Guide to Pain Management in Low-Resource Settings


Download 4.8 Kb.
Pdf ko'rish
bet36/58
Sana26.12.2017
Hajmi4.8 Kb.
#23083
TuriGuide
1   ...   32   33   34   35   36   37   38   39   ...   58

Th
 erapeutic approaches
Is bed rest an appropriate therapeutic  
approach in back pain?
Bed rest is only appropriate for acute radiating pain 
(sciatica), but it should not exceed 1–3 days to avoid 
progressive inactivity and avoidance, which reinforces 
abnormal illness behaviors. For all nonspecifi c  myo-
fascial pain, inactivity would have deleterious physi-
ological eff ects, leading to shortened muscles and 
other soft tissues, joint hypomobility, reduced muscle 
strength, and bone demineralization. Th
 erefore, bed 
rest should not be advised. Th
  e patient should be in-
structed to continue “normal daily activities” as much 
as possible. Any bed rest recommendations would only 
reinforce malcognitive and malconditioned behavior 
(“fear avoidance beliefs”), resulting in a viscous circle 
of bed rest—increased fear of movement—increased 
pain on movement because of muscular decondition-
ing—more bed rest. For these reasons, bed rest is defi -
nitely not recommended as a treatment for nonspecifi c 
back pain.

212
Mathew O.B. Olaogun and Andreas Kopf
What medications are recommended                  
in nonspecifi c back pain?
Unfortunately, many patients with nonspecifi c  back 
pain are treated as in acute specifi c diseases causing 
pain, with long-term prescriptions of nonsteroidal an-
algesics, opioids, and centrally acting muscle relaxants, 
although there is no evidence in the literature for use of 
these drugs for this indication, and a number of guide-
lines do not recommend them. Only a few medications 
are indicated. Tricyclic antidepressants in low to mod-
erate doses are useful to alleviate insomnia, enhance 
endogenous pain suppression, reduce painful dysesthe-
sia, and help the patient’s ability to cope. If a depressive 
disorder is diagnosed, higher doses would be needed. In 
some patients, the anxiolytic and sleep-quality-improv-
ing calcium channel blockers gabapentin or pregabalin 
might be helpful. Other coanalgesics and narcotics may 
only be used if the pain is of malignant, chronic infl am-
matory, or severe degenerative origin.
Are invasive therapeutic techniques      
indicated in nonspecifi c back pain?
In carefully selected patients, such as those with con-
comitant sacroiliacal or facet joint aff ection, local in-
jections might facilitate recovery with physical therapy. 
Local injections into paravertebral soft tissues, specifi -
cally into myofascial trigger points, are widely advocat-
ed. However, study results are rather disappointing.
If conventional analgesics and invasive 
techniques are not recommended, what therapy 
is best for chronic nonspecifi c back pain?
Behavioral and cognitive behavioral multidisciplinary 
pain programs have proven eff ective for many patients, 
but they need dedicated, well-trained personnel and 
rather high fi nancial resources to be eff ective. Th
 erefore, 
prevention of chronic nonspecifi c back pain is the key 
to therapeutic success. Morbid obesity, smoking, gen-
eral fi tness, and job satisfaction should be addressed in 
all patients to avoid development of chronic nonspecifi c 
back pain. Adequate and knowledgeable patient guid-
ance seems to be the most important prophylactic and 
therapeutic instrument in nonspecifi c back pain. Th
 e 
goals of chronic pain management are to relieve dis-
comfort (partially) and (more importantly) to improve 
or restore physical, psychological, and social function. 
Management involves knowing the cause and course of 
the pain, educating patients in simple terms, and select-
ing appropriate “resource-oriented” physical and psy-
chological modalities and techniques. For success, it is 
vital to achieve a “change motivation” in patients and to 
educate them on what can be done as self-care.
Pearls of wisdom
• Chronic nonspecifi c back pain is one of the most 
frequent patient complaints.
•  It is crucial to diff erentiate nonspecifi c back pain 
from specifi c back pain because the therapeutic 
techniques diff er considerably. Th
 is diff erentia-
tion should be made at the earliest possible mo-
ment, because nonspecifi c back pain tends to 
take on a life on its own within a couple of weeks 
or months, resulting in a diffi
  cult-to-treat disease.
• “Red fl ags” help to identify indications for specifi c 
and nonspecifi c pain.
•  In general, opioids, NSAIDs, and central muscle 
relaxants as well as invasive procedures are inef-
fective in nonspecifi c back pain and even have 
the risk to further promote chronic pain develop-
ment. Instead, intensive counseling, patient edu-
cation, physical activation, and behavioral inter-
ventions have been proven to be eff ective.
•  Psychiatric comorbidity is frequent and should 
not be overlooked.
•  An important goal in advanced chronic back 
pain patients is concentration of therapeutic ef-
forts on functional improvement rather than 
pain reduction.
References
[1]  Odebiyi DO, Akinpelu AO, Olaogun MOB. S Afr J Physiother 
2006;62:17–20.
[2]  Olaogun MOB, Adedoyin RA, Ikem IC, Anifaloba OR. Physiother Th
 e-
ory Pract 2004;20:135–42.
[3]  Swagerty DL, Hellinger DO. Am Fam Physician 2001;64: 279–86.
Websites
http://www.rcep7.org/projects/handbook/back.pdf

