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MHD2 > Block 8 (Neuro) - L7, L2, L3 > Flashcards

Block 8 (Neuro) - L7, L2, L3 Flashcards

1
Q

True or false - the brain parenchyma itself does not produce pain.

A

True

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2
Q

What structures in the brain are sensitive to pain?

A
  1. Skin, subcutaneous tissue, muscles, extracranial arteries, periosteum of the skull
  2. Delicate structures of the eye, ear, nasal cavities, and paranasal sinuses
  3. Intracranial venous sinuses and tributaries
  4. Dura at the base of the brain and arteries within the dura and pia-arachnoid
  5. Optic, oculumotor, trigeminal, glossopharyngeal, vagus, first three cervical nerves
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3
Q

What is a primary headache?

A

Condition in which the headache is the primary manifestation and no underlying disease process is present

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4
Q

What is a secondary headache?

A

Condition in which the headache is the secondary manifestation of an underlying disease process

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5
Q

What are the most common headaches?

A
  1. Tension-type
  2. Migraine and variants
  3. Provoked by fever or hunger
  4. Nasal, paranasal, ear, tooth, and eye disease
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6
Q

What are the red flags in a rapid headache evaluation?

A
  1. Split second, unexpected, worst/new, loss of consciousness, vertigo, vomiting
  2. Fever and skin rash
  3. Immunosupressed state
  4. Coagulopathy and anticoagulation
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7
Q

What are diagnoses to have on the differential when a headache involves new/worst/split second/unexpected characteristics, loss of consciousness, vertigo, and/or vomiting?

A

Aneurysmal subarachnoid hemorrhage, cerebellar hematoma

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8
Q

What are diagnoses to have on the differential when a headache involves fever and skin rash?

A

Meningitis

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9
Q

What are diagnoses to have on the differential when a headache involves an immunosuppressed state?

A

Cryptomeningitis and toxoplasmosis

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10
Q

What are diagnoses to have on the differential when a headache involves a person with coagulopathy or anticoagulation?

A

Subdural or intradural hematoma

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11
Q

What is a migraine?

A

A genetic condition in which a person has a predisposition to episodic headaches, GI dysfunction, or neurologic dysfunction; does not require severity to be considered a migraine

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12
Q

What are key clinical questions to ask regarding a migraine?

A
  1. Do you have nausea or feel sick to your stomach with your headache?
  2. Does light bother you more with a headache than without?
  3. Does the headache limit you from working, studying, or doing what you need to do?
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13
Q

What are the typical clinical symptoms associated with migrains?

A
  1. Periodic, usually unilateral and pulsatile
  2. Begin in late childhood or early adult life (from menarche to menopause)
  3. Recur with diminishing frequency throughout life
  4. Usually stereotypical
  5. Most patients will limit activities due to/during the headache
POUND:
Pulsatile
One-day duration
Unilateral
Nausea
Disabling
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14
Q

In which gender are migraines more common?

A

Female (16% vs. 6% in males)

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15
Q

What are typical triggers of migraines?

A
  1. Stress
  2. Lack of sleep
  3. Hunger
  4. Hormonal fluctuations
  5. Certain foods
  6. Alcohol and nitrates
  7. Weather changes
  8. Smokes, scents, fumes
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16
Q

What are the four phases of a migraine?

A
  1. Prodrome
  2. Aura
  3. Pain
  4. Postdrome
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17
Q

Describe the timing of a migraine prodrome.

A

Occurs 6 hours to 48 days before the headache

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18
Q

What are the symptoms seen during the migraine prodrome?

A
  1. Depression
  2. Irritability
  3. Drowsiness
  4. Fatigue
  5. Yawning
  6. Rhinorrhea/lacrimation
  7. Hunger/thirst
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19
Q

What are the symptoms seen during the migraine aura?

