Poliomyelitis: Clinical Stages, Vaccine Prevention, and Acupuncture

Poliomyelitis is caused by the poliovirus, which primarily damages the gray matter of the anterior horn of the spinal cord, leading to spinal nerve paralysis—hence its name. Since it predominantly affects children, it is also known as infantile paralysis. In recent years, the incidence has significantly decreased due to the use of oral polio vaccine (OPV) for prevention.

The primary pathogen causing poliomyelitis is the poliovirus, followed by Coxsackievirus and others. The virus can be classified into types I, II, and III, with type I having the highest pathogenicity. Most infected individuals present with subclinical or mild infections. The main source of transmission is the virus present in the nasal secretions and feces of patients. It spreads through the digestive tract, and in the early stages, it may also be transmitted via droplets. After entering the bloodstream, the virus causes viremia and subsequently invades the central nervous system, leading to disease. It is an epidemic infectious disease.

Key Diagnostic Points

This condition is clinically prevalent in children, with cases occurring throughout the year but a higher incidence in summer and autumn. According to the clinical symptoms and signs, the progression of the disease can be divided into the following four stages:

I. Prodromal Stage

The illness begins with moderate fever, general malaise, and loss of appetite, accompanied by headache, nausea, and vomiting. Approximately 20% of patients present with mild upper respiratory symptoms such as rhinitis and cough, while about 70% experience gastrointestinal symptoms including diarrhea, abdominal pain, and constipation. No significant neurological symptoms are observed. The symptoms resolve within 1–4 days. This phase represents localized viral infection, after which the virus replicates and enters the bloodstream, causing viremia and presenting as low-grade fever. In the majority of cases, the disease does not progress further, resulting in an abortive form.

2. Pre-Paralysis Stage

On the 5th to 9th day of illness, if the virus continues to invade the reticuloendothelial system throughout the body, further replicates, and enters the central nervous system causing pathological changes, the patient’s body temperature rises again (biphasic fever), reaching 38°C–40°C. Symptoms include limb pain, headache, drowsiness, irritability, nuchal rigidity, and urinary retention or incontinence, lasting 1–7 days. At this stage, the cerebrospinal fluid shows increased cell count and protein levels. If the disease process stops here, it is classified as the non-paralytic type.

III. Paralysis Stage

Approximately 1–2% of poliovirus-infected individuals enter the paralytic stage. As fever gradually subsides, paralysis of the muscle groups innervated by specific spinal nerves occurs suddenly. The paralysis is flaccid, asymmetric, with diminished or absent tendon reflexes and no sensory impairment. It ceases to progress after 5–10 days (or after fever resolves). The location and extent of paralysis vary greatly and may involve any part of the body, though the lower limbs are most commonly affected. In about 10% of paralytic cases, the medullary (bulbar) region innervated by the cranial nerves is involved, leading to pharyngeal and palatal paralysis that causes dysphagia and airway obstruction. If the respiratory and circulatory centers are affected, respiratory and circulatory failure can result in death.

IV. Recovery Period

After the progression of paralysis has ceased, recovery begins. Patients with only functional impairment recover relatively quickly, while those with neuronal destruction recover more slowly, and severe cases recover with great difficulty. Generally, the distal functions of the limbs—such as the hands and feet—recover first, gradually extending to the proximal large muscle groups, followed by the reappearance of tendon reflexes. Recovery is faster in the first 1–2 months, slows down after 6 months, and most patients recover within one year. In severe cases, recovery is even slower and more difficult.

The sequelae mainly involve muscle paralysis, spasm, and degeneration. The affected muscle groups and bones may also undergo atrophy, leading to deformities of the limbs and trunk, such as spinal curvature, equinovarus or equinovalgus of the foot, wrist drop, and so on.

Based on the location of the lesion, the severity of paralysis can be classified into the following clinical types:

1. Spinal Cord Pattern (Jisui Xing)

The paralysis is of the lower motor neuron type, flaccid, with decreased muscle tone and diminished tendon reflexes. The distribution of paralyzed muscle groups is asymmetrical, with varying degrees of severity. It is commonly seen in the lower limbs and rarely in the upper limbs. Proximal large muscle groups become paralyzed earlier and more severely than distal small muscle groups. It may affect the neck and back muscles, preventing the patient from holding up the head, sitting up, and turning over.

