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Thalamic pain. Neurology – LiveJournal

Thalamic syndrome is a condition caused by damage to an area of the brain called the thalamic thalamus. The thalamus is a paired formation represented by gray matter and consisting of the anterior tubercle, body and pillow. Refers to the intermediate part of the brain. The nuclei of the optic thalamus are responsible for vision, hearing, tactile sensations, and balance. The thalamus performs the functions of processing information, regulating attention, and coordinating the work of the musculoskeletal system. The part of the brain that coordinates speech, memory, and emotions. Damage to the visual thalamus entails disruption of the described functions.

Main symptoms of thalamic syndrome

The set of symptoms caused by damage to the visual thalamus is otherwise called Dejerine-Roussy syndrome. The painful condition resulting from damage to the thalamus was first described in the 19th century. A detailed definition of the symptoms and causes was given by the French scientists Dejerine and Roussy at the beginning of the 20th century.

The signs of the syndrome are:

loss of pain and skin sensitivity on one side of the body;
increased pain perception threshold with the inability to accurately determine its location;
intense burning pain on one side of the body;
perversion of sensitivity (temperature stimulus is felt as painful, light touches cause discomfort);
loss of sensitivity to vibration effects;
exhaustion and weakening of the muscles of the affected part of the body;
erratic chaotic movements of the fingers of the upper limb;
formation of the so-called thalamic hand: the forearm is bent and turned back, the hand is bent, the distal phalanges are straight with the proximal and middle phalanges half-bent;
unilateral motor coordination disorder;
partial blindness – lack of perception of the right or left half of the visual field;
drooping of one corner of the mouth, unilateral facial paralysis;
impaired concentration.

The patient's psychological state is characterized by mood swings, depression, and suicidal thoughts.

Causes of pathology

Thalamic syndrome is not a disease, but a set of signs and clinical manifestations. The symptom complex can be caused by vascular disorders of the deep branches of the posterior cerebral artery, damage to the ventral posterolateral nucleus of the thalamus. These conditions can lead to:

injury;
malignant brain tumor with metastases in the thalamus;
ischemic stroke;
hemorrhagic stroke.

The origin of hyperpathic pain and severe psycho-emotional disorders accompanying the thalamic syndrome is not fully explained. Other neurological symptoms are caused by the following reasons:

damage to the structures of the cerebellar dentate-thalamic tract;
dysfunction of the medial lemniscus;
damage to the hypothalamic nuclei.

Diagnosis and treatment

Diagnosis is based on a set of measures that involve clinical and instrumental examination methods:

collecting anamnesis, studying patient complaints and determining possible causes of pathology;
checking superficial and deep skin sensitivity;
establishing muscle strength of the limbs;
visual field check;
determination of reactions to auditory, visual and taste stimuli;
computed and magnetic resonance imaging;
cerebral angiography.

Treatment of the pathology - symptomatic and pathogenetic - is based on the use of neuroleptics and antidepressants. A polypharmacotherapy regimen, a combination of drugs: an anticonvulsant, an antidepressant and an opioid, is considered effective. In cases where conservative methods do not bring results, surgical intervention is indicated, during which the doctor destroys the ventrolateral nucleus of the thalamus. The operation is performed using a minimally invasive stereotactic method.

Along with traditional medicine, treatment of thalamic pain syndrome with folk remedies can be effective. Such therapy is aimed at relieving painful symptoms, but does not affect the causes and mechanisms of pathology.

Traditional medicine suggests treating the syndrome by pain relief or by trying to restore sensitivity to the skin, for which the following recipes can be used.

Ginger infusion for bathing (to relieve pain): 50 grams of crushed dry root of the plant are placed in a thermos, poured with a liter of boiling water and infused for one hour. The contents are added to the bath. It is necessary to take water procedures for 15 minutes. Daily use of this infusion for bathing is contraindicated. Before taking a bath with ginger for the first time, you need to determine whether there are any allergic reactions to the plant. With a cotton swab moistened with the prepared solution, wipe a small area of skin on the wrist or elbow and wait 15-20 minutes.
In case of loss of sensitivity, alcohol tincture of dandelions has a healing effect. To prepare it, take 100 grams of the dry matter of the plant and pour half a liter of vodka. Infuse the medicine for a week, leaving the jar in a dark place and periodically shaking the contents. The tincture is used to rub the parts of the body that have lost sensitivity.