A

Can be visual (most common), sensory (numbness/tingling), motor, brainstem (dizziness/diplopia), or cortical (aphasia)

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20
Q

When does the migraine aura occur most commonly?

A

Before the headache; can also be during and after

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21
Q

Describe the timing of a migraine aura.

A

Usually develops over 5-20 minutes and lasts under 60 minutes; the headache usually occurs within 60 minutes

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22
Q

What is an acephalgic migraine?

A

A migraine aura without a headache

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23
Q

What is a common migraine?

A

A migraine without an aura

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24
Q

What causes the migraine aura?

A

Spreading cortical depression

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25
Q

Describe the features of a visual aura of a migraine.

A

Blind spot near the center of vision that prohibits reading; occurs as peripheral, flashing, pulsating bands of light spread out across the visual field

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26
Q

Describe the features of migraine pain (location, onset, duration, associations).

A

May be in the head (most common), abdomen (abdominal migraine), or chest (precordial migraine;

Onset is gradual over minutes to hours

Duration is hours to days

Can be associated with photophobia, phonophobia, nausea, vomiting, osmophobia, thermophobia

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27
Q

Describe the theory of spreading cortical depression (SCD).

A

A genetically susceptible patient has a multifactorial defect in brain metabolism leading to a gain in NMDA-receptor function (excitatory receptor). Activation leads to a burst of focal cerebral activity causing local hyperemia and positive symptoms (usually in the occipital lobe). The burst is followed by a loss of neuronal activity (cortical depression). This advances at 3 mm/min until there is a change in cortical architecture.

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28
Q

What is the Trigeminovascular reflex?

A

Trigeminal nerves wrap around pain sensitive structures, release local neuropeptides, and convey information to the trigeminal nucleus in the brainstem. This is associated with release of neuropeptides including CGRP, substance P, and neurokinin A. This may lead to neurogenic inflammation and evoke vasodilation of pain-producing structures. This creates a feedback loop with the trigeminal pathway.

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29
Q

What are the symptoms and timing of the postdrome?

A

Mood changes (euphoria, fatigue), impaired concentration, scalp/muscle tenderness; present for several hours after the event

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30
Q

What are the aspects of optimizing treatment of acute attacks of migraine?

A
  1. Treat early in the attack when the pain is still mild.
  2. Simple analgesics are considered first line for mild to moderate migraines, followed by triptans.
  3. Use effective doses.
  4. Avoid medications with high overuse potential, especially butalbital-containing medications
  5. Treat associated symptoms
  6. Consider AE and contraindications
  7. Try to minimize the use of medications
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31
Q

Triptans are agonists at ___ receptors.

A

5HT 1BD receptors

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32
Q

What are the contraindications of triptans?

A

Broadly, avoid in those with vascular risk factors

Patients with/at risk for ischemic heart disease, uncontrolled HTN, renal disease, pregnancy, basilar migraine, hemiplegic migraine, within 24 hours of use with ergotamine, if patient is on an MAO inhibitor

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33
Q

What are the AE of triptans?

A
  1. Warm/hot sensations
  2. Tightness
  3. Tingling
  4. Feelings of heaviness or pressure

Occur in nearly any part of the body, most common in face, limbs and chest

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34
Q

What is serotonin syndrome?

A

Severe leg-predominant rigidity, dysautonomia (diarrhea, excessive lacrimation, hyperactive bowel sounds), and encephalopathy characterized by myoclonus, hyperreflexia, and seizures caused by excessive activation of 5-HT 1a and 5-HT2 receptors within 24 hours of medication exposure/change

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35
Q

What drugs can lead to serotonin syndrome?

A 
SSRI, TCA
MAO-B
Ecstasy
Triptans, ergotamine
Lithium, ECT
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36
Q

What are the two ergot alkaloids that can be used for migraines?

A
  1. Ergotamine

2. DHE

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37
Q

What are the side effects of ergotamine?

