8938 0
Amitriptylme
Antidepressants (tricyclics)
Release form
Dragee 25 mgCaps. 50 mg
R-r d/in. 20 mg/2 ml
Table 5 mg, 10 mg
Tablet, p.o., 10 mg, 25 mg
Mechanism of action
The mechanism of the antidepressant action of amitriptyline is associated with the inhibition of the reverse neuronal uptake of neurotransmitters by the presynaptic membranes of nerve endings, which increases the concentration of adrenaline and serotonin in the synaptic cleft and activates postsynaptic impulses. With long-term use, amitriptyline normalizes adrenergic and serotonergic transmission, restores the balance of these systems, disturbed in depressive states. In addition, amitriptyline blocks histamine and M-cholinergic receptors. The high affinity for M-cholinergic receptors determines both the central and strong peripheral cholinergic blocking effects of amitriptyline.Amitriptyline has sedative properties.
Main effects
■ The psychotropic effect develops within 2-3 weeks after the start of use: in anxiety-depressive conditions, anxiety, agitation and depressive symptoms decrease.■ The effectiveness of drugs for bedwetting is obviously associated primarily with peripheral anticholinergic activity.
■ Amitriptyline has a central analgesic effect, which is believed to be due to changes in the concentration of monoamines in the central nervous system (especially serotonin) and effects on endogenous opioid systems. Potentiates the effect of opioid analgesics.
■ During general anesthesia, amitriptyline reduces blood pressure and body temperature.
■ Reduces the secretion of the salivary glands.
■ A clear effect of drugs has been shown in patients with bulimia, both without and with depression.
Pharmacokinetics
Absorption is high. The bioavailability of amitriptyline through various routes of administration is 30-60%, its main metabolite, nortriptyline, is 46-70%. Connection with plasma proteins is up to - 96%, the maximum plasma concentration of 0.04-0.16 mcg/ml is achieved 2.0-7.7 hours after oral administration. At equal doses, when taking capsules, the maximum concentration is lower than when using tablets, which causes less cardiotoxic effect. Volume of distribution - 5-10 l/kg. Therapeutic blood concentrations for amitriptyline are 50-250 ng/ml, for nortriptyline - 50-150 ng/ml. Both compounds easily pass through histohematic barriers, including the blood-brain and placental barriers, and penetrate into breast milk.Amitriptyline is metabolized in the liver with the participation of the enzyme system of cytochromes CYP2C19, CYP2D6, undergoes the processes of demethylation, hydroxylation and N-oxidation, with the formation of active metabolites (nortriptyline, 10-hydroxy-amitriptyline) and inactive compounds. Has a “first pass” effect through the liver. Within 2 weeks, 80% of the administered dose is excreted mainly in the form of metabolites by the kidneys, partially in the feces. T1/2 of amitriptyline - 10-26 hours, nortriptyline - 18-44 hours.
Indications
■ Amitriptyline is effective in patients with chronic pain (especially chronic neurogenic pain: postherpetic neuralgia, post-traumatic neuropathy, diabetic or other peripheral neuropathies).■ Headache and migraine (prevention).
■ Depression, especially with anxiety, agitation and sleep disorders of various natures (endogenous, involutional, reactive, neurotic, medicinal, with organic brain damage, with alcohol withdrawal), the depressive phase of manic-depressive psychosis, schizophrenic psychoses, mixed emotional disorders.
Directions for use and doses
Amitriptyline is prescribed orally, intramuscularly and intravenously.For the prevention of migraines, for chronic pain of a neurogenic nature (including long-term headaches) - from 12.5-25 to 100 mg per day (the maximum dose is taken at night).
Contraindications
■ Hypersensitivity.■ Angle-closure glaucoma.
■ Epilepsy.
■ Prostatic hyperplasia.
■ Atony of the bladder.
■ Paralytic ileus, pyloric stenosis.
■ History of myocardial infarction.
■ Combined use with MAO inhibitors.
■ Pregnancy.
■ Lactation period.
■ Children under 6 years of age (for injection forms - 12 years).
Restrictions on use:
■ coronary heart disease due to tachycardia;
■ arterial hypertension;
■ peptic ulcer of the stomach and duodenum;
■ anxiety-paranoid syndrome with depression (due to the risk of suicide).
Cautions, therapy monitoring
Before starting treatment, it is necessary to determine blood pressure (in patients with low or labile blood pressure, it may decrease even more).During treatment, the peripheral blood picture should be monitored (in some cases, agranulocytosis may develop); during long-term therapy, monitoring the functional state of the liver.
