Guillain-Barré syndrome

Introduction to Guillain-Barre syndrome Guillain-Barré syndrome (GBS) is a serious disease common in the nervous system. The main lesions are in the spinal nerve roots and spinal nerves, which can affect the cranial nerves. Associated with viral infection or autoimmune response. The clinical manifestations are acute, symmetrical, and flaccid limb paralysis. basic knowledge The proportion of illness: the incidence rate is about 0.0001% - 0.0003% Susceptible people: no specific population Mode of infection: non-infectious Complications: Acne, Pulmonary Embolism, Urinary Retention, Anxiety Disorder, Depression

The cause of Guillain-Barre syndrome

So far, the cause of GBS is still not very clear. The earliest thought that infection and poisoning are the cause of the disease, 40% of patients have pre-infection, and the prodromal factors are as follows.

1. Virus and GBS: In 1983, Hurroiz reported 1034 cases of GBS, 70% had prodromal factors, and 2/3 were viral infections, mainly manifested as upper sensation or diarrhea. It is generally believed that cytomegalovirus, EB virus, influenza virus, etc. have There is a great relationship, and there are reports that are closely related to hepatitis virus. Liu Xiumei reported 4 cases of acute hepatitis with GBS in 1988. In addition, Xu Xianhao reported 6/500 of GBS in hepatitis B patients, which was significantly higher than that of the control group. Among the 100 cases of hepatitis B ABSAg positive, GBS There were 17 cases of onset, and 1 case of GBS occurred in 45 cases of the control group.

2. Campylobacter jejuni and GBS: In 1982, Rhodes reported 1 case of GBS. The stool culture and antibody test confirmed that the jejunum is secondary to GBS. In 1984, another scholar reported 56 cases of GBS with Campylobacter jejuni infection, 21 cases in China. In 1993, Jian et al first reported that Campylobacter jejuni infection was the main precursor of GBS in China. 71% of 17 cases of GBS had gastrointestinal infection symptoms, and the positive rate of serum jejunal Igm antibody was 53%, which was higher than that of foreign literature. The relationship between Campylobacter jejuni and GBS has become the focus of GBS research.

3. Vaccination and GBS: a group of 1034 cases of GBS have 4.5% vaccination, more common in influenza vaccine, hepatitis vaccine, measles vaccination after the onset, our department in 1995 admitted a case of hepatitis A vaccine after vaccination GBS.

4. Genetics and GBS: It has been reported that the frequency of A3 and B8 genes in GBS patients is significantly increased, and GBS is considered to have a certain relationship with heredity.

5. Trace elements and GBS: Zhang Xiangjian reported that there are trace elements Zn, Cu, Fe metabolism abnormalities in GBS patients, and it is believed that trace elements are abnormal, which may play a role in the pathogenesis of GBS.

Guillain-Barre Syndrome Prevention

1. The disease is self-limiting, single-phase course, after several weeks or months of recovery, 70% to 75% of patients completely recover, 25% left a slight neurological deficit, 5% died, often died of respiratory failure, jejunum Patients with Campylobacter infection have a poor prognosis, and the prognosis is poor in elderly patients with acute onset or assisted ventilation.

2. Pay attention to personal cleanliness, hygiene, washing hands, avoiding raw food, etc. will reduce the infection of Campylobacter jejuni, thus avoiding acute motor axonal neuropathy.

Guillain-Barre syndrome complications Complications, acne, pulmonary embolism, urinary retention, anxiety, depression

Because patients with this disease often have prolonged bed rest, it is easy to have complicated pneumonia, sepsis, hemorrhoids, deep vein thrombosis, pulmonary embolism, urinary retention, anxiety, depression, etc., and if the lesion involves the respiratory muscles, it can be fatal. .

Guillain-Barré syndrome symptoms Common symptoms Dyspnea, sensory disturbance, dysphagia, reflex, disappearance, muscle agitation, autonomic dysfunction, ataxia, cranial nerve damage, cranial nerve palsy, hypokalemia

First, its clinical features are: 1 to 4 weeks before the symptoms of gastrointestinal or respiratory infections and vaccination history, sudden emergence of severe nerve root pain (to the neck, shoulders, waist and lower limbs), acute progressive symmetry Limb soft palate, subjective sensory disturbance, sputum reflexes weakened or disappeared as the main symptom.

