What causes scarring on the brain. How does brain scarring lead to epilepsy. What are the different types of brain scarring associated with epilepsy. How can epilepsy caused by brain scarring be treated. What are the long-term effects of brain scarring in epilepsy patients.

The Complex Relationship Between Brain Scarring and Epilepsy

Brain scarring, also known as cerebral scarring or encephalomalacia, is a condition where damaged brain tissue is replaced by fibrous tissue. This scarring can have significant implications for neurological function, particularly in relation to epilepsy. Understanding the connection between brain scarring and epilepsy is crucial for both patients and medical professionals.

Can brain scarring always be linked to epilepsy? While brain scarring is a known cause of epilepsy, it’s important to note that not all cases of epilepsy are caused by brain scarring. In fact, approximately 60% of epilepsy cases are idiopathic, meaning the cause is unknown. However, in cases where a structural abnormality in the brain is identified, scarring is often a key factor.

Common Causes of Brain Scarring Leading to Epilepsy

Brain scarring can result from various factors, many of which can potentially lead to epilepsy. Some of the most common causes include:

• Traumatic brain injuries
• Strokes and other vascular problems
• Infections of the nervous system (meningitis or encephalitis)
• Congenital malformations
• Brain tumors
• Metabolic abnormalities

How do these factors contribute to brain scarring? When the brain tissue is damaged due to any of these causes, the body’s natural healing response can sometimes lead to the formation of scar tissue. This scar tissue can disrupt normal neuronal signaling, potentially resulting in seizures and epilepsy.

Types of Brain Scarring Associated with Epilepsy

Several specific types of brain scarring have been identified as potential causes of epilepsy. Understanding these can help in diagnosing and treating epilepsy more effectively.

Cortical Dysplasia

Cortical dysplasia is a condition that occurs during fetal development. It results from the abnormal migration of neurons as the brain’s cortex forms. This can lead to misplaced neurons that signal each other in irregular ways, causing recurring seizures.

Is cortical dysplasia always present from birth? Yes, cortical dysplasia is a congenital condition, meaning it’s present from birth. However, the symptoms, including seizures, may not manifest until later in life.

Hemimegalencephaly

Hemimegalencephaly is a rare and severe form of cortical dysplasia. In this condition, one hemisphere of the brain is significantly larger than the other. This asymmetry can lead to frequent seizures and developmental delays.

Mesial Temporal Sclerosis

Mesial temporal sclerosis involves scarring in the inner portion of the temporal lobe, specifically in the hippocampus. This type of scarring can result from head trauma or brain infections that interrupt oxygen flow to the temporal lobe.

How does mesial temporal sclerosis affect seizure activity? The scarring in the hippocampus and amygdala can lead to temporal lobe epilepsy, characterized by partial (focal) seizures that may spread to other areas of the brain.

The Role of Traumatic Brain Injury in Epilepsy Development

Traumatic brain injury (TBI) is a significant cause of brain scarring that can lead to epilepsy. People who have sustained head injuries from various accidents are at a higher risk of developing seizures or epilepsy compared to those without a history of head trauma.

Does the severity of the head injury correlate with the likelihood of developing epilepsy? Generally, yes. More severe head injuries and multiple traumas to the head increase the risk of developing post-traumatic epilepsy. However, even mild TBIs can sometimes lead to epilepsy, highlighting the importance of proper medical attention for all head injuries.

Metabolic Causes of Brain Scarring and Epilepsy

While structural abnormalities are common causes of brain scarring and epilepsy, metabolic issues can also play a role. One example is GLUT-1 deficiency syndrome, a condition characterized by problems in glucose transport to the brain.

How does GLUT-1 deficiency syndrome lead to epilepsy? The brain relies heavily on glucose for energy. When glucose transport is impaired, as in GLUT-1 deficiency syndrome, it can lead to abnormal brain function and seizures. This condition often affects speech particularly and can be diagnosed through a lumbar puncture.

