What Is Wallenberg Syndrome?

Wallenberg syndrome (Wallenberg syndrome) is a disease caused by medulla oblongata. Clinically, brain nerves such as the glossopharyngeal nerve, vagus nerve and hypoglossal nerve are the main manifestations.

Wallenberg syndrome

Wallenberg syndrome, also known as posterior inferior cerebellar or vertebral artery occlusion syndrome, and dorsal lateral rostral syndrome, is the most common type of brainstem infarction. Causes dizziness, vomiting, nystagmus (vestibular nucleus); cross sensory impairment (damage of the dorsal nucleus of the trigeminal nerve and contralateral cross-linked spinal thalamus tract); ipsilateral Horner sign (damage of the descending sympathetic nerve fibers); drinking water Cough, dysphagia, and hoarseness (impaired nucleus suspected); ipsilateral cerebellar ataxia (damage of the cord or cerebellum). The posterior inferior cerebellar artery has many anatomy variations, and atypical clinical manifestations are common.

Acute treatment principles

(1) Ultra-early treatment: See a doctor immediately after the onset, and strive to dissolve thrombolysis within 3-6 hours of treatment time window, reduce brain metabolism, control brain edema and protect brain cells, and save the ischemic penumbra;
(2) Individualized treatment: take the most appropriate treatment according to the patient's age, type of ischemic stroke, degree of illness, and underlying diseases;
(3) Prevention and treatment of complications such as infection, cerebral heart syndrome, hypothalamic injury, post-stroke anxiety or depression, abnormal antidiuretic hormone secretion syndrome, and multiple organ failure;
(4) Holistic treatment: adopt supportive therapy, symptomatic treatment and early rehabilitation treatment. Preventive interventions for stroke risk factors such as hypertension, diabetes, and heart disease are taken in a timely manner to reduce the recurrence rate and reduce the disability rate.

(1) Symptomatic treatment: including maintaining life functions and managing complications.
The blood pressure rise after ischemic stroke usually does not require emergency treatment. Antihypertensive drugs such as captopril 6.25 can be used when 24/48 systolic blood pressure> 220mmHg, diastolic blood pressure> 120mmHg or average arterial pressure> 130mmHg. 12.5mg, taking; avoid excessive hypotension to reduce cerebral concern pressure, leading to increased cerebral ischemia; high blood pressure (diastolic blood pressure> 140mmHg) can use sodium nitroprusside 0.5-10g / kg.min, maintaining blood pressure at 170-180 / 95-100mmHg level;
People with disturbance of consciousness and respiratory infections should use appropriate antibiotics to control the infection, keep the respiratory tract normal, inhale oxygen and prevent pneumonia, and prevent urinary tract infections and bedsores;
48h-5d after the onset is the peak period of cerebral edema, according to clinical observation or intracranial pressure detection, 250% 20% mannitol, intravenous drip, once every 6-8 hours; or fast urine 40mg intravenous injection, twice daily ; 10% albumin 50ml intravenously; excessive amount of dehydrating agent, long duration is prone to serious adverse reactions, such as kidney damage, hydropower treatment disorders, etc .;
Bedridden patients can be injected subcutaneously with low-molecular-weight heparin 4000IU 1/2 times a day to prevent pulmonary embolism and deep vein thrombosis;
ECG monitoring should be performed within 3 days of onset to prevent fatal arrhythmias (ventricular tachycardia and ventricular fibrillation, etc.) and sudden death. Calcium antagonists and -blockers can be given if necessary.

The blood glucose level should be controlled at 6-9mmol / L. Too high and too low will aggravate ischemic brain damage. If> 10mmol / L, insulin treatment should be given, and care should be taken to maintain water and electrolyte balance

Control seizures in a timely manner, and deal with post-stroke depression or anxiety disorders.

(2) Ultra-early thrombolytic therapy: restore blood flow perfusion in the infarcted area, reduce neuronal damage, and save the ischemic penumbra.

1) Intravenous thrombolytic therapy: Commonly used thrombolytic drugs include:

Urokinase (UK): 500,000-1.5 million IU is added with 0.9% physiological saline 100ml, intravenous drip within 1 hour;