Thalamic syndrome is a complex of neurological symptoms caused by damage to the visual thalamus. Diagnosis of pathology involves the use of clinical and instrumental methods. Treatment is symptomatic and pathogenetic.

Hello, my mother (75 years old) had a stroke in January 2016. She walks, talks, eats well and even thinks quite well :). BUT she complains to the point of tears about pain in her leg and arm, which lost part of their motor function during the stroke. The functions were almost restored, but the pain remained. We live in St. Petersburg, where to go to specialists to choose treatment. The clinic prescribes a mountain of medications, but instead of improving, my blood pressure begins to rise. I know we got away with a slight fright, but it hurts to watch her cradling her hand and suffering from pain in her leg.

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Hello. The cause of pain in the arm and leg on the affected side after a stroke may be the so-called. thalamic pain syndrome (in the absence of pronounced spasticity), in which intense pain syndrome may occur on the side opposite to the lesion in the brain. This may be thalamic pain - as part of the specified syndrome, which occurs when the structures of the thalamus - the so-called visual thalamus - are damaged.

In this case, thalamic pain may have features distinctive from other pain syndromes and be characterized by:

persistent current
have a strong character
a slight painful irritation on the affected side of the body may be perceived as more severe than it actually is
may be burning, resemble “many needles”

For such pain (if it is a thalamic pain syndrome), slightly different groups of drugs are selected to relieve pain (anticonvulsants, antidepressants in small doses, antipsychotics); conventional painkillers (for example, NSAIDs) are often ineffective here.

Again, this is only an assumption based on your description; for a more complete picture and accurate representation, an in-person examination is needed, taking into account previously conducted examinations (if any), and only after that, prescribing therapy.

If you don’t find a solution to your problem, we can look at you and discuss your treatment. Contact us.

You can ask your question and get an answer. Write to email address [email protected]…

A.B.Danilov, O.S.Davydov, Department of Neurology, Federal Faculty of Education and Science, Moscow Medical Academy named after. I.M. Sechenov; Pfizer International LLC

Neuropathic pain is a pain syndrome caused by damage to the somatosensory nervous system due to various reasons. The incidence of neuropathic pain in the population is 6-7%, and at neurological appointments patients with neuropathic pain account for 8-10%. Based on the location of the lesion, peripheral and central neuropathic (CN) pain are distinguished.

CNS is pain associated with a disease of the central nervous system (CNS). The prevalence of this pathology is 50-115 cases per 100 thousand population. CNS is most often observed in diseases such as stroke, multiple sclerosis (MS), as well as spinal cord injuries and syringomyelia. The intensity of pain varies from mild to extremely severe, but even mild pain is often disabling due to its constant presence.

Central post-stroke pain

Central post-stroke pain (CPP) is pain and some sensory disturbances that appear as a result of a cerebral stroke. The optic thalamus and the brainstem are those parts of the brain whose damage during a stroke is most often accompanied by CNS. Intense unbearable pain is observed as part of the so-called thalamic syndrome (superficial and deep hemianesthesia, sensitive ataxia, moderate hemiplegia, mild choreoathetosis) after infarctions in the area of the visual thalamus. The most common cause of central thalamic pain is vascular damage to the thalamus. CPB can also occur with extrathalamic lesions.

