Increased sweating after exposure to cold
Introduction
Introduction A strange sweating phenomenon of syringomyelia is an increase in perspiration after cold, accompanied by a decrease in temperature, excessive fingertips, keratinization of the nails, atrophy, and loss of luster. Because of the pain and temperature loss, it is prone to burns, bumps and trauma. Patients with advanced disease have dysfunction of the stool and recurrent urinary tract infections. The exact cause is still unclear and can be divided into congenital dysplasia and secondary syringomyelia, the latter being rare.
Cause
Cause
(1) Causes of the disease:
The exact cause is still unclear and can be divided into congenital dysplasia and secondary syringomyelia, the latter being rare.
1. Congenital spinal canal insufficiency: This disease is often accompanied by other congenital anomalies such as spina bifida, cervical ribs, scoliosis, and occipital deformity.
2. Abnormal blood circulation of the spinal cord causes ischemia, necrosis and softening of the spinal cord, forming a cavity.
3. Mechanical factors: due to congenital factors, the fourth ventricle outlet obstruction, cerebrospinal fluid from the fourth ventricle to the subarachnoid space is blocked, the cerebrospinal fluid pulse wave down the central tube of the spinal cord, causing the central tube to expand, and break through the central wall to form a cavity .
4. Others, such as spinal cord cystic changes, traumatic myelopathy, radiation-induced myelopathy, spinal cord infarction softening, intraspinal hemorrhage, necrotizing myelitis.
(2) Pathogenesis:
1. There are four general theories about congenital causes:
(1) Gardner's theory of fluid mechanics: In 1958, Gardner reported a large number of cases of Chiari type I malformation with syringomyelia. He speculated that cerebrospinal fluid could not be caused by obstruction in the large area of the occipital region (congenital malformation or arachnoiditis). From the cerebral ventricle, the cerebrospinal fluid will continue to impact the central tube of the spinal cord under the action of the choroid plexus-derived pulsation, causing it to expand and destroy the gray matter around the central tube, forming a cavity. During the operation, the four ventricles and the central tube were also found to be in traffic; in some patients, ventricles were observed, and the contrast agent was observed to enter the central tube through the fourth ventricle; air was injected into the cavity through the skin puncture, and the gas could also overflow into the fourth ventricle; The liquid protein content is low, similar to cerebrospinal fluid. However, there are also different opinions: some patients did not find traffic between the four ventricles and the central canal in angiography, surgery and autopsy; although the contrast agent injected into the lumbar puncture did not flow into the fourth ventricle, the cavity could be developed; some of the cavities were separated from the central canal and were more Room. Some scholars have calculated the pressure of choroid plexus-derived pulsation and found that the pressure is small and it is impossible to cause voids. In addition, this theory cannot explain the occurrence of medullary cavity.
(2) Williams' intracranial and intraspinal pressure separation theory: Since 1969, Williams has conducted a series of studies to determine the pressure in the ventricles, cavities, and subarachnoid space. It is believed that when a person coughs, sneezes and exerts force, it can cause an increase in intracranial and intraspinal venous pressure, which increases the pressure of the subarachnoid space of the cerebral spinal cord. At this time, the normal person passes through the cerebrospinal fluid in the subarachnoid space. Round-trip flow to balance. In patients with mild cerebellar tonsillar palsy, there is a pressure imbalance due to cerebrospinal fluid circulation disorders. Williams found that in the early stages of coughing, the pressure in the subarachnoid space of the waist was higher than in the basal pool, and vice versa. Therefore, he speculated that the cerebellar tonsils may have a flap function. When the subarachnoid pressure of the spinal cord is elevated, the cerebrospinal fluid can push up the sacral tonsils and flow into the cranium; as the subarachnoid pressure of the spinal cord decreases, the cerebellar tonsils reappear. The lower jaw causes the cerebrospinal fluid to not flow back, causing an increase in intracranial pressure, causing cerebrospinal fluid to perfuse from the fourth ventricle to the central canal. This is the pressure difference between the intracranial and spinal cord, the central canal and the spinal cord. Williams refers to the separation of cerebrospinal fluid pressure. This pressure difference has been used repeatedly for many years to form a syringomyelia. The characteristics of high pressure in the cavity were also found by cavity puncture and animal experiments. Some patients have clinical reports of increased symptoms when coughing is exerted. The traffic between the central tube and the cavity of patients with syringomyelia is not always open. It can be closed due to repeated compression of the tissue at the large hole of the pillow and other reasons. Therefore, the cerebrospinal fluid impact theory is proposed in the progress of the cavity. In patients with obvious pressure on the occipital foramen, when the cough is forced, the pressure in the subarachnoid space of the spinal cord suddenly rises, and because it cannot be transmitted to the brain, the spinal cord is transmitted. The inner cavity is transmitted. Because the opening of the cavity is closed or has a flap, the liquid in the cavity cannot flow into the skull, and it is impacted by the gray matter beside the central tube. Over time, the cavity gradually expands upward and forms a medulla on the basis of the syringomyelia. Empty. This indicates that the medullary cavity cannot exist alone, which is consistent with clinical observations.
