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S Afr Fam Pract
ISSN 2078-6190 EISSN 2078-6204
© 2017 The Author(s)
REVIEW
Key Summary Points
• Muscle pain, known as myalgia, can be in one targeted area or
across many muscles, occurring with overexertion or overuse of
these muscles.
• Pain can be classified as acute or chronic pain and further
categorized as nociceptive or neuropathic.
• Causes of muscle pain include stress, physical activity, infections,
hyper or hypo-thyrodism.
• Sprains and strains are the most common types of muscle pains.
• Optimal pain management involves utilizing a combination of
non-opioid, opioid analgesics, adjuvants and non-pharmacologic
strategies.
Introduction
Muscle pain, medically known as myalgia, can be described as
pain that originates in any muscle of the body. The pain can be
in one targeted area or across many muscles, usually occurring
with overexertion or overuse of these muscles.
“Pain, like love, is all consuming: when you have it, not much else
matters, and there is nothing you can do about it. Unlike love,
however, we are actually beginning to tease apart the mystery of
pain.”1
Myalgia may also occur without a primary trauma and this is
frequently associated with a viral infection. The severity of pain
may range from mild to severe, depending on the cause thereof.
It can typically be described as cramping and aching. Signs and
symptoms associated with muscle pain include; redness at the
site of injury, tenderness, swelling and fever.2
Classification of pain
Pain is classified according to its duration and pathogenesis.
Depending on the duration of pain, pain can either be classified
as acute or chronic.
Acute pain:
This type of pain usually arises after obvious tissue damage
and is therefore nociceptive in nature. The pain can be clearly
located and resolves upon healing. It has a protective nature as it
distinctly warns individuals about harmful situations.3
Chronic pain:
Chronic pain usually persists from months to years. The intensity
of the pain no longer correlates with the causal stimuli as there is
changes to the nerve function and transmission. The pain loses
its protective and warning signs and thus serves no purpose.3
Further to this pain can either be classified as nociceptive or
neuropathic:4
Nociceptive pain:
This is known as a very high threshold pain that is activated in
the presence of stimuli. It is the normal physiological pain that is
associated with a warning signal that something is threatening
the person's bodily tissues. It is felt when a person comes into
contact with a stimuli, i.e. hot, cold or sharp. Nociceptive pain
acts as a physiological protective system and signals when there
is impending tissue damage. It requires immediate attention and
Abstract
Muscle pain, also known as myalgia, is most commonly associated with sprains or strains. It frequently presents as redness at the
site of injury, tenderness, swelling and fever. Muscle pain may occur as a result of excitation of the muscle nociceptor due to overuse
of the muscle, viral infections or trauma. The most important endogenous substance released in response to the damaged tissues
or nociceptor nerve endings in regards with muscle pain is adenosine triphosphate (ATP). Optimal pain management involves a
combination of non-opioid, opioid analgesics, adjuvants, as well as non-pharmacologic strategies. Non-opiod analgesics include
paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, which are indicated for mild to moderate pain.
Whereas moderate to severe pain acquires opiod analgesics. This article provides an overview of muscle pain, the management
and treatment thereof.
Keywords: muscle pain, myalgia, sprains, strains, analgesics, opiods, nsaids
South African Family Practice 2017; 59(3):24-32
Open Access article distributed under the terms of the
Creative Commons License [CC BY-NC-ND 4.0]
http://creativecommons.org/licenses/by-nc-nd/4.0
Muscle pain
Omphile Mogole, Ralph Kandiwa, Oyetola Babarinde, Halima Ismail, Nokuthula Dlamini, Letlhogonolo Maluleke,
Quinten Labuschagne, Lucille Malan, Natalie Schellack*
School of Pharmacy, Sefako Makgatho Health Sciences University
*Corresponding author, email: natalie.schellack@smu.ac.za
Muscle pain 25
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action, like pulling your hand off a hot plate within an instant.
Sprains and/or strains, broken bones, lower back pain from disc
disease or injury, and burns are examples of nociceptive pain.1,4,5
Neuropathic pain:
This pain is considered to be maladaptive, and is a disease
state of the nervous system. This type of pain occurs after
there is damage to the nervous system. It is experienced due
to transmission of pain signals in the absence of actual tissue
damage or inflammation, like fibromyalgia, tension headaches
and irritable bowel syndrome. This pathological pain occurs
when there are heightened sensory signals in the central nervous
system and a low threshold of pain.1,4,5
Causes of muscle pain
Muscle pain can be caused by stress, tension or physical activity.
