What causes multiple sclerosis?

A

demyelination
sclerotic plaque that blocks neural transmission

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6
Q

What are clinical manifestations of multiple sclerosis? S&S?

A

Specific to area of CNS involvement
Cycles of exacerbations and remissions

S&S:
Possible immune S&S
fatigue
optic neuritis (FIRST SIGN)
trigeminal neuralgia
widespread neuromusculoskeletal (NMSK) weakness

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7
Q

What is the most common and disabling symptom of MS?

A

Fatigue

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8
Q

What is optic neutitis?

A

Unilateral and painful visual disturbances
vertigo may develop due to connection with vestibular system

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9
Q

What is trigeminal neuralgia?

A

-One of the most widely distributed nerves in the head and face
-sudden and transient shock-like pain
- typically unilateral

(MS S&S)

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10
Q

What can the generalized neuromusculoskeletal weakness with MS cause?

A

-Abnormal speech or swallowing & weak voice
- Especially balance with ataxia (Incoordination) and abnormal muscle tone = FALL RISK
- Bowel and Bladder dysfunction
- Sexual dysfunction
- cognitive dysfunction
-depression due to emotional and pathogenic changes

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11
Q

What percentage of MS cases present with cognitive dysfuntion?

A

More than 50%

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12
Q

What should be a part of the systems review with multiple sclerosis?

A

Hx and Observation
Scan
- resisted testing with multiple joint weakness
- neuro:
*cranial nerves signs (particularly
optic, vestibular, and trigeminal
nerves)
Special Test
- balance tests
- central vertigo
- Lhermitte’s sign

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13
Q

What is Lhermitte’s sign?

A

Neck flexion or cough producing spine and/or LE shock-like pain

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14
Q

What are PT Implications for Multiple Sclerosis? ( What kind of referral is it?)

A

Urgent referral

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15
Q

CVAs are the ___ leading cause of death

A

2nd

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16
Q

CVAs are the ________ cause of long-term disability

A

leading

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17
Q

Which type of CVA is most common?

A

Ischemic

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18
Q

What causes an ischemic CVA?

A

Blocked blood flow, often due to artherosclerosis

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19
Q

What causes an hemorrhagic CVA?

A

a ruptured blood vessel, often due to HTN, aneurysms, and arteriovenous malformations

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20
Q

What are non-modifiable risk factors for a CVA?

A
  • age
  • african americans more than european americans
  • biological women due to longer life span than men
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21
Q

What are modifiable risk factors for a CVA?

A
  • CV disease and HTN
  • diabetes
  • Lifestyle
  • SAD and obesity
  • lack of exercise
  • tobacco use
  • cocaine and possible marijuana use
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22
Q

What is the pathogenesis for CVAs?

A

Disrupted blood flow to the brain

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23
Q

Are stroke symptoms sudden or gradual?

A

Sudden onset

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24
Q

What determines more specific S&S with a CVA?

A

Region of brain

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25
Q

What are general CVA S&S?

A
  • multi-segmental HEMI face and/or extremity numbness and weakness/paralysis
  • visual disturbance
  • speech, swallowing impaired
  • severe HA, WORST Ever
  • dizziness or fall
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26
Q

What is included in our systems review for CVA?

A

Hx and Observation
CV Scans
* Neuro tests: CN signs, UMN signs, Teitelbaum’s CPR for hemispheric lesion, vascular tests for carotid

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27
Q

What are PT implications for a CVA? (What kind of referral?)

A

Emergency Referral

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28
Q

What is the cause of Posterior Circulation Compromise?

A

CVA, pathological joint instabiliity, arthersclerosis, clot or embolism in carotid or vertebrobasialar veins, sudden arterial dissection, tumors

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29
Q

What are examples of pathological joint instability?

A

Collagen, genetic, and autoimmune conditions with AA subluxation

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30
Q

Where is the most common place for a clot or embolism with posterior circulation compromise?

A

Internal carotid

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31
Q

What causes sudden arterial dissection?

A

Excessive rotation/extension/Tx stress such as with a manipulation or trauma

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32
Q

What happens to arteries with posterior circulation compromise?

A

Ischemia of the arteries feeding the inner ear, brain stem, and cerebellum

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33
Q

What can be included with the ischemia of the arteries with posterior circulation compromise?

A
  • Vertebrobasilar insufficiency
  • Posterior cerebral arteries and their branches
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34
Q

What are affected functions of posterior circulation compromise?

