Cerebral swine cysticercosis
Introduction
Introduction to cysticercosis in brain Cerebral cysticercosis is a disease caused by the larvae of the larvae of the swine mites in the central nervous system. It is the most common type of central nervous system parasitic diseases in China. The clinical symptoms of this disease are diverse, often causing serious diseases, and even May be life threatening. The cysticercosis that is parasitic in the ventricular system is of different sizes. It is most common in the fourth ventricle. The lesions can be single or multiple, and can be released from the ventricles or adhere to the ventricle wall. These cysts can easily form flaps or cause meningeal adhesions. Thick and obstructing the ventricle of the ventricles, producing obstructive hydrocephalus, enlargement of the ventricles, and late stage can lead to brain atrophy, intracranial hypertension, cerebral palsy and other serious consequences. basic knowledge Sickness ratio: 0.0001% Susceptible people: no special people Mode of infection: non-infectious Complications: neuromuscular rigidity, straight cerebral palsy
Cause
Causes of cysticercosis in brain
(1) Causes of the disease
Cysticer's cysticercosis is a zoonotic parasitic disease in which humans are infected by eating raw or undercooked pork containing cysticercosis. In the stomach, the cystic wall of the cysticercosis is quickly digested to the small intestine. The intestinal juice and bile function are turned out, and the suction wall and the small hook are fixed on the intestinal wall of the duodenum and jejunum 40 to 50 cm. The head section is deeply buried in the intestinal mucosa, and the worm body is mainly in the intestinal lumen. Taking the digestive food in the intestine as nutrition, the neck section continuously produces segments and forms a chain. With the fertilization of the eggs, the gestational plaque forms, falls off from the chain, and is excreted with the feces. The cysticercosis develops into a tapeworm. Generally, it takes about 8 to 12 weeks. The adult mites are about 2 to 4 m long and divided into 1,000 sections. The general infection is one. Individual infections of 2 to 7 or more can survive for more than 25 years in humans. The terminal host of aphids, the intermediate host is mainly pigs. When the patient suffers from cysticercosis, it becomes an intermediate host. The infection methods include:
1. In vivo infection of patients with current tsutsugamushi disease, due to vomiting or intestinal peristalsis, may cause the aphid gestational tablets and eggs to flow back into the stomach, each section of the gestational section contains about 40,000 eggs.
2. Autologous in vitro infection The hand of a patient with tsutsugamushi disease is contaminated with aphid eggs and infected by oral feeding into the gastrointestinal tract.
3. Allogeneic patients with cysticercosis do not have aphid infection, but are infected with water, vegetables, fruits, etc. contaminated with aphid eggs. After the eggs are swallowed by the intermediate host, they are passed through the gastric juice in their duodenum. The action of bile and other digestive juices, the six hooks in the egg hatch from the embryo membrane after 24 to 72 hours.
Due to the activity of the small hook and the action of the secretion of the six hooks, the six hooks penetrate the intestinal wall, then enter the mesenteric venules and lymphatic circulation, and are sent to various parts of the body. After reaching the parasitic parts, the worms gradually grow up. The middle cell dissolves to form a cavity and is filled with liquid. After 60 days, small hooks and suction cups appear on the cephalic section, and the cysticercosis can mature after about 10 weeks. The cysticercosis parasitic in the human body is different in shape and size due to parasitic parts. The same, generally circular or elliptical, 0.5 ~ 2cm size, 3 ~ 5cm is also more common.
(two) pathogenesis
After entering the brain with the blood flow, the six hooks can be distributed in different parts, causing various pathological changes. The cysticercosis parasitic in the brain parenchyma is generally the size of soybeans, mostly located at the junction of gray matter and white matter, and the white matter parasitic in gray matter. For many, when the worm body survives, only a small amount of fibroblasts and glial cells are seen in the surrounding brain tissue, and the inflammatory reaction is lighter. After the death of the worm, the surrounding inflammatory reaction is more intense, and there are obvious nerve cells, granulocytes, and lymphocytes. Infiltration of cells and plasma cells, followed by different degrees of fibrosis, when the lesions approach the motor center can cause epileptic seizures or loss of vision, visual hallucinations, localized epilepsy, diffuse brain parenchymal involvement can lead to increased intracranial pressure or Qualitative psychosis, severe can lead to extensive destruction of brain parenchyma and cortical atrophy to form dementia.
