.No is easy to discuss the treatment of osteoarthritis and pain control.
It is not, in fact, just take pharmcs
for pain control (fans or synthetic opioids), but to treat and rehabilitate the
individual.
So for the treatment of osteoarthritis of the cervical spine, it seems that
active physical treatment, massage, movements which reactivate the function of
the column and settle the altered posture of the spine are beneficial to the
pain.
In particular:
Physical · Treatment: systematic reviews and randomized trials have found that
therapy with EMF buttons compared to a simulated treatment, the exercise in
relation to stress management and active physiotherapy compared to passive
treatment significantly reduce the pain. Systematic reviews have found
insufficient evidence on the effects of most physical treatments (hot or cold,
traction, biofeedback, spray and stretch)
· Various studies have shown that manipulation and mobilization improves
symptoms compared to other treatments. It still seems that the handling
associated with strengthening exercises significantly reduces pain and increases
patient satisfaction compared to each of the two treatments.
· Muscle relaxant therapy / benzodiazepines: A systematic review identified two
RCTs (159 patients with chronic low back pain or neck pain with spasm acute),
which compared three treatments: cyclobenzaprine (flexiban), diazepam and
placebo. Both studies found that cyclobenzaprine significantly improved symptoms
after two weeks than the other two treatments, but it was not possible to obtain
quantitative data and follow-up about the pain. From a subsequent study (157
subjects with chronic neck pain) found that the eperisone (myonal) significantly
improved pain control after 6 weeks compared to placebo.
· There are insufficient evidence on the effects of analgesics, NSAIDs,
antidepressants and muscle relaxants, although these drugs are widely used as
drugs of first level for neck pain. Many drugs used to treat neck pain are
associated with adverse effects well documented.
In particular, we can say that the use of fans give a limited benefit in time
and not conclusive.
What are the fans?
The nonsteroidal antiinflammatory drugs (NSAIDs) represent a heterogeneous
series of compounds. Were traditionally classified by type of action:
antirheumatic, pain-antifebbrili, reliever. They also wrongly called analgesics
'weak or light'. In fact, some of them, such as ketorolac, have an analgesic
effect that is close to or less equivalent to opiates. Their mechanism of action
is common and the origin of analgesia was due to:
inhibition of prostaglandin synthesis;
hyperpolarization of neuronal membrane;
inhibition of lysosomal enzymes;
depressed levels of oxidizing substances released in the formation of
prostaglandins.
The actions for which NSAIDs are classically exploited are three: analgesic,
antipyretic and antiphlogistic. The analgesic action is predominantly in
peripheral location and exactly at the level of nociceptors. The antipyretic
action consists of inhibition of prostaglandin biosynthesis in the hypothalamic
thermoregulatory center. The anti-inflammatory action is not entirely clear.
Prostaglandins, in addition to proinflammatory activity, increase the action of
biological mediators of inflammation such as histamine and leukotrienes.
Name
Trade Name
Average dose in mg/24 h
Lysine acetylsalicylate
Flectadol
900x4
Acetylsalicylic acid
Aspirin
1000x4
Mefenamic acid
Lysalgo
250x3
Diclofenac
Voltaren
50x3
Diflunisal
Dolobid
500x3
Ibuprofen
Brufen
300x4
Ketoprofen
Orudis
100x3
Ketorolac tromethamine
Tora-Dol / Lixidol
30x4
Metamizole
Painkillers
500x3
Naproxen
Naprosyn
500x2
Nimesulide
Aulin
200x2
Paracetamol
Efferalgan
500x4
Piroxicam
Feldene
20x1
Major side effects of NSAIDs!
Eye on the gastric and duodenal ulcers! Protection should always be used with
antacids or gastric ie pump inhibitors or anti-H2 (eg omeprazole, pantoprazole,
ranitidine)
By interfering with platelet aggregation, they should be administered with
caution in cancer patients with clotting problems, or with a reduced number of
platelets.
Opioids
The drugs are derivatives of opium use old and proven effectiveness. These
substances are also called analgesics opioid analgesics more, narcotics,
morfinosimili.
Morphine is the founder and is the benchmark in the evaluation of analgesic its
other congeners. They represent a stage, almost always obliged, in pain from
cancer. Their potent analgesic activity is due to interaction with opioid
receptors located in certain areas of the CNS and spinal cord along the sensory
pathways of pain. At this level, similar to endorphins (a type of morphine
normally produced by the body), they trigger mechanisms of elimination and
modulation of painful sensations, coming as keys in the lock of pain and
bloccandola.I different pharmacological profile of the individual opioids (
intensity of action, duration of action, side effects) are precisely explained
by the existence of several varieties of different receptors and the ability of
each drug morfinosimile to interact with individual receptors.
They are divided into drugs that act on opioid receptors in three groups
according to the activity:
pure agonists (eg morphine)
agonist-antagonists (eg buprenorphine)
pure antagonists (eg naloxone).
Pure agonists and agonist-antagonists, while sharing a powerful analgesic
activity should never be prescribed at the same time as, competing with the same
receptor, reduce the therapeutic effect. In addition to the note and powerful
anti-pain opioids produce certain other actions and side effects such as:
e-
tranquilizing action
respiratory depression
attenuation of the stimulus of cough
miosis
nausea and vomiting (central effects)
hypertonia of smooth muscle (constipation, impaired urination).
For osteoarthritis and pain from the back.
Clinical evidence
The problem is greater because it is not only to control pain but also to
implement therapeutic interventions relevant surgery, found that shoulder
surgery is not something simple to implement. There are no clinical trials on
the effects of most surgical interventions in shoulder pain. A small randomized
study reported that in subjects with frozen shoulder forced mobilization was
more effective than intra-articular injection of steroids in the short term (3
months).
We found one RCT (30 patients with frozen shoulder divided into 2 groups of 15),
where it was shown that the forced mobilization of the shoulder joint,
associated intraarticular infiltration of hydrocortisone compared with
hydrocortisone alone intraarticular infiltration led to a better recovery many
more (7 / 15 vs 2 / 15 with only infiltration).
Subacromial cortisone infiltration.
A systematic review found limited evidence that subacromial steroid infiltration
increases the range of movements, but no evidence of greater efficacy than
placebo on pain. A randomized study found no evidence of positive effects on
pain or the excursion of movement.
Intra-articular infiltration
Two systematic reviews found no clear evidence that the infiltration of
intra-articular steroids best pain or range of motion compared to placebo. A
small randomized study found that in subjects with frozen shoulder distension of
the glenohumeral joint associated intra-articular infiltration of steroids can
increase the range of movement and reduce the severity of symptoms compared to
only intra-articular steroid infiltration.
NSAIDs and oral steroids.
Little evidence exists about the clinical use of NSAIDs and oral corticosteroids.
For the treatment of osteoarthritis of the knee problem is even more complex and
often only resolvable with prosthetic knee, if there is no relevant neurological
disease in the subject.
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