In elderly people and in patients with cardiovascular diseases, monitoring of heart rate (HR), blood pressure, and electrocardiography readings is indicated. Clinically insignificant changes may appear on the electrocardiogram (smoothing of the T wave, depression of the S-T segment, widening of the QRS complex).
Parenteral use should only be carried out in a hospital setting, under the supervision of a physician, with bed rest in the first days of therapy. Caution should be exercised when suddenly moving to a vertical position from a lying or sitting position.
During the treatment period, ethanol consumption is unacceptable.
Amitriptyline is prescribed no earlier than 14 days after discontinuation of monoamine oxidase inhibitors. It should be taken into account that the therapeutic activity and severity of adverse reactions of amitriptyline are influenced by drugs of many pharmacological groups (see “Interaction”).
If you suddenly stop taking it after long-term treatment, withdrawal syndrome may develop.
In predisposed patients and elderly patients, amitriptyline can provoke the development of drug-induced psychoses, mainly at night (after drug withdrawal, they subside within a few days).
Amitriptyline can cause paralytic ileus, mainly in patients with chronic constipation, in the elderly or in patients forced to remain in bed.
Before performing general or local anesthesia, the anesthesiologist should be warned that the patient is taking amitriptyline.
The anticholinergic effect leads to a decrease in salivary secretion and dry mouth. With long-term use, an increase in the incidence of dental caries is observed. There is a decrease in tear production and a relative increase in the amount of mucus in the tear fluid, which can lead to damage to the corneal epithelium in patients using contact lenses.
The need for riboflavin may increase.
Amitriptyline passes into breast milk and may cause drowsiness in nursing infants.
Children are more sensitive to acute overdose, which is dangerous and potentially fatal for them.
During the treatment period, care must be taken when driving vehicles and engaging in other potentially hazardous activities that require increased concentration and speed of psychomotor reactions.
Prescribe with caution when:
■ chronic alcoholism;
■ bronchial asthma;
■ inhibition of bone marrow hematopoiesis;
■ stroke;
■ schizophrenia (possible activation of psychosis);
■ liver and/or kidney failure;
■ thyrotoxicosis.
Side effects
Anticholinergic cholinergic blocking effects:■ dry mouth;
■ blurred vision;
■ paralysis of accommodation;
■ mydriasis;
■ increased intraocular pressure (only in persons with a local anatomical predisposition - a narrow angle of the anterior chamber);
■ tachycardia;
■ confusion;
■ delirium or hallucinations;
■ constipation, paralytic intestinal obstruction;
■ difficulty urinating;
■ decreased sweating.
From the nervous system:
■ drowsiness;
■ asthenia;
■ fainting;
■ anxiety;
■ disorientation;
■ hallucinations (especially in elderly patients and patients with Parkinson's disease);
■ anxiety;
■ excitement;
■ motor restlessness;
■ manic state, hypomanic state;
■ aggressiveness;
■ memory impairment, depersonalization;
■ increased depression;
■ insomnia, “nightmare” dreams;
■ yawning;
■ asthenia;
■ activation of symptoms of psychosis;
■ headache;
■ myoclonus;
■ dysarthria;
■ tremors of small muscles, especially the arms, hands, head and tongue;
■ peripheral neuropathy (paresthesia);
■ myasthenia gravis;
■ ataxia;
■ extrapyramidal syndrome;
■ increased frequency and intensification of convulsive seizures;
■ changes in the electroencephalogram.
■ tachycardia;
■ heartbeat;
■ dizziness;
■ orthostatic hypotension;
■ nonspecific changes in the electrocardiogram (S-T interval or T wave) in patients who do not suffer from heart disease; arrhythmia; blood pressure lability; intraventricular conduction disturbance (widening of the QRS complex, changes in the P-Q interval, bundle branch block).
From the digestive system:
■ nausea.
Rarely:
■ darkening of the tongue;
■ increased appetite and body weight or decreased appetite and body weight;
■ stomatitis, change in taste (sour-bitter taste in the mouth);
■ hepatitis (including liver dysfunction and cholestatic jaundice);
■ heartburn;
■ vomiting;
■ gastralgia;
■ diarrhea.
From the endocrine system:
■ hypo- or hyperglycemia;
■ impaired glucose tolerance;
■ diabetes mellitus;
■ hyponatremia (decreased vasopressin production);
■ syndrome of inappropriate secretion of antidiuretic hormone.
From the reproductive system:
■ increase in size (swelling) of the testicles;
■ gynecomastia;
■ increase in the size of the mammary glands;
■ disturbances or delay in ejaculation;
■ decrease or increase in libido;
■ decreased potency.
