What Is Brainstem Encephalitis?

Brainstem encephalitis is an inflammatory demyelinating disease that occurs in the brainstem and is rare in clinical practice. It has a 30% -50% chance of being converted into multiple sclerosis, with more sequelae. The characteristics of this disease are: more frequently in young adults; often acute or subacute onset, with progressive exacerbation; about half have a history of upper respiratory tract or intestinal infection before the onset, clinical manifestations with symptoms of brain stem involvement on one or both sides Or signs; fewer changes in cerebrospinal fluid. There is often a history of precursor infections, acute or subacute onset, mainly manifested as multiple cranial nerve damage, ataxia, long bundle sign, and disturbance of consciousness. Pediatric reports are rare, and pediatric brainstem encephalitis with clinical manifestations as cardiovascular features is even rarer.

Brainstem encephalitis

It refers to inflammation that occurs in the brainstem. The etiology and pathogenesis are not clear. It may be viral infection or inflammatory demyelination. Clinical features include: a history of prodromal infection, acute or subacute onset, mainly manifested as multiple cranial nerve damage, ataxia, long bundle sign, and disturbance of consciousness. Pediatric reports are rare, and pediatric brainstem encephalitis with clinical manifestations as cardiovascular features is even rarer.

Brainstem encephalitis

Clinical manifestations of brainstem encephalitis

The severity of brainstem encephalitis symptoms varies widely. Mild encephalitis has the same symptoms as any viral infection: headache, fever, physical weakness, and lack of appetite. Severe symptoms of brainstem brain inflammation are obvious effects on brain function, causing upset, restlessness, and drowsiness. The most serious symptoms are weakness of arm or leg muscles, dual vision (double vision) speech and hearing difficulties, In some cases, drowsiness can turn into a coma.

Mild brainstem encephalitis is common and may not even be noticed. But about a thousand cases of measles can cause mild brainstem encephalitis. The degree of harm depends on the age of the patient and the type of infection that causes brainstem encephalitis.

Brainstem encephalitis in infants and the elderly can be fatal, but brainstem encephalitis in other ages can fully recover, sometimes after a long illness. Although brainstem encephalitis may cause permanent brain damage, the percentage of serious consequences is not high.

1. Symptoms of systemic toxins: fever, headache, body pain, nausea, vomiting, and fatigue. A few have hemorrhoids and myocarditis. The heat course is about 7 to 10 days.

2. Nervous system symptoms: disturbance of consciousness, meningeal irritation. After the second disease day, flaccid paralysis of the cervical and scapular muscles may occur, causing the head to sag and the arm to be unable to lift up, shaking and being helpless. Cerebral nerve and lower limb involvement are rare. Paralysis can be recovered in about 2 to 3 weeks, and about half of the muscles are atrophic. Mild symptoms without obvious neurological symptoms.

Brainstem encephalitis disease types

Grade I manifested as muscle tremor and ataxia, and 5% of patients left with permanent neurological sequelae.

Grade II manifests as muscle tremor and cranial nerve involvement, which can cause sequelae in 20% of patients.

Grade III manifested as rapid cardiopulmonary failure, 80% of patients died, and survivors had severe sequelae.

Brain stem encephalitis diagnosis basis

Brain Stem Encephalitis Blood Picture

Leukocytes of 10,000 to 20,000 have a neutrality.

Brainstem encephalitis

Brainstem encephalitis cerebrospinal fluid pressure

Cerebrospinal fluid pressure is slightly higher, the cell count is generally below 0.2 × 109, and lymphocytes are the majority. Sugar and chloride are normal.

Brain stem encephalitis complement binding test

A double sera titer increase more than 4 times or a single sera titer above 1:16 can confirm the diagnosis.

Brainstem encephalitis hemagglutination inhibition test

A double sera titer increase more than 4 times or a single sera titer above 1: 320 can confirm the diagnosis.

Brainstem Encephalitis Virus Isolation

Virus was isolated from serum and cerebrospinal fluid at the beginning of the disease, but the positive rate was low. After death, the brain tissue can be used to isolate the virus.

Brainstem encephalitis treatment principles

Some of the most dangerous brainstem encephalitis (such as those caused by herpes simplex virus) are now available

Brainstem encephalitis Such as arabinose adenine, or acyclovir, or interferon and other drugs to treat. Although the efficacy of these drugs is still being evaluated, there is always an opportunity to treat dangerous brainstem encephalitis, otherwise the patient will definitely die. Since most other viruses that cause brainstem encephalitis do not respond to antibiotics, the basic treatment is to take some measures to ease the symptoms and allow the body's natural defenses to overcome the infection. In most cases, as long as you stay comfortable, you will be well fed. Sometimes steroids can suppress inflammation. If you are unconscious, feed with a nasogastric tube and use a ventilator to assist breathing. Severe brainstem encephalitis may recover slowly and may require special treatment and study. Basic skills such as speaking clearly.