Diagnostic Approaches for Brain Scarring in Epilepsy Patients

Diagnosing brain scarring in epilepsy patients involves a combination of clinical assessment, imaging techniques, and sometimes genetic testing. The following methods are commonly used:

1. Magnetic Resonance Imaging (MRI): This is the gold standard for visualizing brain structure and identifying areas of scarring.
2. Computerized Tomography (CT): While less detailed than MRI, CT scans can quickly identify major structural abnormalities.
3. Electroencephalogram (EEG): This test measures brain wave patterns and can help locate the origin of seizures.
4. Lumbar Puncture: In some cases, such as suspected GLUT-1 deficiency, analysis of cerebrospinal fluid can be diagnostic.
5. Genetic Testing: While not always conclusive, genetic testing can help identify some inherited forms of epilepsy associated with brain abnormalities.

Are these diagnostic methods always conclusive? While these tests are highly informative, it’s important to note that in some cases, particularly in idiopathic epilepsy, no structural abnormalities may be visible. In such cases, diagnosis relies heavily on clinical symptoms and EEG findings.

Treatment Options for Epilepsy Caused by Brain Scarring

The treatment of epilepsy caused by brain scarring depends on the specific type and location of the scarring, as well as the severity and frequency of seizures. Several treatment options are available:

Medication

Anti-epileptic drugs (AEDs) are often the first line of treatment for epilepsy, regardless of the cause. These medications work by altering brain chemistry to reduce seizure activity.

Dietary Interventions

In some cases, particularly in metabolic disorders like GLUT-1 deficiency syndrome, dietary changes can be highly effective. The ketogenic diet, which is high in fat and low in carbohydrates, has shown significant success in managing certain types of epilepsy.

Surgery

For some patients with localized brain scarring, surgical removal of the affected area can be an effective treatment. This is particularly true for conditions like hemimegalencephaly or certain cases of cortical dysplasia.

Neurostimulation

Devices that stimulate specific nerves, such as the vagus nerve stimulator, can help reduce seizure frequency in some patients.

How effective are these treatments in managing epilepsy caused by brain scarring? The effectiveness of treatment varies depending on the individual case. While many patients achieve good seizure control with medication alone, others may require a combination of treatments. In some cases, particularly those involving surgical intervention, patients may become seizure-free.

Long-Term Prognosis and Management of Epilepsy Due to Brain Scarring

The long-term outlook for patients with epilepsy caused by brain scarring varies widely depending on the underlying cause, the extent of scarring, and the effectiveness of treatment. Some key considerations in long-term management include:

• Regular follow-ups with neurologists to monitor seizure control and adjust treatment as needed
• Ongoing imaging studies to track any changes in brain structure
• Neuropsychological evaluations to assess cognitive function and identify any areas of concern
• Lifestyle modifications to minimize seizure triggers and promote overall brain health
• Psychosocial support to address the emotional and social impacts of living with epilepsy

Can the brain adapt to overcome the effects of scarring? In some cases, yes. The brain has a remarkable ability to adapt, known as neuroplasticity. This is particularly evident in cases where part of the brain is surgically removed, and the remaining healthy tissue takes over some of the lost functions. However, the extent of this adaptation varies greatly between individuals.

Emerging Research and Future Directions in Treating Brain Scarring and Epilepsy

The field of epilepsy research is continually evolving, with new insights into brain scarring and potential treatments emerging regularly. Some promising areas of research include:

Gene Therapy

Researchers are exploring ways to use gene therapy to prevent or reverse brain scarring, potentially offering new hope for patients with genetic forms of epilepsy.

Neuroprotective Agents

Studies are underway to develop drugs that can protect brain cells from damage during and after injuries, potentially reducing the likelihood of scarring and subsequent epilepsy.

Advanced Imaging Techniques

New imaging technologies are being developed to provide even more detailed views of brain structure and function, allowing for earlier and more accurate diagnosis of brain abnormalities.

Personalized Medicine

As our understanding of the genetic and molecular basis of epilepsy grows, there’s increasing focus on developing personalized treatment plans based on an individual’s specific type of brain scarring and genetic profile.

What potential do these emerging treatments hold for epilepsy patients? While many of these approaches are still in the experimental stages, they offer hope for more effective and targeted treatments in the future. The goal is to not only control seizures more effectively but also to prevent or reverse the brain scarring that leads to epilepsy in the first place.

In conclusion, brain scarring plays a significant role in many cases of epilepsy, with various causes and manifestations. While current treatments can effectively manage seizures for many patients, ongoing research promises to bring even more advanced and personalized approaches to treating this complex condition. As our understanding of brain scarring and its relationship to epilepsy continues to grow, so too does the hope for improved outcomes for epilepsy patients worldwide.