A
  • Inner ear / vestibular function
  • brain stem houses cranial nerves and respiratory center
  • Cerebellum regulates coordination
  • The basilar artery most frequently supplies the trigeminal nerve
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35
Q

What are the 5 D’s and 3 N’s of posterior circulation compromise?

A

5Ds
- dysarthria
- dysphagia
- diplopia
- dizziness
- drop attacks - without loss of consciousness

& Ataxia, headache

3N’s
- Nausea
- Nystagmus
- Numbness/ paresthesias in face/extremities

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36
Q

What is ataxia?

A

Incoordination due to cerebellar disorder

** posterior circulation compromise

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37
Q

What is nystagmus?

A

Involuntary rotary eye movement creating a spinning sensation

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38
Q

What are PT implications for posterior circulation compromise? (What kind of referral?)

A

Emergency referral

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39
Q

Why can dizziness happen?

A

Vertigo, Disequilibrium, Pre syncope, Nonspecific

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40
Q

What is presyncope?

A

Near fainting/ light headedness just before LOC without illusion of spinning

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41
Q

What can cause dizziness?

A

High stress or medication

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42
Q

What is the pathogenesis of dizziness?

A

Vasoconstriction reducing posterior circulation to the brain

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43
Q

What are the PT implications for dizziness? ( what kind of referral?)

A

Emergency referral

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44
Q

What is vertigo?

A

The illusion of spinning or rotary motion caused by asymmetries in the vestibular system

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45
Q

What is the most common type of vertigo?

A

BPPV (benign Paroxysmal Positional Vertigo)

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46
Q

What makes up 90% of vertigo episodes?

A

Peripheral vertigo

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47
Q

What is the primary etiology of BPPV?

A

Unknown

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48
Q

What can be a secondary etiology of peripheral vertigo?

A

TBI (traumatic Brain Injury), migraine HAs, ischemia, or anything causing an accumulation of fluid

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49
Q

What is the pathogenesis of vertigo?

A

Crystals become free floating in semi-circular canals

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50
Q

What would we do to review for vertigo?

A

Progressive vestibular tests on CV scan

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51
Q

What makes up 10% of vertigo?

A

central vertigo

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52
Q

What primarily causes central vertigo?

A

CVA or tumor

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53
Q

What secondarily causes central vertigo?

A

-Trauma creating a TBI or upper cervical instability
-infection
- Demyelination like with MS
- migraine HAs

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54
Q

What is the pathogenesis of central vertigo?

A

Due to ischemia to cerebellum or brainstem

55
Q

Which type of vertigo is treatable by PT?

A

Peripheral vertigo

56
Q

Which type of vertigo is an emergency?

A

Central Vertigo

57
Q

When does central vertigo happen?

A

At rest

58
Q

What is dysequilibrium?

A

Unsteadiness without illusion of spinning

59
Q

What is the balance triad with dysequilibrium?

A

3 primary afferent systems contributing to postural perception and control

  • somatosensory system
  • vestibular system
  • visual pathways
60
Q

Where does the balance tried mostly happen?

A

The somatosensory system

61
Q

What is a part of the somatosensory system with the balance triad?

A

Pressure, pain, position, motion, vibration, temp throughout the body in muscles, joints, skin, fascia, ligaments, etc

**esp in the LE and trunk

62
Q

What is the etiology of dysequilibrum?

A

aging - biomechanical restrains
progressions of neuromusculoskeletal diseases

63
Q

What causes biomechanics restraints with aging? (dysequilibrium)

A

Less ROM and strength, insufficient joint receptors

64
Q

What is the pathogenesis of dysequilibrium?

A

Dysfunction of the balance triad

65
Q

What are the implications for PT with dysequilibrium?

A

Begin a trial of PT, assess and treat MSK condition to improve somatosensory function, assess and treat the balance triad basically with balance training

  • potential urgent referral for vestibular or vision component
66
Q

Where can non-specific dizziness come from?

A

Phychophysiological or cervical origins

67
Q

What are some psychophysiological examples with non-specific dizziness?

A

Psychological disorders such as anxiety phobias and depression

68
Q

What is the pathogenesis of psychophysiological dizziness?

A

Vasoconstriction with SNS response

69
Q

What are clinical manifestations and S&S of phychophysiological dizziness?