(3) Infiltration of spinal cord parenchyma in cerebrospinal fluid: In 1972, Ball found a significant widening of the perivascular space in the spinal cord parenchyma during autopsy of syringomyelia. He injected ink into the cavity to spread along the perivascular space and formed some localized parts. The small pool, especially the white matter on the dorsal side of the spinal cord, is obvious. It is speculated that due to the malformation of the occipital macropore, the pressure of the venous pressure and the subarachnoid space of the spinal cord are repeatedly increased, and the spinal cord is long-term, so that the perivascular space is gradually enlarged, and the cerebrospinal fluid is infiltrated to form a cavity. In 1979, Aboulker proposed that the axon tissue is permeable to water, and the cerebrospinal fluid can penetrate into the spinal cord along the nerve tissue. Clinically, it has been reported that patients who have no communication between the fourth ventricle and the central tube during surgery can develop the cavity in the delayed cerebrospinal fluid imaging, and some of the cavity is away from the central tube, and is mostly near the posterior corner of the spinal cord surface.
(4) Circulatory Disorder Theory: Netsky found vascular abnormalities in the medulla in patients with syringomyelia, especially in the posterior horn. He speculates that with age, circulatory disorders can occur around abnormal blood vessels leading to voids. The spinal cord has a protective mechanism for the perfusion or impact damage of the cerebrospinal fluid. The glial fibrosis proliferates. These fibers affect the blood supply to the parenchymal spinal cord. Ischemia may be one of the causes of cavity development and progression. Congenital abnormalities in the spinal cord parenchyma (mainly in the posterior horn) are not the only factors in the pathogenesis. Congenital anomalies in the posterior horn of the spinal cord, combined with abnormalities in the occipital macropore and venous pressure, make the cerebrospinal fluid easily invade from the posterior root of the congenital anomaly, forming a cavity in the area, which can be communicated with the central tube as the cavity expands. The central tube is gradually enlarged, and finally it can communicate with the fourth ventricle.
2. Acquired causes: caused by factors such as spinal cord tumor, arachnoiditis and trauma. Trauma can cause necrosis in the central part of the spinal cord, resulting in the accumulation of exudate and destruction products, resulting in increased osmotic pressure and fluid retention. As the intramedullary pressure increases, the surrounding tissue can be destroyed and the cavity can be gradually enlarged. In animal experiments, it was found that some tiny cysts appeared near the broken end of the spinal cord, and it is speculated that the rupture and confluence of these cysts may be the cause of cavity formation. Syringomyelia after arachnoiditis is mainly caused by ischemia and venous thrombosis. Syringomyelia caused by spinal cord tumors is mainly related to the secretion of protein fluid by tumor cells.
The pathogenesis of syringomyelia is complicated, and malformation or obstruction of the occipital macropore is one of the important factors leading to the formation of cavities. Due to the different causes, physical fitness and compensatory capacity of each person, the formation and development of cavities are also different. Therefore, different causes should be discussed and comprehensively analyzed according to clinical characteristics and different disease periods.
Syringomyelia occurs mostly near the central canal of the cervical and upper thoracic segments, close to the posterior horn of one side, forming a tubular cavity that can continue multiple spinal segments and does not necessarily communicate with the central canal. In the cross-section of the spinal cord, it can be seen that the hollow cavity occupies most of the medulla, and the dorsal side of the anterior horn can also be involved, and the anterior and posterior commissure structures are often destroyed. With the further development of the cavity, the relief angle can also be affected, even including the ventral side of the sling. The void can be confined to one side of the spinal cord and can also occupy both sides. The shape of the cavity is different, and there may be multiple cavity cavities in the same plane of the spinal cord, which may be separated from each other or connected to each other. Some of this disease exists at the same time as the medullary cavity. The cavity is extended to the pons and midbrain. Cavity below the lumbar region is less common. In a few cases, small holes are seen at the end of the spinal cord and coexist with the spina bifida.