Epilepsy Causes | Johns Hopkins Medicine

In some 6 out of 10 cases, epilepsy is idiopathic — meaning the cause is
unknown. In other cases, epilepsy can be traced to an abnormality of the
structure or function of the brain. These abnormalities can arise from
traumatic brain injuries, strokes and other vascular problems, infections
of the nervous system (meningitis or encephalitis), congenital
malformations, brain tumors or metabolic abnormalities.

Regardless, doctors can treat most epilepsy with medication, diet, nerve
stimulation or, in some instances, surgery.

What You Need to Know

• Some epilepsies are caused by problems in the early formation
  of the fetal brain; others by inborn metabolic problems or
  early oxygen deprivation that leads to scarring.
• Other epilepsies occur as a result of brain trauma, stroke,
  infection, tumor or genetic susceptibility. Still others have
  no apparent cause.
• About 3 out of 10 people with epilepsy have structural changes
  in the brain that cause chronic seizures. These changes can be
  present at birth (congenital) or acquired later in life.
• Researchers are exploring the impact of genes in epilepsy but
  the association is complex, and genetic testing may not
  identify a specific cause.

GLUT-1 Deficiency Syndrome

GLUT-1 deficiency syndrome is an example of an epilepsy caused by a
metabolic problem. GLUT-1 deficiency syndrome is characterized by problems
in the transport of glucose to the brain. Speech may be particularly
affected. A lumbar puncture can help diagnose the condition.

GLUT-1 deficiency can be treated with a ketogenic diet, one high in fat and
protein and low in sugar and carbohydrates. Children who start the diet
early and stick with it can see great improvement. If seizures still occur,
the doctor may also prescribe medication.

Cortical Dysplasia

As a fetus develops in the womb, cells called neurons migrate from the
innermost parts of the brain and organize themselves to form the brain’s
outer layer, or cortex. If this process occurs in an irregular way,
cortical dysplasia cells can result. The misplaced neurons signal one
another in abnormal ways, and the result is recurring seizures.

Treatment for seizures due to cortical dysplasia typically begins with
anti-seizure medications. Surgery may be recommended if these medicines do
not adequately control the seizures.

Hemimegalencephaly

One rare example of cortical dysplasia is called hemimegalencephaly.
Present at birth, this condition is characterized by one hemisphere (half)
of the brain that is larger than the other. Hemimegalencephaly can cause
frequent seizures and developmental delays.

Surgeons can remove the affected side of the brain, allowing the healthy
hemisphere to adapt and assume the functions of the other side. This
healing process is known as neuroplasticity, the ability of healthy brain
tissue to compensate for damaged areas.

Mesial Temporal Sclerosis

The temporal lobe is a part of the brain under the temples on the side of
the head. When scars form in the inner, or mesial, portion of the temporal
lobe known as the hippocampus, the result is mesial temporal sclerosis.

Head trauma or brain infection can also interrupt the flow of oxygen to the
temporal lobe, causing its brain cells to die. Scar tissue can form within
the hippocampus and amygdala, areas in the brain that govern short-term
memory and emotions. A person with this condition can develop a form of
temporal lobe epilepsy with

partial (focal) seizures

that can spread and affect other areas of the brain.

Treatments can include anti-seizure medications, a low-carb diet, surgery
or nerve stimulation.

Traumatic Brain Injury

People who have sustained head injuries from falls, car crashes, sports
injuries and other accidents are more likely to experience seizures or
epilepsy than those without a history of head injuries. The more times a
person has had a trauma to the head, the more likely he or she is to have
seizures. Genetics may also play a role in the development of
post-traumatic epilepsy. Treatment may include medications, diet, surgery
or neurostimulation.

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How to Diagnose Arachnoiditis : Arachnoiditis is an inflammation of the arachnoid membrane of the brain or spinal cord. Primary diagnosis of arachnoiditis will require an MRI of the brain or an MRI of the spinal cord and a consultation with a neurologist. As an additional examination, the doctor may prescribe:

• MRI of the brain with contrast
• CT scan of the brain
• Electroencephalogram (EEG)
• additional consultation with an infectious disease specialist.

Which doctor treats arachnoiditis: A neurologist deals with conservative treatment of arachnoiditis. The surgical treatment of arachnoiditis is performed by a neurosurgeon.