Recombinant tissue-type plasminogen activator (rt-PA): 0.9mg / kg once; the maximum dose is less than 90mg, 10% of the dose is given by intravenous bolus first, and the remaining dose is continuously injected intravenously for about 60 minutes; rt -PA is a serine protease located on human chromosome 8 (8p12), which can catalyze lysogen into plasmin, and has the ability to dissolve fibrin clots contained in cerebral thrombosis; some clinical control studies suggest that symptoms appear for 3 hours Intravenous rt-PA intravenous injection can reduce the disability and mortality of ischemic stroke, and its high cost restricts its application. Anti-coagulants and anti-platelet drugs can no longer be used within the first 24 hours of using rt-PA. CT showed no bleeding at 24 hours and can be treated with anti-coagulation and anti-platelets. Stroke patients receiving UK and rt-PA thrombolytic therapy must be performed in a hospital with the ability to diagnose stroke and manage bleeding complications. Intravenous thrombolysis with streptokinase (SK) is not recommended, as it can cause bleeding. When severe headaches, vomiting, and sudden elevation of bleeding occur during the menstrual process, the UK or rt-PA should be stopped immediately and a CT examination should be performed.
· Thrombolytic indications: Acute ischemic stroke without coma. Within 3 hours of onset, it can be extended to 6 hours under the guidance of MRI; age 18 years; CT does not show low-density lesions, and intracranial hemorrhage has been ruled out; The patient and his family agree.
· Absolute contraindications: A single attack or rapid improvement of TIA and mild symptoms; Medical history and physical examination are consistent with subarachnoid hemorrhage; Bp is still> 185 / 110Hg after two antihypertensive treatments; Edema, mass effect, tumor and arteriovenous malformation; the patient had received or received trauma within 14 days, had arterial puncture within 7 days, and had active internal bleeding; was on anticoagulants or had been used 48 hours before stroke Heparin treatment; history of rickets includes blood disease, hemorrhagic quality, coagulopathy or history of coagulation inhibitors (PT> 15s, APTT> 40s, INR> 1.4, platelet count> 100/109 / L).
· Thrombolytic complications: Secondary blood from the infarct: UK is a non-selective fibrinolytic agent, which activates thrombus and plasma fibrinogen, which has the potential risk of inducing bleeding. The coagulation time and prothrombin time should be measured after administration; Thrombolysis can also lead to fatal reperfusion injury and cerebral edema; The rate of thrombolysis and reocclusion is as high as 10% -20%, and the mechanism is unclear.
2) Arterial thrombolytic therapy-As an emergency treatment for stroke, superselective interventional arterial thrombolysis can be performed under DSA direct vision. Intravenous infusion of urinary hormone enzyme arterial thrombolysis with a small dose of heparin may be beneficial to patients with stroke in the middle cerebral artery distribution area where symptoms occur for 3-6 hours.
(3) Brain protective treatment: A variety of brain protective agents have been suggested for application. Medication before initiation of ischemic waterfall can reduce ischemic brain injury by reducing brain metabolism and interfering with cytotoxic mechanisms caused by ischemia. Including free radical scavengers (peroxide dismutase, barbiturate, vitamin E and vitamin C, 21-aminosteroids, etc.), as well as opioid receptor blockers naloxone, voltage-gated calcium channel blockers , Excitatory amino acid receptor blockers and magnesium ions. At present, early (<2h) head or systemic hypothermia treatment is recommended. The drug can be citicoline, a novel free radical scavenger edaravone, early (<4h) 10% albumin, cyclophosphamide Combined with colchicine. However, many brain protective agents are effective in animal experiments, and the clinical efficacy is poor or ineffective, and sufficient evidence is still needed.
(4) Anticoagulation therapy: It does not appear effective in most complete stroke cases and does not seem to affect the stroke process that has occurred. In order to prevent thrombus expansion, progressive stroke, occlusion after thrombolytic therapy, etc., it can be applied for a short time. Commonly used drugs include heparin, low-molecular-weight heparin, and warfarin. During the treatment, the clotting time and prothrombin time should be detected, and vitamin K, protamine sulfate and other antiseptics should be prepared to deal with possible bleeding complications.
(5): By degrading fibrinogen and enhancing fibrinolytic system activity to inhibit thrombosis. The drugs that can be selected include batroxobin, defibrase, ankerose, and lumbrokinase defibration therapy. The first dose of batroxobin is 1.BU, and the next day is 5BU. It is given intravenously for a total of 3 to 4 times. .

(6) Antiplatelet therapy: Large-scale, multicenter randomized controlled clinical trials have shown that aspirin 100-300mg / d within 48 hours of onset of unselected patients with acute cerebral infarction can reduce mortality and relapse rate, and is recommended for application. However, do not use them at the same time when thrombolytic or anticoagulant treatment is used, it can increase the risk of bleeding. Antiplatelet agglutinating agents such as ticlopidine and clopidogrel can also be used.
(7) Stroke units should be established in conditional hospitals. SU is composed of multi-disciplinary physicians, nurses and therapists. After professional training, the first aid, treatment, nursing and rehabilitation of strokes should be organically integrated, so that patients can get timely, Standardized diagnosis and treatment can effectively reduce the mortality and disability, improve the prognosis of patients, improve the quality of life, shorten the length of hospital stay and reduce costs, and are conducive to post-discharge management and community treatment. Patients with moderate or severe stroke, such as large-scale cerebral infarction, cerebellar infarction, vertebrobasilar main infarction, and unstable cerebral infarction patients should be treated with SU.
(8) Vasodilators should not be used or used with caution in the acute phase of cerebral infarction. The blood vessels in the ischemic area are paralyzed and excessively perfused, which can lead to stealing blood in the brain and aggravating cerebral edema. The brain cell nutritional agent cerebrolysin should not be used in the acute phase of stroke. It can increase the oxygen consumption of ischemic and hypoxic brain cells and aggravate brain cell damage. It should be used in the subacute phase of stroke (2 to 4 weeks). Traditional Chinese medicine preparations, such as ginkgo biloba, ligustrazine, panax notoginseng, kudzu root, salvia miltiorrhiza and hirudin, all have functions of activating blood circulation and removing stasis; large-scale, multicenter, randomized controlled clinical trials and meta-analysis should be provided to provide valid and powerful evidence .
(9) Surgical treatment: For patients with large cerebral infarction on the curtain with severe cerebral edema, mass effect and signs of cerebral hernia formation, craniotomy can be performed; patients with cerebellar infarction causing brain stem compression to worsen the condition through aspiration. Cerebellar tissue and posterior cranial fossa decompression can save lives.
(10) Rehabilitation treatment: should be carried out early and follow the principle of individualization, formulate short-term and long-term treatment plans, select treatment methods in stages and according to local conditions, conduct targeted physical and skill training for patients, reduce disability, and improve neural function Recovery, improvement of quality of life and reintegration into society.
(11) Preventive treatment: Preventive treatment should be carried out as soon as possible for those with clear risk factors for ischemic stroke, such as hypertension, diabetes, atrial fibrillation, and carotid stenosis. The antiplatelet drugs aspirin 50-100mg / d and ticlopidine 250mg / d have a positive effect on the secondary prevention of stroke, and are recommended to be used; there should be an intermittent period in long-term medication, and those with bleeding tendency should be used with caution.