A

Extremely nauseating, causes uterine contractions (DHE has less of these_

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38
Q

What are the contraindications of ergots?

A

Ischemic cardiac, cerebrovascular, or peripheral vascular disease, collagen vascular disease or vasculitis, cardiac valvular disease, uncontrolled hypertension, use within 24 hours of triptan therapy, hemiplegic/basilar migraine, prior evaluation of patients with risk factors for CAD, renal or hepatic impairment, pregnancy/breastfeeding, >60 y/o

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39
Q

When should preventive therapy be considered for migraines?

A
  1. Incidence of attacks > 2-3 per month
  2. Attacks are severe and impair normal activity
  3. Patient is psychologically unable to cope with attacks
  4. Optimal therapies have failed or produced serious AE
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40
Q

What are some alternative therapies for migraines?

A
  1. Avoid triggers
  2. Relaxation, biofeedback, acupuncture
  3. Physical therapy
  4. Dietary/vitamin supplementation
  5. Botulinum toxin (only for chronic migraine headache)
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41
Q

Cluster headaches are more common in ___ (gender). Peak incidence occurs at ___ (age). Often associated with heavy ___ use. More common in ___ (months). Commonly occur at ___.

A

Men; 40-49 y/o; smoking and alcohol; spring and autumn; night

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42
Q

Describe the timing of cluster headaches.

A

Last 6-12 weeks
Occur every year or two
1-4 attacks/day lasting 20 minutes to 3 hours
Rapid onset over 15-30 minutes

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43
Q

Where are cluster headaches localized?

A

Unilateral (invariably); can switch sides in subsequent attacks

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44
Q

What are two issues associated with cluster headaches?

A

Partial Horner’s and unilateral rhinorrhea

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45
Q

How are cluster headaches treated?

A

Treatment is limited by headache duration (short); oral medications are not great. Effective medications include inhaled oxygen, injectable sumatriptan, nasal spray triptans, intranasal lidocaine, and intranasal DHE. Prednisone may also help.

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46
Q

What is the most common form of headache?

A

Tension-type headaches

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47
Q

What are the clinical features of tension-type headaches?

A
  1. Bilateral pain lasting >30 minutes, usually 4-6 hours
  2. Band-like head pain with a pressing or tightening quality
  3. Mild to moderate intensity
  4. Not aggravated by routine activity
  5. No nausea/voiting
  6. Phonophobia and photophobia can occur, but not both
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48
Q

How are tension-type headaches treated?

A
  1. Screen for depression and sleep disorders
  2. May respond to TCAs (amitriptyline)
  3. Physiotherapy, biofeedback
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49
Q

What is trigeminal neuralgia?

A

Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting 1+ divisions of the trigeminal nerve.

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50
Q

What is the peak incidence of trigeminal neuraliga?

A

60-70 y/o, unusual before 40 y/o

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51
Q

What is the most common disease associated with trigeminal neuralgia?

A

MS

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52
Q

Trigeminal neuralgia is usually worse with ___.

A

Talking or eating (many patients go to the dentist first)

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53
Q

Compare trigeminal neuralgia and cluster headaches.

A

TN usually involves the jaw and is lightening-like; cluster headaches are usually behind the eye and last much longer

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54
Q

What is the first line treatment for TN?

A

Carbamazepine

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55
Q

What is temporal arteritis?

A

Systemic vascular disease with inflammation of median and large arteries of the neck

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56
Q

When should temporal arteritis be on the differential?

A

New or different headache in patients > 60 y/o; may report temple pain.

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57
Q

What causes the jaw claudication seen in temporal arteritis?

A

Ischemia of temporalis and masseter muscles

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58
Q

Temporal arteritis can lead to ___ from ischemic optic neuropathy.

A

Vision loss

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59
Q

What is the gold standard for diagnosis of temporal arteritis?

A

Biopsy (can also use elevated inflammatory markers)

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60
Q

How is temporal arteritis treated?