Some medical conditions known to cause muscle pain include.6-10
• Infections
• Hyper or hypo-thyrodism
• Hypokalemia
• Autoimmune conditions e.g. lupus
• Side effects of certain medications (i.e. the Statins)
Pathophysiology of muscle pain
Muscle pain may occur as a result of excitation of muscle
nociceptor due to overuse of the muscle, inflammation and or
trauma. When the impact has occurred, endogenous substances
are released in response to damaged tissues or nociceptor nerve
endings. Some of these substances include;11
• Potassium ion
• Prostaglandin E2
• Bradykinin
• Serotonin
• Neuropeptides e.g. substance P
• Somatostatin
• Adenosine triphosphate
Of all substances released the most important one involved in
muscle pain is adenosine triphosphate (ATP) which is released
from muscle cells at high concentrations after damage to the
muscles. The increased levels of substances released from the
damaged tissues stimulate the nociceptors directly. The pain
experienced during movements of these damaged tissues are as
a result of the low threshold of sensitized muscle nociceptors.11-13
In the case of muscle inflammation the level of substance
P and nerve growth factor (NGF) increases, which in turn leads to
hyperalgesia known as increased sensitivity to painful stimuli in
the affected muscle.11,13
Sprains and strains are the most common types of muscle pains
and is especially frequent in the elderly. Sprains occur as a result
of overstretching of the ligaments. This can be caused by twisting
of joints. The most regularly affected parts of the body are the
ankles and wrists. This is usually followed by pain, swelling and at
times bruising. Strains on the other hand are the overstretching
of muscle or tendons.4,14
Management of muscle pain
Non-Pharmacological Management
The non-pharmacological treatments for muscle pain are
illustrated in Figure 1.
Treatment modalities include the following
Transcutaneous electrical stimulation (TENS)
TENS is a non-invasive procedure used in rehabilitation to
modulate pain.15 Electrical currents are delivered through the
skin to activate central inhibitory pathways decreasing central
excitability. Activation of the descending inhibitory pathways
from the midbrain and brainstem leads to inhibition of the
nociceptive neurons in the spinal cord. This is used for acute and
chronic pain.16-17
Acupuncture
It is a traditional Chinese-based therapeutic method which
involves the insertion of small, solid needles into specific
points in the body in order to improve health or modify painful
states.18 There are several postulated mechanisms of action.
Acupuncture are indicated for chronic pain unresponsive to
standard therapy. Acupuncture may work via same mechanisms
of other complimentary therapies (placebo, diversion etc).19
Thermal modalities
Thermotherapy is the therapeutic use of heat, usually greater
than that of body temperature, to the body.20 Thermal modalities
are classified as superficial thermotherapy (the application of a
device that is used primarily to heat structures to 1 cm deep) and
deep thermotherapy (the application of a device that causes a
tissue temperature rise at 3 – 5 cm deep). Superficial heating
modalities include; dry hot packs, moist hot packs and paraffin
baths. Deep heat modalities include therapeutic ultrasound.20
Non-Pharmacological Treatment Modalities
TENS
• Non-invasive
• Used in
rehabilitation to
modulate pain
• Acute and
chronic pain
• Therapeutic use
of heat:
◦ Superficial
heating (dry
hot or moist
hot packs and
paraffin baths)
◦ Deep heating
(ultrasound)
• Insertion of small
needles into
specific points on
the body
• Chronic pain,
unresponsive to
standard therapy
Acupuncture Thermal Modalities
[TENS: Transcutaneous Electrical Stimulation]
Figure 1: Non-pharmacological treatments of muscle pain
S Afr Fam Pract 2017;59(3):24-3226
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Pharmacological management
Optimal pain management involves utilizing a combination
of non-opioid, opioid analgesics, adjuvants and non-
pharmacologic strategies. The approach must be adapted such
that it is possible in resource limited areas as well. Treatment
guidelines should therefore consider the acute and chronic
phase of the pain state, and recommend the appropriate
pharmacologic or non-pharmacologic treatment using evidence
based recommendations. They should also indicate when a
single mode of treatment is appropriate and when multiple
modes are required .21-23
The multimodal approach to pain management involves
administering two or more analgesics with different mechanisms
of action. The routes of administration may also be different. This
approach as aimed at providing a synergistic effect of analgesia
using the lowest possible doses of these medications than if they
were used alone.24
Non-opioid analgesics
The following non-opioid related medicines are available for
managing pain in children: paracetamol, and the non-steroidal
anti-inflammatory drugs (NSAIDs), for example naproxen,