213
Guide to Pain Management in Low-Resource Settings, edited by Andreas Kopf and Nilesh B. Patel. IASP, Seattle, © 2010. All rights reserved. Th
  is material may be used for educational 
and training purposes with proper citation of the source. Not for sale or commercial use. No responsibility is assumed by IASP for any injury and/or damage to persons or property 
as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material herein. Because of the rapid advances in the 
medical sciences, the publisher recommends that there should be independent verifi cation of diagnoses and drug dosages. Th
  e mention of specifi c pharmaceutical products and any 
medical procedure does not imply endorsement or recommendation by the editors, authors, or IASP in favor of other medical products or procedures that are not covered in the text.
Guide to Pain Management in Low-Resource Settings
Arnaud Fumal and Jean Schoenen
Chapter 28
Headache
How is headache classifi ed?
Headache is a leading reason for medical consultation 
and particularly for neurological consultation. A tre-
mendous range of disorders can present with headache. 
A systematic approach to classifi cation and diagnosis 
is therefore essential both for clinical management and 
research. Headache disorders were poorly classifi ed and 
defi ned until 1988. At that time, the International Head-
ache Society (IHS) published its International Clas-
sifi cation of Headache Disorders (ICHD-1), in which 
headaches were classifi ed into 13 major groups. Th
 is 
headache classifi cation with operational diagnostic cri-
teria was an important milestone for clinical diagnosis 
and is accepted worldwide. Its second edition (ICHD-
2) has fi ne-tuned the classifi cation of diff erent specifi c 
headaches and expanded the number of groups to 14 
(Table 1). For each disorder, explicit diagnostic criteria 
are provided. Th
 ese diagnostic criteria are very use-
ful for the clinician because they contain exactly what 
needs to be obtained from the patient while taking the 
history. Nevertheless, it is surprising and disappointing 
that headache patients remain poorly diagnosed and 
treated in most countries.
Th
 ere are four groups of primary headache 
disorder: (1) migraine, (2) tension-type headache, (3) 
trigeminal autonomic cephalalgias, and (4) other pri-
mary headache. Th
  e criteria for the primary headaches 
are clinical and descriptive and, with a few exceptions 
(i.e., familial hemiplegic migraine) are based on head-
ache features and the exclusion of other disorders, not 
etiology. In contrast, secondary headache are classifi ed 
based on etiology and are attributed to another disorder. 
Because primary headaches are the most common, this 
discussion focuses on the diagnosis and management 
of those syndromes. Th
  e epidemiology and experiences 
of patients with headache disorders in the developing 
world are uncertain, because the majority of research 
on headache disorders comes from a limited number of 
high-income countries. Where sought, regional varia-
tion in the incidence, prevalence, and economic burden 
of headache disorders has been found. Social, fi nancial, 
and cultural factors can all infl uence the experience 
of the individual headache suff erer, and patients in re-
source-poor settings could presumably experience an 
even greater impact of these infl uences.
What are important issues for   
non-headache specialists?
Caring for a patient complaining of headaches requires 
above all a thorough history taking and physical exami-
nation that includes a neurological examination. First, 
one needs to distinguish primary from secondary head-
aches. To evaluate the likelihood of a secondary, symp-
tomatic headache, the most crucial feature, besides 
clinical examination, is the duration of the headache 
history. Patients with a short history require prompt at-

