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