Second, its specific clinical manifestations are

1. Dyskinesia: The most common symptoms of the disease are the most common symptoms of the disease. It usually starts from the lower limbs and gradually affects the trunk muscles, the upper limbs and the cranial nerves. The muscle tension is low, and the proximal end is often heavier than the distal end, usually in a few days. The disease progressed to a peak within 2 weeks, and the critically ill patients rapidly aggravated within 1-2 days, with complete paralysis of the extremities, respiratory muscles and swallowing muscle paralysis, difficulty breathing, swallowing disorders, and life-threatening.

2. Sensory disorder: generally lighter than dyskinesia, but common, abnormal limbs such as wood, tingling, burning sensation, etc., can appear before or at the same time, about 30% of patients have muscle pain, feeling really rare , in the form of gloves and socks.

3. Reflex disorder: The quadriplegia reflex is mostly symmetry weakening or disappearing, the abdominal wall and cremaster reflex are normal, and a few patients may have pathological reflexes due to vertebral body beam involvement.

4. Autonomic dysfunction: often sweating in the initial or recovery period, sweat odor is strong, may be the result of sympathetic stimulation, a small number of patients may have short-term urinary retention in the early stage, may be due to temporary imbalance of autonomic function of the bladder Or the spinal nerves that control the external sphincter are damaged, the stool is often secret, and some patients may have unstable blood pressure and tachycardia.

5. Cranial nerve symptoms: Half of the patients have cranial nerve damage, with tongue, pharynx, vagus nerve and peripheral paralysis of one or both sides of the nerve, followed by oculomotor, trochlear, abductor nerve, occasional optic nerve head edema, possible For the optic nerve itself inflammatory changes or cerebral edema, it may also be significantly increased with cerebrospinal fluid protein, blocking the arachnoid villi, affecting the absorption of cerebrospinal fluid.

Third, GBS can have variants, and the current report is gradually increasing. The understanding of variant GBS will help the diagnosis of GBS and prevent misdiagnosis. The main variant GBS is as follows:

1. Fisher syndrome: Fisher syndrome was first reported by Fisher in 1956. It has 5 major features: 1 bilateral extraocular muscle paralysis; 2 bilateral symmetrical cerebellar ataxia; 3 deep reflex disappeared; 4 cerebrospinal fluid protein cell separation 5 is good afterwards, the first Fisher syndrome in China was reported by the author in 1979, and the domestic report has gradually increased.

2. Ataxia type: Sun Shizhen reported 1 case of ataxia-type GBS, mainly showing unstable walking, hands are not active, deep feeling of obvious obstacles, sputum reflex disappeared, finger nose, rotation, and knee squat test are not allowed , RomDerg's sign is positive, cerebrospinal fluid protein cells are separated.

3. Muscle tremor type: Xu Xianhao reported 2 cases of this type of disease, with multiple limbs, abdominal wall, scapula and other muscles as the main symptoms, the examination was fasciculation, cerebrospinal fluid protein cells were separated, confirmed by electrophysiology and muscle biopsy. GBS.

4. Pharyngeal-neck-arm neuropathy: only the pharynx, neck and arm muscle spasm, no lower limbs, protein cells, and action potentials suggest demyelinating lesions.

5. Paraplegic type: manifested in both lower limb paralysis, lower extremity tendon reflex disappeared, upper limbs and cranial nerves are not tired, electrophysiological examination is in line with GBS.

6. Double-sided sacral type: with bilateral 9,10 cranial nerve palsy as the main performance, while the sputum reflex is low, cerebrospinal fluid protein cells are separated.

7. Posterior cranial nerve type: The main manifestation of bilateral 9.10 cranial nerve palsy, sputum reflex is weakened, or there is a terminal type of pain sensation, and cerebrospinal fluid protein cells are separated.

8. Low potassium type: a group of 39 cases in China reported that there were 9 cases of potassium type (27.05%) in GBS, 2~3mmol/L of blood potassium, and hypokalemia in electrocardiogram. Other symptoms were the same as GBS, and potassium supplementation was invalid. In addition to various types, there are also reports of conduction beam type; pyramidal beam type; autonomic dysfunction type and so on.

Guillain-Barre syndrome check

1. Cerebrospinal fluid examination: protein is elevated, the number of cells is not high or slightly elevated, showing "protein-cell separation".

2. The white blood cell count and classification can be increased when the infection is combined.

3. There are abnormal electrocardiograms in severe cases, common sinus tachycardia and T wave changes, and QRS wave voltage is increased (may be caused by abnormal autonomic function).

