Schilder-Stengl Symptom

Schilder-Stengl symptom: description and characteristics

Schilder-Stangl symptom, also known as Stangl syndrome or asymbolia dolorosa, is a neurological disorder that involves a lack of perception of pain. This symptom was described in 1932 by American neurologist and psychiatrist Paul Schilder and named after him.

Although pain is an important feature that helps prevent injury, the Schilder-Stengl symptom causes impairment of this function. Patients with this symptom cannot feel pain, although they can feel other types of tactile sensations such as pressure, temperature, and texture. This can lead to injuries and damage that patients do not notice because they do not feel pain.

The cause of the Schilder-Stengl symptom is not fully understood, but it is thought to be due to damage to the brain structures responsible for processing pain signals. This can be caused by a variety of factors, including head injury, infection, or tumor.

Treatment of the Schilder-Stengl symptom can be difficult because patients are unable to communicate their pain. In some cases, patients may use visual cues to report injury or pain. In other cases, treatment is aimed at reducing the likelihood of injury or damage.

The Schilder-Stengl symptom is a rare disorder, and not all neurologists and psychiatrists may be familiar with it. If this disorder is suspected, consultation with a specialist experienced in working with this symptom is necessary.

Although the Schilder-Stengl symptom is rare, studying it may help us better understand how pain is processed in the brain and develop new treatments for pain and neurological disorders.

Schilder-Stengl symptom: understanding and features

Schilder-Stengl symptom, also known as Schilder-Stengl syndrome or asymbolia dolorosa, is a rare neurological condition that is characterized by loss of the ability to sense and experience pain. This symptom was first described by the American neurologist and psychiatrist Paul Fedorovich Schilder and the German neurologist Albert Stengl at the end of the 19th and beginning of the 20th centuries. The Schilder-Stengl symptom is a rare neurological disorder and occurs mainly in clinical practice.

One of the main characteristics of the Schilder-Stengl symptom is asymbolia, that is, the absence of an emotional or physical reaction to pain. Patients suffering from this symptom may be insensitive to pain, unresponsive to injury, or unaware of serious medical conditions that require treatment. This distinguishes the Schilder-Stengl symptom from other disorders associated with pain perception.

Although the exact cause of the Schilder-Stengl symptom remains unknown, it is thought to be related to damage or dysfunction of certain areas of the brain responsible for processing pain signals. Possible causes include head injury, infection, tumors, or autoimmune diseases. However, a deeper study of this symptom is necessary to fully understand its mechanisms.

Diagnosis of the Schilder-Stengl symptom can be difficult because there are no specific laboratory tests or educational methods that can definitively confirm its presence. Diagnosis is based on a thorough analysis of the patient's medical history, clinical observations, and exclusion of other possible causes of lack of pain perception.

Treatment of the Schilder-Stengl symptom is difficult due to its rarity and limited research. Symptomatic therapies are generally used to relieve symptom-related problems, such as preventing injury and controlling conditions that may lead to pain. Physiotherapy and psychological support may also be helpful for patients suffering from the Schilder-Stengl symptom.

In conclusion, the Schilder-Stengl sign is an interesting and rare neurological entity. This condition, characterized by a lack of pain perception, raises many questions among the medical community. Despite the fact that the causes and mechanisms of development of this symptom are not completely clear, further research and study of its characteristics will help expand our knowledge about the functioning of the brain and pain mechanisms.