Parasitic in the subarachnoid space, cysticercosis in the brain pool often occurs in a string, there are many no-heads in the capsule, because there are gaps around, the resistance is small, so the volume is larger, the largest resembling grapes, called grape-like cysticercosis, pole Easy to rupture, such cysticercosis can cause arachnoiditis, form thickening of the meninges, adhesions, severe cases can cause cerebrospinal fluid absorption disorders, produce traffic hydrocephalus, cysticercosis in the spinal cord can cause symptoms of compression, dyskinesia .
The histopathological morphology of cerebral cysticercosis can be divided into three phases: live cysticercosis, denaturing cysticercosis and depressive cysticercosis, and multiple cysticercosis parasitized in the brain tissue of the same patient. Different, it is possible to see pathological changes in various periods.
1. The cystic sac of the cystic sac, the body and the sac are all intact, the head sucker, the apex is obvious, the small hook under the apex is obvious, the wall is thin, and can be divided into three layers: the inner layer is inflammatory cells. The middle layer is a fibrous layer containing collagen fibers and reticular fibers, and the outer layer is a villus layer, adjacent to brain tissue with glial cell proliferation, intimal hyperplasia and inflammatory cell infiltration.
2. The internal structure of the denaturing cystice stage is still visible, but the wall of the capsule has different degrees of adhesion to the surrounding inflammatory reaction layer, the wall of the cyst wall becomes loose, the fiber breaks, vacuoles appear under the surface layer, cell edema, inflammatory reaction The fibroblasts in the layer increased, the fibrous layer became thicker, the hairs were broken by electron microscopy, the mitochondria were denatured and condensed, the reticular fibers underneath were thickened, and the glycogen particles in the cells under the surface layer were dissolved.
3. The head of the cysticercosis cyst, the body and the sac structure are blurred, pink, sometimes only the calcareous body is seen, the vascular proliferation of the inflammatory reaction layer is obvious, the electron microscope sees most of the villi disappear, and the mitochondria disintegrate. It can also be expressed as a inflammatory block. Finally, the complete liquefaction of the cysticercosis is surrounded by vacuolated fibrous tissue. The inflammatory cells are reduced or have no inflammatory reaction, and the lesion is partially or completely calcified. From the accumulated necropsy data, the patient has brain essence. Infected with a large number of cysticercosis, its inflammatory reaction is intense and obvious, and the brain tissue is extensively edematous and hyperemia, the brain volume is enlarged, the sulcular gyrus is shallow, the ventricular system is often reduced, and the cranial suture can be separated in children, such as cystic sac in the cisterna magna. Pool, cerebellum pons and other parts, often accompanied by secondary proliferative arachnoiditis, adhesions and thickening, cerebellar tonsils can be congested, edema and hemorrhage, brain tissue can appear softening, nerve cell variability necrosis.
Prevention
Cerebral cysticercosis prevention
Cerebral sac cysticercosis has been involved in more than 20 provinces in China, of which the northeastern region and the Yellow River Basin are high-incidence zones, and it is not uncommon in some provinces in the southwest. Therefore, this disease needs to be strengthened in China.
Prevention of this disease should start from eliminating the source of infection and cutting off the route of transmission.
1. Advocate and popularize the medical knowledge of cysticercosis, make people understand the importance of eating habits, change the habit of eating half-baked pork, and prevent rice pork from entering the body.
2. Strict manure management to eliminate eggs.
3. The most important thing is to strictly implement the food management law, strengthen the health quarantine of pork foods, and prohibit the listing of pork with cysticercosis; in addition, it is also important to manage the treatment of pigs, such as captivity, timely treatment of pig intestinal mites, Slaughter pigs with cysticercosis are buried or used as industrial raw materials.