214
Arnaud Fumal and Jean Schoenen 
•  Is the pain on one or both sides?
•  Is it aggravated by physical activity?
• Th
 e presence of trigger zones and lancinating 
quality suggest a neuralgia.
•  Is a migraine aura present?
•  Very importantly, are there accompanying symp-
toms such as nausea, hypersensitivity to light and 
sound, or autonomic symptoms such as tearing, 
stuff y nose, sweating, ptosis, or miosis?
Th
  e next question is whether the patient has one 
or more diff erent kinds of headache. Th
  is must be eluci-
dated skillfully. Th
  e reason for the consultation must be 
made clear. Is it because the usual headache is getting 
worse, or is it because of a new kind of headache? We 
have to keep in mind that if headache is the fi fth  most 
common complaint seen in United States emergency de-
partment, the minority of these patients have a second-
ary cause for headache, and an even smaller number have 
a grave and potentially catastrophic cause for headache, 
such as meningitidis or subarachnoid hemorrhage.
In clinical practice, it is known that patients 
may not easily identify and recall certain features of 
their headaches, such as the presence and type of aura 
symptoms, specifi c associated symptoms, and the coex-
istence of several types of headache. Th
  erefore, the use 
of monitoring instruments becomes crucial in the di-
agnosis of these disorders. Using headache diaries and 
calendars, the characteristics of every attack can be re-
corded prospectively, increasing the accuracy of the de-
scription and making it possible to distinguish between 
coexisting headache types.
Moreover, headache diaries provide the phy-
sician with information concerning other important 
features, such as the frequency and temporal pattern 
of attacks, drug intake, and the presence of trigger fac-
tors. Use of acute drugs can be checked for optimal dos-
ing. Frequent use (10 days or more per month) of acute 
medication is an alert for medication overuse headache. 
Th
  e diary could even be sent to headache patients before 
their fi rst consultation at the headache center as it can 
improve the clinical diagnosis from the fi rst interview.
What is essential to know         
about migraine?
Migraine is the commonest cause of severe episodic re-
current headache. Migraine aff ects approximately 12% 
of Western populations, and prevalence is higher in fe-
males (18%) than males (6%). Migraine is a recurrent 
tention and may need quick complimentary investiga-
tions, while those with a longer headache history gen-
erally require time and patience rather than speed and 
imaging. Patients with a headache history of more than 
2 years defi nitely have a primary headache disorder. Red 
fl ags (see Table 2) that should alert to the possibility of a 
secondary headache include pain of sudden onset, fever, 
marked change in pain character or timing, neck stiff -
ness, pain associated with neurological disturbances, 
such as cognitive dysfunction or weakness, and pain 
associated with local tenderness, for example of the su-
perfi cial temporal artery.
Patients with recent onset headache or with 
neurological signs require at the least brain imaging 
with computed tomography (CT) or magnetic reso-
nance imaging (MRI). To classify primary headaches, 
the following questions are crucial:
•  Frequency and duration of attacks.
• Headache severity.
Table 1
Tension-type headache (episodic form): 
general diagnostic criteria (ICHD-2)
General Diagnostic Criteria 
A. Headache lasting from 30 minutes to 7 days
B. At least 2 of the following pain characteristics:
Bilateral location
Pressing/tightening (non-pulsating) quality
Mild or moderate intensity
Not aggravated by routine physical activity such as walking or 
climbing stairs
C. Both of the following:
1. No nausea or vomiting (anorexia may occur)
2. No more than one of photophobia or phonophobia
D. Not attributed to another disorder
Table 2
Migraine with aura diagnostic criteria (ICHD-2)
Diagnostic Criteria for Migraine without Aura
A. At least 5 attacks fulfi lling criteria B–D
B. Headache attacks lasting 4–72 hours (untreated or unsuccess-
fully treated)
C. At least 2 of the following pain characteristics:
Unilateral location
Pulsating quality
Moderate or severe intensity
Aggravation by or causing avoidance of routine physical activity 
(e.g., walking or climbing stairs)
D. During headache at least one of the following:
1. Nausea and/or vomiting
2. Photophobia and phonophobia
E. Not attributed to another disorder