ibuprofen and mefenamic acid. They adequately treat mild
pain and moderate-to-severe pain in combination with other
medicines, particularly opioids, to provide more effective relief
and reduce adverse effects.25
Paracetamol
Paracetamol is one of the drugs of choice in pain
management, due to its excellent safety profile and lack of
any significant side-effects.26 It acts as a prodrug, with an
active cannabinoid metabolite. In the brain and spinal cord,
paracetamol follows deacetylation to its primary amine
(p-aminophenol) which is conjugated with arachidonic acid
to form N- arachidonolylphenolamide, a compound known
as an endogenous cannabinoid. The involved enzyme is fatty
acid amide hydrolase. N-arachidonolylphenolamide is an
agonist at the Transient Receptor Potential Cation Channel,
Subfamily V, Member 1 (TRPV1) receptors and an inhibitor of
cellular anandamide uptake, which leads to increased levels of
endogenous cannabinoids, inhibiting cyclooxygenases in the
brain at concentration that are probably not attainable with
analgesic dosages of paracetamol. It is of interest to note that
a cannabinoid-1 receptor antagonist, given at a dosage level
that completely prevents the analgesic activity of a selective
cannabinoid receptor agonist, completely inhibits the analgesic
activity of paracetamol as well. This fact allows us to explain the
mechanism of action of paracetamol in more detail. Despite
this finding, however, the definite proof that the analgesic
and antipyretic effects of paracetamol are dependent on COX-
inhibition is still unclear. Hence, it works effectively when is
combined with codeine for more effective control of moderate-
to-severe pain and discomfort.27
Paracetamol is available orally, in several tablet and liquid
formulations however the dosage should be guided by the age
and general condition of the patient.28
Non-steroidal anti-inflammatory drugs
Non-Steroidal Anti-inflammatory agent (NSAIDs) competitively
inhibit the cyclo-oxygenase (COX) enzyme, the enzymes
facilitate the bioconversion of arachidonic acid to inflammatory
prostaglandins. This results in the blockade of prostaglandin
synthesis and subsequently dampened inflammatory
responses.29-30 COX-1 and 2 are isozymes that only vary genetically.
NSAIDs have three pharmacological preferred attributes i.e.
analgesia, anti-inflammatory and anti-pyretic activity. They
generally have similar analgesic properties but selection is
based on their receptor selectivity. COX-1 receptor activation
produces gastric effects that mediate hyper-secretion of gastric
acid, thinning of the lumen and propagate the development of
gastric ulcers. These medicines have various formulations.31
The only over the counter (OTC) available pain medications is
aspirin (S0) and paracetamol (S2) and requires no prescription.
The NSAID ibuprofen is S2 when intended for the treatment
of post traumatic conditions such as pain, swelling and
inflammation, for a maximum period of five days without a
prescription. All other NSAIDs are S3 and can only be obtained
via a prescription from a physician (Act 101 of 1965).
It is important to note that NSAIDs have ceiling analgesic effects
but the Cyclooxygenase -2 mediated anti-inflammatory effects
are dose dependant.33 COX-2 is not detected in most normal
tissues, but its expression is rapidly induced by stimuli such as
proinflammatory cytokines (IL-1b, TNFα), lipopolysaccharides,
mitogens and oncogenes (phorbol esters), fibroblast growth
factor, epidermal growth factor, (luteinizing hormone, LH) and
fluid-electrolyte hemostasis, resulting in increased synthesis of
PGs in inflamed and neoplastic tissues.29
The non-steroidal anti-inflammatory drugs (NSAIDs), such as
asprin, ibuprofen, diclofenac, ketorolac and mefenamic acid,
have analgesic and anti-inflammatory properties, which are
useful in the management of pain.27
Ibuprofen is one of the most frequently used NSAIDs for mild
and moderate pain.34 The medicine has gained advantage in
the market as is available as an over-the-counter medication
for fever reduction, as well as pain relief. Studies have shown
ibuprofen to be superior in terms of its safety profile, compared
to ketorolac. However, ketorolac has been used as a single agent
for the treatment of postoperative pain, especially when used as
an adjuvant to opioid analgesia.35
If pain is constantly present, analgesics should be administered
on a regular time schedule, i.e. ‘by the clock’, whereby the
medicine is administered at a fixed time interval with dosages
tailored according to the patient’s pain, with the next dosage
given before peak time effect of the previous dosage has worn
off. This will result in more predictable and consists level of
analgesia. 23,25
Muscle pain 27
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Aspirin and paracetamol are very popular as over the counter
pain medication.1 Selection of analgesic used is determined by
the side effect profile and severity of pain.