A

Motion sickness
giddiness
feeling removed from their body
sensations of floating
subjective postural imbalances with normal balance testing

70
Q

What are the PT implications of psychophysiological dizziness? (what kind of referral?)

A

Urgent physiological consult

71
Q

What is the pathogenesis of cervicogenic dizziness?

A

Abnormal afferent input from the neck to the TCN - hypersensitivity

72
Q

What are the clinical manifestations and S&S of Cervicogenic dizziness?

A

Dizziness with neck motion
other TCN symptoms
No illusion of spinning or nystagmun

73
Q

What are the PT implications of cervicogenic dizziness?

A

Begin a trial of PT to assess and address cervical dysfunction

74
Q

What is cervical myelopathy?

A

Slow, gradual and often progressive ischemic compression on cord

75
Q

T/F cervical spine is the most common area of the spine for myelopathy?

A

FALSE
- LEAST common

76
Q

What is the etiology of cervical myelopathy?

A

Most commonly due to degenerative spinal changes

  • lax and buckling ligamentum flavum
  • age-related joint changes
  • age related disc changes
  • vertebral body collapse / fx
  • pathological instability (i.e. spondylolisthesis)
77
Q

What is cervical myelopathy NOT due to?

A

Trauma

78
Q

How much of the time is cervical myelopathy malignant?

A

20% of the time

79
Q

What can happen with cervical myelopathy but is RARE?

A

Central disc herniation

80
Q

What is the history of cervical myelopathy?

A

Slow, gradual and often progressive onset

81
Q

What will we find with our observation with cervical myelopathy?

A

Not acute so not likely to splint
- increased tone or spasticity
- incoordination

82
Q

What can we expect with A/PROM with cervical myelopathy?

A
  • Primarily limited with UE neuro symptoms into neck ext
  • other neck directions may be limited and symptomatic
83
Q

What will we find with PA stress tests for cervical myelopathy?

A

Possibly positive for neuro symptoms

84
Q

What is the CPR for myelopathy?

A

Cooks CPR (+)

85
Q

What neuro S&S do we expect with cervical myelopthy?

A

Primarily in bilateral UEs
- multi segments diminished to light and sharp touch plus to vibration, temp, and/or, 2 pt discrimination
- multi segmental hyperrefexia or clonus with DTRs
- loss of proprioception
- positive UMN tests like hoffman’s babinski, etc and superficial reflexes
- dural mobility negative due to gradual onset

86
Q

Where can cervical myelopathy extend to if it is more severe?

A

trunk and bilateral LEs

87
Q

What are PT implications for cervical myelopathy?

A

MD referral - EMERGENCY
Stabilize pt

88
Q

What is meningitis?

A

An infection leading to inflammation of the brain and spinal cord meningeal membranes

89
Q

What is the incidence of meningitis?

A

Rare

90
Q

What population is viral meningitis most common in?

A

Adults

91
Q

What is viral meningitis caused by?

A

Enteroviruses from GI tract

92
Q

What population is bacterial meningitis most common in?

A

young children

93
Q

What is the most common cause of bacterial meningitis?

A

Streptococcus pneumonia

94
Q

What are staph infections associated with?

A

Surgery, central lines, and trauma

95
Q

What are the clinical manifestations for recent viral meningitis?

A

Infection and GI S&S

96
Q

What are the clinical manifestations for recent bacterial meningitis?

A

Infection and respiratory S&S

97
Q

What are additional S&S of meningitis?

A

Constitutional
neck pain/stiffness
photophobia
HA

98
Q

What are S&S of increased intracranial pressure with meningitis?

A
  • Altered mental status
  • varied UMN deficits (including CN VI Abducens that is susceptible)
  • Diplopia
  • Painful eye motion
  • seizures
99
Q

What are S&S for review with meningitis to help up RULE it OUT?

A

Jolt Accentuation of HA test
- HA worsened by neck rotation 2-3x in a second
- most sensitive clinical test to RULE OUT meningitis

100
Q

What are the best clinical tests to rule IN meningitis?

A

While supine:
* Kernig test: low back and posterior thigh pain with combined hip flexion and knee extension
* Brudzinskin test - neck flexion produces hip and knee flexion

101
Q

What are the PT implications with meningitis?

A

Emergency Referral

102
Q

What is the mean age for a brain tumor?

A

60 years old

103
Q

Brain tumors are the ___ most common primary tumor in children

A

2nd

104
Q

What is the most common brain tumor in adults?

