The role of antidepressants in the treatment of chronic pain syndrome. Antidepressants: which are better? Overview of Antidepressants in the Treatment of Chronic Pain
![The role of antidepressants in the treatment of chronic pain syndrome. Antidepressants: which are better? Overview of Antidepressants in the Treatment of Chronic Pain](https://i0.wp.com/mif-ua.com/frmtext/NMIF/2012/420_2012/026/026_1.jpg)
I. Acute, chronic and pathological pain. Pathophysiological and clinical features of chronic pain. The main types of chronic pain syndromes. Neurochemistry of chronic pain.
acute pain- a symptom of any sudden onset pathology or tissue damage. Acute pain syndrome can be called physiological, since it performs a certain protective function and, signaling the development of pathological processes in tissues, contributes to the development of adaptive complex reactions in the body. Therapy of acute pain is usually aimed at eliminating the cause that provokes this pain, or at reducing its algogenic effect (blockade).
Chronic or recurrent pain
has a multicomponent origin, which is based not only on pathophysiological, but also on closely interacting psychological and social factors. Chronic pain is also called pathological pain, due to the fact that it has a pathogenic significance for the body, and, causing dysfunction of the central nervous system, mental and emotional disorders, leads to damage to internal organs.
Chronic (pathological) pain is an independent disease with a primary pathological process in the somatic sphere and secondary dysfunction of the peripheral and central nervous system.
Main differences in chronic (pathological) pain:
u duration (at least 3 - 6 months),
u increasing the patient's resistance to ongoing therapy,
u the absence of direct dependence on the identification and elimination of the cause that caused it.
Types of chronic pain:
1) Pain as a result of continuous prolonged exposure (herniated disc).
2) Pain after an acute injury but lasting much longer than the normal healing period (causalgia, regional pain syndrome, phantom pain).
3) Pain without a specific, visible, appreciable cause (muscle tension headaches, migraine).
§ chronic pain is an independent disease, in the pathogenesis of which psycho-emotional and social factors play a leading role. With this type of pain, there may be no direct relationship between the pain and the underlying cause.
§ Common mediator systems lie in the mechanisms of development of chronic pain and depression.
§ According to epidemiological studies, there is a strong link between depression and chronic pain.
Various classifications of chronic pain are known.
Most of them are based on the localization of the pain syndrome.:
o headaches,
o neck and back pain,
o facial pain,
o limb pain,
o chest pain,
o abdominal pain,
o pain in the pelvis.
There are also pain somatic origin, neurogenic And psychogenic pain.In the mechanisms of development of chronic pain, regardless of its location and origin, the mediator systems of the brain and spinal cord are of great importance:
v Serotonergic
v Noradrenergic
v Dopaminergic
v GABAergic
v Peptidergic (opioid and non-opioid).
Numerous clinical and experimental studies have established:
- Intrathecal administration of serotonin causes analgesia and inhibits the activity of neurons in the dorsal horns of the spinal cord, caused by pain stimulation.
- When serotonin reuptake inhibitors are injected into certain areas of the brain (large raphe nucleus), which promotes the release of serotonin from synaptic terminals, an analgesic effect develops.
- Selective destruction of descending serotonergic pathways enhances the pain response.
When studying the influence of the adrenergic mediator system, similar results were obtained. It was found that norepinephrine modulates pain signals, both at the suprasegmental and spinal levels. As a result, adrenergic receptor blockers increase pain sensitivity, and agonists (clopheline) inhibit the activity of nociceptive neurons in response to pain stimulation.
II. Chronic pain and depression.
According to the results of numerous clinical and epidemiological studies, it has been established that there is a close relationship between chronic pain and depression. The prevalence of depression among patients with chronic pain range from 30 to 87%. According to some researchers, depression is the leading factor in reducing the ability to work in patients with chronic pain, or the most significant motivation for seeking medical help. The relationship between depressive disorders and chronic pain does not seem to be unambiguous, and there are various alternative versions of their causal relationship:
1) Chronic pain is the cause of depression.
2) Patients with depression are more likely to perceive pain.
3) Chronic pain and depression are indirectly related to other intermediate factors (disability).
III. Pharmacotherapy for chronic pain. adjuvant therapy. The use of antidepressants in the treatment of chronic pain.
The main groups of drugs used in the drug therapy of chronic pain syndromes:
1. Analgesics
opioids,
non-opioid.
2. adjuvant analgesics.