Spinal compression and degeneration is often the inevitable result of the expansion of the cavity. The spinal cord of the cavity is fusiform, the color is lightened, and the soft membrane is reduced. The cavity can be located at the center or on one side, or biased to the front or the back, so that the gray matter of the spinal cord, the lateral cord, and the posterior cord are denaturing. The wall of the cavity is smooth, and it is a proliferating gelatinous and nerve fiber that tends to be denatured. The color becomes white and the surrounding nerve fibers are edematous. In the late stage of syringomyelia, the spinal cord tissue is thin and can cause obstruction of the spinal canal.
According to the pathological condition, syringomyelia can be divided into two types: one is traffic syringomyelia, that is, syringomyelia and fourth ventricle, subarachnoid cerebrospinal fluid communication, often combined with cerebellar tonsil sputum type I and type II deformity. It may be caused by some abnormal factors in the growth and development process. For example, the central canal of the spinal cord may be under the pressure of high cerebrospinal fluid, and the fluid continuously leaks into the peripheral nerve tissue, causing it to continuously expand and form a local The other type is non-communicative syringomyelia, and the cavity is not in contact with the cerebrospinal fluid circulation. Its formation is related to intramedullary tumors, traumatic paraplegia and some degenerative diseases.
Examine
an examination
Related inspection
Temperature and sweating pilocarpine sweating test sweat electrolyte test
Clinical manifestations:
The age of onset is 31 to 50 years old, and children and the elderly are rare. More men than women, had a family history report. There are three aspects of the clinical manifestations of syringomyelia, and the degree of symptoms is closely related to the development of the cavity. The general course of disease progresses slowly, and the early symptoms are mostly segmental, affecting the upper limb first. When the cavity is further enlarged, the gray matter in the marrow and the white matter conduction bundle outside it are also involved, and the conduction beam dysfunction occurs below the cavity. Therefore, the symptoms of early patients are more limited and mild, and late symptoms are widespread and even paraplegic.
1. Sensory symptoms: According to the cavity located in the cervical and upper thoracic segments of the spinal cord, one side or the center, there is a segmental sensory disturbance of the unilateral upper limb and the upper thoracic segment, often characterized by segmental dissociative sensory disturbance. Pain, temperature loss or disappear, deep feeling exists. This symptom can also be bilateral.
2. Motor symptoms: the neck and thoracic cavity affect the anterior horn of the spinal cord, and there is a symptom of flaccid part of the upper limb on one or both sides. It is characterized by muscle weakness and decreased muscle tone, especially in the two-handed intermuscular muscle and interosseous muscle atrophy. In severe cases, the claw-shaped hand deformity appears. When the descending root of the trigeminal nerve is affected, the central side feels like central pain and temperature sensation, and the facial separation sensation is so-called "onion-like distribution" with weak chewing muscle strength. If the vestibular cerebellar conduction bundle is involved, dizziness, nausea, vomiting, gait instability, and nystagmus may occur. On one or both sides of the lower extremity, the upper part of the motor was paralyzed, the muscle tension was hyperthyroidism, the abdominal wall reflex disappeared and the Babinski sign was positive. Late cases are more severe.
3. Autonomic nerve damage symptoms: Cavity involving the spinal cord (neck 8 cervical and chest 1 chest) lateral sympathetic spinal cord center, the presence of Horner syndrome. The lesions may damage the corresponding segments, the limbs and the trunk skin may have abnormal secretions, and hyperhidrosis or hypohidrosis is the only sign of abnormal secretion. Less sweat can be confined to one side of the body, called "half side sweating", and more often seen on one side of the upper body, or one side of the upper limb or half of the face. Usually corneal reflexes can also weaken or disappear, because neurotrophic keratitis can cause bilateral corneal perforation. Another strange phenomenon of sweating is the increase in perspiration after cold, accompanied by a decrease in temperature, excessive fingertips, keratinization of the nails, atrophy, and loss of luster. Because of the pain and temperature loss, it is prone to burns, bumps and trauma. Patients with advanced disease have dysfunction of the stool and recurrent urinary tract infections.
diagnosis:
According to the characteristics of chronic onset and clinical manifestations, there are segmental separation sensory disturbances, motor neuron dyskinesia in upper limbs, and motor neuron dyskinesia in lower limbs. Combined with the performance of imaging, the diagnosis can be further clarified.
