| disease | Polio |
| alias | Polio, Poliomyelitis, Polio, Infantile Paralysis |
Poliomyelitis (commonly referred to as polio) is an acute infectious disease caused by the poliovirus. Its clinical manifestations primarily include fever, sore throat, and limb pain, with some patients developing flaccid paralysis. During outbreaks, the majority of cases are asymptomatic or non-paralytic. Children are more susceptible than adults, and before widespread vaccination, infants and young children were particularly affected, hence its alternative name "infantile paralysis." The main lesions occur in the spinal cord gray matter, and severe cases may result in paralytic sequelae. Since the widespread adoption of vaccines in the late 1950s, the incidence of polio has significantly declined. Following the eradication of smallpox in the 1970s, polio has been designated as the next disease targeted for elimination by the end of this century.
bubble_chart Epidemiology
The disease is commonly seen in temperate zones, occurring sporadically throughout the year but more frequently in summer and autumn, potentially leading to minor or major outbreaks. In tropical regions, the incidence rate is similar across all seasons. The disease occurs worldwide, but its incidence has significantly decreased in areas with widespread vaccination, almost to the point of elimination (e.g., Finland, Switzerland, the Netherlands, and other Northern European countries). In China, the average incidence rate from 1976 to 1980 had already dropped to 0.7 per 100,000. Particularly in large and medium-sized cities where the vaccination rate among infants and young children exceeds 80%, the incidence has declined rapidly. For example, in Jiangsu Province, the rate decreased from 10.51 per 100,000 in 1956 to 0.2 per 100,000 in 1982. However, outbreaks still occur in areas without vaccination. Historically, type 1 was the most common, but in recent years, types 2 and 3 have become more prevalent. During outbreaks, asymptomatic latent infections and mild cases without paralysis are more frequent. In tropical regions, densely populated areas, and places without widespread vaccination, children aged 1–5 still have the highest incidence rate. Since the widespread adoption of vaccination among infants and young children, the age of onset has gradually increased worldwide, with school-aged children and adolescents being the most affected, and adult cases have also risen. Cases among infants under one year old have also increased.
The source of the pestilence is patients and asymptomatic carriers, with the latter being not only numerous but also difficult to detect and control, thus playing a significant role in the spread and outbreaks of the disease. Among children, the ratio of paralysis cases to latent infections and non-paralysis cases can be as high as 1:1,000, and among adults, it can reach 1:75. During outbreaks, infection rates in childcare facilities can soar to 100%. As early as 3–5 days before the onset of symptoms, the virus can be shed in the nasopharyngeal secretions and feces of patients. The virus is primarily shed in the throat during the first week of illness, so the period of transmission via droplets is short. In contrast, the virus is shed in feces not only early (up to 10 days before illness) and in large quantities but can also persist for 2–6 weeks, or even as long as 3–4 months. Therefore, contamination of food and water by feces, leading to oral ingestion, is the primary mode of transmission. Hands, objects, toys, clothing, and flies directly or indirectly contaminated with the virus can all serve as vectors. Contaminated drinking water often triggers outbreaks.After infection, the body develops long-lasting immunity to the same type of virus. Specific IgM appears earliest in the serum, followed by IgG (neutralizing antibodies) after two weeks. Secretory IgA is produced in saliva and the intestines. Neutralizing antibody levels peak 2–3 weeks after the onset of illness and gradually decline over 1–2 years but remain at a certain level, providing protection not only against the same type of virus but also offering some cross-protection against other types. Additionally, the virus has two antigens, C and D. The C antibody appears early after illness but declines within 1–2 weeks, while the D antibody appears later, peaking at two months and lasting for about two years, with type specificity. Specific antibodies can be transmitted from mother to newborn via the placenta (IgG) and breast milk (containing secretory IgA). This passive immunity gradually diminishes within six months after birth. Most older children acquire active immunity through latent infections, leading to a renewed increase in antibody levels. By adulthood, most individuals have developed a certain level of immunity.