Complication
Complications of cysticercosis in brain Complications , neuromuscular rigidity, tonic cerebral palsy
Cysts can be parasitic in the brain, or parasitic on the skin, muscles, eyes, tongue and heart, so you can have multiple systemic symptoms and signs.
Symptom
Cerebral cysticercosis symptoms Common symptoms Increased intracranial pressure, irritability, nausea, meningeal irritation, subcutaneous nodular response, retarded dementia
1. Clinical classification In 1986, the editorial department of the Chinese Journal of Neuropsychiatry was divided into 6 types and several subtypes according to the clinical manifestations of cysticercosis in China. In 1994, Ge Lingyun and Kong Qingan and others in the monograph of the nervous system cysticercosis The disease is divided into 9 types, which are described as follows:
(1) Epilepsy type: Epilepsy is a prominent symptom. The form of seizure can be a general episode, a small episode, a psychomotor episode or a localized seizure. The diversity of the seizure form and the ease of conversion are characteristics of this type.
The pia mater type (subarachnoid type) is mainly composed of meningeal lesions without obvious brain parenchymal lesions, which can be further divided into:
1 meningitis type: manifested as meningeal irritation, cerebrospinal fluid has an inflammatory reaction.
2 skull base adhesion type: can show increased intracranial pressure, head CT scan or ventriculography showed that the ventricles are generally enlarged, or the intracranial pressure is not high and there is other manifestations of arachnoid adhesions.
(2) Brain parenchyma: mainly based on brain parenchymal damage, can be further divided into:
1 increased intracranial pressure: manifested as increased intracranial pressure and symptoms and signs of diffuse brain damage, CT showed that the ventricles became smaller.
2 normal intracranial pressure: normal intracranial pressure, manifested as symptoms of brain parenchymal damage, such as dementia, mental symptoms or localized damage.
(3) ventricle type: more intracranial pressure increased, often Bruns sign, positioning signs are not obvious, the diagnosis is based on ventriculography, and distinguishes lateral ventricle type, three ventricle type and four ventricle type.
(4) Mixed type: There are two types of clinical symptoms and signs.
(5) Asymptomatic type: no obvious brain symptoms, however, objective examination showed evidence of significant damage.
2. The current clinical manifestations of several types of this disease are summarized as follows
(1) Epilepsy type: It is the most common type of cysticercosis in cerebral pigs, accounting for 59% of the total number of cases. Among them, epilepsy is the first symptom, accounting for 46.1%, and epilepsy as the only symptom, accounting for 40.1% (Wei Gangzhi, etc.) , 1988).
Seizures often start in young adults. The common types of seizures are generalized tonic-clonic seizures, simple partial seizures and complex partial seizures, and a few are epileptic continuous states. The same patient can have two episodes and can be converted to each other. The frequency of seizures varies widely, and can occur several times in a few months or several times in a month.
Electroencephalography shows focal or multifocal slow wave activity, diffuse slow waves, spikes or spikes, slow-synchronous waves or periodic unilateral distribution.
(2) Increased intracranial pressure: common in patients with a large number of cysticercosis invading brain tissue, increased intracranial pressure may be progressive, but also more acute onset, with headache, jet vomiting and varying degrees of optic disc edema The main clinical manifestations, increased intracranial pressure may be due to diffuse damage caused by a large number of cysticercosis, including inflammatory reactions and edema around the lesion.
Cerebrospinal fluid examination, in addition to elevated intracranial pressure, the number of cells often increased slightly.
(3) Meningoencephalitis type: It is more common in the early stage when a large number of cysticercosis invades the brain. At this time, cysticercosis has entered the subarachnoid space through the ventricular system, or invades the pia mater. Generally, the onset is more urgent, and the course of disease is slow. However, when this type is classified as chronic meningitis, the brain parenchyma often has diffuse damage. The clinical manifestations are mainly meningeal irritation, headache, neck stiffness, fever, irritability and lethargy can occur.