A

Steroids

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61
Q

What are the clinical features of pseudotumor cerebri?

A
  1. ICP >/= 250 mm H2O
  2. No localizing features
  3. No mass lesion or enhancement
  4. Normal CSF content
  5. No CVT (central venous thrombosis)

Headaches are the presenting features in most cases; can also have pulsatile tinnitus, transient visual obscuration

62
Q

What are the most common patients with pseudotumor cerebri?

A

Young female with increased BMI

63
Q

What is seen on physical exam in pseudotumor cerebri?

A

Papilledema

64
Q

How is pseudotumor cerebri treated?

A

Acteazolamide, topiramate, surgery

65
Q

What type of headache can occur after a spinal tap?

A

Low-pressure headache

66
Q

What is a primary exertional headache?

A

Pulsating headache lasting from 5 minutes to 48 hours and occurring only during or after physical activity

67
Q

What type of patients get exertional headaches?

A

Younger patients (10-48 y/o), usually male

68
Q

How are primary exertional headaches treated?

A

Beta-blockers, indomethacin

69
Q

Why are lower motor neuron signs seen?

A

Lower motor neuron signs are seen in a limb if some of its muscles are innervated by anterior horn cells (lower motor neurons) affected at the level of the spinal cord lesion.

70
Q

Why are upper motor neuron signs seen?

A

Upper motor neuron signs are seen in a limb if a more rostral spinal cord lesion affects the corticospinal tract descending to the anterior horn cells which innervate the muscles in that limb.

71
Q

Compare the clinical signs of upper and motor neuron lesions regarding weakness.

A

UMN: more diffuse
LMN: more focal

72
Q

Compare the clinical signs of upper and motor neuron lesions regarding atrophy.

A

UMN: mild, general
LMN: severe, focal

73
Q

Compare the clinical signs of upper and motor neuron lesions regarding atrophy VERSUS weakness.

A

UMN: severe weakness with relatively mild atrophy
LMN: Severe atrophy with milder weakness

74
Q

Compare the clinical signs of upper and motor neuron lesions regarding fasciculations.

A

UMN: never seen
LMN: may be present

75
Q

Compare the clinical signs of upper and motor neuron lesions regarding muscle tone.

A

UMN: increased (spasticity) - except in spinal or neurogenic shock
LMN: decreased

76
Q

Compare the clinical signs of upper and motor neuron lesions regarding muscle stretch reflex.

A

UMN: increased - except in spinal or neurogenic shock
LMN: decreased to absent

77
Q

Compare the clinical signs of upper and motor neuron lesions regarding clonus.

A

UMN: may be present - except in spinal or neurogenic shock
LMN: never present

78
Q

Compare the clinical signs of upper and motor neuron lesions regarding pathological reflexes (Babinski sign).

A

UMN: may be present - except in spinal or neurogenic shock
LMN: absent

79
Q

What roots innervate the deltoid and biceps muscles?

A

C5-C6

80
Q

What roots innervate the triceps muscles?

A

C7-C8

81
Q

What roots innervate the interossei and flexor digitorum muscles?

A

C8-T1

82
Q

What roots innervate the iliopsoas (hip flexor) and quadriceps?

A

L2-L4

83
Q

What roots innervate the tibialis anterior (foot dorsiflexor)?

A

L4-L5

84
Q

What roots innervate the gastrocnemius (foot plantar flexor)?

A

S1-S2

85
Q

What is radicular (root) pain?

A

Lightning, stabbing, shooting, or electrical pain in the dermatomal distribution of a dorsal root.

86
Q

What does the presence of radicular pain indicate?

A
  1. Dorsal root inflammation

2. Compression by an extramedullary lesion

87
Q

In addition to radicular pain, an extramedullary lesion may also cause what type of pain? An intramedullary lesion may cause what type of pain?

A

Constant, dull, local pain

Diffuse pain or no pain at all

88
Q

How is radicular pain treated?