The poliovirus belongs to the genus Enterovirus of the family Picornaviridae. These viruses share certain physicochemical and biological characteristics, appearing as small spherical particles under electron microscopy, with a diameter of 20–30 nm and an icosahedral symmetry. The viral particle consists of a single-stranded positive-sense RNA genome at its core, surrounded by 32 capsomeres forming the outer capsid. This viral nucleocapsid is naked, lacking an envelope. The nucleocapsid contains four structural proteins: VP1, VP3, and VP0, which is cleaved into VP2 and VP4. VP1 is the major exposed protein, containing at least two epitopes that can induce the production of neutralizing antibodies. VP1 has a specific affinity for human cell membrane receptors (possibly located on chromosome 19) and is associated with the virus's pathogenicity and virulence. VP0 is ultimately cleaved into VP2 and VP4, which are internal proteins closely associated with RNA. VP2 and VP3 are semi-exposed and antigenic. The molecular structure of human enteroviruses is generally similar. Poliovirus has been extensively studied at the molecular level, revealing that its genome consists of approximately 7,450 nucleotides, divided into three regions: a 5′ terminus of 743 nucleotides, followed by a coding region of about 6,625 nucleotides, and a 3′ poly(A) tail of variable length, which is related to RNA infectivity. The 5′ end is linked to a small viral protein (VPg), which is involved in initiating RNA synthesis. Since poliovirus lacks an envelope and its outer coat does not contain lipids, it is resistant to ether, ethanol, and bile salts. The virus remains stable within a pH range of 3.0–10.0 and is resistant to gastric and intestinal fluids, facilitating its growth and replication in the intestines. The virus exhibits strong survival capabilities outside the human body, persisting in sewage and feces for 4–6 months. It can survive for extended periods under low temperatures, remaining viable for years at -20°C to -70°C. However, it is highly sensitive to heat and desiccation, being inactivated immediately by boiling or within half an hour at 56°C. Ultraviolet light can kill the virus within 0.5–1 hour. Various oxidizing agents (bleach, hydrogen peroxide, chloramine, potassium permanganate, etc.), 2% iodine tincture, formaldehyde, and mercuric chloride are effective disinfectants. The virus is inactivated in water containing 0.3–0.5 ppm free chlorine within 10 minutes. Solutions of 1:1000 potassium permanganate, 2% iodine tincture, and 3–5% formaldehyde can rapidly inactivate the virus, while acetone and phenol act more slowly. Notably, 70% alcohol and 5% Lysol are ineffective as disinfectants, and antibiotics and chemical drugs also have no effect. Currently, humans are considered the only natural hosts of poliovirus because human cell membranes possess a receptor with specific affinity for the viral VP1 protein. Experimental infections have shown that only chimpanzees and monkeys are susceptible. Certain strains can cause disease in suckling mice. Lower primates are less likely to develop nervous system infections but are more prone to intestinal infections. In tissue culture, human embryonic kidney, lung, and amniotic membrane cells, as well as monkey kidney cells, are highly sensitive to the virus. It can also be easily cultured in HeLa cells, which possess a common receptor for all three poliovirus serotypes. The virus causes cytopathic effects such as cell rounding and detachment.
After the poliovirus enters the human body through the oral, pharyngeal, or intestinal mucosa, it can reach local lymphoid tissues such as the tonsils, pharyngeal lymphoid tissues, and intestinal aggregated lymphoid tissues within one day, where it grows and replicates, and is then excreted locally. If the body produces a sufficient amount of specific antibodies at this stage, the virus can be contained locally, resulting in an asymptomatic infection. Otherwise, the virus further invades the bloodstream (primary viremia) and reaches various non-neural tissues by the third day, such as the respiratory tract, intestines, skin mucosa, heart, kidneys, liver, pancreas, and adrenal glands, where it replicates, particularly in systemic lymphoid tissues. Between the fourth and seventh days, the virus re-enters the bloodstream in large quantities (secondary viremia). If the specific antibodies in the bloodstream are sufficient to neutralize the virus by this time, the disease progression halts here, resulting in abortive poliomyelitis, which presents only with upper respiratory and intestinal symptoms without neurological involvement. In a small number of patients, due to the high virulence of the virus or insufficient neutralizing antibodies in the blood, the virus may cross the blood-brain barrier via the bloodstream and invade the central nervous system. Severe cases may develop paralysis. Occasionally, the virus may also spread to the central nervous system via peripheral nerves. Specific neutralizing antibodies do not easily reach the central nervous system or the intestines, so the virus persists longer in the cerebrospinal fluid and feces. Therefore, the presence, timing, and quantity of specific antibodies in the bloodstream are critical factors determining whether the virus can invade the central nervous system.
Various factors can influence the outcome of the disease, such as cold exposure, fatigue, local irritation, injury, surgery (e.g., vaccinations, tonsillectomy, tooth extraction), and immunodeficiency, all of which may contribute to the onset of paralysis. Pregnant women are more prone to paralysis if infected, and older children and adult patients tend to have more severe conditions, with a higher incidence of paralysis. Among children, boys are more likely than girls to develop severe cases, often presenting with paralysis.