CPP develops within 1 year after stroke in 8% of patients. The prevalence of stroke is high - about 500 cases per 100 thousand population, thus, the absolute number of people with post-stroke pain is very significant. The onset of pain can be soon after a stroke or after a certain time. In 50% of patients, pain occurs within 1 month after a stroke, in 37% - in the period from 1 month to 2 years, in 11% - after 2 years from the moment of stroke. CP is felt in a large part of the body, such as the right or left side; however, in some patients the pain may be localized (in one arm, leg, or face). Patients most often characterize the pain as burning, aching, tingling, tearing. CPP is often accompanied by other neurological symptoms such as hyperesthesia, dysesthesia, numbness, changes in sensitivity to heat, cold, touch and/or vibration. Pathological sensitivity to heat and cold is the most common and serves as a reliable diagnostic sign of CNS; 70% of patients with CLP are unable to perceive a difference in temperature in the range from 0° to 50°C. The phenomenon of allodynia, characteristic of neuropathic pain, occurs in 71% of patients.

Treatment of CPP

In the treatment of CPP, the effectiveness of amitriptyline (daily dose 75 mg) has been shown, which was higher when it was prescribed immediately after the onset of pain. Selective serotonin reuptake inhibitors are ineffective in the treatment of CPP. Carbamazepine was also ineffective in three placebo-controlled studies. Attempts to treat CP with non-steroidal anti-inflammatory drugs have been unsuccessful. Data on the use of opioid analgesics are inconclusive. Prospects for treatment are associated with the use of anticonvulsants, preliminary studies of which have shown encouraging results. The most reliable evidence for the effectiveness of anticonvulsants in the treatment of CPP comes from studies of pregabalin (Lyrica). The drug is registered by the FDA (USA) based on data from controlled clinical studies for the treatment of pain in diabetic neuropathy and postherpetic neuralgia, as well as CNS (data obtained in a model of spinal cord injury). To evaluate the effectiveness and safety of Lyrica, a 4-week randomized, controlled placebo study was conducted, which, in addition to patients with other pathologies, included patients with CPP. By the end of the 4th week of therapy, a significantly greater decrease in the visual analogue scale (VAS) value was noted than in the placebo group in patients receiving Lyrica at a dose of 150, 300 and 600 mg. In patients receiving Lyrica, the quality of life and health status reliably and significantly improved, while in the majority of patients in the placebo group it even worsened. Due to the flexible dosing regimen, the drug was well tolerated.

Despite certain advances in the field of therapy for CPP, treating such patients remains a challenge. Taking into account the different pathophysiological mechanisms of CPP, rational polypharmacotherapy is increasingly being discussed, i.e. use of drug combinations (antidepressant + anticonvulsant + opioid).

MS pain

Although pain has not traditionally been considered a major problem in patients with MS, recent evidence suggests that this complication occurs in 45-56% of patients. The pain is localized in the lower extremities and can involve the arms. Most often it is bilateral pain. The most typical descriptions of pain in MS are “sharp”, “burning”, “stabbing”. In most patients, the pain is intense. Pain is almost always combined with other sensory disturbances: increased sensitivity to mechanical and temperature stimuli. Trigeminal neuralgia occurs at older ages, in later stages of the disease and occurs in 4-5% of cases with MS. It should be emphasized that dysesthesia is very characteristic of MS. In addition, Lhermitte's symptom is characteristic of this group of patients - when the head is tilted forward, a sudden transient pain occurs, reminiscent of an electric shock, which quickly spreads down the back and radiates to the legs.

Treatment of pain in MS

In the treatment of neuropathic pain syndrome in MS, amitriptyline, lamotrigine, carbamazepine, and gabapentin were used, which showed good effects. However, an analysis of the literature has shown that there are still few such works, the number of patients in groups is also small and there are practically no large-scale evidence-based studies. Lamotrigine, topiramate, and gabapentin were effective in small studies for the treatment of symptomatic trigeminal neuralgia in MS. Two double-blind, placebo-controlled studies on the use of cannabinoids (dranibinol and Sativex) for neuropathic pain in patients with MS were recently completed. Patients noted a decrease in pain intensity, but in most cases there were adverse reactions such as drowsiness, dizziness and incoordination. All researchers unanimously recognize the need for well-designed, controlled studies of pharmacological agents to treat pain in these patients.