From the blood system:
■ agranulocytosis;
■ leukopenia;
■ thrombocytopenia;
■ purpura;
■ eosinophilia.
Allergic reactions:
■ skin rash;
■ itching of the skin;
■ urticaria;
■ photosensitivity;
■ swelling of the face and tongue.
Other effects:
■ hair loss;
■ tinnitus;
■ swelling;
■ hyperpyrexia;
■ enlarged lymph nodes;
■ urinary retention;
■ pollakiuria;
■ hypoproteinemia.
Local reactions (with intravenous administration):
■ thrombophlebitis;
■ lymphangitis;
■ burning sensation;
■ skin reactions.
Overdose
Symptoms: effects develop 4 hours after an overdose, reach a maximum after 24 hours and last 4-6 days. If an overdose is suspected, especially in children, the patient should be hospitalized.From the side of the central nervous system:
■ drowsiness;
■ stupor;
■ coma;
■ ataxia;
■ hallucinations;
■ anxiety;
■ psychomotor agitation;
■ decreased ability to concentrate;
■ disorientation;
■ confusion;
■ dysarthria;
■ hyperreflexia;
■ muscle rigidity;
■ choreoathetosis;
■ seizures.
From the cardiovascular system:
■ decrease in blood pressure;
■ tachycardia;
■ arrhythmia;
■ violation of intracardiac conduction;
■ changes in the electrocardiogram (especially QRS) characteristic of intoxication with tricyclic antidepressants;
■ shock, heart failure; in very rare cases - cardiac arrest.
Others:
■ respiratory depression;
■ shortness of breath;
■ cyanosis;
■ vomiting;
■ mydriasis;
■ increased sweating;
■ oliguria or anuria.
Treatment: gastric lavage, administration of activated carbon, laxatives (overdose when taken orally); symptomatic and supportive therapy; for severe symptoms caused by blockade of cholinergic receptors, administration of cholinesterase inhibitors (the use of physostigmine is not recommended due to the increased risk of seizures); maintaining body temperature, blood pressure and water-electrolyte balance.
Monitoring the functions of the cardiovascular system for 5 days (relapse may occur after 48 hours or later), anticonvulsant therapy, artificial ventilation and other resuscitation measures are indicated. Hemodialysis and forced diuresis are ineffective.
Interaction
Synonyms
Amizol (Slovenia), Amirol (Cyprus), Adepren (Bulgaria), Amineurin (Germany), Amiton (India), Amitriptyline (Germany, Indonesia, Poland, Slovak Republic, France, Czech Republic), Amitriptyline Lechiva (Czech Republic), Amitriptyline Nycomed (Norway), Amitriptyline-AKOS (Russia), Amitriptyline-Grindeks (Latvia), Amitriptyline-LENS (Russia), Amitriptyline-Slovakofarm (Slovak Republic), Amitriptyline-Ferein (Russia), Apo-Amitriptyline (Canada), Vero- Amitriptyline (Russia), Novo-Triptin (Canada), Sarotene (Denmark), Sarotene retard (Denmark), Triptisol (India), Elivel (India)G.M. Barer, E.V. Zoryan
When conducting differentiated therapy for pain syndromes of non-cancerous origin, it is important to remember the fundamental differences between acute and chronic pain:sharp pain evolutionarily is a protective mechanism for exo- or endogenous damage and is transmitted by the nociceptive system
chronic pain more often it represents an inadequately high, prolonged and persistent response to certain damaging factors and can be transmitted both nociceptively and exist on the basis of pathological interneuronal circulation of impulses mainly at the central level - neuropathic pain.
Based on these ideas, traditionally used in the treatment of nociceptive pain analgesics or non-steroidal anti-inflammatory drugs (NSAIDs). Drugs are used to treat neuropathic pain, antidepressants and antiepileptic drugs (ADs and AEDs) that affect the neurotransmitter system.
In patients with neuropathic pain syndrome:
available complaints for burning, stabbing, shooting or aching pain, accompanied by trembling, paresthesia, and a feeling of numbness
characteristic allodynia– the feeling of pain evoked by normal, non-painful stimuli
the pain usually gets worse at night or during physical activity
When establishing chronic pain syndrome (CPS) (with the exception of CPS of cancer origin), it is necessary to determine which type of it (peripheral neuropathic pain, central neuropathic pain or pain not associated with neuropathy) the patient has, which will influence therapeutic tactics:
Peripheral neuropathic pain
Complex local pain syndrome
Neuropathy caused by HIV
Idiopathic peripheral neuropathy
Infection
Metabolic disorders
Alcohol, toxins
Diabetic neuropathy
Nutrient deficiency
Nerve compression
Phantom limb pain
Postherpetic neuralgia
Trigeminal neuralgia, etc.