The most prominent pathological changes in poliomyelitis occur in the central nervous system (the virus has neurotropic toxicity), with lesions characterized by scattered and multifocal asymmetry. These lesions can involve the cerebrum, midbrain, medulla oblongata, cerebellum, and spinal cord, with the spinal cord being the most affected, followed by the brainstem, particularly the motor neurons. The cervical and lumbar segments of the spinal cord's anterior horn cells are most commonly damaged, leading to the clinical presentation of limb paralysis. Most brainstem centers and cranial nerve motor nuclei can be affected, with lesions frequently observed in the reticular formation, vestibular nuclei, and cerebellar roof nuclei. The cerebral cortex is rarely involved, and even if lesions occur in the motor area, they are mostly mild. Occasionally, lesions may appear in the sympathetic ganglia and peripheral nerve ganglia, with scattered inflammatory foci visible on the leptomeninges, while the arachnoid membrane is rarely affected. The cerebrospinal fluid shows inflammatory changes. In non-paralytic cases, neurological lesions are generally mild.
bubble_chart Pathological Changes
Early microscopic examination reveals chromatolysis in the neuronal cytoplasm, disappearance of Nissl's bodies, and the presence of eosinophilic inclusions, accompanied by surrounding tissue congestion, edema, and perivascular cellular infiltration—initially with neutrophils, later dominated by monocytes. In severe cases, the nucleus becomes pyknotic, leading to cell necrosis, which is eventually cleared by phagocytes. Paralysis primarily results from irreversible severe lesions in the nerve cells. The extent and distribution of neuronal lesions determine the presence, severity, and degree of recovery of paralysis in clinical manifestations. Long-term paralysis leads to atrophy of muscles, tendons, and subcutaneous tissues in the affected areas, and may also impair skeletal growth. Apart from nervous system lesions, degenerative and proliferative changes are observed in the intestinal wall's lymphoid tissue and other lymph nodes, occasionally accompanied by focal myocarditis, interstitial pneumonia, and congestion with cloudy swelling in the liver, kidneys, and other organs—mostly due to severe hypoxia before death. Clinical symptoms are closely related to nervous system lesions.
bubble_chart Clinical Manifestations
The incubation period is generally 5–14 days (3–35 days). Clinical symptoms vary in severity, with milder cases being more common. Many individuals may show no symptoms at all but can still shed the virus in nasopharyngeal secretions and stool while producing specific antibodies. These cases are referred to as asymptomatic, concealed, or subclinical infections. A small number of patients may develop flaccid paralysis. Based on the progression of the disease in paralytic patients, the clinical stages are as follows (see Figure 11-7):
**(1) Prodromal Stage** The onset may be gradual or abrupt. Most patients experience low-grade or moderate fever, lack of strength, and malaise, accompanied by symptoms of upper respiratory tract infection such as sore throat and cough, or gastrointestinal symptoms like anorexia, nausea, vomiting, constipation, diarrhea, and abdominal pain. No obvious neurological abnormalities are observed at this stage. These symptoms may last from a few hours to 3–4 days. Some patients experience a rapid drop in temperature and recover (referred to as the abortive type), while others progress to the pre-paralytic stage.
**(2) Pre-paralytic Stage** Symptoms of this stage may appear at the onset of the illness, immediately after the prodromal stage, or following a brief interval (about 1–6 days) between the intermediate stage [second stage]. Fever may recur (known as biphasic fever, seen in 10–30% of patients, mostly children), accompanied by neurological symptoms such as headache, muscle pain in the neck, back, and limbs, and sensory hypersensitivity. Affected children resist being held or moved and cry when touched. When sitting up, they cannot bend forward or flex due to neck and back stiffness, supporting themselves with their arms behind in a characteristic tripod posture. They also cannot touch their knees with their chin (kiss-the-knee sign). The child’s face may be flushed, with profuse sweating, indicating sympathetic nerve dysfunction. Most are mentally agitated, prone to crying or anxiety, and may occasionally shift from agitation to lethargy or drowsiness. Neck stiffness and positive Kernig’s and Brudzinski’s signs may appear due to neck and back muscle pain. Tendon reflexes and superficial reflexes may weaken or disappear in the late stage [third stage], but paralysis is absent. Cerebrospinal fluid abnormalities are often present by this stage. Typically, symptoms resolve within 3–4 days as fever subsides (non-paralytic type). This stage may sometimes last over ten days. A few patients develop paralysis by the end of this stage and enter the paralytic stage.