Adjuvant analgesics (“coanalgesics”)
- a heterogeneous group of drugs that provide analgesia either for specific pain syndromes or neutralize the side effects of opioids, which allows them to prolong their analgesic effect. These include drugs that do not have direct analgesic properties, but acquire them under certain circumstances (antihistamines, tranquilizers, anticonvulsants, etc.). Chronic (pathological) pain is precisely the conditions under which the use of adjuvant agents leads to a positive effect. Among the latter, a significant place belongs to antidepressants.
In wide clinical practice, unfortunately, the prescription of antidepressants by doctors is motivated only by the desire to cause a sedative effect and, thereby, create a favorable background for the main therapy (analgesics). Meanwhile, it is known that the use of antidepressants has a positive effect in 50-60% of patients with CHD. More than 60 clinical trials have proven the analgesic effect of antidepressants in the treatment of most CHD.
Antidepressants have an analgesic effect through three main mechanisms. :
1. Reduce depression.
2. Potentiate the action of analgesics or endogenous opiate peptides.
3. They have their own analgesic properties, which consist in a long-term prolongation of the synaptic activity of norepinephrine and serotonin.
A common indication for the use of antidepressants is HBS , but some pain syndromes are an obligate indication for their appointment.
These include :
· neurogenic pain syndromes (diabetic neuropathy, herpetic neuropathy, causalgia, etc.),
· some types of primary headaches (muscle tension headache, migraine, abuse headache, etc.).
IV. Pharmacotherapy with antidepressants of CHD.
Antidepressants are used in the treatment of chronic pain syndrome.
Antidepressants - inhibitors of neuronal uptake of neurotransmitters:
v indiscriminate;
v electoral.
Nondescript antidepressants include tricyclic And four-cycle antidepressants.
1. Tricyclic antidepressants:
amitriptyline,
imipramine,
clomipramine.
The pharmacological action of this group of drugs is to inhibit the reuptake of norepinephrine and serotonin, which leads to the accumulation of these neurotransmitters in the receptor area. The initial dose of tricyclic antidepressants is 10 to 25 mg in the evening, at bedtime, followed by an increase in daily dose of 10-25 mg every 3-7 days to a maximum of 75 mg (migraine, tension headaches) to 150 mg (neuropathic pain). An analgesic effect is possible by the end of the first week, a psychotropic effect occurs in 2-3 weeks - mood improves, working capacity increases, anxious expectation of pain disappears. Treatment lasts several months with gradual withdrawal.
Side effects:
a)cholinergic:
o dry mouth,
o Blurred and blurred vision
o constipation,
o urinary retention,
o sinus tachycardia,
o dizziness.
b)histaminergic:
o drowsiness,
o weight gain.
c)adrenergic:
o orthostatic hypotension,
o cardiotoxicity.
2. Quadricyclic antidepressants:
· maprotiline-ludiomil,
· mianserin-lerivon.
They are characterized by a predominant effect on the noradrenergic transmitter system. Efficacy data available Mianserina (Lerivona) in the treatment of muscle tension headaches. The drug has a sedative effect. Mianserin is used with good effect for pain in the lower back at a dose of 10 to 30 mg per day.
The drugs in this group have minimal side effects:
o drowsiness,
o weight gain,
o orthostatic hypotension.
Selective serotonin reuptake inhibitors:
§ fluoxetine-prozac,
§ venflaxin,
§ nefazodon,
§ sertraline-zoloft,
§ paroxetine-paxil.
In the treatment of chronic pain, the role of selective inhibitors is controversial and there are few clinical trials demonstrating their effectiveness in neurogenic pain. Fluoxetine (Prozac) is best known for the treatment of headaches: migraine and, especially, chronic tension headaches. It is recommended to take 1 capsule (20 mg) 1 time per day for 6-8 weeks. A good effect according to domestic authors (A.M. Vein, T.G. Voznesenskaya and others) was obtained in 65% of patients. Fluoxetine causes a statistically significant reduction in the frequency of seizures and their duration.
Selective inhibitors have minimal anticholinergic and a-drenergic
some blocking activity.
Side effects:
o nausea,
o vomiting,
o anxiety
o worry,
o sexual dysfunction,
o headaches,
o arousal.
The table shows various groups of antidepressants that differ in their mechanism of action.
Antidepressants (thymoanaleptics, thymoleptics)
Table 1.