Central neuropathic pain
Multiple sclerosis
Myelopathy
Parkinson's disease
Post-stroke pain, etc.
Pain not associated with neuropathy or non-neuropathic (elements of neuropathic pain may overlap with the main symptoms)
Arthritis
Osteoarthritis
Chronic lumbar pain
Chronic neck pain
Fibromyolgia
Post-traumatic pain, etc.
NB!!!Transmission of pain impulses through the spinal cord and brain:
carried out with the participation of excitatory and inhibitory neurotransmitters
limited by the degree of activity of sodium and calcium channels.
Norepinephrine, serotonin and to the greatest extent gamma-aminobutyric acid(GABA) are physiological inhibitors of pain transmission.
Antidepressants And antiepileptic drugs reduce the severity of pain by influencing these neurotransmitters and ion channels.
Tricyclic antidepressants (TCAs):
affect pain transmission at the level of the spinal cord, inhibiting the reuptake of norepinephrine and serotonin, which, when accumulated, inhibit the transmission of pain impulses
H1-receptor agonism and associated sedation correlate with the analgesic effects of TCAs
Amitriptyline is also effective in patients with acute pain.
TCAs can be conveniently divided into secondary and tertiary amine derivatives:
secondary amines(nortriptyline, desipramine) quite selectively block the neuronal uptake of norepinephrine
tertiary amines(amitriptyline, imipramine) almost equally inhibit the uptake of norepinephrine and serotonin, and also have a pronounced anticholinergic effect
“New antidepressants” venlafaxine and duloxetine:
inhibit neuronal reuptake of norepinephrine and serotonin without affecting other neuroreceptors
do not have anticholinergic effects
Mechanism of action of bupropion associated with blockade of dopamine reuptake (the other mechanisms of action of the drug are not fully understood).
Antiepileptic drugs (AEDs):
inhibit excitation in neurons
enhance inhibition processes
These drugs affect:
voltage-gated sodium and calcium ion channels
ligand-gated ion channels
specific receptors for glutamate and N-methyl-D-aspartate
excite glycine and GABA receptors
Clinical effectiveness of AD and PEP in chronic heart disease
Neuropathic pain
1. The effectiveness of TCAs in the treatment of neuropathic pain has been confirmed in clinical studies.
2. Other ADs show variable effects in this pathology
Nonselective ADs or ADs with noradrenergic activity are most effective for neuropathic pain.
Amitriptyline and nortriptyline have the largest evidence base of all ADs in the treatment of neuropathic and non-neuropathic pain syndromes.
The effect of TCAs correlates with their antidepressant effects.
Drugs with serotonergic activity (such as fluoxetine) are usually ineffective in the treatment of CHD.
3. Traditionally, AEDs are used in the treatment of patients with neuropathic pain, and the first generation drug carbamazepine is used most often, especially in the presence of:
trigeminal
postherpetic neuralgia
pain syndrome due to diabetic neuropathy
Frequency of pain relief in trigeminal neuralgia while taking carbamazepine fluctuates, according to various authors, in the range of 58–90%, and for diabetic neuropathy reaches 63%, which, along with economic accessibility, determines the widespread use of the drug in these diseases.
4. Second generation AEDs also have a convincing basis for their effectiveness in neuropathic pain. In clinical studies, gabapentin was more effective than placebo in patients with diabetic neuropathy and postherpetic neuralgia. Pregabalin has similar properties.
5. Lamotrigine has demonstrated effectiveness in:
trigeminal neuralgia
neuralgia associated with HIV infection
post-stroke pain syndrome
nonspecific refractory neuropathic pain
Long-term use of lamotrigine is largely limited by the risk of life-threatening skin reactions.
6. AD and AEDs are generally comparable in effectiveness for chronic heart disease; there are differences only in the use and tolerability of drugs within these groups.
Non-neuropathic pain
1. In most cases, TCAs are effective for various non-neuropathic pain syndromes (although the severity of their action may decrease over time); other ADs and AEDs do not demonstrate activity in these conditions.
2. ADs have an average degree of effectiveness in reducing the severity of pain and anxiety, improving sleep and the general condition of patients with fibromyalgia.
3. Fluoxetine has a significant effect in pain syndrome associated with fibromyalgia at a dose of 80 mg/day and does not have such an effect at a dose of 20 mg/day.