Brain stem encephalitis disease care

1. Prevention of infection: reduce infection-causing factors, patients with nasal feeding due to swallowing difficulties,

Brainstem encephalitis Low resistance, coupled with eating without mouth, prone to oral infections, oral saline and 0.1% acetic acid for oral care every day. Keep the indoor air fresh and sunny, disinfect once a day with ultraviolet light, and wipe the bed unit and the floor with a disinfectant solution to keep the patient's skin clean and dry.

2. Nursing during ventilator-assisted breathing:

(1) Closely observe vital signs and mechanical ventilation, auscultate the lungs every 2h and make detailed records. Observe whether the breathing and the ventilator are synchronized. When the ventilator alarms, it is necessary to find the cause immediately and eliminate it in time.

(2) Ensure that the pipeline of the ventilator circuit is unobstructed, sterilize daily, and dump the water in the collection bottle in time to prevent its countercurrent from causing bacteria to multiply.

(3) Regular dripping of normal saline plus chymotrypsin and dexamethasone into the airway to humidify the airway to ensure that there is no obstruction and it is also conducive to diluting sputum, which is easily sucked out and reduces pulmonary complications.

(4) Ultrasonic atomized inhalation 6 times a day, encourage voluntary coughing, assist in back patting, and use body position drainage to make sputum drain smoothly.

3. Medication care: long-term application of glucocorticoids can cause a variety of side effects, mainly infection, diabetes, increased blood pressure, exacerbation of ulcers, osteoporosis, etc. During the medication, closely observe the patient for skin infections, vomiting and other symptoms, and regularly Check blood, urine glucose and other related laboratory tests, and pay attention to the rebound phenomenon during the reduction. When applying biological preparations such as neurotrophic drugs, it is easy to cause allergic reactions and increase the number of inspections. The use of gamma globulin can cause leukopenia, pay attention to review blood routines, and notify the doctor in time if any bad hair is found.

4. Diet care: Reasonable diet is closely related to physical rehabilitation. Due to long-term nausea and vomiting, dysphagia caused gastrointestinal dysfunction and water-electrolyte imbalance, coupled with high fever in a high consumption state to significantly reduce weight, nasal feeding was provided with a high-protein, high-nutrition, high-vitamin liquid diet combined with intravenous fluid replacement.

Clinical data of brainstem encephalitis

Patient, female, 35 years old, farmer in suburb of Hengyang, Hunan. Because of walking weakness, blurred vision for 5 days, worsening companionship

Brainstem encephalitis Speechlessness, drowsiness for 2 days, was admitted to the emergency department on November 24, 2005. On the morning of November 20, 2005, after working in house in a town in Guangzhou, the patient was unable to walk when he went upstairs. His vision was blurred in the afternoon without fever, chills, headache, dizziness, cough, sore throat, nausea, Vomiting and other symptoms. On the morning of November 21, the patient walked to a town hospital in Guangzhou and the treatment of "upper respiratory infection" was invalid. On the afternoon of November 22, the patient developed inability to walk and needed support, and his speech was unclear and mentally poor. He was returned to the local county people's hospital in Hunan for treatment. Examination: lethargy, sluggish response, unclear speech, crooked mouth angle to the left, right tongue extension, right upper and lower limb muscle strength IV, normal left and upper limb muscle strength, pathological reflex (-). CT scan of the skull showed no abnormalities. According to the "cerebral infarction" treatment, his condition did not improve, so he was transferred to the intensive care unit of the Department of Neurology of our hospital in the afternoon of November 24 to diagnose and treat the severe cerebral infarction. Physical examination at admission: T36.7 , P86 times / minute, R20 times / minute, BP105 / 71mmHg drowsiness, poor speech, right eyelid drooping slightly, right adduction and left eye abduction restricted, and right nasolabial sulcus slightly changed Shallow, tongue extension, right side deviation, bilateral pharyngeal reflexes weakened, no abnormalities in heart, lungs, and abdomen. The muscle strength of the upper left and lower limbs is increased by IV, the muscle strength of the upper right and lower limbs is increased by III. , Finger nose and rotation test and sensory function test can not cooperate. Soft neck, grams and bruce's sign (-), right pasteur sign (+), left pasteur sign (-). Laboratory examination: Blood routine: Total WBC: 10.4 × 109 / L, normal classification; electrolyte, liver, kidney function, blood lipid, blood glucose and blood gas analysis were normal. On the morning of November 25, the patient developed drowsiness, complete aphasia, a marked decrease in limb muscle strength, a right upper limb muscle strength of 0, a left upper, lower limb, and right lower limb muscle strength of grade II. Skull MRI showed that the midbrain and the pontine junction saw a slightly longer T1 and longer T2 signal, the border was not clear, and no significant compression was seen in the midbrain aqueduct and the fourth ventricle; the brain MRI enhancement: abnormal brainstem signals, No significant enhancement was seen, considering brainstem infarction. On November 26, the patient was in a shallow coma. The lumbar puncture cerebrospinal fluid pressure was 95mmH2O. The appearance was colorless and clear. Pan's test (+), total protein quantitative 0.58g / L, white blood cell count 76 × 106 / L, and mononuclear cells 90%. 10% of multiple nuclear cells, 2.59mmol / L glucose, 117mmol / L chloride, so diagnosis of brainstem encephalitis, administer 10mg intravenous drip of dexamethasone, once a day, at the same time antiviral, anti-infective treatment, etc. On December 2, the patient became awake, but his speech was ambiguous. His right upper limb muscle strength was Grade II, his right lower limb muscle strength was Grade 0, and his left upper and lower limb muscle strength was Grade II-III. After 14 days, dexamethasone was changed to oral prednisone 30mg / day, and the dose was gradually reduced. The patient was discharged due to financial difficulties on the 20th day of admission. Physical examination at discharge: limited right adduction and left eye abduction, tongue extension Right deviation, double upper limb muscles III-IV, double lower limb muscles