4. Electrophysiological examination: evidence of slowing of motor and sensory nerve conduction velocity (NCV), denervation or axonal degeneration, early detection of only F wave or H reflex delay or disappearance (F wave abnormality represents nerve proximal or nerve root damage) For the diagnosis of segmental lesions, multiple nerves should be examined. Demyelinating lesions can be seen with slowing of NCV, prolonged latent latency, normal or mild abnormalities, and axonal lesions with reduced distal amplitude.

5 Sural nerve biopsy: Demyelinating and inflammatory cell infiltration can be seen. This result is only for reference.

Diagnosis of Guillain-Barre syndrome

diagnosis

Acute onset, symmetrical limb flaccid paralysis, may be associated with bilateral VII or IX, X cranial nerve palsy, CSF has protein cell separation phenomenon, neuroelectrophysiological examination can reduce the nerve conduction velocity to diagnose this disease.

AIDP diagnostic criteria

(1) There is often a history of pre-infection, which is acute onset, progressively aggravated, and peaks in about 2 weeks.

(2) Symmetrical limbs and medullary innervation muscles, facial muscle weakness, severe cases may have respiratory muscle weakness, quadriplegia reflexes reduced or disappeared.

(3) may be associated with mild sensory abnormalities and autonomic dysfunction.

(4) Protein-cell separation occurs in cerebrospinal fluid.

(5) Electrophysiological examination suggests prolonged motor nerve conduction latency, slower conduction velocity, F wave abnormality, conduction block, and abnormal waveform dispersion.

(6) The course of disease is self-limiting.

AMAN diagnostic criteria

Referring to the AIDP diagnostic criteria, the salient feature is that neurophysiological examinations suggest that almost pure motor nerves are involved and are significantly impaired by motor axonal injuries.

AMSAN diagnostic criteria

Referring to the AIDP diagnostic criteria, the salient feature is that neurophysiological examination suggests significant impairment of sensory and motor axonal damage.

MFS diagnostic criteria

(1) Acute onset, the condition reaches a peak within a few days or weeks. (2) Clinically, the main symptoms are extraocular tendon, ataxia and sputum reflex, and the limb muscle strength is normal or mildly decreased. (3) Protein-cell separation occurs in cerebrospinal fluid. (4) The course of disease is self-limiting.

Diagnostic criteria for acute pan-autonomic neuropathy

(1) Acute onset, rapid progress, reaching a peak in about 2 weeks. (2) Extensive sympathetic and parasympathetic dysfunction, without or accompanied by mild limb weakness and paresthesia. (3) Cerebrospinal fluid protein and cell separation may occur. (4) The course of disease is self-limiting. (5) Exclude other causes.

ASN diagnostic criteria

(1) Acute onset, rapid progress, peaking at around 2 weeks. (2) Symmetrical limb paresthesia. (3) There may be cerebrospinal fluid protein-cell separation. (4) Neurophysiological examination suggests sensory nerve damage. (5) The course of the disease is self-limiting. (6) Exclude other causes.

Differential diagnosis

1. Polio: After a few days of fever, the body temperature does not return to normal when there is paralysis, often involving one side of the lower limbs, no sensory disturbances and cranial nerve involvement, CSF cell protein separation can be seen 3 weeks after the disease, pay attention to identification.

2. Hypokalemia paralysis: GBS has a history of pre-infection and autoimmune reaction, hypokalemia type periodic spasm has hypokalemia, history of hyperthyroidism, the former acute or subacute onset, progress no more than 4 weeks, Quadriplegia often starts from the lower extremities, the proximal end is more obvious, the latter onset is fast (hours to 1 day), recovery is fast (2 to 3 days,) limbs flaccid paralysis, GBS may have respiratory muscle paralysis, cranial nerves Loss, sensory disturbance (peripheral type) and pain, hypokalemia type periodic paralysis, GBS cerebrospinal fluid protein cell separation, electrophysiological examination early F wave or H reflex delay, exercise NCV slow, hypokalemia periodicity normal Electrophysiological examination EMG potential amplitude decreased, electrical stimulation can be unresponsive, GBS blood potassium is normal, hypokalemia type periodic blood potassium is low, potassium supplementation is effective.

3. Functional : According to the neurological signs are not fixed, sputum reflexes and mental incentives are identified.

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