4. Among AEDs, duloxetine and pregabalin are considered effective for fibromyalgia.
5. ADs have a significant (but weak) effect on chronic lumbar pain. AD with predominant serotonergic activity has the least effect.
Information about medications that can be used for CHD
Antidepressants
1. TCA
Adverse adverse reactions (ADRs): dry mouth, constipation, urinary retention, sedation, weight gain
Amitriptyline, imipramine 10–25 mg; increase by 10–25 mg/week to a dose of 75 to 150 mg at night
NPR: Pronounced anticholinergic effect, cannot be used in old age
Desipramine, nortriptyline 25 mg in the morning or at night; increase by 25 mg/week to 150 mg/day
NPR: Less pronounced anticholinergic effect
2. SSRIs (selective serotonin reuptake inhibitors)
Fluoxetine, paroxetine 10–20 mg/day, up to 80 mg/day for fibromyalgia
Adverse reactions: nausea, sedation, decreased libido, headache, weight gain; for chronic heart disease the effect is weak
3. “New” antidepressants
Bupropion 100 mg/day, increase by 100 mg/week to 200 mg twice a day
ADRs: anxiety, insomnia or sedation, weight loss, seizures (at dose above 450 mg/day)
Venlafaxine 37.5 mg/day, increased by 37.5 mg/week to 300 mg/day
Adverse reactions: headache, nausea, increased sweating, sedation, hypertension, seizures; serotonergic effects at a dose below 150 mg/day; serotonin and noradrenergic effects at doses above 150 mg/day
Duloxetine 20–60 mg/day in 1–2 doses for depression, 60 mg/day for fibromyalgia
Adverse reactions: nausea, dry mouth, constipation, dizziness, insomnia
Antiepileptic drugs
I generation
Carbamazepine (Finlepsin) 200 mg/day, increase by 200 mg/week to 400 mg 3 times/day (1200 mg/day)
Adverse reactions: dizziness, diplopia, nausea, aplastic anemia
Phenytoin 100 mg at night, dose increased weekly to 500 mg at night
Adverse reactions: nausea, dizziness, ataxia, slurred speech, anxiety, hematopoietic disorders, hepatotoxicity
II generation
Gabapentin 100–300 mg at night, increased by 100 mg every 3 days to 1800–3600 mg/day for 3 doses
Adverse reactions: drowsiness, fatigue, dizziness, nausea, sedation, weight gain
Pregabalin 150 mg at night for diabetic neuropathy; 300 mg 2 times a day for postherpetic neuralgia
Adverse reactions: drowsiness, fatigue, sedation, dizziness, nausea, weight gain
Lamotrigine 50 mg/day, increased by 50 mg every 2 weeks up to 400 mg/day
Adverse reactions: drowsiness, constipation, nausea, rarely life-threatening skin reactions
Living with 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 living with pain unbearable. But the good news is that these conditions can be separated. Effective medications and psychotherapy help relieve 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 react 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 decreased functioning of the brain and body. Chronic pain conditions worsen as neurochemical changes in the body increase susceptibility to pain. An overwhelming feeling of pain causes irritability, depression and can lead to suicide for those who no longer believe in the possibility of getting rid of pain.
What are the consequences of depression associated with 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 accompanying 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 had pain that lasted longer than a year.
Half of US residents who went to the doctor for severe pain were depressed
On average, about 65% of people with depression report feeling pain
People whose pain limits their independence are also more likely to develop depression.
Since depression in patients with chronic pain goes unnoticed, it therefore remains without proper treatment. Painful symptoms and complaints of the patient occupy all the attention of the doctor. As a result, the patient develops a state of depression, sleep is disturbed, the patient loses appetite, energy and reduces physical activity, which provokes 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 experiencing pain. Typically, 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 related to family problems
Fatigue
Fear of getting hurt
Worries about your financial situation
Irritability
Concern about legal issues
Deterioration in physical condition
Decreased sexual activity
Sleep dysfunction
Social self-isolation
Rapid weight gain or loss
Worry about work
Mood swings
Why is depression (in almost every way) the same as chronic pain?
Some of the similarities between these diseases can be explained using biology. Depression and chronic pain rely 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 give you the strength to cope with life's losses, such as loss of sleep, social life, personal relationships, sexual performance, loss of job or income. These same life losses can cause you to feel depressed.
In this case, depression increases the feeling of pain and reduces the ability to fight these problems. If you were previously used to dealing with stress through exercise, then with chronic pain, you will not be able to do this.