**(3) Paralytic Stage** Limb paralysis usually appears 3–4 days (range: 2–10 days) after onset. Paralysis may occur suddenly or follow a brief period of muscle weakness. Tendon reflexes are often the first to weaken or disappear. Paralysis in different areas may develop sequentially over 5–10 days and gradually worsen, though mild cases may stop progressing after 1–2 days. Early paralysis may be accompanied by fever and muscle pain, but in most patients, paralysis ceases to progress once body temperature drops. Clinically, it can be classified into the following types:
**1. Spinal Paralysis** Manifesting as flaccid paralysis with reduced muscle tone and absent tendon reflexes, the distribution is irregular and asymmetrical, potentially affecting any muscle or muscle group. Since lesions often occur in the cervical or lumbar spinal cord, limb paralysis—especially in the lower limbs—is common. Proximal large muscle groups (e.g., deltoid, anterior tibial muscles) are more severely and earlier affected than distal small muscles of the hands and feet. Trunk muscle paralysis may prevent the head from staying upright, with neck and back lack of strength, making sitting up or turning over impossible. Paralysis severity is graded as follows: - **Grade 0 (complete paralysis):** No muscle contraction upon stimulation. - **Grade 1 (near-complete paralysis):** Slight tendon or muscle contraction detectable by touch but no movement. - **Grade 2 (grade III paralysis):** Limbs cannot be lifted but can move on a flat surface. - **Grade 3 (grade II paralysis):** Limbs can be lifted voluntarily but cannot bear pressure. - **Grade 4 (grade I paralysis):** Limbs can be lifted voluntarily and bear some pressure. - **Grade 5:** Normal muscle strength.
Severe cervicothoracic spinal cord lesions can affect respiratory movements due to paralysis of the diaphragm and intercostal muscles (respiratory muscles), clinically manifesting as shallow and rapid breathing, weak voice, weak cough, and intermittent speech. Physical examination may reveal limited chest expansion (paralysis of intercostal muscles) and paradoxical inward movement of the upper abdomen during inspiration (diaphragmatic paralysis). By tightly binding the chest to observe diaphragmatic movement or pressing the upper abdomen to assess intercostal muscle activity, the strength of their movements can be distinguished. Under X-ray fluoroscopy, paradoxical upward movement of the diaphragm during inspiration can be seen in cases of diaphragmatic paralysis. Occasionally, urinary retention or incontinence (bladder muscle paralysis) and constipation (intestinal or abdominal muscle paralysis) may occur, often coexisting with lower limb paralysis, and are more common in adults. Sensory abnormalities are rarely observed.
2. Bulbar paralysis (brainstem paralysis or bulbar palsy) is often severe and usually coexists with spinal paralysis, manifesting with the following symptoms.
⑴ Cranial nerve palsy: Commonly involves the 7th, 9th, 10th, and 12th cranial nerves. Palsy of the 7th cranial nerve alone often causes deviation of the mouth, presenting as a crooked mouth, drooping eyelid, or incomplete eyelid closure. Paralysis of the soft palate, pharynx, and vocal cords results from damage to the 9th, 10th, and 12th cranial nerves, leading to nasal or hoarse speech, choking on water or nasal regurgitation, dysphagia, and pharyngeal mucus accumulation, with a constant risk of asphyxia. Physical examination may reveal an inability to elevate the soft palate, deviation of the uvula to the unaffected side, loss of the pharyngeal reflex, and tongue protrusion toward the affected side. Oculomotor disturbances and eyelid drooping occur with damage to the 3rd, 4th, and 6th cranial nerves. Neck weakness, drooping shoulders, and head tilting backward are seen with damage to the 11th cranial nerve.
⑵ Respiratory center damage: Primarily involves lesions in the ventrolateral reticular formation of the medulla oblongata. Symptoms include shallow, weak, and irregular breathing, occasional double inhalations and breath-holding, progressively prolonged respiratory pauses, and even respiratory arrest, with thready and rapid pulse and elevated blood pressure (later dropping). Initial anxiety and restlessness may progress to confusion, unconsciousness, and severe respiratory failure.
⑶ Vasomotor center damage: Mainly involves lesions in the ventromedial reticular formation of the medulla oblongata. Early signs include facial flushing, thready and irregular pulse, later turning weak, hypotension, skin cyanosis, cold and clammy extremities, and circulatory collapse. The patient transitions from extreme dysphoria and restlessness to unconsciousness.
3. Spinobulbar type: More common, combining symptoms of both the above types.
4. Cerebral type: Extremely rare. May present as dysphoria, insomnia, or drowsiness, with possible convulsions, unconsciousness, and spastic paralysis. Severe hypoxia can also cause altered consciousness.