If the cervical and thoracic spinal cord is involved, the diaphragm and intercostal muscles (respiratory muscles) become paralyzed, impairing respiratory movement. This may present with bradypnea, nasal flaring, a weak voice, interrupted speech, and weakened cough. When the abdominal muscles are paralyzed, the patient is unable to contract them during sneezing or coughing, and may also experience intractable constipation, urinary retention, or urinary incontinence.

2. Brainstem Type

The lesion occurs in the medulla oblongata and lower pons, affecting the cranial nerve nuclei as well as the respiratory and vasomotor centers in the ventral reticular formation of the medulla. Cranial nerve palsy is present, with damage most commonly involving the sixth (CN VI) and tenth (CN X) cranial nerves. The ninth (CN IX), eleventh (CN XI), fourth (CN IV), and sixth (CN VI) may also be affected. Palsy of the seventh cranial nerve (CN VII) presents as facial paralysis. Palsy of the ninth (CN IX) and tenth (CN X) cranial nerves manifests as impairment of swallowing and laryngeal muscles. On examination, the soft palate cannot be elevated, the uvula is deviated toward the healthy side, the pharyngeal reflex is absent, and the tongue protrudes toward the affected side. Other cranial nerve palsies will present with corresponding symptoms.

Vasomotor center paralysis: This condition results from damage to the medial aspect of the reticular formation. Initially, the patient presents with facial flushing, irritability, arrhythmia, and a thin, rapid, irregular pulse. Subsequently, blood pressure drops, the complexion becomes grayish, and the extremities grow cold. In severe circulatory failure, consciousness deteriorates to coma.

**Respiratory Center Paralysis:** Caused by damage to the lateral portion of the reticular formation, leading to respiratory failure with diminished respiratory effort, irregular rhythm (manifesting as double inspiration/gasping breathing), severe hypoxia with cyanosis, and in severe cases, convulsions and coma.

3. Cerebral Pattern

In isolated cases, symptoms of brain damage may manifest, including high fever (hyperpyrexia), drowsiness (somnolence), altered consciousness, coma, and convulsions (seizures).

IV. Mixed Pattern

It is commonly seen that spinal paralysis is combined with bulbar paralysis, and the symptoms of both may appear simultaneously.

5. Complications

Patients with respiratory disorders may develop complications such as aspiration pneumonia and atelectasis. Those with high fever may experience hypertension and azotemia. Intestinal paralysis can lead to constipation, acute gastric dilatation, ulcers, and bleeding. In acute cases, myocarditis may occur. Urinary retention can result in urinary tract infections. Long-term paralysis may cause bone decalcification, leading to hypercalcemia, as well as urinary tract and biliary stones.

Examination

General blood routine changes are typically minimal, with white blood cells possibly slightly increased. In early-stage cases, cerebrospinal fluid (CSF) protein levels are mildly elevated, usually ranging from 300 to 1,500 mg/L. After 1 week, levels may rise to 1,000–1,500 mg/L. Approximately 95% of cases show CSF abnormalities. In the pre-paralytic stage, lymphocyte counts are mildly increased (≤100/μL), while granulocyte counts are relatively low (100–300/μL). CSF chloride levels are normal, and glucose levels are normal or slightly elevated. The erythrocyte sedimentation rate (ESR) is accelerated in about 30–50% of patients.

Serological examination: IgM positivity, or positivity for both neutralizing antibodies and complement-fixing antibodies, indicates recent infection. If neutralizing antibodies are positive while complement-fixing antibodies are also positive, it suggests past infection.

Viral isolation: Viruses can be isolated from throat swabs taken during the first week of illness and from stool specimens collected within one month.

Treatment

I. Acupoints and Needling Techniques

1. **BL23 (Shenshu)**: Located 1.5 *cun* lateral to the lower border of the spinous process of the 2nd lumbar vertebra. Use a 30-gauge, 2 *cun* filiform needle. After routine local disinfection, insert perpendicularly to the skin to a depth of 1–1.8 *cun*. Needling sensation: local distension and pain, or electric shock-like radiation down the lower limb.

2. GB30 (Huantiao): Located on the lateral aspect of the lower buttock, at the junction of the lateral one-third and middle one-third of the line connecting the most prominent point of the greater trochanter of the femur and the sacral hiatus. Using a 30-gauge, 3-cun filiform needle, after routine local disinfection, insert into the greater sciatic foramen to a depth of approximately 2–2.8 cun. Needle sensation: local distension and pain, or an electric sensation radiating to the lower limb.