Scientists compared people with chronic pain and depression with those who suffered only chronic pain without symptoms of depression and found the following facts. People with chronic pain reported:
More severe pain
Inability to control your life
Unhealthy methods of dealing with illness
Since depression and chronic pain are closely related to each other, they are often treated together. Moreover, it has been proven that a certain medicine can treat both depression and pain.
Is there a cure for depression and chronic pain that can be used throughout your life?
Both chronic pain and depression can last a lifetime. Accordingly, the best medicine for both diseases is one that can be taken throughout your life.
Since there is a relationship between these diseases, it is natural that the treatment should be interrelated.
Can antidepressants relieve pain and depression?
Since pain and depression are caused by the same nerve endings and neurotransmitters, antidepressants are used to treat both conditions. Antidepressants affect the brain to reduce the threshold for pain perception.
There is ample evidence of the effectiveness of tricyclic antidepressants, such as Evaline and doxepin. However, due to side effects, their use is often limited. Recently released antidepressants, selective serotonin and norepinephrine reuptake inhibitors (Cymbalta, Effexor), provide good results with few side effects.
How can you relieve pain and depression through exercise?
Most people with chronic pain avoid exercise. But if you don't exercise, your risk of injury or increased pain increases. Playing sports is one of the most important stages of treatment, provided that physical exercises have been selected for you under the supervision of your doctor.
Exercise is also a good treatment for depression as it has the same effect as antidepressants.
Few people pay attention to periodic back pain. Some are sure that it was just fatigue, a pulled muscle, or a draft 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 shock-absorbing properties. 
They become less elastic, the joints are pressed too tightly 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 changes that occur in the spine are associated with excessive load placed on it. The vertebrae put pressure on each other and, as a result, become displaced, causing irreversible changes in the structure and joints.
The causes of chronic back pain include the following:
- Work involving constant sitting (office employees, drivers);
- Insufficient activity, sedentary lifestyle;
- Age-related changes;
- Overweight;
- Bad habits (smoking);
- Untreated past injuries;
- Scoliosis.
Chronic pain that does not stop for three months or more may indicate the development of a serious illness and requires treatment at the clinic. The treatment process is usually long 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 medications, 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 influencing the nervous system, medications reduce 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 and exercises at this stage.
Treatment with antidepressants is based on the mechanism of retention of neurotransmitters in brain tissue. It is strictly forbidden to take them uncontrollably. At some stage, the patient may become dependent. Therefore, when prescribed by a doctor, you must strictly adhere to the recommended dose and duration of use.
Therapy
In the treatment of chronic pain syndrome, drugs of the tricyclic group have proven effective, the most famous of which is Amitriptyline. Your doctor will tell you how to take amitriptyline correctly for chronic back pain. But most importantly, it is worth paying attention to the following points:
- A high dose, as for 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 muscle corset.
This disease develops as a result of infections, toxic effects, injuries and professional activities. In the acute form, the patient is prescribed bed rest, conservative treatment and antidepressants.
Chronic tension in the back muscles can provoke involuntary contractions of one or an entire group of muscles, which are accompanied by sharp, ongoing 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 tries to independently limit the mobility of a weakened muscle in a certain area of the spinal column.
In such cases, the doctor may prescribe drugs from the trazodone group of drugs, in particular Trittico for chronic back pain. The antidepressant has a hypnotic effect and eliminates sleep disorders.
After stabilization of sleep and general mood, the quality of life increases, the physical and mental state returns to normal. Emotional attitude is very important for dealing with chronic pain and the desire to get rid of it.
Remember that painkillers for chronic back pain should be taken strictly as prescribed by your doctor. Self-medication and uncontrolled use of pills can be dangerous to health.
An excellent way to get rid of pain and maintain muscle tone will be advice from Alexandra Bonina.
If you want to get more information like this from Alexandra Bonina, check out the materials on 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 therapeutic purposes. This article is not a substitute for medical advice from a doctor (neurologist, therapist). Please consult your doctor first to know the exact cause of your health problem.
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S.S. Pavlenko. Regional pain center. Novosibirsk
I. Concept of acute, chronic and pathological pain. Pathophysiological and clinical features of chronic pain. The main types of chronic pain syndromes. Neurochemistry of chronic pain.
Typically, acute pain is a symptom of some sudden pathology or tissue damage. Acute pain 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. Treatment of acute pain is usually aimed at eliminating the cause that caused this pain, or at minimizing 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, since 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 considered an independent disease with a primary pathological process in the somatic sphere and secondary dysfunction of the peripheral and central nervous system. Its main differences are the duration (at least 3 - 6 months), increased patient resistance to the therapy, and the absence of a direct dependence on the identification and elimination of the cause that caused it.