Opioid analgesics
Opioid analgesic will provide analgesia for moderate to severe
pain, for the vast majority and with a wide margin of safety.36
This group includes the following examples: codeine, morphine,
oxycodone, methadone, fentanyl and pethidine. Opioids can be
divided into weak and strong opioids. Weak opioids are used
alone or in combination with other analgesics, in management
if moderate pain. Strong opioids are usually reserved for severe
pain.3
Opioids are the third-step in the pain treatment ladder and the
recommended treatment of moderate or severe pain.37 One of
the undesirable effects which is of great concern in healthcare is
dependence, which is associated with prolonged use of opioids.
Concomitant administration of an opioid with ibuprofen can
reduce the amount of opioid analgesic required for pain control.
Pethidine, morphine and fentanyl
A variety of opioids are available for use; however, there is
insufficient evidence to support a preference of one opioid
over another.38-39 Pethidine does not provide good analgesia
compared to morphine and should not be used long-term
because of the possible accumulation of its toxic metabolite,
nor-pethidine, that can result in seizures. Fentanyl provides
approximately equal analgesic effects to morphine, and can be
used for rapid analgesia over short periods of time if morphine is
contra-indicated. Opioids are the most commonly administered
intravenous agents for moderate to severe pain. The opioid
dosage that effectively relieves pain can differ, and should be
based on a pain severity assessment. However, the long-term
use of opioids is associated with constipation; therefore, a
combination of a stool softener and stimulant laxative can be
Table 1: Formulations, dosages and side-effects of various pain medications
Drug Formulations Dosages Side effects
Paracetamol Tablets
Suppositories
Intravenous Solutions
1-4 g/daily 1g q 6 hourly Hypersensitivity skin reactions: neutropenia,
thrombocytopenia
Nephrotoxicity
Hepatoxicity
Non-specific NSAIDs
Ibuprofen Tablets
Topical patch
Topical Gel
Oral syrup
200-400 mg q 4-6 hourly Same as for diclofenac
Indomethacin Capsules 25-50 mg q 6-8 hourly CNS effects: Dizziness drowsiness, mental confusion,
headache in less than 10% to patients
Corneal deposits
Ketaprofen tablets 200 mg daily with food Same as Diclofenac
Diclofenac Tablets
Intramuscular Injection
Topical Gel
Suppositories
Topical patch
Oral: 25-50 mg q 8hourly, to
maximum of 150 mg/day
Intramuscular: 75 mg q 12 hourly,
maximum of 150mg/day for
2 days only
Suppositories: 100 mg daily
GIT: Gastric erosion ,peptic ulceration
Hypersensitivity reactions: Skin rashes, pruritus
and angioedema
Renal toxicity
Piroxicam Tablets
Topical Gel
40mg/day Same as Diclofenac
Naproxen Tablets 500 mg q 12 hourly Same as Diclofenac
Mefanemic Acid Oral syrups
Tablets
Suppositories
500 mg q 8 hourly
COX-2 Inhibitors
Celecoxib Tablets
Capsules
100-200 mg q 12 hourly GIT: Nausea , dyspepsia, diarrhoea , flatulence
Steven-Johnsons Syndrome
Hypersensitivity reaction: Toxic epidermal
necrolysis
Renal toxicity
Etoricoxib Tablets
Capsules
60-90 mg q 12 hourly Same as for Celecoxib
Meloxicam Tablets
Capsules
7.5 mg q 12 hourly or 15 mg daily Same as for Celecoxib
S Afr Fam Pract 2017;59(3):24-3228
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used as prophylaxis when it is anticipated that these agents will
be used over an extended period of time. 38-39
Morphine is well established as the first-line strong opioid and
is available in both immediate-release and prolonged-release
formulations. Immediate-release tablets are used to individualise
patient dosages and have an adequate dosage for pain control.