A. Monoamine oxidase (MAO) inhibitors |
|
A) irreversible MAO inhibitors: § Nialamid, § Phenelsine | b) reversible MAO inhibitors: § befolum, § Feprosidnin HCL |
B. Neuronal uptake inhibitors: |
|
A) non-selective neuronal uptake inhibitors: | b) selective neuronal uptake inhibitors: |
2. four-cycle antidepressants : § maprotilin, § Mianserin | § Burtriptyline, § Fluoxetine § Nefazodon, § Paroxetine § Sertralin, § Venflaxin. |
IN. Antidepressants differentgroups: § cephedrinum, § Citalopram, § Tryptophan. |
|
D. Drugs of other pharmacological groups with antidepressant action: § Ademetionin. |
V. Evaluation of the effectiveness of the use of antidepressants in the treatment of CHD.
In a review of the current literature on the use of antidepressants for analgesia (Onghena, Van Houdenhove, 1992) in placebo-controlled studies, it is known:
1. among the population of patients with chronic kidney disease receiving antidepressants, on average, the effect occurs in 74%.
2. when using antidepressants, the magnitude of the analgesic effect is independent of the predominantly organic or psychological basis of the pain.
3. The magnitude of the analgesic effect does not depend on the antidepressant activity of the drug, the presence of masked depression, and the use of antidepressants as sedatives. As a result, antidepressants with a more pronounced sedative effect should be used in patients with sleep disorders to reduce the risk of addiction to hypnotics.
4. there is no obvious advantage in choosing selective antidepressants (serotonin or norepinephrine). Antidepressants with low selectivity in the inhibition of monoamine reuptake have a large analgesic effect.
Efficacy versus complications ratio of antidepressants (McQuay et al. 1996)
Chronic pain syndromes | NNT (number needed to treat) NNT - the number of patients who need to be treated in order to achieve a certain effect) |
||
Pain reduction (>50%) | Minor side effects | Big Side Effects |
|
Diabetic neuropathy | 19,6 |
||
Postherpetic neuralgia | 19,6 |
||
Atypical facial pain | |||
Central pain | |||
Imipramine | |||
Desipramine | |||
Combined TCAs | |||
Paroxetine | |||
fluoxetine | 15,3 | ||
Mianserin |
Pain is the number one reason patients seek medical attention. It accompanies most diseases and pathological conditions. On the one hand, pain is an adaptive reaction aimed at mobilizing the body's defenses, however, intense acute or chronic pain itself becomes a powerful pathogenic factor, leading to a sharp limitation in activity, sleep disturbance, significantly reducing the patient's quality of life.
On May 17-19, Uzhgorod hosted the VI scientific and practical conference "Carpathian Reading", within the framework of which a school of clinical neurosciences was held, dedicated to the diagnosis and treatment of pain syndromes in neurology and strokeology.
The report "Post-stroke pain syndrome" was made by V.N. Mishchenko (Institute of Neurology, Psychiatry and Narcology, Kharkov).
In the modern world, cerebrovascular diseases are a huge medical and social problem. This is due to the high level of morbidity, mortality and disability of the population. In the structure of vascular diseases, the leading place belongs to cerebral stroke - 150-200 cases per 100 thousand of the population. Every year, about 16 million people suffer from a stroke for the first time, and about 7 million people die as a result of it. Only 10-20% of stroke survivors return to work, and 20-43% of patients require outside help.
A fairly common consequence of a cerebral stroke is post-stroke pain, which is noted by 11 to 53% of patients. The most common types of chronic pain after a stroke are musculoskeletal pain - in 40% of cases, pain in the shoulder joint - 20%, headache - 10%, central post-stroke pain (CPBP) - 10%, painful spasticity - 7%.
Central post-stroke pain is a pain syndrome that develops after an acute cerebrovascular accident. It is characterized by pain and sensory disturbances in those parts of the body that correspond to the area of the brain damaged by the vascular focus. Central post-stroke pain belongs to the group of chronic pain disorders, which are combined into the concept of "central neuropathic pain" (Henriett K., Nanna B. et al., 2009).
Central neuropathic pain occurs as a direct consequence of damage or disease affecting the central somatosensory system, as well as as a result of pathological effects on the spinothalamocortical pathways of the central nervous system.
The most common causes of central neuropathic pain are: ischemic and hemorrhagic strokes, multiple sclerosis, spinal cord injury, vascular malformations, syringomyelia, space-occupying lesions of the brain and spinal cord, epilepsy, brain infection (encephalitis). Among all nosological forms of damage to the nervous system, the prevalence of neuropathic pain in cerebral stroke is 8-10% (Yakhno N.N., Kukushkin M.L., Davydov O.S., 2008).