Chronic pain can be of three types:
- Pain resulting from continuous long-term exposure (herniated disc).
- Pain following an acute injury, but lasting well beyond the normal healing period (causalgia, regional pain syndrome, phantom pain).
- Pain without a specific, visible, noticeable cause (muscle tension headaches, migraines).
- Chronic pain is an independent disease, in the pathogenesis of which psycho-emotional and social factors are of leading importance. With chronic pain, there may be no direct connection between the pain and the cause that caused it.
- The mechanisms of development of chronic pain and depression involve common mediator systems.
- According to epidemiological studies, there is a strong connection between depression and chronic pain.
There are different classifications of chronic pain. Most of them are based on the localization of the pain syndrome: headaches, neck and back pain, facial pain, pain in the limbs, chest pain, abdominal pain, pain in the pelvic area.
There are also pains of somatic origin, neurogenic and psychogenic pain.
In the mechanisms of development of chronic pain, regardless of its location and origin, important importance is given to the mediator systems of the brain and spinal cord:
- Serotonergic
- Noradrenergic
- Dopaminergic
- GABAergic
- Peptidergic (opioid and non-opioid).
As a result of numerous clinical and experimental studies, the following has been established:
- Intrathecal administration of serotonin causes analgesia and inhibits the activity of dorsal horn neurons of the spinal cord caused by painful stimulation.
- When serotonin reuptake inhibitors are introduced into certain areas of the brain (the raphe nucleus magnum), which promotes the release of serotonin from synaptic terminals, an analgesic effect develops.
- Selective disruption of descending serotonergic pathways enhances the pain response.
Similar results were obtained when studying the influence of the adrenergic mediator system. It turned out that norepinephrine modulates pain signals both at the suprasegmental and spinal levels. Therefore, adrenergic receptor blockers increase pain sensitivity, and agonists (clonidine) inhibit the activity of nociceptive neurons in response to pain stimulation.
II. Chronic pain and depression.
Numerous clinical and epidemiological studies have established that there is a close connection between chronic pain and depression. Data on the prevalence of depression among patients with chronic pain range from 30 to 87%.
Some researchers consider depression to be the leading factor in decreased ability to work in patients with chronic pain, or the most significant motivation when seeking medical help.
However, the connection between depressive disorders and chronic pain does not seem clear, and there are various alternative versions of their cause-and-effect relationships:
- Chronic pain is a cause of depression.
- Patients with depression are more likely to experience pain.
- Chronic pain and depression are indirectly linked by other intervening factors (disability).
III. Pharmacotherapy of chronic pain. Adjuvant therapy. Use of antidepressants in the treatment of chronic pain.
In the drug therapy of chronic pain syndromes, two main groups of drugs are used:
- Analgesics (opioid and non-opioid)
- Adjuvant analgesics.
Adjuvant analgesics, or “coanalgesics,” are a heterogeneous group of drugs that provide analgesia either for specific pain syndromes or neutralize the side effects of opioids, allowing 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 represents precisely those conditions in which the use of more adjuvant agents leads to a positive effect. Among the latter, a significant place belongs to antidepressants.
Unfortunately, in widespread clinical practice, 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 chronic heart disease. Data from more than 60 clinical trials show the analgesic effect of antidepressants in the treatment of most CHD.
Antidepressants are believed to have an analgesic effect through three main mechanisms:
- Reduce depression.
- Potentiate the effect of analgesics or endogenous opiate peptides.
- They have their own analgesic properties, which consist in a long-term prolongation of the synaptic activity of norepinephrine and serotonin.
CBP is a general indication for the use of antidepressants, but some pain syndromes are an obligatory indication for their use. 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 for CHD.
The table shows different groups of antidepressants that differ in their mechanism of action.
In the treatment of CHD, antidepressants are used - inhibitors of neuronal uptake of neurotransmitters: non-selective and selective.
The first group includes tricyclic And four-cycle antidepressants.
1. Tricyclic antidepressants(amitriptyline, imipramine, clomipramine).
Their pharmacological action 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 from 10 to 25 mg in the evening, before bed, followed by an increase in the daily dose by 10-25 mg every 3-7 days to a maximum of 75 mg (migraine, tension headaches) to 150 mg (neuropathic pain ). By the end of the first week, an analgesic effect is possible, at 2-3 weeks a psychotropic effect occurs - mood improves, ability to work increases, and anxious anticipation of pain disappears. Therapy is carried out for several months with gradual withdrawal.