In addition to elevated brain pressure, the number of cells in the cerebrospinal fluid examination increased to varying degrees, lymphocytes and eosinophils increased, protein content increased, sugar, chloride can reduce the changes similar to tuberculous meningitis, but this type The positive rate of serum and cerebrospinal fluid cysticercosis immunoassay was the highest.
(4) ventricle type: the immature cysticercosis can enter the ventricular system through the choroid plexus. The initial worm body is small in size, matures after 10 weeks, and is suspended in the cerebrospinal fluid in the ventricle, and moves with the flow of cerebrospinal fluid, so it can be moved in. The third ventricle enters the fourth ventricle through the midbrain water tube. The cystic worm passes through the narrow midbrain water pipe. It may be due to the pressure of the cerebrospinal fluid flow rate and the larvae wall is still thin, containing liquid, and the worm body is flexible and deformable. It can pass through a narrow channel smaller than the diameter of cysticercosis. When entering the fourth ventricle, the worm continues to grow, and some of them have not easily passed through the median and lateral holes and remain in the fourth ventricle. When you live, it can cause sudden increase of intracranial pressure, but once the blockage is eliminated, the symptoms of increased intracranial pressure will also be relieved. When the cystic sac of the fourth ventricle accumulates at the bottom of the fourth ventricle, it can induce sudden spiraling and nausea. , vomiting, nystagmus, forced head position and even double vision, ataxia and drowsiness are called Bruns sign, which is a characteristic symptom of this type.
Most of the cysticercosis is single-shot. For example, Zhang Yongfu et al. (1993) reported that 31 cases of intraventricular cysticercosis confirmed by surgery were single, but some patients also had several to more than 10 cysticercosis in the ventricular system. Most of them are located in the fourth ventricle, and patients with this type have symptoms of elevated intracranial pressure.
(5) Skull base adhesion type: cysticercosis enters the occipital pool through the median or lateral hole of the fourth ventricle, and moves to the brain pool with cerebrospinal fluid circulation. The cysticercosis can continue to increase in this volume, and the cyst wall is in contact with the arachnoid membrane. It causes an inflammatory reaction and forms a local arachnoid and adhesion to the brain tissue. Brain lesions can cause the entire ventricular system to expand, leading to obstructive hydrocephalus and simultaneous damage to the brain.
(6) Mental disorders: patients with mental retardation, light manifestations of memory loss, decreased ability to work, slow response, feelings of indifference; severe behavior is weird, restless restlessness, hallucinations, delusions eventually stupor or dementia, This type is caused by a large number of cysticercosis in the frontal lobe, especially in the frontal lobe, which causes extensive damage to the brain parenchyma, or due to long-term high intracranial pressure hydrocephalus, which causes the cortex to be extensively compressed and thinned.
(7) intraspinal type: this type is rare, cysticercosis can be located in the spinal cord, spinal or nerve roots, mostly single hair, cysticercosis into the spinal canal pathway may be the cerebral system of cysticercosis, into the fourth ventricle through the pillow The large pool enters the subarachnoid space of the spinal canal; it may also be the circulation of the six hooks into the spinal canal through the blood circulation. There are cases of cysticercosis found in the horsetail area in China (Wei Gangzhi et al., 1988). The clinical manifestations of this type are based on the capsule. The parasitic parts of the insects are different, and the symptoms of the spinal cord vary.
(8) Asymptomatic type: Although this type of patient has been confirmed to have cysticercosis in the brain, even the blood and cerebrospinal fluid cysticercosis immunoassay is also positive, but there are no symptoms and signs in the clinic. This type of patient should be thoroughly examined. Then determine if it should be treated.
(9) Mixed type: There are two types of clinical symptoms and signs.
Examine
Examination of cysticercosis in brain
Laboratory tests that aid diagnosis include:
1. General laboratory examination of stool for routine inspection of mites and adult stalks, direct smear method, preferably by natural precipitation method or centrifugal sedimentation method to check eggs, eggs are round outer shell is very thin Colorless and transparent, it is easy to rupture and fall off. The eggs found in the stool are mostly six-clawed, brown or tan.