Prolonged-release oral formulations improve patient compliance
by allowing longer dosing intervals. Oral morphine solution is
usually used for persistent pain and when patients are unable to
swallow tablets.39
The use of a pain scale to manage pain is a crucial part of effective
opioid therapy because these medicines do not have a so-called
ceiling effect. Therefore it is imperative to ensure an appropriate
dosage that provides effective analgesia with manageable side-
effects. A suitable opioid antagonist, such as naloxone, should
also be available in the healthcare for the management of
adverse effects or opioid-related complications.23
When pain management is no longer needed, slow withdrawal
of opioids may be necessary to prevent abstinence syndrome,
with continuous monitoring of the vital signs. This may require
tapering the daily dosage whilst monitoring the level of pain,
and with continuous reassessment to ensure that the patient is
pain free.39
Combination Opioid Formulations
When pain management by paracetamol and NSAIDs is
inadequate, combination agents are usually employed.
Hydrocodone and oxycodone have been increasingly used in
combination with paracetamol.37 These agents proved to be
more effective in post-surgical injuries and exhibit increased pain
relief compared singular usage of NSAIDs. Caution is indicated
in patients that have a previous problem with drug abuse and
seizures as some patients on antidepressants (SSRIs, MOA) have
experienced seizures with concomitant use of these agents.31
Table 2: Formulations, receptors and doses of opioids
Opioids Formulation Receptors it works on Doses
Morphine Tablets
Intravascular injection
Subdermal patch
Oral syrup
mu-(µ) and kappa-(k) opioid receptors PO 5-30 mg ,3-4hrly
IM 5-10mg 3-4 hourly
IV 1-2.5mg 5 – 10mnts up
to 15mg
Hydromorphine Tablets mu-(µ) and kappa-(k) opioid receptors 4-8mg every 24 hours
Codeine Tablets
Oral syrup
Partial agonist on k-receptors and µ receptors,
full agonist on delta (δ)receptor
PO 30 -60mg 4-6 hours
Hydrocodone Tablets mu-(µ) and kappa-(k) opioid receptors 5-10mg 4-6 hours
Fentanyl Intravascular solution
Transdermal Patch
mu-(u) receptor IV 25-50mcg/h
IM 50-100mcg/h
Transdermal 25mcg/h every
72 hours
Methadone Oral linctus
intramuscular
delta (δ) receptor PO 10-25mg 3-4hrly
IM 10-25mg 8-12 hourly
Mild to moderate pain
Moderate pain
Severe pain
Non-opioid analgesics:
Aspirin, paracetamol or ibuprofen;
With / without an adjuvant*
Weak opioid analgesics:
Codeine, dextropropoxyphene,
tramadol or buprenorphine);
With / without a non-opioid, such as
aspirin, paracetamol or ibuprofen;
With / without an adjuvant*
Strong opioid analgesics:
Morphine, hydromorphone,
oxycodone, buprenorphine or
tapentadol*;
With / without a non-opioid, such as
aspirin, paracetamol or ibuprofen;
With / without an adjuvant*
[*Examples of adjuvants include corticosteroids, antidepressants, hypnotics and anticonvulsants/antiepileptic agents.]
Pers
isten
t or w
orse
ning
pain
Figure 2: The World Health Organization’s three-step analgesic ladder3
[*Examples of adjuvants include corticosteroids, antidepressants, hypnotics and anticonvulsants/antiepileptic agents.]
Muscle pain 29
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Adjuvant Therapy
Adjunctive therapy is sometimes necessary to manage the
side-effects of medications for pain, provide symptom relief,
treat anxiety and manage related or underlying conditions.
This is because patients with chronic pain are more likely to
report anxiety, depression neuropathic pain and significant
activity limitations. Examples of adjuvant medicines include
corticosteroids, anxiolytics, antidepressants, hypnotics and
anticonvulsants/antiepileptic agents.23,40
A step-wise approach
The World Health Organization’s (WHO) ‘analgesic ladder’
serves as the mainstay of treatment for the relief of pain
together with psychological and rehabilitative modalities. This
multidimensional approach offers the greatest potential for
maximising analgesia and minimising adverse effects.23,40
According to the WHO, the key concepts to the effective
management of pain are as follows:23,40
• By mouth: If possible analgesics should be given by mouth.
• By the clock: Analgesics should be given at fixed time intervals
and the dosage should be titrated according to the patient’s
pain, and the next dosage should be given before the previous
dosage has fully worn off.
• For the individual: The choice and dosages of the analgesics
should be tailored to the needs and circumstances of the
particular patient.
• By the ladder: The well-known WHO ladder, illustrated in Figure
2, advocates a step-wise approach to the use of analgesics, as
explained below.
Step 1: Non-opioids (e.g. aspirin, paracetamol or ibuprofen) are
used for mild to moderate pain.