A

Analgesics, anti-inflammatory medications, or nerve block procedures, in addition to surgical removal of causative lesions

89
Q

How is chronic root pain treated?

A

Anticonvulsants (gabapentin, carbamazepine) or antidepressants (duloxetine, amitriptyline)

90
Q

What happens when there is a spinal cord lesion in the spinothalamic tract?

A

Pain and temperature deficit in the CONTRALATERAL body

91
Q

A suspended pattern of pain and temperature deficit with sacral sparing indicates what type of lesion?

A

Intramedullary (disrupts the decussating spinothalamic fibers)

92
Q

A sensory deficit of pain and temperature up to a level with sacral involvement indicates what type of lesion?

A

Extramedullary

93
Q

What happens when there is a spinal cord lesion in the dorsal column pathways?

A

Ipsilateral position sense and vibration deficits

94
Q

Compare the pain seen in intra- vs. extra-medullary lesions.

A

I: diffuse or none
E: radicular

95
Q

Compare the sensory loss seen in intra- vs. extra-medullary lesions.

A

I: suspended
E: to a level or sacral

96
Q

Compare the sacral sparing seen in intra- vs. extra-medullary lesions.

A

I: present
E: absent

97
Q

True or false - a spinal cord lesion at a certain level can be approximated by the vertebral level.

A

False - the bony vertebral column is longer than the spinal cord

98
Q

What is a transection or transverse myelopathy?

A

Complete or nearly complete lesion encompassing the cross-sectional extent or breadth of the spinal cord at one, or a few adjacent, levels.

99
Q

What is a transection or transverse myelitis?

A

Complete or nearly complete lesion encompassing the cross-sectional extent or breadth of the spinal cord at one, or a few adjacent, levels caused by inflammation or infection

100
Q

What types of signs are seen in transection/transverse myelopathy?

A

Dermatomal sensory loss
LMN signs
UMN signs may be present in the limbs innervated by LMNs caudal or inferior to the level of the lesion

101
Q

What may be seen when a transection myelopathy is caused by severe, acute trauma?

A

Spinal or neurogenic shock (UMNs will emerge later than expected)

102
Q

In addition to severe acute trauma, what are other causes of transverse myelopathy?

A

Extramedullary lesions: tumors (especially vertebral metastases), spinal stenosis, extradural hemorrhage, abscess

Severe spinal cord ischemia

103
Q

What is spinal stenosis?

A

Spinal cord compression from degeneration of the bony spinal column and herniated intervertebral discs

104
Q

What can cause transverse myelitis?

A

Viral infections, reactions to vaccines, autoimmune demyelination of the spinal cord (e.g. MS)

105
Q

What is Brown-Sequard syndrome?

A

AKA - hemisection

A lesion affecting approximately the left or right half of the spinal cord cross-section at one level

106
Q

What are the presenting signs of a Brown-Sequard lesion?

A
  1. Contralateral pain and temperature deficit
  2. Ipsilateral deficit of vibration and position sense
  3. Ipsilateral weakness with LMN and UMN signs if there is involvement of the anterior horn cells and corticospinal tract on one side
107
Q

What are common causes of a hemisection?

A

Trauma, extramedullary tumors, herniated discs with degenerative disease of the bony spine

108
Q

What is syringomyelia?

A

Spinal cord lesion caused by a syrinx (cavity) within or near the center of the cord (intramedullary lesion)

109
Q

Syringomyelia usually occurs in which levels of the spinal cord?

A

Cervical or thoracic

110
Q

What are the presenting signs of syringomyelia?

A
  1. Disruption of decussating STT leads to pain and temperature deficit over the affected dermatomes; sacral dermatomes are spared = suspended sensory level with sacral sparing (vest-like)
  2. Weakness may occur if the anterior horn cells or corticospinal tract get involved

Dorsal columns are spared (preserved vibration and position sense)

111
Q

What are some causes of syringomyelia?