Cerebrospinal fluid cytology examination of normal or light, moderately elevated cells, general eosinophils, lymphocytes and monocytes increased, meningeal encephalitis type increased significantly, and even eosinophils predominance, but the total number of cells Below 500×106/L, the protein content is light, moderately elevated, sugar can be reduced, and chloride is normal.
2. Subcutaneous muscle biopsy The cystic nodules extracted by subcutaneous muscle biopsy can be observed by tableting method. The thicker connective tissue outer capsule is first cut, the inner capsule is removed, and the inner capsule is cut open, and the cystic fluid is released. Between the two slides, gently flatten, look for the head section under a low magnification microscope, the untreated person is a live cysticercosis
3. Serum and cerebrospinal fluid cysticercosis immunological detection Currently, clinical use of serum and cerebrospinal fluid specific antibodies to assist diagnosis, the commonly used methods are as follows.
(1) Enzyme-linked immunosorbent assay (ELISA): Zhang Xinghu et al (1997) reported that the specificity and sensitivity of this method for serum detection antibodies were 89.1% and 69.7%, respectively, cerebrospinal fluid specificity was negative, sensitivity was 40%, Knowing the number of cysticercosis and the lesion site can affect the results of ELISA. The more the number of worms, the higher the ELISA reaction intensity, the higher the serum antibody titer of meningeal encephalitis type, and the early and late stage of cysticercosis infection. The ELISA may be negative. The positive rate of the method used by the Shandong Institute of Parasitic Diseases to diagnose cysticercosis is 90%. In view of the fact that this method can produce false positives, it is suggested that a negative control can be set in the same test to help judge the results of the test. .
(2) Indirect hemagglutination test (THA): The result of a large series of tests in China, the seroprevalence rate was 87.2%, the cerebrospinal fluid was 84.0% (Wei Gangzhi et al., 1988), and the other reported seroprevalence rate was 79.9% (Li Zhirong) Et al., 1987), the majority of meningitis type is positive.
(3) Cysticer's complement fixation test: the positive rate of cerebrospinal fluid was 80.2%, and the serum was 68.6%.
At present, there are reports on the detection of serum and cerebrospinal fluid antibodies and the detection of cerebrospinal fluid circulating antigen by dot enzyme-linked immunosorbent assay (Dot-ELISA), which is to be popularized.
CT and MR examination of the brain is an important means to diagnose cysticercosis in brain, but the number of cysticercosis parasitic in the brain tissue varies, and the position is different. The cysticercosis is in the stage of live cystice, degenerative and dead pathology. The changes are different, so the imaging performance is diverse, and the performance of the disease in imaging is generally divided into several types.
1. CT findings of cysticercosis in brain
(1) Multiple cystic low-density lesions with small and uniform cystic parenchyma distribution, mostly located in the cortex or near cortex, sometimes only one lesion, 0.3 to 2 cm in diameter, if the number is large and densely present Causes the ventricle to be compressed or displaced to the opposite side, and is enhanced in a ring-like enhancement.
(2) multiple nodular type: plain sweep is scattered in multiple irregular low-density shadows, or low-density and high-density mixed nodular, and nodular or annular enhancement occurs in the enhanced low-density shadow, suggesting cysticercosis Edema has formed a granuloma.
(3) Giant capsule type: plain scan is a low-density round or oval lesion, generally 5 to 8 cm in diameter. The large capsule itself is not strengthened, and the surrounding fibrous tissue is ring-reinforced. This type can exist simultaneously with the small capsule type. More common in the early stages of infection.
(4) ventricle type plain scan showed intracranial cystic space-occupying lesions, which were round or oval, generally larger, and the density was the same as that of cerebrospinal fluid. When the position was changed, the position of the lesion in the ventricle was also changed, and the enhancement was not enhanced. Cysts can be found in any part of the ventricular system, but more common in the fourth ventricle, and more obstructive hydrocephalus.