Side effects:
- Cholinergic: dry mouth, blurred vision, constipation, urinary retention, sinus tachycardia, dizziness.
- Histaminergic: drowsiness, weight gain.
- Adrenergic: orthostatic hypotension, cardiotoxicity.
2. Quadruple cyclic antidepressants(maprotiline-ludiomil, mianserin-lerivone). They have a predominant effect on the noradrenergic transmitter system. There is evidence of the effectiveness of Mianserin (Lerivon) in the treatment of muscle tension headaches. In addition, the drug is convenient when it is necessary to obtain a sedative effect. In our practice, Mianserin was used with good effect for pain in the lower back at a dose of 10 to 30 mg per day.
Drugs in this group have minimal side effects, which include drowsiness, weight gain and orthostatic hypotension.
Selective serotonin reuptake inhibitors (fluoxetine-Prozac, venflaxine, nefazodone, sertraline-Zoloft, paroxetine-Paxil).
The role of selective inhibitors in the treatment of chronic pain is controversial and there are few clinical trials to prove their effectiveness in neurogenic pain.
Fluoxetine (Prozac) is best known for the treatment of headaches: migraines and, especially, chronic tension headaches. Prescribed 1 capsule (20 mg) 1 time per day for 6-8 weeks. According to Russian authors (A.M. Vein, T.G. Voznesenskaya, etc.), a significant effect was obtained in 65% of patients. It has been proven that fluoxetine causes a statistically significant reduction in the frequency of attacks and their duration.
Selective inhibitors have minimal anticholinergic and α-adrenergic blocking activity and thus minimal side effects (nausea, vomiting, anxiety and restlessness, sexual dysfunction, headaches, agitation).
V. Evaluation of the effectiveness of the use of antidepressants in the treatment of chronic heart disease.
According to recent reviews of the use of antidepressants for analgesia (Onghena, Van Houdenhove, 1992) in placebo-controlled studies:
- On average, among the population of patients with chronic heart disease receiving antidepressants, the effect occurs in 74%.
- The magnitude of the analgesic effect when using antidepressants is independent of the predominantly organic or psychological basis of pain.
- The magnitude of the analgesic effect does not depend on the antidepressant activity of the drug, the presence of masked depression, or the use of antidepressants as sedatives. Therefore, antidepressants with a more pronounced sedative effect should be used in patients with sleep disorders to reduce the risk of addiction to hypnotics.
- There is no obvious advantage in choosing selective antidepressants (serotonin or norepinephrine). However, antidepressants with low selectivity in inhibiting monoamine reuptake have a greater analgesic effect.
Antidepressants
(thymoanaleptics, thymoleptics)
|
A. Monoamine oxidase inhibitors (MAO) A) irreversible MAO inhibitors: Nialamid, Phenelsine |
|
B. Neuronal uptake inhibitors:
|
|
B. Antidepressants of different groups: Cephedrinum, Citalopram, Tryptophan. |
|
D. Drugs of other pharmacological groups with antidepressant effects: Ademetionin. |
TRICYCLIC ANTIDEPRESSANTS
|
The initial dose is from 10 to 25 mg in the evening, before bed, followed by an increase in the daily dose by 10-25 mg every 3-7 days to a maximum of 75 mg (migraine, tension headaches) to 150 mg (neuropathic pain). By the end of the first week, an analgesic effect is possible; at 2-3 weeks, a psychotropic effect occurs. The duration of treatment is several months with gradual withdrawal. Side effects: 1. Cholinergic: dry mouth, blurred and blurred vision, constipation, urinary retention, sinus tachycardia, dizziness. 2. Histaminergic: drowsiness, weight gain. 3.Adrenergic: orthostatic hypotension, cardiotoxicity. |
Efficacy versus complications of antidepressants (McQuay et al. 1996)
| Chronic pain syndromes | NNT (number needed to treat) NNT - number of patients, which must be treated to achieve a certain effect) |
||
| Pain reduction (>50%) | Minor side effects | Big side effects | |
|
Diabetic neuropathy |
3 | 2,8 | 19,6 |
|
Postherpetic neuralgia |
2,3 | 6 | 19,6 |
|
Atypical facial pain |
2,8 | - | - |
|
Central pain |
1,7 | 2 | - |
|
Imipramine |
3,7 | - | - |
|
Desipramine |
3,2 | - | - |
|
Combination TCAs |
3,2 | - | - |
|
Paroxetine |
5 | - | - |
|
Fluoxetine |
15,3 | - | - |
|
Mianserin |
- | - | - |