Diagnosis
Differential diagnosis
Night sweats: It is a disease name of Chinese medicine. It is a symptom characterized by abnormal sweating after going to sleep and sweating after waking up. "Pirates" have the meaning of stealing. Ancient medical thieves sneak around in the night to describe the disease card. When people fall asleep or just close their eyes and fall asleep, sweat sneak out like a thief. Night sweats have physiological and pathological points. The effect of traditional Chinese medicine on the treatment of night sweats by umbilical therapy is very significant. Patients with night sweats should pay attention to self-care, strengthen physical exercise, and rational diet therapy.
Hyperhidrosis: A disease caused by excessive secretion of sweat glands due to excessive sympathetic stimulation. Sympathetic innervation dominates the body's sweating. Under normal circumstances, the sympathetic nerve regulates the body's body temperature by controlling sweating, but the patient's sweating and facial flushing completely lose normal control. Hyperhidrosis and facial flushing make the patient daily. In helplessness, anxiety or panic.
Clinical manifestations: The age of onset is 31 to 50 years old, and children and the elderly are rare. More men than women, had a family history report. There are three aspects of the clinical manifestations of syringomyelia, and the degree of symptoms is closely related to the development of the cavity. The general course of disease progresses slowly, and the early symptoms are mostly segmental, affecting the upper limb first. When the cavity is further enlarged, the gray matter in the marrow and the white matter conduction bundle outside it are also involved, and the conduction beam dysfunction occurs below the cavity. Therefore, the symptoms of early patients are more limited and mild, and late symptoms are widespread and even paraplegic.
1. Sensory symptoms: According to the cavity located in the cervical and upper thoracic segments of the spinal cord, one side or the center, there is a segmental sensory disturbance of the unilateral upper limb and the upper thoracic segment, often characterized by segmental dissociative sensory disturbance. Pain, temperature loss or disappear, deep feeling exists. This symptom can also be bilateral.
2. Motor symptoms: the neck and thoracic cavity affect the anterior horn of the spinal cord, and there is a symptom of flaccid part of the upper limb on one or both sides. It is characterized by muscle weakness and decreased muscle tone, especially in the two-handed intermuscular muscle and interosseous muscle atrophy. In severe cases, the claw-shaped hand deformity appears. When the descending root of the trigeminal nerve is affected, the central side feels like central pain and temperature sensation, and the facial separation sensation is so-called "onion-like distribution" with weak chewing muscle strength. If the vestibular cerebellar conduction bundle is involved, dizziness, nausea, vomiting, gait instability, and nystagmus may occur. On one or both sides of the lower extremity, the upper part of the motor was paralyzed, the muscle tension was hyperthyroidism, the abdominal wall reflex disappeared and the Babinski sign was positive. Late cases are more severe.
3. Autonomic nerve damage symptoms: Cavity involving the spinal cord (neck 8 cervical and chest 1 chest) lateral sympathetic spinal cord center, the presence of Horner syndrome. The lesions may damage the corresponding segments, the limbs and the trunk skin may have abnormal secretions, and hyperhidrosis or hypohidrosis is the only sign of abnormal secretion. Less sweat can be confined to one side of the body, called "half side sweating", and more often seen on one side of the upper body, or one side of the upper limb or half of the face. Usually corneal reflexes can also weaken or disappear, because neurotrophic keratitis can cause bilateral corneal perforation. Another strange phenomenon of sweating is the increase in perspiration after cold, accompanied by a decrease in temperature, excessive fingertips, keratinization of the nails, atrophy, and loss of luster. Because of the pain and temperature loss, it is prone to burns, bumps and trauma. Patients with advanced disease have dysfunction of the stool and recurrent urinary tract infections.
diagnosis:
According to the characteristics of chronic onset and clinical manifestations, there are segmental separation sensory disturbances, motor neuron dyskinesia in upper limbs, and motor neuron dyskinesia in lower limbs. Combined with the performance of imaging, the diagnosis can be further clarified.