The concept of central post-stroke pain was first proposed by Edinger in 1891. After 15 years, Dejerine and Roussy in their famous work "Thalamic Syndrome" described the central post-stroke pain. It was characterized as strong, persistent, paroxysmal, often unbearable, arising on the side of hemiplegia, in which treatment with painkillers did not give an effect. Pathological examination revealed lesions in the thalamus and in the posterior tubercle of the internal capsule in 3 out of 8 patients. In 1911, Head and Holmes described in detail the loss of sensation and pain in 24 patients with a stroke, the clinical symptoms of which indicated damage to the thalamus and were accompanied by central pain. In 1938, Riddoch described the clinical manifestations of pain of thalamic and extrathalamic origin.
From the standpoint of pathophysiology, central neuropathic pain occurs when the CNS is damaged with the involvement of nociceptive structures, which leads to a change in nociceptive neurons, as well as to a decrease in the activity of antinociceptive descending influences. A possible mechanism for the development of central post-stroke pain is a functional imbalance between the lateral and medial parts of the nociceptive system, as well as a violation of the control of cortical and thalamic structures over incoming pain information. CPIB can occur when the somatosensory pathways of the brain are affected at any level, including the medulla oblongata, thalamus, and cerebral cortex.
Thus, in the pathophysiology of central post-stroke pain, the following play an important role:
1. Central sensitization causing chronic pain.
2. Violation in the form of hyperexcitability and activity in the spinothalamic tract.
3. A lesion in the lateral thalamus that interrupts inhibitory pathways and causes disinhibition of the medial thalamus (disinhibition theory).
4. Changes in the thalamus, since it plays the role of a pain generator and there is a loss of inhibitory GABA-containing neurons and activation of microglia.
According to MacCoulan et al., 1997, the incidence of central post-stroke pain depends on the location of the stroke. As a rule, it occurs with a lateral infarction of the medulla oblongata (Wallenberg's syndrome) and with damage to the posteroventral part of the thalamus.
Thalamic infarction is characterized by a triad of symptoms: anterograde amnesia, impaired perception of information, and spatial disturbances. With a heart attack in the area of blood supply of the paramedian thalamic-subthalamic arteries, an acute impairment of consciousness is observed. Hypersomnia is possible: patients are awake, but may fall into a deep sleep soon after cessation of stimulation. They experience apathy, indifference, lack of motivation. Oculomotor vertical paresis is revealed.
With a large infarction focus in the paramedial thalamus, aphasia, transient or persistent dementia joins. Lesions located symmetrically in the paramedial thalamus cause a disinhibition syndrome, including manic delirium, infantilism, or Kluver-Bucy syndrome.
The clinical picture of CPIB is characterized by its occurrence immediately after a stroke or several months after it. Pain occurs in the right or left side of the body, although in some patients it may be local: in one arm, leg or face. It is chronic, severe, persistent. Sometimes it occurs spontaneously or is caused by the action of an irritant. Patients characterize it as burning, aching, chilling, squeezing, penetrating, shooting, excruciating, debilitating. An obligatory symptom of CPIB is a violation of sensitivity: temperature, pain, less often tactile or vibrational, according to the type of hypesthesia or hyperesthesia. Pain significantly affects the quality of life of patients, disrupts sleep, and impairs the effectiveness of rehabilitation.
Neuropathic pain syndrome is characterized by a symptom complex of specific sensory disorders, such as allodynia (appearance of pain in response to a non-painful stimulus), hyperalgesia (increased sensitivity to a painful stimulus), hyperesthesia (increased response to a tactile stimulus), hypesthesia (loss of tactile sensitivity), hypalgesia (decrease pain sensitivity), feeling of numbness, crawling.
Among the diagnostic criteria for central post-stroke pain, obligatory and auxiliary ones are distinguished.
The mandatory diagnostic criteria of the CPIB include:
1. Localization of pain according to the lesion in the central nervous system.
2. History of stroke and onset of pain at the same time as the stroke or later.
3. Confirmation of the presence of a CNS lesion on imaging, or negative or positive sensory symptoms that are limited to the area corresponding to the lesion.
4. Other causes of pain, such as nociceptive or peripheral neuropathic pain, are ruled out or considered unlikely.
Auxiliary diagnostic criteria:
1. No causal relationship to movement, inflammation, or other types of local tissue damage.
2. Pain sensations are burning, aching, pressing, tingling. Possible pain, resembling an insect bite, electrical discharge, painful cold.
3. Presence of allodynia or dysesthesia when exposed to cold or touch.
The following system is used in evaluating clinical cases for compliance with the CPIB criteria:
1. Exclusion of other potential causes of pain. There are no other obvious causes of pain.
2. The pain has a clear and anatomically justified localization. It is localized unilaterally to the CNS focus on the body and/or face, or unilaterally on the body with contralateral involvement of the face.