Symptoms of arachnoiditis

Arachnoiditis is a condition characterized by severe burning pain and neurological complications. Arachnoiditis is caused by inflammation of the arachnoid membrane, one of the 3 membranes that cover the brain and spinal cord. Inflammation causes constant irritation, scarring and fusion of nerve roots and blood vessels. The predominant symptom of arachnoiditis is chronic and persistent pain in the lower back, legs, or, in severe cases, throughout the body. Additional features include:

• numbness or weakness in the legs
• goosebumps and false tactile sensations
• severe pain with spasms
• muscle cramps and uncontrollable twitching
• decreased bowel and bladder control
• sexual dysfunction.

As the disease progresses, symptoms may become more severe or chronic. Most patients with arachnoiditis have significant disability.

Causes of arachnoiditis

There are 3 main causes of arachnoiditis.

Injury or consequences of surgery. Arachnoiditis has long been recognized as a rare complication of spinal surgery (especially after repeated and complex surgeries) or spinal injury. Arachnoiditis can develop after lumbar punctures (especially with concomitant bleeding into the cerebrospinal fluid), as well as due to progressive spinal stenosis or chronic degenerative disease of the intervertebral disc.

Consequences of exposure to chemicals during myelogram. In recent years, myelograms have come under scrutiny as a possible cause of arachnoiditis. A myelogram is a diagnostic test in which an x-ray contrast agent is injected into the area surrounding the spinal cord and nerves. Then the tissues “stained” with contrast appear on X-ray, CT or MRI. The data is used by doctors to diagnose diseases of the spine.

There is current concern that exposure (particularly repeated exposure) to certain contrast agents used in myelograms may cause arachnoiditis. Similarly, there are concerns that preservatives in epidural steroid injections may cause arachnoiditis, especially if the drug is accidentally released into the cerebrospinal fluid.

Infection. Arachnoiditis can also be caused by certain infections that affect the spine, such as meningitis or tuberculosis.

How arachnoiditis is diagnosed

Diagnosis of arachnoiditis includes various methods of examination, such as:

Neurological examination: a neurologist examines the patient, assesses the presence of symptoms such as headaches, seizures, sensory disturbances, impaired coordination.

MRI of the brain allows you to get more detailed information about the state of the brain, arachnoid and brain vessels, which allows you to identify signs of inflammation of the arachnoid.

Spinal tap: This test removes samples from the cerebrospinal fluid (cerebral spinal fluid or cerebrospinal fluid) to analyze the content of proteins, cells, glucose and other substances, which can help in the diagnosis of inflammation of the arachnoid.

CT of the brain can be used to detect changes in the structures of the brain and meninges, but may be less sensitive than MRI.

An electroencephalogram (EEG) helps detect abnormalities in the electrical activity of the brain, such as seizure activity, which may be associated with arachnoiditis.

Treatment

There is no specific cure for arachnoiditis. Treatment options focus on pain relief and are similar to other chronic pain conditions and include:

• spinal cord stimulation is one of the best treatment options. For stimulation, a special device is used that transmits an electrical signal to the spinal cord to relieve pain
• intravenous infusions of lidocaine. One of the properties of lidocaine is a powerful anti-inflammatory effect
• ketamine infusions. Ketamine is a type of anesthetic that helps relieve pain
• low-dose naltrexone is used as an anti-inflammatory agent in the treatment of chronic pain
• pain medicines such as non-steroidal anti-inflammatory drugs, corticosteroids (by mouth or injection), anti-spasmodics, anticonvulsants (to help with burning pain), and in some cases narcotic pain relievers. Some of these drugs can be given through an intrathecal pump, which is implanted under the skin and delivers drugs directly into the spinal cord
• physiotherapy.

Surgery is not recommended for arachnoiditis because it causes scar tissue to develop and exposes an already irritated spinal cord to more trauma.

Unfortunately, this condition can lead to serious disability. This not only negatively affects vitality, but can also cause mental stress. Treatment options should focus on relieving pain and maintaining quality of life.

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Actinomycosis: causes, symptoms, diagnosis and treatment.

Definition

Actinomycosis (radio-fungal disease, pseudomycosis, actinobacteriosis, deep mycosis) is a chronic purulent, non-contagious disease caused by radiant fungi actinomycetes – more precisely, these are fungus-like organisms, similar in structure and activity to bacteria.