（四）Stage of convalescence and sequelae: 1–2 weeks after the acute phase, paralyzed limbs usually begin recovering from the distal end, and tendon reflexes gradually normalize. The first 3–6 months show faster recovery, followed by slower progress. If recovery does not occur within 1–2 years, it becomes a sequela. Without active treatment, chronically paralyzed limbs may develop muscular rigidity, atrophy, and deformities, such as equinovarus or equinovalgus foot, spinal deformities, etc. Poor blood supply may lead to local edema, hindered bone development, and severely impaired mobility. Intestinal and bladder paralysis mostly recover after the acute phase, rarely leaving sequelae. Respiratory muscle paralysis usually begins recovering within 10 days and eventually fully resolves. Very rarely, long-term reliance on a ventilator is needed. Recovery from cranial nerve damage takes time but rarely leaves sequelae.
Post-polio syndrome: Some patients with paralysis, after full or partial recovery, may experience new weakness, myalgia, fatigue, and atrophy in the originally paralyzed muscle groups years after the acute phase. Other muscle groups may also be affected, progressing slowly and rarely causing disability. About 20–30% of paralyzed patients develop this syndrome, mostly 25–35 years after the acute phase, likely due to further physiological depletion of already damaged motor units.
Since the widespread use of the oral attenuated live vaccine (OPV), poliomyelitis cases caused by wild strains have nearly disappeared in some countries. For example, in the United States, there are 5 to 10 paralysis cases annually, most of which are related to OPV. Among these, about 15% occur in immunocompromised individuals, affecting both vaccine recipients and their close contacts. The onset typically occurs 20 to 29 days after vaccination, mostly following the first dose. Cases caused by Polio types 2 and 3 are more common than those caused by type 1, with occasional multi-type infections. It is estimated that one case occurs per 2.6 million vaccine doses administered, while the incidence in individuals with congenital immunodeficiency is 2,000 times higher than in healthy vaccine recipients. However, the risk varies among different types of immunodeficiencies. Poliomyelitis in immunocompromised individuals has the following characteristics: a prolonged incubation period of up to 30 to 120 days, a protracted course of illness, paralysis that may progress over several weeks, possible accompanying chronic meningoencephalitis and progressive neurological damage, and signs of both upper and lower motor neuron impairment. These individuals may also shed the virus in their stool for extended periods and generally have a poorer prognosis.
bubble_chart Auxiliary Examination
(1) Cerebrospinal Fluid Abnormalities mostly appear before paralysis. The fluid appears slightly turbid, with mildly increased pressure and cell count (25–500/mm3). In the early stage, neutrophils predominate, later replaced by monocytes, which rapidly return to normal after fever subsides. Glucose may be slightly elevated, chloride levels are mostly normal, and protein is mildly increased and persists longer. In a few patients, spinal fluid may remain normal throughout.
(2) Peripheral Blood Picture White blood cell counts are mostly normal but may increase in the early stage or with secondary infections, predominantly neutrophils. Erythrocyte sedimentation rate (ESR) rises during the acute phase.
(3) Virus Isolation or Antigen Detection Within the first week of onset, the virus can be isolated from the nasopharynx and feces, with fecal positivity lasting 2–3 weeks. Isolation from blood or cerebrospinal fluid in the early stage is more significant. Tissue culture is the standard isolation method. In recent years, PCR has been used to detect enterovirus RNA, offering faster and more sensitive results than tissue culture.
(4) Serological Tests Type-specific immune antibody titers peak by the end of the first week, with specific IgM rising faster than IgG. Neutralization tests, complement fixation tests, and ELISA can detect specific antibodies, with neutralization tests being the most common due to their prolonged positivity. A fourfold or greater increase in paired serum titers confirms the diagnosis. Complement fixation tests turn negative faster; if negative while neutralization tests are positive, it suggests past infection. If both are positive, recent infection is indicated. Recently, immunofluorescence for antigen detection and ELISA for specific IgM monoclonal antibodies have aided early diagnosis.
During the epidemic season, if susceptible individuals develop symptoms such as profuse sweating, dysphoria, hypersensitivity, sore throat, neck, back, and limb pain, stiffness, and loss of tendon reflexes after contact with patients, this disease should be suspected. The prodromal phase should be differentiated from general upper respiratory tract infections, epidemic common cold, gastroenteritis, etc. Patients in the pre-paralysis stage should be distinguished from various viral encephalitis, purulent meningitis, tuberculous meningitis, and epidemic encephalitis B. The appearance of flaccid paralysis aids in diagnosis.
bubble_chart Treatment Measures
(1) Acute phase treatment
1. General treatment: Bed rest and isolation for at least 40 days after onset, avoiding fatigue. Local dampness-heat compresses can be applied to areas with muscle pain to alleviate discomfort. Paralyzed limbs should be positioned functionally to prevent deformities such as wrist or foot drop. Pay attention to nutrition and fluid balance; large doses of vitamin C and B complex can be administered orally. For early-stage patients with high fever and severe toxic symptoms, intramuscular injection of gamma globulin (3–6 ml daily for 2–3 days) may be considered. Severe cases may be given oral prednisone or intravenous hydrocortisone, usually for 3–5 days. Antibiotics should be added in cases of secondary infection.