Spinal cord injury pain

Between 27 and 94% of spinal injury patients experience chronic moderate to severe pain. Damage to the spinal cord occurs both due to direct impact on it and due to pathological changes in the surrounding tissues. Some injuries are due to medical conditions, such as stroke or cancer, or surgery, but most are due to traumatic exposure. Every year in different countries, from 15 to 40 people per 1 million population suffer from a spinal injury. This occurs more often at a young age and mainly in men (4 times more often than in women). The number of people living with a spinal injury is 70-90 per 100 thousand population. Neuropathic pain after spinal injury is most often characterized by patients as:

pinching;
tingling;
shooting;
exhausting;
pulling;
annoying;
burning;
intermittent, shooting “like an electric shock.”

When the spinal cord is damaged, pain can be localized, unilateral or diffuse bilateral, affecting the area below the level of the lesion. Pain in the perineal area often becomes particularly intense. The pain is constant and has a burning, stabbing, tearing, and sometimes crampial character. Against this background, paroxysmal focal and diffuse pain of different nature may occur. The Lhermitte symptom, well known in practice (paresthesia with elements of dysesthesia during movement in the neck), reflects the increased sensitivity of the spinal cord to mechanical stress in conditions of demyelination of the posterior columns.

Therapy of pain syndrome in spinal cord injury

Pain therapy for spinal injury includes pharmacotherapy, physiotherapy, surgical treatment, psychological rehabilitation, and social support. However, at present there is no convincing data obtained in evidence-based studies that could be considered ready-made recommendations for treatment. However, more drugs are being tried to treat this severe pain syndrome. Preliminary studies have shown the effectiveness of intravenous infusions of lidocaine, amitriptyline, carbamazepine, lamotrigine, valproate and topiramate. The use of these drugs has often been associated with a high incidence of adverse events. Several pilot controlled placebo studies have shown the effectiveness of gabapentin administered at 1800-2400 mg/day (course of treatment - 8-10 weeks).

Recently, the results of a large-scale and evidence-based study of another anticonvulsant, Lyrica (pregabalin), in the treatment of CNS due to spinal cord injury were published. The objective of the study was to evaluate the effect of Lyrica (pregabalin) on neuropathic pain associated with spinal cord injury. This 12-week multicenter study was conducted with patients randomized into 2 groups: Lyrica at a dosage of 150-600 mg/day (70 patients) and placebo (67 patients). Patients were allowed to continue taking previously prescribed pain medications. The main criterion for the effectiveness of therapy was the total VAS score, which was analyzed using the patients’ daily diaries for the last 7 days of observation. Additional efficacy criteria included data on the time to onset of analgesic effect, the Short Form of the McGill Pain Questionnaire (SF-MPQ), the Sleep Disturbance Severity Rating Scale, the Mood Rating Scale, and the Patient Global Impression Scale.

The VAS pain level before the start of therapy was 6.54 points in the group of patients receiving pregabalin and 6.73 in the placebo group. At the end of the 12-week course of therapy, significant differences were obtained in the group receiving Lyrica therapy (pain level decreased according to VAS to 4.62 points) in comparison with the placebo group (VAS 6.27 points; p<0,001). Положительный обезболивающий эффект терапии Лирикой наблюдался уже на 1-й неделе лечения и продолжался на протяжении всего исследования. Средняя суточная доза Лирики составила 460 мг. Лирика показала достоверно большую эффективность по результатам анализа краткой формы болевого вопросника Мак-Гилла (SF-MPQ) в сравнении с плацебо. Скорость наступления противоболевого эффекта была ≥30 и ≥50% в группе пациентов, получавших прегабалин, в сравнении с группой плацебо (p<0,05). В группе пациентов, принимавших Лирику, наблюдалось значительное улучшение нарушенного сна (p<0,001) и снижение уровня тревожности (p<0,05). Наиболее характерными нежелательными явлениями были умеренно выраженная и обычно непродолжительная сонливость и головокружение. Таким образом, Лирика в дозировке от 150 до 600 мг/сут оказалась эффективной в купировании ЦНБ, одновременно улучшала качество сна и общее самочувствие, снижала уровень тревожности у пациентов с травмой спинного мозга. Эти результаты согласуются с данными по эффективности и безопасности Лирики, полученными из описанного выше исследования на смешанной группе больных с ЦПБ и болью вследствие спинальной травмы.