A

Metastatic

105
Q

What are 50% of metastatic brain tumors from?

A

The lung

**others from breast and melanoma (skin)

106
Q

What is the pathogenesis of brain tumors?

A

Compression of cerebral tissue, at times erosion of bone with tumor growth

107
Q

What can brain tumors lead to?

A

Edema and ICP

108
Q

When are brain tumors most asymptomatic? Why?

A

In early stages due to brain’s ability to adapt to slow growing tumors

109
Q

What are S&S of brain tumors?

A
  • Cancer S&S plus specific S&S related to the area of the brain
  • HA that is increased with activities further increasing ICP
110
Q

What kind of neurological symptoms are present with a brain tumor?

A
  • Uni or bilateral with varied UMN S&S based on area of brain affected
  • Cranial nerve VI (abducens)
  • diplopa
  • painful eye motion
  • seizures
  • speech impairment
111
Q

What is the incidence of horner’s syndrome

A

Rare

112
Q

What is the etiology of Horner’s syndrome?

A
  • pancoast tumor in apical portion of lung that compresses sympathetic ganglion at cervicothoracic junction
  • intracranial pathology
  • conditions influencing carotid artery and venous sinus
113
Q

What is the pathogenesis of horner’s syndrome?

A

Interruption of sympathetic nerve supply to the eye

114
Q

What are clinical manifestations / S&S of Horner’s Syndrome?

A

Ipsilateral
* Ptosis (droopy eye lid)
* Miosis (Constricted pupil)
* Lack of facial sweating
* Possibly pain in T2-4 dermatomal region due to shared spinal nerve innervation in the area of the Pancoast tumor

115
Q

Where is the thyroid?

A

Anterior, lower neck on both sides of trachea

116
Q

What are the functions of the thyroid?

A
  • Regulate metabolism
  • increase protein synthesis
  • calcium and phosphate balance with bone, kidney, and GI tract together
117
Q

What is the thyroid regulated by?

A

hypothalamus and pituitary gland

118
Q

What do hormones act on?

A

ALL body tissues

119
Q

What are the different types of thyroid disorders?

A

Hypo or hyper active

120
Q

Why is it harder to detect thyroid disorders in older individuals?

A

It masquerades as other illnesses due to multi-system influence

121
Q

What are the risk factors for thyroid disorders?

A

Biological women, particularly in middle ages more than men

  • increases with age
122
Q

What does hyperthyroidism do?

A

elevates metabolic activity in every system

123
Q

What is the most common form of hyperthyroidism?

A

Grave’s disease (autoimmune condition)

124
Q

What is the pathogenesis of hyperthyroidism?

A

Increased hormonal secretion

125
Q

What are clinical manifestations and S&S for review with hyperthyroidism?

A
  • Possible immune S&S
  • Symmetric enlargement of thyroid and possible dysphagia
  • exophthalmos (eye protrusion)
  • proximal muscle weakness
  • higher metabolic activity
126
Q

What are some examples of things that can happen with higher metabolic activity as a result of hyperthyroidism?

A
  • Heat and exercise intolerances, excessive sweating and fatigue
  • Weight loss despite increased appetite
  • nervousness, hyperactivity, insomnia, and mood alterations
  • palpitations and tremors
    -low endurance
127
Q

What does hypothyroidism do?

A

Slows body’s metabolism

128
Q

What is the most common thyroid disorder in north america?

A

Hypothyroidism

129
Q

What is hypothyroidism from?

A
  • Genetic or autoimmune
  • possible damage from surgical ablation, radiation therapy, or medications
130
Q

What is the pathogenesis of hypothyroidism?

A

Decreased hormonal secretion

131
Q

What are some clinical manifestations and S&S for review with hypothyroidism?

A

Possible autoimmune S&S
Lower metabolic activity
large and spinal joint pain/stiffness
proximal weakness

132
Q

What are some examples of lower metabolic activity with hypothyroidism?

A
  • slow and steady weight gain
  • myxedema
  • fatigue and lethargy
  • cold intolerances
  • dry skin, hair, and nails
133
Q

What is myxedema with hypothyroidism? What causes it?

A

Collection of non-pitting boggy edema, particularly around supraclaviciular fossa, eyes and distal extremities

  • due to build up of sugars and proteins attracting and retaining water
  • may also thicken oral and throat structures thus impairing swallowing, breathing, and speech

CLIN MED EXAM 2 (4 decks)

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