3. History of stroke. Neurological symptoms developed suddenly; the pain appeared simultaneously with the stroke or later.
4. Identification of clear and anatomically justified disorders during clinical neurological examination. During this examination of the patient, a violation of sensitivity (with a positive or negative sign) is detected in the painful area. The pain is localized in the zone of sensitive disorders, and its location can be anatomically justified by the localization of the lesion in the central nervous system.
5. Identification of the corresponding vascular focus using neuroimaging methods. When conducting CT or MRI, a pathological focus is visualized, which can explain the localization of sensitivity disorders.
Thus, the diagnosis of CPIB is based on the history of the disease, the results of a clinical and neurological examination. Information about the onset of pain, its nature, the presence of dysesthesia or allodynia, and sensory disturbances are taken into account. A visual analog scale is used to assess pain, as well as neuroimaging data (CT or MRI of the brain).
According to the recommendations of the European Federation of Neurological Societies on the pharmacotherapy of neuropathic pain syndrome (2010), the following groups of drugs are used in the treatment of CPIB: antidepressants, anticonvulsants (Ca channel agonists - gabapentin, pregabalin; Na channel blockers - carbamazepine), opioid analgesics, local drugs drugs (lidocaine, etc.), NMDA receptor antagonists (ketamine, memantine, amantadine), as well as neurostimulation.
Based on the extensive experience of doctors dealing with this problem, as well as data from placebo-controlled studies, it has been established that the most effective approach in the treatment of CPIB is the prescription of antidepressants.
The mechanism of action of antidepressants is to block the reuptake of neuronal monoamines (serotonin, norepinephrine) in the central nervous system. The greatest analgesic effect was observed in amitriptyline. Pronounced analgesic properties have duloxetine, venlafaxine, paroxetine. The development of an analgesic effect in the treatment of patients with pain syndromes with antidepressants is associated with an increase in the tonic activity of the antinociceptive system, which occurs as a result of serotonin- and noradrenergic inhibition of nociceptive neurons due to inhibition of monoamine reuptake by presynaptic endings. This leads to the accumulation of mediators in the synaptic cleft and an increase in the efficiency of monoaminergic synaptic transmission. In addition to the actual analgesic effect, antidepressants potentiate the effect of narcotic analgesics by increasing their affinity for opioid receptors.
There were 17 studies examining the efficacy and safety of 10 antidepressants in the treatment of neuropathic pain syndrome. In the course of these studies, it was found that there is no significant difference in the effectiveness of antidepressants with different mechanisms of action. Venlafaxine and duloxetine, both serotonin and norepinephrine reuptake inhibitors, have been shown to be effective in the treatment of diabetic polyneuropathy. Trazodone (Trittico) at a dosage of 50-300 mg / day has shown in a number of studies its effectiveness in the treatment of pain in conditions such as fibromyalgia (Molina-Barea R. et al., 2008), diabetic neuropathy (Wilson R.C., 1999), migraine pains (Brewetton T.D. et al., 1988), chronic pain (Ventafridda V. et al., 1988, Fig. 1).
Thus, at a dose of up to 225 mg/day, Trittiko was not inferior in analgesic effect to amitriptyline in the treatment of pain in oncological practice. At the same time, taking Trittiko provided severe oncological patients with a significantly shorter hospital stay, the ability to lead an active lifestyle without pain and side effects that occur when taking amitriptyline (Fig. 1).
Trazodone is a modern alternative to amitriptyline in the complex treatment of patients with chronic pain syndrome.
The Board of the World Congress on Neuropsychopharmacology (Canada, Montreal, 2002) defined trazodone (Trittico) as an atypical antidepressant with a predominant sedative and anxiolytic effect, the first and only representative of type 2 serotonin receptor antagonists and serotonin reuptake inhibitors (SARI) in Ukraine. According to its pharmacological parameters, trazodone belongs to the group of serotonin receptor antagonists (5-HT) and selective serotonin reuptake inhibitors (SSRIs). Of all the types of medicinal effects characteristic of it, the blockade of serotonin receptors is more pronounced than the inhibition of serotonin reuptake. Trazodone (Trittico) acts as an antagonist at the serotonin 2A receptor subtype and as a partial agonist at the 5-HT1A receptor. This leads to its use in depression, sleep disturbance, anxiety, sexual dysfunctions. The drug also has a pronounced effect on alpha-1-adrenergic receptors and inhibits the reuptake of serotonin less powerfully (Stephen M., Stahl M., Fig. 2).