Syringomyelia pain

It is generally accepted that syringomyelia is characterized by disorders of pain sensitivity, leading to hypoesthesia and so-called painless burns. However, pain syndrome with syringomyelia occurs in 50-90% of cases. The clinical picture of pain can be varied. Patients complain of radicular pain in the arms, pain in the interscapular region, and sometimes in the back. 40% experience dysesthesia, burning pain, which is quite painful and significantly maladjusts the patients. Hyperesthesia and allodynia in the hands are characteristic, along with malnutrition and vegetative-trophic disorders.

Treatment of pain due to syringomyelia

Therapy for neuropathic pain in syringomyelia is still empirical. There are no controlled studies on the use of pharmacological drugs yet. The most appropriate is rational polypharmacotherapy: the combined use of antidepressants, anticonvulsants, lidocaine (topically) and opioids.

In conclusion, treatment of CNB is challenging. Not all drugs used have proven effectiveness in the treatment of this syndrome. However, currently the most studied drugs are antidepressants, anticonvulsants, opioid analgesics and local anesthetics. Among them there are drugs whose effectiveness has been proven in numerous controlled studies, while others have received preliminary results. Almost no evidence has been accumulated on combination therapy for neuropathic pain in general and CNS in particular. Today, there is an obvious need for further research to identify the optimally effective combinations of drugs, select doses and the safest combinations, as well as to evaluate the pharmacoeconomic aspects of therapy.

Pain syndrome in thalamic syndrome belongs to the group of “central” pains. It is one of the most severe manifestations of indomitable pain, which is extremely difficult to relieve.

The main cause of thalamic pain syndrome is ischemic stroke with the localization of the focus of ischemia in the visual thalamus. The disease can also develop with brain tumors that cause compression of the thalamus, disruption of blood and cerebrospinal fluid circulation in the area of this structure. Other causes of thalamic pain syndrome are thrombosis of the thalamic-geniculate artery, which supplies the posterior and lateral parts of the thalamus (specifically, its ventroposteriomedial and ventroposteriolateral nuclei), as well as hemorrhages in this organ.

The basis of the pain syndrome is damage to the passage of impulses carrying different types of sensitivity, as a result of which they are mixed, and the nociceptive (pain) system becomes predominant.

Symptoms

The thalamus is a structure where the pathways of various types of sensitivity intersect. It is the “coordinator” of impulses received from the sensory organs (except for the olfactory analyzer), receiving information along the sensory and motor pathways and transmitting them to the desired area of the cortex of the right or left hemisphere. In addition, structure is important for maintaining a sufficient level of consciousness, concentration, and sleep and wakefulness.

Therefore, when this organ is damaged, the following symptoms occur:

first – a short-term disturbance of movements (paralysis or paresis) in one half of the body, after which the range of movements in the affected half of the body is normalized or remains minimally changed;
extremely intense, burning pain in different, alternating areas in one half of the body. They are accompanied by a very strong negative emotional connotation; have weather dependence;
continuous headaches;
unpleasant sensations disproportionate to the stimulus during tactile or mechanical stimulation in the affected half of the body. Even a slight touch to a limb on one side causes discomfort in a person, even to the point of pain. These sensations do not have precise localization, last a long time, and radiate to nearby areas of the body or limbs;
disturbances in eye movement, especially looking up or down, or a combination of both;
speech disorders - if the dominant hemisphere was affected.

Additional symptoms may include depressive disorders, fatigue, attention deficit, insomnia, spatial orientation problems, and sometimes hallucinations.