2. Management of respiratory impairment: Severe cases often exhibit respiratory impairment, leading to hypoxia and carbon dioxide retention, which are frequently the main causes of death. First, the cause of respiratory impairment must be identified (see Table 11-10), and active resuscitation measures should be taken. Airway patency must be maintained. Sedatives should be used cautiously in patients with hypoxia and dysphoria to avoid exacerbating respiratory or swallowing difficulties. Antibiotics should be administered early to prevent secondary lung infections. Close monitoring of blood gas changes and electrolyte imbalances is essential, with prompt correction as needed.
Table 11-10 Causes of respiratory impairment in poliomyelitis
| Spinal-type paralysis | Bulbar-type paralysis | Pulmonary complications | Other factors |
| Due to lesions in cervical and thoracic spinal nerve cells, causing paralysis of respiratory muscles (primarily intercostal muscles, diaphragm, and accessory respiratory muscles) | ① Lesions of the 9th–12th cranial nerves, leading to pharyngeal and vocal cord paralysis, laryngeal muscle paralysis, choking cough, dysphagia, accumulation of oral secretions, and aspiration ② Lesions of the respiratory center, causing shallow and irregular breathing, cardiovascular dysfunction (due to vasomotor center damage), high fever (increasing oxygen consumption), etc. | Pneumonia, atelectasis, pulmonary edema, etc. | Severe muscle pain, gastric distension, excessive use of sedatives, and improper tracheostomy or ventilator settings |
For bulbar paralysis with dysphagia, the patient’s head should be lowered, and they should be placed in a right lateral position with the bed elevated 20–30 degrees to facilitate postural drainage. Strengthen suctioning to maintain airway patency; tracheostomy should be performed early if necessary; correct hypoxia; provide nutrition via gastric tube. Artificial ventilation is contraindicated for respiratory impairment caused solely by dysphagia.
For spinal paralysis affecting respiratory muscle function, artificial ventilation should be used to assist breathing. If respiratory muscle paralysis and swallowing difficulties coexist, tracheostomy should be performed as early as possible, accompanied by endotracheal positive-pressure ventilation.
For respiratory center paralysis, artificial ventilation should be used with respiratory stimulants. Circulatory collapse should be actively managed as shock.
(2) Promoting recovery from paralysis: Drugs that enhance nerve conduction, such as dibazol and galantamine, have limited efficacy and are rarely used now. After fever subsides and paralysis ceases to progress, the following therapies should be initiated early:
1. Acupuncture Treatment Suitable for patients who are young, have a short disease course, and show no significant limb atrophy. Acupuncture points can be selected based on the paralysis area. For the upper limbs, common points include cervical Jiaji points, Jianzhen (SI9), Dazhui (GV14), Shousanli (LI10), Shaohai (HT3), Neiguan (PC6), Hegu (LI4), and Houxi (SI3), with 2–3 points selected each time. For the lower limbs, common points include the area 1 inch lateral to the lumbar spine, Huantiao (GB30), Zhibian (BL54), Tiaoyue, Yusu, Biguan (ST31), Yinlian, Siqiang, Futu (ST32), Chengfu (BL36), Yinmen (BL37), Jizhong, Yanglingquan (GB34), Zusanli (ST36), Jiexi (ST41), Taixi (KI3), Juegu (GB39), Fengshi (GB31), Chengshan (BL57), Luodi, etc. Based on the main muscle groups involved in the paralyzed limb, select 3–4 relevant points, which can be rotated and alternated each time. Treatment is administered once daily, with 10–15 sessions constituting one course. A 3–5 day interval is recommended between courses. Initially, strong stimulation is used to achieve effects, followed by moderate stimulation, and weak stimulation for consolidation. Electroacupuncture or hydro-acupuncture may be used. For hydro-acupuncture, select 1–2 points each time to inject vitamin B1, γ-aminobutyric acid, or an invigorating blood and resolving stasis Chinese medicinals compound formula (e.g., Chinese Angelica, Carthamus, Sichuan Lovage Rhizome preparation), with 0.5–1.0 ml per point.
2. Tuina therapy On the paralyzed limb, perform rolling manipulation back and forth for 8–10 minutes, knead and relax the joints for 3–5 minutes, rub the relevant spine and limbs 5–6 times, and locally apply scrubbing manipulation to generate heat. Perform once daily or every other day, and family members can be taught to do it at home.