Step 2: Weak opioids (e.g. codeine phosphate, dihydrocodeine,
tramadol and buprenorphine) are recommended for moderate
pain, used alone or in combination with one of the non-opioids
mentioned in step 1.
Step 3: Strong opioids (morphine, hydromorphone, oxycodone,
buprenorphine and tapentadol) may be used alone or in
combination with a non-opioid (from the first step) for severe
pain.
If the patient’s pain is already severe, it is recommended that
the physician should move to the third level of the ladder
immediately, rather than starting with the first two.
As illustrated by Figure 2, opioids play an important role in the
management of, not only acute and chronic pain, but also in the
management of moderate to severe pain.23,40
However, certain barriers limit the effective use of opioids in the
management of pain:
• Concerns about the use of opioids from health care workers,
family members and patients; these concerns may be related
to the side-effects and risk of dependence when using the
opioids.
• Development of tolerance to the chronic use of opioids.
In instances where muscle pain does not subside with the use
of mentioned analgesics, an alternative interventional therapy
is muscle relaxants, where the relief of muscle spasms may also
reduce pain and discomfort.41
Skeletal muscle relaxants are classified into two main categories
namely, antispasticity and antispasmodic medications.
Antispascitic medications (e.g. baclofen) acts on the spinal cord
or on the skeletal muscles itself to better muscle hypertonicity
and involuntary spasms. Antispasmodic medications lessons
muscle spasms through alterations of central nervous
conduction. These agents are divided into benzodiazepines and
nonbenzodiazepines.41
A new skeletal muscle relaxant in South Africa is Myprocam®.
The active ingredient is cyclobenzaprine, a nonbenzodiazepine
antispasmodic agent, which blocks nerve impulses recognized
as pain. Cyclobenzaprine is structurally related to the tricyclic
antidepressants, like amitriptyline and nortriptyline. It is
categorized as a muscle relaxant with a mechanism of action
not fully understood, but is thought to be an agonist of the α2
receptor at the descending noradrenergic neurons within the
supraspinal area of the brain stem. Some evidence also revealed
seretonergic antagonism of the 5-HT2 receptors.41-42
Myprocam® is often combined with analgesics like ibuprofen or
naproxen and is used in addition to rest and physical therapy for
short-term relief of muscle spasm associated with acute, painful
musculoskeletal conditions. The recommended adult dose is a
15 mg capsule, taken once daily. Some patients may require up
to 30 mg per day, administerd as one Myprocam® 30 mg capsule,
taken once daily, or as two Myprocam® 15 mg capsules, taken
once daily.42-43
Side effects include dizziness and drowsiness. Other
anticholinergic effects such as dry mouth, blurred vision,
constipation and urinary retention will be expected due to
activity on cholinergic receptors. Cardiac arrhythmias like QTc
prolongation is likely to arise and should be used with caution
in patients with a history of arrhythmias or who are using any
medications prolonging the QTc interval. Myprocam is contra-
indicated in patients older than 65 years, or in patients with
impaired liver function.41-43
Adequate evidence for the effectiveness of the prolonged use of
Myprocam® is not available and therapy for longer periods of use
is seldom warranted, the duration of use should hence only be
for short periods of not more than three weeks.41-43
Conclusion
Muscle pain, or myalgia can be in one targeted area or across
many muscle. The severity of muscle pain can range from mild
to severe depending on the cause. It usually occurs with overuse
of the muscles, inflammation or trauma causing excitation
of muscle nociceptor but is also frequently associated with
a viral infection. The effective management of patients with
muscle pain is through a step-wise approach, offering the
greatest potential for maximum analgesia and the minimum
adverse effects. Non-Pharmacological and pharmacological Figure 2: The World Health Organization’s three-step analgesic ladder3
[*Examples of adjuvants include corticosteroids, antidepressants, hypnotics and anticonvulsants/antiepileptic agents.]
S Afr Fam Pract 2017;59(3):24-3232
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management are often applied for patients with chronic or
recurrent muscle pain associated with medical disease or injury.
Pharmacological management, depending on the severity
of muscle pain, may include OTC medicines such as aspirin,
ibuprofen and/or paracetamol or prescription medicine such
as other NSAIDs (diclofenac, naproxen, mefenamic acid etc)
or opioids for moderate to severe muscle pain. Adjunctive
therapy is sometimes necessary to manage the side-effects of
medications, provide symptom relief, treat anxiety or to manage
related or underlying conditions.
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