A

Severe spinal cord injury, traumatic cervical spinal cord hemorrhage resorbtion, intramedullary tumors, impaired CSF flow (typically from Chiari malformation)

112
Q

What does the anterior spinal artery supply?

A

Anterior 2/3 of the spinal cord

113
Q

What can cause occlusion of the anterior spinal artery?

A

Atherosclerotic disease of the aorta, complication of surgery for an aortic aneurysm, aortic dissection in a patient with HTN (leads to thrombosis and occlusion), transverse myelopathy

114
Q

Where does severe spinal cord ischemia occur typically?

A

Lower thoracic or upper lumbar spinal cord

115
Q

What are the presenting signs of severe spinal cord ischemia?

A
  1. Corticospinal tract involvement - paraplegia with UMN signs in the lower limbs
  2. Thoracic level of sensory loss without sacral sparing to pain and temperature

Vibration and position sense remain normal

116
Q

What are common initial symptoms of severe spinal cord ischemia?

A

Back or radicular pain

117
Q

What is a classic cause of posterolateral syndrome (subacute combined degeneration)?

A

B12 deficiency

118
Q

What happens in a B12 deficiency in the spinal cord?

A

Demyelination and degeneration of the white matter, usually at thoracic levels; combined degeneration refers to the dorsal and lateral columns both being involved

119
Q

What are the presenting signs of posterolateral syndrome (subacute combined degeneration)?

A
  1. Vibration and position sense are reduced or lost in the lower limbs (unsteadiness, falling)
  2. Positive Romberg sign
  3. Spastic paraparesis from involvement of the corticospinal tract

Pain and temperature are not affected

120
Q

What are two other rare causes of posterolateral syndrome (subacute combined degeneration)?

A

Copper deficiency, HIV

121
Q

What is amyotrophic lateral sclerosis (ALS)?

A

Degenerative disease where upper and lower motor neurons are selectively and progressively destroyed for unknown regions

122
Q

What are the presenting signs of ALS?

A
  1. Initial LMN signs in the upper limbs and UMN signs in the lower limbs
  2. Sensory pathways are unaffected
  3. Bowel and bladder functions remain normal
  4. No radicular pain
  5. Prominent fasciculations
123
Q

What are some clinical manifestations of ALS?

A

Fine hand movements impaired, interosseous muscle wasting, foot drop, early fatigue on walking, head drop, drooling, tongue wasting, difficulty chewing/swallowing/speaking

124
Q

What causes tabes dorsalis?

A

Syphilis

125
Q

What happens in tabes dorsalis?

A

Lesions of the dorsal roots and dorsal spinal cord

Causes severe radicular pains in the lower limbs
Dorsal columns degenerate, impairing vibration and position sense in the lower limbs
Most sensory fibers degenerate at the dorsal roots, creating loss of all sensation in the lower limbs
Reflexes are lost (arcs disrupted)
Strength remains intact because motor neurons and corticospinal tracts are spared

126
Q

What are Charcot joints?

A

Severe traumatic injury and deformation of ankle joints due to sensation loss

127
Q

Describe the process of normal muscle contraction.

A
  1. Lower motor neurons are depolarized and fire APs.
  2. When the AP reaches the motor neuron terminal, calcium influx facilitates presynaptic release of ACh from vesicles.
  3. ACh binds at nicotinic AChR in the end plate of the post-synaptic muscle membrane, activating ion channels and creating an EPP.
  4. The EPP typically exceeds the threshold for a muscle fiber AP, which spreads through the muscle fiber, causing contraction.
128
Q

What limits the effect of ACh and its EPP?

A

Synaptic AChE

129
Q

What happens to ACh release during repetitive muscle contractions?

A

Lesser amounts of ACh are released and the EP amplitudes are decreased. However, they still remain above the threshold for generating muscle fiber APs and adequate muscle contraction is still achieved. This is the safety factor at NMJs.