3. Functional exercise For paralyzed limbs that are too heavy to move, tuina can be performed first to promote blood circulation in the affected limb, improve muscle nutrition and nerve regulation, and enhance muscle strength. For limbs that can make slight movements but have very poor muscle strength, assist with passive movements such as extension, flexion, abduction, and adduction. When the limb can move but muscle strength is still weak, encourage the patient to perform active movements, engage in physical therapy, and use therapeutic tools to strengthen muscles and correct deformities.
4. Physical therapy Hydrotherapy, electrotherapy, wax therapy, phototherapy, etc., can be used to relax the affected muscles, improve local blood flow, and promote the absorption of inflammation.
5. Others Cupping (fire cupping, water cupping, air cupping) and Chinese medicinals fumigation, washing, or external application can be used to promote the recovery of paralyzed limbs. There are also reports of using acupoint stimulation ligation therapy to enhance muscle strength in limbs paralyzed for a long time. Deformed limbs can be fixed with wooden boards or gypsum, or corrected surgically.
The severity of each epidemic varies, with a fatality rate of 5–10%, mostly due to respiratory failure. In areas with vaccination, not only does the incidence decrease, but the condition is also milder, with rare fatalities.
Persistent fever often indicates the potential onset of paralysis. However, the height of the fever, the severity of symptoms, and the number of cells in the cerebrospinal fluid are unrelated to whether paralysis occurs or its severity. Paralysis does not progress after the fever subsides. The prognosis is poor for those with bulbar palsy or respiratory muscle paralysis. The timing of muscle function recovery in paralysis is related to the extent of nerve damage; muscle fibers whose nerve cells have already necrotized cannot regain function, and muscle strength recovery relies on compensation from undamaged muscle groups. Muscle strength recovers fastest in the first few weeks after the illness, then gradually slows. If no recovery occurs within 1–2 years, it often becomes a permanent sequela.
The polio vaccine has excellent immunization effects.
(1) Active immunization The earliest used was the inactivated polio vaccine (Salk vaccine). Intramuscular injection provides certain protection for susceptible individuals, and since it does not contain live virus, it is also very safe for immunocompromised individuals. Some countries have achieved significant results in controlling and nearly eradicating polio by using only the inactivated vaccine. However, the immunity induced by the inactivated vaccine is short-lived, requiring repeated injections, and it does not induce local immunity. Additionally, its preparation is costly, which are its drawbacks. In recent years, improvements in the formulation have been made. Administering three doses at the 2nd month, 4th month, and 12th–18th months can induce antibodies against all three types in 99% of recipients, lasting for at least 5 years.
The attenuated live vaccine (Sabin vaccine, Oral polio-virus vaccine, OPV) is currently more widely used. This live vaccine virus, after multiple passages in tissue culture, has little or no toxicity to the human nervous system. When taken orally, it can replicate in the intestinal tissues of susceptible individuals, rapidly increasing homologous neutralizing antibodies in the body. At the same time, it induces the production of secretory IgA, enhancing immunity in the intestines and pharynx, which can eliminate invading wild strains and interrupt their transmission in the population. Moreover, the live vaccine virus can be excreted, infecting contacts and indirectly immunizing them, thus providing better immunization effects. A trivalent sugar pill vaccine has now been developed, which can be stored for 5 months at 2–10°C, 10 days at 20°C, and only 2 days at 30°C, so refrigeration (4–8°C) is still necessary. The primary target group for oral vaccination is susceptible children aged 2 months to 7 years, but susceptible individuals of other ages and adults should also take the vaccine. Mass vaccination is best conducted in winter and spring, administered in 2 or 3 doses on an empty stomach. Hot water should not be used to swallow the vaccine, as it may inactivate the virus and render it ineffective. The sugar pill vaccines are categorized as type 1 (red), type 2 (yellow), type 3 (green), a mixed type 2 and 3 vaccine (blue), and a mixed type 1, 2, and 3 vaccine (white). Starting at 2 months of age, the vaccine is administered in three oral doses, either sequentially with one pill of type 1, 2, and 3 each time or one pill of the mixed type 1, 2, and 3 vaccine each time. The latter has been shown to provide better immunization, require fewer doses, and reduce the risk of fistula disease, so China has gradually shifted to using the trivalent mixed vaccine. Each oral dose should be spaced at least 4–6 weeks apart, preferably 2 months, to avoid potential interference. To boost immunity, the vaccine can be repeated annually for 2–3 consecutive years, with another dose before starting school at age 7. Type-specific antibodies typically develop about 2 weeks after oral vaccination, peak within 1–2 months, and gradually decline thereafter. After 3 years, half of the children show significantly reduced antibody levels.