3. BL37 (Yinmen): Located at the midpoint of the line connecting BL36 (Chengfu) and BL40 (Weizhong), between the biceps femoris and semitendinosus muscles, 6 cun below BL36 (Chengfu). Use a gauge 30, 2-cun filiform needle. After routine local disinfection, insert perpendicularly to a depth of approximately 1.8 cun. Needle sensation: Local distension and pain, or radiation toward the foot.

4. **BL40 (Weizhong)**: Located on the posterior aspect of the knee, at the midpoint of the popliteal crease. Use a 30-gauge, 2.0-cun filiform needle. After routine local disinfection, insert obliquely upward approximately 1.8 cun. Needling sensation: local distention and pain, or radiation toward the foot.

5. BL57 (Chengshan): Located at the midpoint of the gastrocnemius muscle belly, approximately midway between BL40 (Weizhong) and BL60 (Kunlun). A 2-cun filiform needle of gauge 30 is inserted perpendicularly to a depth of about 1.8 cun after routine disinfection of the local area. Needling sensation: local distension and pain.

**6. ST36 (Zusanli):** Located 3 cun directly below ST35 (Dubi), and 1 finger-breadth (middle finger) lateral to the anterior border of the tibia. Use a 30-gauge, 1.5 cun filiform needle. Routinely disinfect the local area. Insert perpendicularly to a depth of approximately 1.3 cun. Needling sensation: local distension and pain, or radiation toward the dorsum of the foot.

7. SP6 (Sanyinjiao): Located on the lower portion of the anteromedial aspect of the lower leg, 3 cun above the tip of the medial malleolus, in the depression posterior to the medial border of the tibia. Using a 30-gauge, 1.5 cun filiform needle, after routine local disinfection, insert obliquely toward GB39 (Xuanzhong) to a depth of approximately 1.3 cun. Needling sensation: local distension and pain.

8. Motor area, upper 1/5 and middle 2/5 of the sensory area: For acupoint location method, refer to the section on cerebral thrombosis.

2. Methods

For patients with paralysis in one leg, apply the above seven acupoints on the affected side only; for both legs affected, apply the 14 acupoints bilaterally. In children under 6 years of age, needles are not retained after insertion. For children aged 6–14, retain the needles appropriately for about 20 minutes, with one manipulation (twirling) midway. If accompanied by upper limb paralysis, add contralateral scalp acupuncture at the motor area and the upper 1/5 and middle 2/5 of the sensory area while needling the lower limbs. For quadriplegia, apply bilateral lower limb acupoints together with bilateral scalp acupuncture at the motor area and the upper 1/5 and middle 2/5 of the sensory area. Scalp needles are retained for 40 minutes, with manipulation every 20 minutes; lower limb acupoints may be retained appropriately or not. Treatment is administered once daily, with 10 sessions constituting one course. A 5-day rest is taken before the next course.

Appendix: Anterior Thigh Muscle Block

This treatment is mainly indicated for patients in the paralysis phase. Prepare a 5 mL sterile syringe fitted with a No. 6 sterile intramuscular injection needle. Aspirate 10 mg (1 mL) of Vitamin B1, 500 µg (1 mL) of Vitamin B12, 2 mg (1 mL) of Galantamine, and 1 mL of Moschus (Shexiang) Injection for use.

Method: Expose the infant’s thigh at the prominence of the adductor muscle group on the upper inner side, or at the abdomen.

The targeted area is located 2-3 cun inferior and medial to the inguinal ligament. The operator gently lifts the anterior thigh muscles with the left hand, performs routine disinfection of the local skin, and holds the prepared needle with medication in the right hand. Insert the needle approximately 2 cm into the lifted region, aspirate to confirm no blood return, then slowly inject the medication. Upon needle removal, apply pressure with a sterile cotton ball to prevent leakage of the medicinal liquid or bleeding. Treatment is administered once daily, with 10 sessions constituting one course. If no improvement is observed after 10 sessions, switch to acupuncture therapy.