130
Q

___ is an autoimmune disorder of the presynaptic NMJ. ___ is an autoimmune disorder of the postsynaptic NMJ.

A

Lambert-Eaton myasthenic syndrome;

Myasthenia gravis

131
Q

What does the immune system attack in MG?

A

AChRs

132
Q

What is seen on EM in MG?

A

Loss of normal architecture and folding of the post-synaptic NMJ

133
Q

What is an important factor in the etiology of MG?

A

Thymus (most patients have some abnormality - glandular enlargement, hyperplasia, thymoma)

134
Q

When does MG present?

A

Any age

135
Q

What are the signs and symptoms of MG?

A
  1. Fatigue and weakness of skeletal muscles (difficulty chewing, talking, climbing stairs, watching a movie, etc.)
  2. Initial symptoms: ptosis, diplopia, dysarthria, dysphagia
136
Q

What is not affected in MG?

A

Sensation, muscle stretch reflexes, cognition, and higher cortical functions

137
Q

What is ocular myasthenia?

A

A restricted form of MG in which patients only have ptosis or diplopia

138
Q

What is neonatal myasthenia?

A

Symptoms in healthy newborns of mothers with MG until the Ab wash out of their system

139
Q

What is a myasthenic crisis?

A

Profound weakness causing quadriplegia, with the patient unable to speak, swallow, or breathe, typically triggered by a serious infection or other systemic illness

Note - sensation and reflexes remain normal

140
Q

What is on the differential in addition to MG?

A
  1. Extensive infarction of the brain stem (hyperreflexia would be noted)
  2. Guillain-Barre syndrome (areflexia and sensory impairment)
  3. Acute paralysis from a SC lesion (spares CN, localizing level of sensory loss)
141
Q

How is MG diagnosed?

A
  1. Clinical history
  2. Positive edrophonium (Tensilon) test
  3. EMG - repetitive nerve stimulation or single fiber jitter analysis demonstrates NMJ abnormalities typical of MG
  4. Presence of serum AChR
142
Q

What is the most specific diagnostic test for MG?

A

Presence of serum AChR antibodies

143
Q

How is MG treated?

A
  1. Oral anticholinesterase drugs (pyridostigmine)
  2. Immunosuppressant drugs (corticosteroids, azathioprine, mycophenolate, cyclosporine)
  3. Thymectomy (younger patients)
144
Q

What is an AE of anticholinesterase drugs?

A

Cholinergic crisis (weakness, sweating, salivation, diarrhea, excessive urination)

145
Q

How is a myasthenic crisis treated?

A

IVIG or plasmaphoresis

146
Q

What are the signs and symptoms of Lambert Eaton?

A

Muscle fatigue and weakness of the proximal muscles of the shoulders and hips, as well as the trunk (mimicks weakness seen in myopathy)

Autonomic symptoms - dry mouth, orthostatic hypotension, erectile dysfunction

No sensory deficits, cognitive symptoms, or pain
Do not usually involve the eyes, swallowing, or speech

147
Q

What happens to muscle stretch reflexes in Lambert Eaton?

A

Appear decreased, but reappear along with improved strength after a brief period of isometric exercise

148
Q

The majority of patients with Lambert Eaton have a ___ related to the autoimmune problem.

A

Small cell carcinoma of the lung

149
Q

How is Lambert Eaton diagnosed?

A
  1. EMG - repetitive nerve stimulation and other tests

2. Ab to voltage-gated calcium channel

150
Q

What is the target of the immune system in Lambert Eaton?

A

Voltage-gated calcium channels

151
Q

How is Lambert Eaton treated?

A
  1. Search for and treat small cell carcinoma of the lung
  2. Guanidine or 3,4-diaminopyridine (enhance ACh release)
  3. Immunosuppressants and plasmapheresis

MHD2 (34 decks)

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