Headache
215
headache manifesting in attacks lasting between 4 and 
72 hours. Typical features of this headache are unilateral 
location, pulsating quality, moderate or severe intensity, 
aggravation by routine physical activity, and association 
with nausea and/or photophobia and phonophobia (see 
Table 3 for diagnostic criteria of migraine without aura 
from the ICHD-2).
Th
  e headache may be preceded in 15–20% of pa-
tients by an aura, so-called migraine with aura. Th
 e aura 
may last between 5 and 60 minutes. Th
  e most common 
type is visual aura, causing scotomas, teichopsia, forti-
fi cation spectra, and photopsias. It can also comprise 
other neurological symptoms such as focal paresthe-
sias, speech disturbances and, in hemiplegic migraine, a 
unilateral motor defi cit.  Th
  e heterogeneity of the clini-
cal phenotype of migraine is underestimated. Despite a 
common diagnostic denominator, some clinical features 
such as type of aura symptoms, pain intensity, presence 
of prodromes, coexistence of migraine with and without 
aura, or associated symptoms such as vertigo, may char-
acterize subgroups of patients bearing diff erent underly-
ing pathophysiological and genetic mechanisms.
In migraine, premonitory symptoms and trig-
ger factors are manyfold, and they may vary between 
patients and during the disease course. Th
 e most 
frequently reported premonitory symptoms are fa-
tigue, phonophobia, and yawning. Concerning trig-
ger factors, the most common ones are stress, the 
perimenstrual period, and alcohol. Overuse of acute 
antimigraine drugs, in particular of combination anal-
gesics and ergotamine, is another underestimated fac-
tor leading to chronifi cation.
If the migraine is a benign condition, the se-
verity and frequency of attacks can result in signifi cant 
disability and reduced quality of life, even between at-
tacks. Although migraine is one of the most common 
reasons for patients to consult their doctor, and despite 
its enormous impact, it is still under-recognized and 
undertreated. Th
  is lack of recognition has various rea-
sons. On the one hand, there are no biological markers 
to confi rm the diagnosis, and many doctors lack knowl-
edge, time, interest, or all three, to manage migraineurs. 
On the other hand, there is no cure for migraine, and, 
although eff ective therapies do exist, they have only par-
tial effi
  ciency or are not accessible to all. Finally, percep-
tion of migraine may vary between cultures, some of 
which tend to negate or trivialize its existence. As a re-
sult, a proportion of aff ected individuals do not seek (or 
have given up on) medical help.
Migraine is a neurovascular disorder (i.e., both 
neuronal and vascular factors are involved) in which ge-
netic susceptibility renders the brain hyperresponsive to 
stimuli and probably metabolically vulnerable, setting a 
“migraine threshold” on which trigger factors may act 
to precipitate an attack. Th
  e consensus is now that the 
migraine aura is caused by the neuron-glial phenome-
non of so-called “cortical spreading depression,” where 
a brief front of neuronal depolarization (“scintillations”) 
is followed by a wave of arrest of neuronal activity due 
to hyperpolarization; both spread over the cortex with a 
velocity of 3–5 mm/minute.
Th
 e migraine headache probably results from 
activation of the trigeminovascular system, the major 
pain-signaling system of the visceral brain composed of 
nociceptive aff erents belonging to the visceral portion of 
the ophthalmic nerve (V1) and surrounding meningeal 
blood vessels. Th
 e precise pathogenic relationship be-
tween aura and migraine headache is not fully clarifi ed.
Table 3
Typical symptoms of migraine and tension-type headache
Migraine
Tension-Type Headache
Sex ratio (F:M)
2 to 3:1
5:4
Pain
 
Type
Pulsating
Pressing/tightening (non-pulsating) quality
 
Severity
Moderate to severe
Mild or moderate intensity
 Site
Unilateral
Bilateral
Aggravated by routine physical activity Yes
No
Duration of attack
4 to 72 h
30 minutes to 7 days
Autonomic features
No
No
Nausea and/or vomiting
Yes
No
Photophobia and/or phonophobia
Yes, both
No more than one of photophobia or phonophobia

216
Arnaud Fumal and Jean Schoenen 
What are the options for acute 
migraine treatment?
During the last decade, the advent of highly eff ective 
5-HT
1B/1D
 agonists, the triptans, has been a major break-
through in treatment. Triptans are able to act as vaso-
constrictors via vascular 5-HT
1B
 receptors and to inhibit 
neurotransmitter release at the peripheral as well as at 
central terminal of trigeminal nociceptors via 5-HT
1D/B
 