(5) meningitis type: plain scan sees the cerebral cistern or lateral fissure with cystic low-density shadow, enhances the posterior sac wall lightly, if the brain arachnoid has been adhered and thickened, it can be strengthened, and the ventricle system is symmetrically enlarged. .
(6) Multiple calcification type: Late stage performance of cysticercosis infection for more than several years, cysticercosis death and calcium deposition, calcification plaque diameter 0.2 ~ 0.4cm, round, no edema around, enhanced no enhancement, calcification in the lesion In the process, the wall of the capsule and the head section are first calcified.
(7) Hybrid type: The imaging performance of the above different types.
It is worth noting that patients with cysticercosis in the brain may have abnormal CT scans of the brain, and only ring or nodular enhancement occurs when strengthening.
2. MRI findings of cysticercosis in brains and brains The T1 weighted images of live cysticercosis in the brain parenchyma are long-signal, ranging in size from 0.3 to 1 m, or even just a dot. The larger lesions may be slightly longer. Nodules or blocky shadows of the signal, the lesion boundary is generally unclear, the T2 weighted image shows a relatively uniform long T2 signal, and there are few edema or only mild edema around it. The enhanced scan T1-weighted image appears in the same lesion. Ring-enhanced, peripheral edema is also more obvious, cysticercosis in the degeneration of brain parenchyma, T1 weighted image is a block-like long T1 signal, the lesion diameter is also slightly larger, can be single or multiple, and the lesion and brain tissue boundaries are not Clear; the T2-weighted image is a long signal, and the center signal is unevenly mixed. The enhanced T1-weighted image is circularly enhanced in the original lesion. Sometimes the enhanced comma-like head segment is visible, and the circumferentially enhanced peripheral edema area is obviously enlarged. The cystic larvae degenerate and release allogeneic protein, and the cystic worms in the brain parenchyma are dead and calcified. Both T1 and T2 weighted images have a round-like low signal. The enhanced scan can show the glial hyperplasia in the calcified group. Systemic cysticercosis In the fourth ventricle, the T1 weighted image was expanded in the fourth ventricle, and the cystic worm showed a long T1 signal, and the cephalic section showed a small dot-like high signal; the T2-weighted cystic worm showed a long T2, and the cephalic section showed a point-like low signal. Intraventricular cysticercosis is often accompanied by obstructive hydrocephalus.
Diagnosis
Diagnosis and identification of cysticercosis in brain
Diagnostic criteria
Patients from high incidence areas of cysticercosis should be asked whether there is a history of aphids in the past, whether white mites have been discharged in the stool, whether subcutaneous nodules have been found, and whether they have eaten uncooked pork and eating habits. Etc. Physical examination includes the nervous system such as the fundus and retina, extraocular muscles and limbs with abnormal hypertrophy or subcutaneous nodules.
Seizures and/or multifocal, diverse central nervous system symptoms, history of constipation, or subcutaneous nodules confirmed by biopsy as cysticercosis, and serological positive of cerebrospinal fluid are important diagnoses of this disease Based on the pathological diagnosis of cystic nodules and skull CT, a typical cystic opioid image of magnetic resonance is the basis for diagnosis.
Because the clinical manifestations of cysticercosis in brain sinus are complex and diverse, in addition to detailed medical history and careful physical examination, brain imaging examination and detection of serum and cerebrospinal fluid cysticercosis are extremely important. It is difficult to affirm the diagnosis of some diseases. Diagnostic treatment can be considered to aid diagnosis.
Differential diagnosis
The cerebral cysticercosis is complicated and variable. In clinical work, it is often confused with the following diseases:
1. Other brain parasitic diseases such as echinococcosis, cerebral schistosomiasis, brain amebiasis, and toxoplasmosis, mainly rely on epidemiological characteristics, specific immunodiagnosis and typical imaging examination to distinguish .
2. Non-parasitic infectious diseases of the brain such as encephalitis, brain abscess, brain tuberculosis, etc.
3. Non-infectious diseases of the brain such as epilepsy, cerebral infarction, cerebral vascular malformation, tuberous sclerosis and multiple sclerosis.
4. Brain tumors and brain metastases.