The frequency of the disease is approximately 0.1-0.3 cases per 100,000 population per year.

Causes of actinomycosis

Disease-causing actinomycetes are present in the soil and can enter the body only through damaged skin, mucous membranes, and much less often through the oropharynx and nasopharynx (with inhaled air and with food). Actinomycetes that enter the body in the vast majority of cases do not cause the development of the disease, but form colonies (drusen) on the mucous membranes of the oral cavity, in the gastrointestinal tract, on the tonsils as a saprophytic flora. If the integrity of the mucosa is violated, they enter the lymph or bloodstream and, with reduced immunity, begin to actively multiply.

These microorganisms are always present in the human microbiota, being activated under the influence of various factors, which include severe infectious diseases, weakened immunity, diabetes mellitus, oncological diseases, etc.

Classification of the disease

Actinomycosis is divided into two types according to the way of infection introduction :

• primary — manifested by exogenous infection;
• secondary – occurs after the spread of infection in the body with blood or lymph flow from the primary focus, which can be carious teeth, inflamed tonsils, appendix, fecal stones, intrauterine devices, chronic inflammatory processes in the chest, abdomen, pelvis and etc.

There are several forms of actinomycosis:

• cervicofacial actinomycosis (jaw actinomycosis), when periodontal pathologies become the cause of the development of the disease. This is perhaps the most common form of the disease;
• thoracic or pulmonary actinomycosis develops against the background of chest trauma, chronic obstructive pulmonary disease, tuberculosis, AIDS, after aspiration of oral secretions;
• Abdominal actinomycosis appears to be the result of rupture of the diverticulum/appendix mucosa or trauma;
• actinomycosis of the urinary system;
• genital actinomycosis is a focal form and is a complication associated with the installation of certain types of intrauterine devices;
• pararectal actinomycosis occurs with inflammatory diseases of the rectum, purulent processes in the perineum;
• Generalized actinomycosis develops extremely rarely when the infection spreads from primary foci throughout the body.

In addition, localization isolated actinomycosis of the skin, ENT organs, central nervous system, lymph nodes, tongue and odontogenic actinomycotic osteomyelitis. Rare localizations include actinomycosis of the brain and spinal cord, pericardium, auricle, middle ear, mastoid process, tonsils, nose, thyroid gland, orbit of the eye, salivary glands, liver, bladder, large and small labia (after bartholinitis and piercing) .

By stages of the development of the disease:

• infiltrative stage – the formation of edema and dense infiltrate without clear boundaries;
• stage of abscessing – the formation of small abscesses, suppuration of granulomas with the addition of pain;
• fistulous stage – rupture of granuloma capsules, formation of fistulous passages with access to the pleura, abdominal cavity, etc. (depending on the location of the focus), the pain is insignificant;
• stage of scarring – the formation of scar tissue at the site of inflammation, the reduction or disappearance of symptoms of the disease.

Symptoms of actinomycosis

The duration of the incubation period can last up to several years.

Cervical-facial actinomycosis

Actinomycetes are always present in dental plaque, tartar, periodontal pockets, in carious cavities of teeth.

Inflammatory processes in the oropharynx (periodontal disease, tonsillitis, inflammation of the salivary glands, etc.), as well as damage to the oral mucosa contribute to the development of actinomycosis.

The process usually begins as a slightly painful or painless small, flat, hard swelling. Subsequently, areas of softening appear, which are resolved through fistulas with the release of purulent contents. The cheeks, tongue, pharynx, salivary glands and, in extremely advanced cases, the skull bones, pia mater, and brain may be affected.

Thoracic actinomycosis manifests as a cold. The patient experiences general weakness, his temperature rises to subfebrile values, a dry cough appears. Then the disease begins to resemble tuberculosis – the cough becomes wet with the release of mucopurulent sputum interspersed with blood. Gradually, the actinomycotic infiltrate spreads from the focus to the surface with the formation of fistulous tracts. Not only the lungs, pleura and bronchi are affected, but also the lymph nodes, sternum, ribs. Moreover, actinomycetes can go far beyond the borders of the chest, spreading to the abdominal and maxillofacial zones.

The thoracic form also includes actinomycosis of the armpits and mammary glands.