Thus, due to the unique complex multifunctional action on the receptor profile, trazodone provides a powerful antidepressant and anxiolytic effect in combination with the restoration of sleep disorders, including those caused by SSRIs.
Trazodone (Trittico) has a powerful proven antidepressant effect, which is very important for post-stroke patients. According to different authors, the incidence of post-stroke depression ranges from 25 to 79%. Moreover, it is important to note that its development is possible both in the early and late periods after a stroke, although the maximum frequency of depressive episodes is recorded in the recovery period of ischemic stroke.
Trazodone (Trittico) is characterized by a pronounced anti-anxiety effect, starting from the first days of therapy. In a double-blind, placebo-controlled, randomized study in which 230 patients took part, trazodone was shown to be effective and well tolerated in generalized anxiety disorder. The patients were divided into 3 groups. Group 1 received imipramine 143 mg/day, group 2 received trazodone 225 mg/day, and group 3 received diazepam 26 mg/day. After 8 weeks of therapy, 73% of patients in the imipramine group, 69% in the trazodone group, 66% in the diazepam group, and only 47% in the placebo group noted a moderate or significant improvement in their condition (Fig. 3).
The study confirmed that trazodone was highly effective and significantly better tolerated than other drugs.
The effectiveness of Trittico in the treatment of patients with frontotemporal dementia has been proven. The use of the drug at a maximum dose of 250 mg / day (dose titration begins with 50 mg) for 9 weeks leads to a noticeable improvement in symptoms: a decrease in arousal, irritation, depression, normalization of eating behavior.
Trittiko is characterized by excellent tolerability, comparable to SSRIs, which is very important for stroke patients and ensures high adherence to this therapy. The drug does not cause an anticholinergic effect, agitation, sleep disturbance, sexual dysfunction, orthostatic hypotension, weight gain, ECG changes, inhibition of platelet aggregation. There may be minor gastrointestinal disturbances, such as nausea, vomiting, diarrhea, and possible drowsiness.
Dosing of Trittiko is carried out as follows. During the 1-3rd day, 50 mg is prescribed at bedtime (1/3 of the table), which improves sleep. On the 4-6th day, the dose is 100 mg at bedtime (table 2/3), which causes an anxiolytic effect. From the 7th to the 14th day for an antidepressant effect, the dose is increased to 150 mg at bedtime (table 1). And from the 15th day, to consolidate the antidepressant effect, the dose of 150 mg is retained or increased to 300 mg (Table 2).
Thus, Trittico (trazodone) is the first and only representative of the SARI class in Ukraine, which has the world's largest evidence base and has established itself as an effective antidepressant for the elimination of symptoms of depression, anxiety, sleep disorders, as well as in the treatment of patients with chronic pain syndrome.
Prepared by Tatyana Chistik
Any origin. Their analgesic effect is not associated with the antidepressant effect itself.
They are comparable in effectiveness with folk remedies http://golovnieboli.ru/drugie-stati/narodnye-sredstva-ot-golovnoj-boli. The most widely used antidepressants are amitriptyline and imipramine (melipramine).
Imipramine is first prescribed at 10 mg / day, then the dose is increased every week until the effect is achieved (maximum up to 150 mg / day). The drug, to a lesser extent than amitriptyline, gives a sedative effect, but due to the pronounced anticholinergic effect and adverse cardiac effects, many patients cannot take it for a long time.
Tricyclic antidepressants, especially amitriptyline, can reduce heart rate variability, exacerbate cardiovascular autonomic dysfunction, and increase orthostatic hypotension. Therefore, they are prescribed with caution to persons with diseases of the cardiovascular system, autonomic neuropathy.
Serotonin reuptake inhibitors (attention - selective) block the uptake exclusively of serotonin.
Citalopram (Cipramil) and Paxil, but not fluoxetine, may have an independent analgesic effect in some types of neuropathic pain - diabetic polyneuropathy.
Sometimes for headaches, a combination in the treatment of low doses of three cyclic antidepressants with some selective serotonin reuptake inhibitors with a short half-life (citalopram) is possible. Citalopram does not inhibit the activity of the microsome and liver enzymes, so its combination with tricyclic drugs is safer.
However, with a general good tolerance, SSRIs often cause side effects from the stomach, intestinal tract, and may even increase the risk of gastric bleeding (especially when taking NPS in parallel). Also, they are able to cause sexual dysfunction (erection dysfunction in men, anorgasmia in women), only aggravating the headache, and patients with autonomic neuropathy may be especially sensitive to this side effect.