Oral vaccination rarely causes adverse reactions, with occasional reports of grade I fever or diarrhea. Individuals with active subcutaneous node disease, severe rickets, chronic heart, liver, or kidney diseases, or acute fever should temporarily avoid vaccination. Some reports suggest that after repeated passages in the human intestine, the vaccine virus strain may increase in neurovirulence for monkeys. In recent years, countries widely using OPV have identified cases of paralysis confirmed to be caused by the vaccine strain, mostly occurring in immunocompromised individuals. Therefore, it is now widely agreed that attenuated live vaccines should not be used in immunocompromised individuals, whether due to congenital immunodeficiency or secondary immunodeficiency caused by medication, infection, or tumors. Contact with OPV recipients should also be avoided. Some suggest that such patients should first receive the inactivated vaccine, followed by the attenuated live vaccine as a booster, but most advocate using only the inactivated vaccine.
(2) Passive immunization For unvaccinated young children, pregnant women, healthcare workers, immunocompromised individuals, or those who have undergone local surgeries such as tonsillectomy and have had close contact with patients, gamma globulin should be administered intramuscularly as soon as possible. The pediatric dose is 0.2–0.5 ml/kg, or placental globulin at 6–9 ml, once daily for 2 consecutive days. Immunity can last for 3–6 weeks.
(3) Isolation of patients: Patients should be isolated for at least 40 days from the onset of illness. During the first week, both respiratory and enteric isolation measures should be emphasized. Excreta should be mixed and disinfected with 20% bleaching powder. Tableware should be soaked in 0.1% clarified bleaching powder solution or boiled for disinfection, or exposed to sunlight for two days. Floors should be disinfected with limewater. The hands of contacts should be soaked in 0.1% clarified bleaching powder solution or disinfected with 0.1% peracetic acid. Close contacts who are susceptible should be placed under quarantine observation for 20 days.
(4) Maintain daily hygiene It is very important to regularly maintain environmental hygiene, eliminate flies, and cultivate hygienic habits. During the epidemic of this disease, children should avoid crowded places, prevent excessive fatigue and catching cold, and postpone various preventive injections and non-urgent surgeries to avoid turning an abortive infection into a paralytic type.
It is commonly seen in patients with medullary respiratory paralysis and can be complicated by bronchitis, pneumonia, atelectasis, acute pulmonary edema, azotemia, hypertension, etc. In the acute phase, approximately one-fourth of patients exhibit abnormal electrocardiograms, indicating myocardial lesions, which may be directly caused by the virus or secondary to severe hypoxia. Gastrointestinal paralysis may be complicated by acute gastric dilation, gastric ulcers, and intestinal paralysis. Urinary retention is prone to concurrent urinary tract infections. In cases of long-term severe paralysis and prolonged bed rest, skeletal atrophy and decalcification may lead to complications such as hypercalcemia and urinary tract stones.
However, it needs to be differentiated from the following diseases:
(1) Infectious polyradiculoneuritis or Guillain-Barré syndrome: More common in older children, sporadic onset, afebrile or with low-grade fever, accompanied by grade I upper respiratory tract inflammation symptoms. Gradually presents with flaccid paralysis, ascending and symmetrical, often accompanied by sensory disturbances. The cerebrospinal fluid shows increased protein with few cells as a characteristic feature. Paralysis recovers relatively quickly and completely, with few sequelae.
(2) Familial periodic paralysis: Rare, afebrile, sudden onset of paralysis, symmetrical, rapidly progressive, and may involve the whole body. During attacks, hypokalemia is present, and recovery is rapid after potassium supplementation, but recurrence is possible. A family history is often present.
(3) Peripheral neuritis: May be caused by post-diphtheritic neuritis, intramuscular injection injury, lead poisoning, vitamin B1 deficiency, herpes zoster infection, etc. Medical history and physical examination can aid in differentiation, with no changes in cerebrospinal fluid.
(4) Other viral infections causing mild paralysis: Such as Coxsackie or echovirus infections, which are clinically difficult to differentiate. However, the presence of typical symptoms like chest pain or rash may assist in differentiation. Confirmation relies on viral isolation and serological tests.
(5) Epidemic encephalitis B: Should be differentiated from the encephalitic type of this disease. Epidemic encephalitis B mostly occurs in summer and autumn, with acute onset and frequent consciousness disturbances. Both peripheral blood and cerebrospinal fluid predominantly show neutrophilic granulocytosis.
(6) Pseudoparalysis: Infants and young children may exhibit limited limb movement due to injury, fracture, arthritis, or subperiosteal hematoma caused by vitamin C deficiency. Careful examination is required for differentiation.
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