receptors. Th
 e site of action relevant for their effi
  ca-
cy in migraine is still a matter of controversy; possibly 
their high effi
  cacy rate is due to their capacity of acting 
at all three sites, contrary to other antimigraine drugs. 
Sumatriptan, the fi rst triptan, was followed by several-
second generation triptans (zolmi-, nara-, riza-, ele-, 
almo-, and frovatriptan), which were thought to correct 
some of the shortcomings of sumatriptan. A large me-
ta-analysis of a number of randomized controlled trials 
performed with triptans confi rms that the subcutane-
ous auto-injectable form of sumatriptan (6 mg) has the 
best effi
  cacy, whatever outcome measure is considered. 
Diff erences between oral triptans do exist for some out-
come measures, but in practice each patient has to fi nd 
the triptan that gives the best satisfaction.
At present, the major reason for not considering 
triptans as fi rst-choice treatments for migraine attacks 
is their high cost, and in some patients their cardiovas-
cular side eff ects. However, stratifying care by prescrib-
ing a triptan to the most disabled patients has been 
proven cost-eff ective. In severely disabled migraineurs, 
the effi
  cacy rate of injectable sumatriptan for a pain-free 
outcome at 2 hours is twice that of ergot derivatives or 
NSAIDs taken at high oral doses and of i.v. acetylsalicyl-
ic acid lysinate. Th
  e therapeutic gain tends to be clearly 
lower for simple analgesics or NSAIDs, such as acet-
aminophen (1000 mg p.o.), eff ervescent aspirin (1000 
mg), or ibuprofen (600 mg), than for oral triptans, when 
severe attacks are considered.
For mild and moderate attacks, however, it has 
proven diffi
  cult to show superiority of oral triptans in 
randomized controlled trials. Combining analgesics 
or NSAIDs with an antiemetic and/or with caff eine or 
administering them as suppositories clearly increas-
es their effi
  cacy, often up to that of oral triptans. Re-
cently, combining a triptan plus an NSAID as a single 
tablet for acute treatment of migraine resulted in more 
favorable clinical benefi ts compared with either ther-
apy used alone, with an acceptable and well-tolerated 
adverse-eff ect profi le.
As expected, the triptans have not solved pa-
tients’ problems. Th
  ere is room for more effi
  cient  and 
safer oral acute migraine treatments. As triptans are con-
traindicated in patients with cardiovascular disorders, 
non-vasoconstricting agents are the holy grail in acute 
therapy research. Serotonin 5-HT
1F
-receptor agonists 
and a novel calcitonin gene-related peptide (CGRP) an-
tagonist are currently being investigated, with promis-
ing results. Treatment algorithms should be inspired by 
Table 4
Red fl ags in the diagnosis of headache
Red Flags
To Consider
Possible Investigation(s)
Sudden-onset headache
Subarachnoid hemorrhage, brain bleeding, 
mass lesion (especially posterior fossa)
Neuroimaging, lumbar puncture (after neuro-
imaging)
Worsening-pattern headache
Mass lesion, subdural hematoma, medica-
tion overuse
Neuroimaging
Headache with systemic illness (fever, 
neck stiff ness, cutaneous rash)
Meningitidis, encephalitis, Lyme disease
systemic infection, collagen vascular disease, 
arteritis
Neuroimaging, lumbar puncture, biopsy, blood 
tests
Focal neurologic signs, or symptoms 
other than typical visual or sensory aura
Mass lesion, arteriovenous malformation, 
collagen vascular disease
Neuroimaging, collagen vascular evaluation
Papilledema
Mass lesion, pseudotumor, encephalitis, 
meningitidis
Neuroimaging, lumbar puncture (after neuro-
imaging)
Headache triggered by cough, exertion 
or Valsalva
Subarachnoid hemorrhage, mass lesion
Neuroimaging, consider lumbar puncture
Headache during pregnancy or post-
partum
Cortical vein/cranial sinus thrombosis, 
carotid dissection, pituitary apoplexy
Neuroimaging
New headache type in a patient with 
cancer, Lyme disease or HIV
Metastasis, meningoencephalitis, opportu-
nistic infection
For all neuroimaging and lumbar puncture
Source: Bigal ME, Lipton RB. Headache Pain 2007;8:263–72.

Headache
217
personal experience, by the local pharmacoeconomic 
situation, as well as by the available literature.
Download 4.8 Kb.

Do'stlaringiz bilan baham:
1   ...   32   33   34   35   36   37   38   39   ...   58




Ma'lumotlar bazasi mualliflik huquqi bilan himoyalangan ©fayllar.org 2024
ma'muriyatiga murojaat qiling