With poor tolerance, ineffectiveness of only one tricyclic antidepressants, it is possible to use uptake inhibitors and serotonin and noradrenaline, for example, venlafaxine (effexor), up to 225 mg / day, duloxetine 60 mg / day.
The article was prepared and edited by: surgeonVideo:
Healthy:
Related articles:
- Almost everyone gets a headache sooner or later. Headaches are in the top 20 most...
- It seems that special if the head hurts. Yes, every second it hurts. But the pain is...
- Headaches (HA) can occur with repeated intake of various substances. The so-called...
Few people pay attention to recurrent pain in the back. Some are sure that it's just fatigue, pulled a muscle or blew through the wind. But, when chronic back pain becomes a constant companion, we can talk about the presence of serious pathologies.
Causes of the disease
The most common cause of pain is, as a result of which the intervertebral discs lose their cushioning properties. They become less elastic, the joints are pressed too hard against each other.
As a result, the surface of the vertebrae is erased or dense growths begin to form on it, which in medical terminology are called osteophytes.
The ongoing changes in the spine are associated with the excessive load exerted on it. The vertebrae press against each other and, as a result, shift, causing irreversible changes in the structure itself and the joints.
Some of the causes of chronic back pain include:
- Work related to permanent sitting (office employees, drivers);
- Lack of activity, sedentary lifestyle;
- Age changes;
- Overweight;
- Bad habits (smoking);
- Past unhealed injuries;
- Scoliosis.
Chronic pain that does not stop for three months or more may indicate the development of a serious illness and require a visit to the clinic. The treatment process is usually lengthy and will require the patient to adhere to a certain regimen, as well as lifestyle changes.
How to get rid
To alleviate the patient's condition, the attending physician may prescribe analgesic drugs, glucocorticoids, tranquilizers, or antidepressants.
Antidepressants for chronic back pain are prescribed to normalize sleep and the general psychological state of the patient (disappearance of irritability, nervousness, neuroses, etc.).
By acting on the nervous system, drugs lower the pain threshold, improve a person’s internal mood, motivating him to and.
During an exacerbation, it is better to adhere to bed rest and exclude gymnastics at this stage and.
Treatment with antidepressants is based on the mechanism of retention of neurotransmitters in brain tissues. It is absolutely impossible to take them uncontrollably. At some stage, the patient may become addicted. Therefore, when prescribing a doctor, it is strictly necessary to observe the recommended dose and duration of administration.
Therapy
In the treatment of chronic pain syndrome, drugs of the tricyclic group have proven their effectiveness, the most famous of which is Amitriptyline. How to take amitriptyline for chronic back pain correctly, the attending physician will tell. But most importantly, you should pay attention to the following points:
- A high dose, as in depression, is not required. To alleviate the condition, 1, less often 2, tablets per day is enough;
- Treatment of chronic back pain is a long process, you will need to take the drug for at least 6 months, a year or more;
- Taking antidepressants may cause side effects.
In recent years, new generation drugs from the SSRI and SNRI groups have appeared, which, according to the principle of action, are not inferior to amitriptyline, have the same analgesic effect, but are safer for other human organs.
Chronic with the formation of painful nodules as a result of inflammation can lead to complete atrophy of the muscular corset.
This disease develops as a result of infections, toxic effects, injuries and professional activities. In the acute form, the patient is shown bed rest, conservative treatment and antidepressants.
Chronic tension of the back muscles can provoke involuntary contractions of one or an entire group of muscles, which are accompanied by a sharp incessant pain for a short period of time.
If such contractions are regular, then we can talk about chronic spasm of the back muscles. Spasms occur because the body is trying to independently limit the mobility of a weakened muscle in a certain area of \u200b\u200bthe spinal column.
The doctor in such cases may prescribe drugs from the trazodone drug group, in particular Trittiko for chronic back pain. The antidepressant has a hypnotic effect and eliminates sleep disturbances.
After stabilization of sleep and general mood, the quality of life improves, the physical and mental state returns to normal. Emotional state is very important for dealing with chronic pain and the desire to get rid of them.
Remember that painkillers for chronic back pain should be taken strictly according to the doctor's prescription. Self-medication and uncontrolled use of pills can be dangerous to health.
A great way to get rid of pain and keep muscles in good shape will help advice from Alexandra Bonina.
If you want to get more information about this from Alexandra Bonina, check out the materials at the links below.
Denial of responsibility
The information in the articles is for general information purposes only and should not be used for self-diagnosis of health problems or for medicinal purposes. This article is not a substitute for medical advice from a doctor (neurologist, internist). Please consult your doctor first to know the exact cause of your health problem.