Advanced cases of thoracic actinomycosis can result in the death of the patient.

In the abdominal form of , the intestines (most often the caecum and appendix) and peritoneum are affected. The disease is characterized by pain, distension in the abdomen, fever, vomiting, diarrhea or constipation, and exhaustion of the body. One or more granulomatous lesions develop in the peritoneum, causing symptoms of partial intestinal obstruction. Intestinal fistulas may extend to the outer abdominal wall.

Actinomycosis of the urinary system

Due to urolithiasis, as well as chronic infectious and inflammatory diseases of the urinary system.

Genital actinomycosis

Bloody vaginal discharge, pelvic or lower abdominal pain. Weight loss is often associated and body temperature rarely rises.

The initial (primary) focus can be localized in any organ or tissue of the patient’s body.

Diagnosis of actinomycosis

Detection of actinomycetes in sputum, pharyngeal or nasal swabs is of no diagnostic value, since they are present in the norm and in healthy people. Therefore, for research, a fistula discharge is taken or a percutaneous puncture of the affected organ is performed.

Conventional microscopy of the test material can reveal drusen of actinomycetes, which allows a preliminary diagnosis. The diagnosis is considered preliminary, since drusen are detected only in 67-72% of cases in patients with actinomycosis.

Examination of punctures of other organs and tissues (except bone marrow)

Examination of punctates obtained from tumors, pretumor, tumor-like formations of various localization: liver, kidneys, lungs, retroperitoneal tumors, o…

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Subsequent immunofluorescence reaction with specific antigens is aimed at determining the type of actinomycetes.

The biomaterial is inoculated on transparent nutrient media.

Culture of wound exudates and tissues for microflora and determination of sensitivity to antimicrobial drugs

Synonyms:
Wound/tissue Culture. Aerobic Bacteria Identification and Antibiotic Susceptibility testing.
Brief description of the study “Sowing of wound discharge and tissues for microflora and determination of sensi. ..

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Microscopic examination of a Gram-stained smear.

Gram Stain. Bacterioscopic examination of different smears

Synonyms: Gram-stained smear analysis.

Microscopic (bacterioscopic) examination of Gram-stained smear.

Brief description of the study Microscopic examination of a smear, stained …

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Ultrasound of the abdominal organs is performed.

Comprehensive ultrasound examination of the abdominal organs (liver, gallbladder, pancreas, spleen)

Scanning of the internal organs of the abdominal cavity to assess its functional state and the presence of pathology.

RUB 3,090

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Chest x-ray.

Plain chest x-ray

X-ray examination of the structure of the lungs to diagnose various pathologies.

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CT of the brain and other methods of instrumental imaging, taking into account the clinical picture of the disease.

CT scan of the brain and skull

Scanning of the brain, skull and surrounding tissues, which allows diagnosing various pathologies.

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Fistulography of a fistula is an important X-ray method for diagnosing actinomycosis, the essence of which is the introduction of a contrast agent into the fistulous passages, followed by fluoroscopy of these passages. The method allows to determine the prevalence of the pathological process.

When actinomycosis is localized in the urinary system, fistulography is used in conjunction with urography and barium enema, which provide more detailed information about the extent of the disease.

A general blood test allows you to identify an infectious and inflammatory process.

Clinical blood test: general analysis, leukoformula, ESR (with microscopy of a blood smear in the presence of pathological changes)

Synonyms: Complete blood count, UAC. Full blood count, FBC, Complete blood count (CBC) with differential white blood cell count (CBC with diff), Hemogram.
Brief description of the study CBC: general a…

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Clinical urinalysis is performed to assess the condition of the urinary system.

General urinalysis (Urine analysis with sediment microscopy)

Method of determination

Determination of physical and chemical parameters is carried out on an automatic analyzer using the “dry chemistry” method.

Hardware microscope…

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Biochemical analysis of blood is necessary to identify the pathological state of organs and tissues affected by actinomycosis: glucose, plasma histamine, total bilirubin, direct bilirubin, cholesterol and its fractions (lipid profile).

Glucose (in the blood) (Glucose)

Research material

Serum or blood plasma. If it is not possible to centrifuge the sample 30 minutes after collection for serum/plasma separation…

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Plasma histamine (Histamine, plasma)

The test is used in the diagnosis of histamine-producing carcinoid tumors, laboratory confirmation of anaphylactic reactions.

