Decreased piloerection reflex

Introduction Sympathetic chain syndrome can be characterized by loss of function, such as weakening of standing hair reflex. Sympathetic chain syndrome is a clinical syndrome in which multiple causes cause long-term recessive existence. When the ganglion damage is severe and the compensatory ability is weakened, typical symptoms appear, which are often delayed in diagnosis and treatment, and are occasionally found in autopsy. Due to the different sympathetic ganglia, the clinical manifestations are not the same, but all have common clinical symptoms. Such as pain, sensory disturbances, vascular dysfunction, etc.

Cause

(1) Causes of the disease

Many causes can cause sympathetic chain syndromes, such as various acute and chronic infections, systemic or local infections, various endogenous and exogenous poisonings, as well as trauma, spinal degenerative diseases, tumors, vascular diseases and chronic Irritating lesions, etc.

(two) pathogenesis

This disease is caused by different sympathetic ganglia, which leads to the corresponding clinical manifestations. Pathological changes vary with the primary disease, caused by infectious inflammation, intracellular vacuolization and steatosis, with hyperplasia of the interstitial and surrounding tissues, edema and infiltration, poisoning and sepsis cause visible ganglion cell necrosis.

an examination

Laboratory examination

(1) routine and biochemical examination of hematuria is associated with the primary disease.

(2) There is no specificity in routine examination of cerebrospinal fluid.

2. Other auxiliary inspections

(1) Skull limb imaging examination has differential diagnosis significance.

(2) Drug and toxicant detection also has the significance of differential diagnosis.

3. Commonly used methods for detecting plant function

(1) Eye reflex

Close your eyes on your back and gently press the sides of the eye with your fingers. After 3 to 4 seconds (with mild pain), start a few pulses (15 seconds), record the pulse rate per minute, and compare with the pulse rate before the test. Comparison. Normal people can reduce 4-7 times/min after inspection. If the patient is reduced by 12 times/min or more, the vagal tone is increased, and the vagal tone is significantly increased by 18-24 times/min. Such patients are particularly prone to syncope, and there is a possibility of cardiac arrest during treatment. In addition to slow heart rate, pulse strength is often weakened, clinically can be black, dizziness, nausea and even vomiting, commonly known as vagal nervous system. Conversely, if the pulse is increased after pressing the eyeball, it is called an inversion reaction, indicating that the patient has increased sympathetic tone.

(2) White striate

Use bamboo sticks or nails to lightly and quickly across the skin (the lower limbs are more obvious), white lines appear within 8 to 20 seconds, lasting 3 to 5 minutes. This is due to vasoconstriction caused by neurological reflexes, indicating increased sympathetic excitability.

(3) Red striate

Use a bamboo stick to apply a little pressure across the skin, and red lines will appear in normal 3 to 5 seconds for 8 to 30 minutes. If the red pattern is wider and lasts longer, it may be related to increased parasympathetic excitability. In severe cases, it can appear 1 to 2 minutes across the skin and lasts 1 to 12 hours. Causes skin bulging, edema, vasodilation and blood oozing. Skin scratches can also occur in normal people, and only when there is a long duration, or a reaction occurs in both light and heavy strokes, there is a clinical reference.

(4) lying test

Let the patient lie flat and count the pulse for 1 minute; then sit up and count the pulse for 1 minute. The pulse from the lying position to the standing position is increased by 10 to 20 times/min, which is an increase in sympathetic excitability. If the position is from 10 to 20 times/min, the parasympathetic excitability is enhanced.

(5) vertical hair reflection

Ice cubes or other cold irritants are placed on the back of the patient's neck or on the axillary skin for a few seconds. It can be seen that the vertebral muscles contract and the skin follicles bulge in a chicken skin-like appearance. The reflection is affected by sympathy and is governed by segments. According to the response of different parts, sympathetic dysfunction can be diagnosed. For example, C8-T3 dominates the head and neck, T4-7 dominates the upper limbs, T8-9 dominates the trunk, and T10-L2 dominates the lower limbs.

(6) Micro-sweating assay

Skin moisture is associated with the function of sweat glands. Warm sweating is mainly related to the ambient temperature, which can regulate the body temperature. Neuropathic sweating is primarily controlled by autonomic function. The sweat glands are dominated by the postganglionic fibers of the cholinergic sympathetic nerves. By monitoring the neurogenic micro-sweat gland secretion of the skin, the sympathetic tone can be determined in time.

(7) Micro nerve electrode method

The silicon carbon micro-neural electrode has a tip diameter of 0.1, which can be inserted into a single nerve cell. In the shielded environment of the copper mesh, it is amplified by an electronic instrument and directly leads to the impulse of the sympathetic nerve. This is one of the most direct ways to judge sympathetic function.

(8) Diagnostic sympathetic block

It is the most commonly used method in the clinic. Selectively block the sympathetic nerves that govern the lesions. If the pain is relieved quickly, the affected area will be changed from cold and damp to comfortable warmth, facial skin temperature will rise, and sweating will decrease, indicating the occurrence of the pain. It is closely related to sympathetic nerves.

(9) Other

ECG R2R interval method, blood hormone concentration determination.

Differential diagnosis

Facial reflex hyperthyroidism: Sympathetic chain syndrome, the skin may have irritating symptoms, such as increased sweating and hyperfibrillation. Sympathetic chain syndrome is a clinical syndrome in which multiple causes cause long-term recessive existence. When the ganglion damage is severe and the compensatory ability is weakened, typical symptoms appear, which are often delayed in diagnosis and treatment, and are occasionally found in autopsy. Due to the different sympathetic ganglia, the clinical manifestations are not the same, but all have common clinical symptoms. Such as pain, sensory disturbances, vascular dysfunction, etc.

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