Brainstem encephalitis Grade III, negative pathological signs, reexamination of cerebrospinal fluid: pressure 180mmH2O, colorless, clear, Pan's test (-), cerebrospinal fluid protein quantification 0.23g / L, white blood cell count 16 106 / L, monocyte-based, glucose 3.4 mmol / L, chloride 128 mmol / L. Follow-up on January 17, 2006: The patient is still walking unsteadily and needs support. Check: Shenqingyuli, normal memory, directional power, calculation power, normal eye movements, bilateral nasolabial sulcus symmetry, tongue extension slightly to the right, limb muscle strength and muscle tension is normal, double pasteurization sign, depth Feeling the check is normal. The bilateral finger-nose test was slightly worse, with Romberg's sign opening eyes (+) and closing eyes (+). EEG is normal; visual and brainstem auditory evoked potentials are examined: the right eye VEP latency is prolonged and the amplitude is within the normal range; the left eye VEP latency and the amplitude are within the normal range; the right ear BAEP waveform is poorly differentiated, and the left ear BAEP I, III, amplitude, normal incubation period; electromyographic examination of the extremities: the left general peroneal nerve motor conduction amplitude decreased. Follow-up on March 15, 2006, the patient walked normally and recovered completely. Examination was normal.

Discussion: The clinical manifestations of brainstem encephalitis are diverse, but they lack typical symptoms and signs and are easily misdiagnosed. In this case, the patient started with sudden limb paralysis. There was no history of infection before the onset and no history of fever during the course of the disease. CT scan of the skull showed no abnormalities.

Brainstem encephalitis MRI enhancement: brainstem abnormal signals, no obvious enhancement, consider brainstem infarction. Therefore, the clinical misdiagnosis was severe cerebral infarction. The causes of misdiagnosis may be: (1) the incidence of cerebral infarction in young adults has increased in recent years; (2) clinicians rely heavily on imaging findings such as skull CT and MRI in patients with sudden limb paralysis and unconsciousness; (2) before the onset of illness The absence of a history of infection and the absence of a history of fever during and after the onset of disease have led to the possibility of neglecting inflammatory diseases. The literature reports that the characteristics of brainstem encephalitis are as follows: 1. It can occur at any age, and most of them are young adults. 2. Most patients have a history of upper respiratory tract infection or other viral infections 1 to 4 weeks before the onset of illness. 3. Sudden onset, often early onset of mental symptoms and disturbance of consciousness, usually bilateral cerebral palsy in a short period of time, accompanied by one or both limb dyskinesias and sensory disorders, but long bundle signs are rare, symptoms and The signs are less confined to a certain part, 4. Cerebrospinal fluid is basically normal, the protein is slightly increased, and the cells are mainly lymphocytes and monocytes. 5. The course of the disease is often self-limiting, and most of it improves or heals after 7-8 weeks of treatment. 6. Early hormone treatment is effective and the prognosis is good. 7. The abnormal rate of skull CT and MRI is low. In this case, the treatment of cerebral infarction was not effective. After the cerebrospinal fluid was found abnormal, the patient was fully treated with dexamethasone and other treatments according to brainstem encephalitis. We speculate that the pathogenesis of the disease may be the direct invasion and damage of the virus or the immune damage after the virus infection. Masaaki Odaka and other researchers believe that many Bickerstaff patients with brainstem encephalitis are associated with axonal changes in Guillain-Barre syndrome, suggesting that the two diseases are similar, and they belong to the same disease spectrum.