I will be very grateful if you click on one of the buttons
and share this material with your friends :)
Living in constant pain is a terrible burden. But, if depression is also added to the feeling of pain, then this burden becomes even more terrible.
Depression makes the pain worse. It makes life with pain unbearable. But the good news is that these states can be separated. Effective medications and psychotherapy help to get rid of depression, which in turn makes the pain more bearable.
What is chronic pain?
Chronic pain is pain that lasts much longer than simple pain. If the feeling of pain becomes constant, the body may respond to it in different ways. The phenomenon of chronic pain can be characterized as abnormal processes in the brain, low energy levels, mood swings, muscle pain, and a decrease in the capacity of the brain and body. The state of chronic pain worsens as neurochemical changes in the body increase susceptibility to pain. An overwhelming sense of pain causes irritability, depression and can lead to suicide in those who no longer believe in the possibility of getting rid of pain.
What are the consequences of depression on the background of chronic pain?
If you suffer from chronic pain and at the same time suffer from depression, then you are in a difficult situation. Depression is one of the most common mental illnesses associated with chronic pain. Often it worsens the patient's condition and the course of his treatment. Below are some statistics:
According to the American Pain Association, about 32 million people in the United States have had pain that lasted for more than a year.
Half of the people in the United States who went to the doctor with a problem of severe pain were depressed
On average, about 65% of people with depression complain of feeling pain.
People whose pain limits their independence are more likely to develop depression as well.
Since depression in patients with chronic pain goes unnoticed, it, accordingly, remains without proper treatment. Pain symptoms and complaints of the patient occupy all the doctor's attention. As a result, the patient develops a state of depression, sleep is disturbed, the patient loses appetite, energy and reduces physical activity, which provoke pain.
Is depression and pain a vicious circle?
Pain causes an emotional reaction in every person. If you feel pain, it is most likely that you also feel anxious, irritable, and agitated. And these are normal feelings when feeling pain. Usually, when the pain subsides, the emotional reaction subsides.
But with chronic pain, you feel constant tension and stress. Over time, a constant state of stress results in various mental disorders associated with depression. Symptoms common to chronic pain and depression include:
Constant anxiety
Confused thoughts
Reduced self-esteem
Stress associated with family problems
Fatigue
Fear of getting hurt
Worry about financial situation
Irritability
Worry about legal matters
Physical deterioration
Decreased sexual activity
Sleep dysfunction
Social self-isolation
Rapid weight gain or loss
Work anxiety
mood swings
Why is depression (almost on every count) the same as chronic pain?
Some overlaps of these diseases can be explained with the help of biology. Depression and chronic pain depend on the same neurotransmitter, a chemical produced in the brain that travels between nerve cells. Depression and pain also share common nerve cells.
The impact of chronic pain on a person's life can also cause depression. Chronic pain can empower you to deal with life's losses, such as loss of sleep, social life, personal relationships, sexual opportunities, loss of a job or income. These same life losses can cause you to become depressed.
In this case, depression increases the feeling of pain and reduces the ability to deal with these problems. If before you used to deal with stress through exercise, then with chronic pain, you will not be able to do this.
Researchers compared people with chronic pain and depression with those with only chronic pain without depressive symptoms and found the following facts. People with chronic pain have:
More intense pain
Inability to control your life
Unhealthy methods of dealing with the disease
Since depression and chronic pain are closely related to each other, they are often treated in combination. Moreover, it has been proven that a certain medicine can treat both depression and pain.
Is there a lifelong cure for depression and chronic pain?
Both chronic pain and depression can last a lifetime. Accordingly, the best remedy for both diseases is one that can be taken for a lifetime.
Since there is a relationship between these diseases, it is natural that the treatment should be interconnected.
Can antidepressants relieve pain and depression?
Since pain and depression are caused by the same nerve endings and neurotransmitters, antidepressants are used in the treatment of both conditions. Antidepressants affect brain function in ways that lower the pain perception threshold.
There is ample evidence for the effectiveness of tricyclic antidepressants such as Evalin and doxepin. However, due to side effects, their use is often limited. Recently released antidepressants, selective serotonin and norepinephrine reuptake inhibitors (Tsimbalta, Effexor), give good results with few side effects.
How can pain and depression be relieved through exercise?
Most people with chronic pain avoid sports. But, if you do not play sports, the risk of injury or pain increases. Playing sports is one of the most important stages of treatment, but provided that the physical exercises were chosen for you under the supervision of your doctor.
Exercise is also a good treatment for depression because it has the same effect as antidepressants.