Diagnostics

Diagnosis of thalamic pain syndrome involves:

examination by a neurologist who will evaluate all types of sensitivity, determine the range of movements in the limbs, and diagnose oculomotor disorders;
performing magnetic resonance imaging, which allows you to clearly visualize foci of ischemia and hemorrhages in the thalamus, as well as determine their cause (in the case of a tumor, when thalamic syndrome is its first manifestation).

Treatment methods

Treatment tactics for thalamic pain syndrome include one or more areas such as:

prescribing symptomatic drug therapy;
transcranial electrical stimulation;
radiosurgery.

Treatment with analgesic drugs has long proven to be ineffective. Based on the extensive experience of doctors, as well as research data, it has been proven that pain is reduced when using a combination of a tricyclic antidepressant and an anticonvulsant.

Transcranial electrical stimulation can achieve some analgesic effect. A small electric current passed through electrodes placed on the scalp can reduce the severity of pain by activating endorphin structures in the brain.

These approaches bring only a partial and temporary effect. Currently, only stereotactic radiosurgery provides the best results. This is a procedure consisting of targeted exposure of radioactive rays strictly to the pathological focus. As a result, the structure that causes intense pain in half the body—in the case of thalamic syndrome, the posterior ventrolateral nucleus of the thalamus—is destroyed.

Application of Gamma Knife

The posterior ventrolateral nucleus of the thalamus is a structure that is a kind of relay that switches impulses from tactile, taste, pain, visceral and temperature sensitivity. It is clearly divided into zones corresponding to parts of the body. If a certain area of the ventral posterior nuclei is destroyed, the flow of pain impulses from the corresponding half of the body will stop, which will be noticeable within 3-4 weeks after surgery.

Such an intervention can be carried out using a unique radiosurgical device - the Gamma Knife. It is a special installation that provides targeted exposure to a high dose of radiation to a specific area. In this case:

no incisions required;
the procedure is carried out in consciousness (without anesthesia), as it is painless;
One procedure is sufficient to ensure destruction of the ventroposteriolateral nucleus, since its diameter is much less than 3.5 cm;
surrounding tissues receive virtually no radiation;
there is no intraoperative bleeding, since the radiation acts on the cells from the inside, without cutting or cauterizing them.

The reliability, accuracy and effectiveness of the Gamma Knife have made it the gold standard in radiosurgery. It has been used for a relatively short time only in our country, but in developed countries the experience of using the device reaches several decades.

Help your relative who has suffered a stroke or has a brain tumor get rid of terrible pain! Contact Gamma Clinic!

... Dejerine and Roussy in 1906 described intense unbearable pain within the so-called thalamic syndrome (superficial and deep hemianesthesia, sensitive ataxia, moderate hemiplegia, mild choreoathetosis) after infarctions in the area of the visual thalamus (its ventroposteriomedial and ventroposteriolateral nuclei).

In the reference book “Neurological symptoms, syndromes, symptom complexes and diseases” E.I. Gusev, G.S. Burd, A.S. Nikiforov"; Moscow, “Medicine” 1999. – 880 p.; p.323 we read the following about Dejerine-Roussy syndrome:

«…
Thalamic posterolateral syndrome.
Dejerine-Roussi syndrome
The consequence is damage to the lateral part of the thalamus, including its posterolateral ventral nucleus. On the opposite side, constant paroxysmal, intensifying, burning pain is observed (see. Förster's symptom), hyperpathy (see. Ged-Holmes' sign), which may extend beyond the midline. Burning, vaguely localized pain intensifies in paroxysms with irritation of the integumentary tissues and emotional stress. It is combined with a decrease in superficial and especially deep sensitivity, sensitive hemiataxia, pseudoastereognosis, transient hemiparesis, while the hand mainly suffers, hyperkinesis of the type is possible in it choreoathetosis(see), characterized by a phenomenon known as thalamic arm(cm). Sometimes there is also a depletion of spontaneous facial reactions. while voluntary facial movements remain intact. Instability of attention and orientation is common. There may be changes in speech, manifested by impaired intelligibility, monotony, literal paraphasia, and loss of sonority. Hemianopsia is possible. The syndrome most often occurs due to circulatory disorders in the basin of the thalamogeniculate artery, which arises from the posterior cerebral artery. described in 1906 by French doctors neuropathologist J. Dejerine (1849 - 1917) and pathologist G. Roussy (1874 - 1948).”