**【Commentary】**

**Sequelae of Infantile Paralysis (Polio)** To date, there is no specific effective treatment for the sequelae of poliomyelitis. For mild cases of unilateral leg paralysis, early application of **anterior thigh muscle group block therapy** during the paralytic stage yields good results; in most mild patients, significant improvement or full recovery can be achieved within 10 sessions. However, for more severe cases involving unilateral, bilateral, or quadriplegia, when the anterior thigh muscle group block proves ineffective, **acupuncture** should be adopted instead. For patients with bilateral lower limb paralysis, using only limb acupoints produces some effect but remains unsatisfactory; the addition of **scalp acupuncture (head needling)** markedly enhances therapeutic outcomes. Nevertheless, even with meticulous treatment, severe cases may still retain partial sequelae. For those with residual sequelae, surgical interventions such as **catgut embedding**, **ligation**, **tendon transfer**, or **tendon lengthening** may be considered—but these must be performed as early as possible, as delayed intervention makes correction difficult once skeletal deformity has occurred. In general, timely and appropriate treatment can restore partial function in most patients. Patients should be advised to persist in rehabilitative exercises to facilitate early functional recovery.

Etiology and Clinical Manifestations of Poliomyelitis

Poliomyelitis, historically termed infantile paralysis, is an acute infectious disease caused primarily by the poliovirus, a neurotropic enterovirus that selectively attacks motor neurons in the anterior horn of the spinal cord. What causes poliomyelitis in children is the fecal‑oral transmission of wild poliovirus, though non‑polio enteroviruses such as Coxsackievirus and echovirus can occasionally produce similar paralytic syndromes. Upon entering the central nervous system, the virus destroys gray matter, leading to flaccid paralysis of affected muscle groups. The symptoms of infantile paralysis range from mild, nonspecific febrile illness (abortive poliomyelitis) to aseptic meningitis and, in severe cases, irreversible paralysis of the limbs, respiratory muscles, or both. The incubation period averages 7–14 days, and paralysis typically develops within days of prodromal symptoms. Because the disease predominantly strikes children under five years of age, it earned the colloquial name “infantile paralysis,” although older individuals remain susceptible. Recognition of these clinical features is crucial for early diagnosis and containment, especially in regions where vaccination coverage is suboptimal.

Vaccine Efficacy and Global Control Strategies

Widespread immunization has dramatically reduced poliomyelitis incidence worldwide. Oral polio vaccine effectiveness stems from its ability to induce both humoral and intestinal immunity, thereby interrupting transmission. The live attenuated Sabin vaccine, administered orally, mimics natural infection and stimulates robust secretory IgA responses in the gut, preventing viral replication and shedding. This property made OPV the cornerstone of the Global Polio Eradication Initiative. Consequently, prevention of poliomyelitis with vaccine has been remarkably successful: cases fell from an estimated 350,000 in 1988 to fewer than 100 in 2023. However, the oral vaccine itself can rarely revert to neurovirulence, causing vaccine‑derived poliovirus (VDPV) outbreaks in under‑immunized populations. Inactivated polio vaccine (IPV) is now used in many countries to eliminate this risk while maintaining humoral protection. Despite these advances, the question is polio still a threat today remains relevant: wild poliovirus is endemic only in Afghanistan and Pakistan, but VDPV circulates in multiple nations, and any interruption of vaccination could trigger resurgence.

Contemporary Challenges and the Path to Eradication

Although substantial progress has been made, the eradication campaign faces persistent obstacles. Is polio still a threat today is answered affirmatively by ongoing transmission of both wild and vaccine‑derived strains in regions with conflict, weak health systems, or vaccine hesitancy. To achieve global eradication, prevention of poliomyelitis with vaccine must reach every child, requiring innovative delivery strategies and sustained political commitment. The oral polio vaccine remains indispensable for outbreak response due to its ease of administration and ability to induce intestinal immunity, but its use must be carefully phased out as wild virus disappears. Meanwhile, surveillance for acute flaccid paralysis (AFP) is critical to detect all polio cases, regardless of cause. The ultimate goal—a polio‑free world—demands that what causes poliomyelitis in children be eliminated through universal vaccination, rigorous monitoring, and rapid containment of any emerging strains. Success will also depend on addressing the symptoms of infantile paralysis in affected survivors, many of whom require lifelong rehabilitative care. Only by maintaining high immunization coverage and adapting to epidemiological changes can humanity consign polio to history.