Chapter 49 Fibromyalgia Flashcards
KEY POINTS 1. Fibromyalgia can be considered a discrete condition as well as a construct to help explain how/why individuals have multifocal pain and other somatic symptoms in spite of the lack of nociceptive input (i.e., peripheral damage/inflammation) that adequately accounts for the pain. 2. The primary abnormality identified to date in FM and related pain syndromes is an increased gain or volume control in CNS pain processing (i.e., secondary hyperalgesia/allodynia). 3. It is likely that
Fibromyalgia (FM)
a medical condition that appears to
involve disordered afferent processing and which may be associated with multiple symptoms including: chronic widespread pain, fatigue, sleep disturbances, cognitive alterations, mood disturbances, dysesthesias, stiffness, poor balance, oral and ocular symptoms (e.g., keratoconjunctivitis sicca), headaches, sexual dysfunction, impaired physical function, and
psychological distress
The core symptoms seen
in FM and many other “central” pain syndromes are
multifocal pain, fatigue, insomnia, cognitive or memory problems, and, in many cases, psychological distress.
Common disorders that may coexist with fibromyalgia
include
regional musculoskeletal pain syndromes (e.g., low back pain, temporomandibular joint disorder [TMD]), chronic fatigue syndrome, irritable bowel syndrome (IBS), irritable bladder syndrome or interstitial cystitis, headaches, vulvodynia, and pelvic pain (often attributed to endometriosis).
when individuals have multifocal pain combined with other somatic symptoms
in clinical practice, it is useful to consider a fibromyalgia-like
or central sensitivity syndrome
the most reproducible pathogenic features of Fibromylagia
Evidence of augmented pain and sensory processing
PATHOPHYSIOLOGY
OF FIBROMYALGIA
Once a diagnosis of fibromyalgia is established, the
most consistently detected objective abnormalities involve pain and sensory processing systems.
One of the earliest findings
is that tenderness in FM is not confined to tender points, but extends throughout the entire body.
Theoretically, such diffuse tenderness could be due to
psychological (e.g., hypervigilance) or neurobiological factors (i.e., factors that can lead to temporary or permanent amplification of sensory input)
FM patients display a decreased threshold
to
heat, cold, and electrical stimuli
There are two different specific pathogenic mechanisms
in FM that have been identified using experimental pain
testing:
(1) decreased descending analgesic activity, and
(2) increased wind-up or temporal summation
diffuse noxious inhibitory controls (DNIC)
application of
analgesic effect produced by an intense painful stimulus for 2 to 5 min produces generalized
whole-body analgesia
The DNIC response is thought to be partly mediated
by
descending opioidergic and serotonergic-noradrenergic
pathways.
The biochemical and imaging
findings suggesting increased activity of endogenous opioidergic systems are consistent with
the anecdotal experience
that opioids are generally ineffective in FM and
related conditions
efficacious in treating FM and related conditions
any type of compound that simultaneously raises both serotonin and norepinephrine
(tricyclics, duloxetine, milnacipran, tramadol)
individuals
with FM may have evidence of wind-up, indicative of
central sensitization
patients with
FM have approximately threefold higher concentrations of
substance P in CSF compared with normal controls
Another neurotransmitter in pain processing that likely
plays some role in FM is
the excitatory neurotransmitter
glutamate. CSF levels of glutamate are twice as high in FM patients than controls
a strong genetic and
familial component to the development of fibromyalgia
First-degree relatives of individuals with fibromyalgia display
an eightfold greater risk of developing fibromyalgia
than those in the general population
affective spectrum disorder, and more recently central sensitivity syndromes and chronic multi-symptom illnesses.
familial and personal coaggregation of functional pain syndromes was originally
Neural Influences on Pain and Sensory Processing
Facilitation
Increase Substance P, Glutamate and EAA, Serotonin (5HT2a, 3a), Nerve Growth Factor, CCK
Neural Influences on Pain and Sensory Processing
Inhibition
- Descending anti nociceptive pathways (Decrease NE, Serotonin, Dopamine)
Increase Opioids, GABA, Cannabanoids, Adenosine
DIAGNOSIS AND ASSESSMENT
OF FIBROMYALGIA
The ACR research criteria for FM require that an individual
have both a history of chronic widespread pain and
over 11 of a possible 18 tender points on examination
optimal treatment of fibromyalgia supports a
multifaceted program comprising pharmacologic therapy and nonpharmacologic therapy (education, exercise, and cognitive behavioral therapy).
Pregabalin
an alpha-2-delta ligand
and antiepileptic drug. is a g-aminobutyric acid (GABA) analog antiepileptic drug that binds to the a-2-d subunit of calcium channels.
duloxetine
milnacipran
a selective serotoninnorepinephrine reuptake inhibitor (SNRI),
Antidepressants.
amitriptyline
Tricyclic Antidepressants (TCAs)
The effectiveness of
TCAs, especially amitriptyline and cyclobenzaprine, in
treating the symptoms of pain, poor sleep, and fatigue
associated with fibromyalgia
Cyclobenzaprine
centrally acting muscle relaxant structurally similar to amitriptyline, has been used to
treat the musculoskeletal pain and sleep disturbances
associated with FM.
Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)
SNRIs tend to be better tolerated than older TCAs. Venlafaxine tends to have clinically significant effects on norepinephrine reuptake only at higher doses and thus may be beneficial in FM when used at these higher
doses
Milnacipran also demonstrated benefit in FM
including
improvements in fatigue, physical functioning, and
discomfort
Centrally Acting Agents. g-Hydroxybutyrate,
a GABA precursor with strong sedative qualities, has been
shown to be beneficial in FM
Pramipexole
a dopamine agonist used for Parkinson’s
disease and restless leg syndrome that has been shown in
one controlled study to improve pain and sleep in FM
patients treated with concomitant analgesics
pure opioids
anecdotal experience has not found this class of analgesics to be effective.
Tramadol
a compound that exerts weak analgesic effects by binding to the m-opioid receptor, but the majority of its analgesic effects likely stem from serotonin/norepineprhine
reuptake inhibition. Tramadol appears to possess some beneficial effects in the management of FM both alone and as a fixed-dose combination with acetaminophen.
exercise is beneficial in FM for both
physical symptoms and functional capacity.
crucial for optimal
adherence to regimens
The use of low-intensity, low-impact programs and the
ability to individualize the protocol
Catastrophizing,
or the belief that the worst possible outcome is going to occur, has been associated with pain severity, decreased functioning, and affective distress in FM
Relaxation techniques
commonly part of cognitive behavioral therapy (CBT) for FM. progressive muscle
relaxation (PMR), autogenic training, guided imagery, and
meditation.
multicomponent treatment reduces
pain, fatigue, and depressive symptoms, and improves
quality of life and physical fitness post-treatment