Definition of Dejerine-Roussy syndrome in the “Large Explanatory Dictionary of Psychiatric Terms by V.A. Zhmurova":

«…
Thalamic syndrome (Dejerine-Roussi)
– pain in half of the body is combined with hemianesthesia, hemiataxia, choreatic hyperkinesis and a peculiar position of the hand (“thalamic hand”). Particularly characteristic are sharp, painful, causalgic-type pains, which the patient cannot always clearly localize. Phenomena of dysesthesia are also noted in response to an injection, touching, exposure to cold, heat, as well as a long aftereffect after the end of stimulation. The pain is intensified by various kinds of stimuli: touch, bright lighting, sharp knocking, traumatic emotional impressions. The thalamic hand looks like this: the forearm is bent and pronated, the hand is flexed, the fingers are extended and sometimes continuously move, as a result of which elaborate and quickly crumpling poses of the entire hand arise. Sometimes violent laughter and crying, paresis of facial muscles, disturbances of smell and taste, and autonomic disorders are observed. The disorder occurs when the optic thalamus is damaged (usually due to impaired blood circulation in the branches of the posterior cerebral artery).”

According to modern concepts, if Dejerine-Roussy syndrome develops as a result of an infarction in the area of the visual thalamus, then it belongs to the so-called central post-stroke pain (as already indicated, the most common cause of central thalamic pain is vascular damage to the thalamus).

Dejerine-Roussy syndrome as part of central post-stroke pain develops within 1 year after stroke in 8% of patients. Since the prevalence of stroke is approximately 500 cases per 100 thousand population, the absolute number of people with post-stroke pain is very significant. The onset of pain can be soon after a stroke or after a certain time. In 50% of patients, pain occurs within 1 month after a stroke, in 37% - in the period from 1 month to 2 years after a stroke, in 11% - after 2 years from the moment of a stroke. Central post-stroke pain is felt in a large part of the body, for example, in the right or left half; however, in some patients the pain may be localized, such as in one arm, leg, or face. Patients most often characterize the pain as “burning”, “aching”, “pinching”, “tearing”. Post-stroke pain can be intensified by various factors: movement, cold, heat, emotions. In contrast, in other patients these same factors may relieve pain, especially heat. Central post-stroke pain is often accompanied by other neurological symptoms such as hyperesthesia, dysesthesia, numbness, changes in sensitivity to heat, cold, touch and/or vibration. Pathological sensitivity to heat and cold is the most common and serves as a reliable diagnostic sign of central post-stroke pain. According to studies, 70% of patients with central post-stroke pain are not able to feel the difference in temperature in the range from 0 to 500C. The phenomenon of allodynia, characteristic of neuropathic pain, occurs in 71% of patients.

Principles of treatment. For central post-stroke pain (Dejerine-Roussy syndrome) effectiveness shown amitriptyline (dose 75 mg per day), and its effectiveness is higher in cases of administration immediately after the onset of pain and lower in cases of late administration of the drug. Selective serotonin reuptake inhibitors despite a more favorable safety profile in the treatment of central post-stroke pain, they are ineffective. Carbamazepine is also ineffective (according to three placebo-controlled studies; it significantly reduced pain only when assessing 3 weeks of therapy, but overall it was ineffective after treatment). Attempts to treat central neuropathic pain with non-steroidal anti-inflammatory drugs in unsuccessful. Data on use are also inconclusive opioid analgesics: Some positive effects are accompanied by side effects. The prospects for treatment are associated with the use of anticonvulsants, preliminary studies of which have shown encouraging results (pregabalin, gabapentin). Given the different pathophysiological mechanisms in some cases, central neuropathic pain is increasingly discussed. rational polypharmacotherapy, i.e. combination of drugs - antidepressant + anticonvulsant + opioid .