Histamine – biogenic…

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Total bilirubin (Bilirubin total)

Synonyms: Total blood bilirubin; Total serum bilirubin.
Totalbilirubin; TBIL.
Brief characteristics of the analyte Bilirubin total
Bilirubin is a pigment…

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Bilirubin direct (Bilirubin conjugated, bound; Bilirubin direct)

Direct bilirubin is a water-soluble conjugated form of bilirubin produced in the liver and excreted in the bile. The test is used to assess liver function, in …

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Lipid profile screening

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It is necessary to carry out differential diagnostics with tuberculosis, nocardiosis, tumor processes, true mycoses.

Which doctors to contact

A dermatologist is primarily involved in the diagnosis and treatment of actinomycosis. However, depending on the localization of the process, consultations may be required.
pulmonologist,
gastroenterologist, dentist,
urologist,
gynecologist.

Treatment of actinomycosis

Features of the development of the disease and the variety of its clinical manifestations require complex treatment, which includes anti-inflammatory, immunomodulatory, restorative agents, surgical and physiotherapeutic treatment. Due to the formation of antibiotic resistance, it is often difficult to select antibiotics. Therefore, it is necessary to take into account the microflora accompanying actinomycosis in order to select the most effective drugs, and treatment should be carried out in 2-3-week courses.

Local treatment consists in the treatment of fistulous passages with antiseptics (hydrogen peroxide, miramistin, iodinol, etc.).

A very important part of the treatment is intramuscular immunotherapy with actinolysate, a preparation made from actinomycetes.

Actinolysate affects the immune system, stimulating the production of antibodies that destroy actinomycetes, and also increases the body’s resistance.

Surgical treatment is carried out with a deep location of the focus of actinomycosis and with insufficient effectiveness of conservative treatment, but only outside the exacerbation of the inflammatory process, after drug therapy, including drainage of fistulous tracts. In some cases, with large lesions of the lungs, a lobe of the lung is removed entirely. In the postoperative period, anti-inflammatory and immune therapy continues.

After the end of therapy, the patient should be observed by a doctor for 6-12 months, since some forms of actinomycosis may recur.

Complications

Complications caused by actinomycosis largely depend on the location of the inflammation focus.

With abdominal actinomycosis, partial or complete intestinal obstruction, the formation of abscesses, the development of hepatitis and pyelonephritis can be observed.

Thoracic actinomycosis increases the risk of formation of malignant neoplasms in the area of ​​localization of the inflammatory process.

With actinomycosis of the genitourinary system, hydronephrosis develops due to narrowing of the ureter.

Involvement of the middle ear can lead to mastoiditis (inflammation of the mastoid process of the temporal bone), actinomycosis of the central nervous system, and inflammation of the meninges.

In addition, with prolonged actinomycosis, chronic intoxication, anemia, amyloidosis of internal organs, and adhesions develop in the body.

Prevention of actinomycosis

There is no specific prevention of this disease. Non-specific prevention includes compliance with disinfectant measures for skin injuries, hygiene, sanitation of the oral cavity, timely treatment of diseases of the gastrointestinal tract, genitourinary system, pararectal region and skin, compliance with the terms of the use of intrauterine devices.

Before taking antibiotics for any reason, you should consult your doctor – this will reduce the risk of developing antibiotic resistance.

Sources:

1. Agayeva N.A. Actinomycoses as chronic granulomatous diseases // Biomedicine. – 2018. – No. 1. – S. 14-15.
2. Kulakov A.A. Surgical dentistry / ed. Kulakova A. A. – M.: GEOTAR-Media, 2021. – 408 p.
3. Kazakova A.V., Lineva O.I., Trupakova A.A., Kiyashko I.S., Kuznetsova L.V., Petyanova V.A. Generalized actinomycosis of the pelvic organs. Clinical case // Obstetrics, Gynecology and Reproduction. 2022;16(3):317-323.

IMPORTANT!

The information in this section should not be used for self-diagnosis or self-treatment. In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For diagnosis and proper treatment, you should contact your doctor.
For a correct assessment of the results of your analyzes in dynamics, it is preferable to do studies in the same laboratory, since different laboratories may use different research methods and units of measurement to perform the same analyzes.

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