Definition And Epidemiology
- Paralytic poliomyelitis is an acute viral infectious disease caused by the wild poliovirus that selectively destroys the anterior horn cells of the spinal cord and brain stem.
- It presents as a characteristic Acute Flaccid Paralysis (AFP) syndrome.
- Only 1-2% of individuals infected with the poliovirus develop paralytic disease.
- Historically in India, the median age at onset was 18 months, with peak transmission occurring between July and September.
- Following major immunization initiatives, India was declared polio-free in March 2014, with endemicity now restricted to Afghanistan and Pakistan.
Clinical Manifestations
Acute Presentation
- Prodrome: A febrile illness just prior to the onset of paralysis is a hallmark finding. Fever is invariably present at the onset of flaccid paralysis but typically resolves the following day.
- Progression: Sudden onset of paralysis that progresses rapidly, usually reaching maximum severity in less than 4 days (occasionally 4 to 7 days).
- Pain: Severe myalgia and backache are prominent features. Associated signs of meningeal irritation, such as the tripod sign, may be present.
- Provocative Factors: There may be a history of a recent intramuscular injection or minor surgical intervention prior to the onset of weakness.
Neurological Examination
- Symmetry: Paralysis is classically asymmetrical and patchy.
- Distribution: Proximal muscle groups are more severely involved compared to distal groups.
- Tone And Reflexes: Profound hypotonia and diminished or absent deep tendon reflexes in the affected limbs.
- Sensory System: Sensations remain entirely intact; there is no sensory loss.
- Cranial Nerves: Affected only in bulbar and bulbospinal variants.
- Autonomic Function: Bladder and bowel involvement are distinctly absent.
Differential Diagnosis
Paralytic poliomyelitis must be differentiated from other causes of Acute Flaccid Paralysis.
Distinguishing Features Of Acute Flaccid Paralysis Etiologies
| Feature | Poliomyelitis | Guillain-Barré Syndrome | Transverse Myelitis | Traumatic Neuritis |
|---|---|---|---|---|
| Fever At Onset | High; always present at onset | Not common | Rarely present | Absent |
| Symmetry | Asymmetrical, proximal | Symmetrical, distal | Symmetrical, lower limbs | Asymmetrical |
| Sensations | Severe myalgia; no sensory loss | Cramps, tingling, hypoanaesthesia | Anaesthesia below lesion level | Pain in gluteal region |
| Deep Tendon Reflexes | Decreased or absent | Absent | Absent early; hyperreflexia late | Decreased or absent |
| Bowel/Bladder | Absent | Transient late dysfunction | Present early | Absent |
| Cerebrospinal Fluid | Lymphocytic pleocytosis | Albuminocytologic dissociation | Variable | Normal |
Investigations
Stool Examination For Virus Isolation (Gold Standard)
- Diagnosis is definitively confirmed by the isolation of wild poliovirus from stool samples.
- Two stool specimens (approximately 8 grams each) must be collected 24 to 48 hours apart.
- Samples must be collected ideally within 14 days of paralysis onset and transported under strict cold chain conditions.
- Human rhabdomyosarcoma (RD) and L20B cell lines are utilized for virus isolation.
Other Modalities
- Cerebrospinal Fluid (CSF): Transparent appearance. Shows mild protein elevation (40-65 mg/dL) and pleocytosis (200-300 cells/mm³) that is initially polymorphonuclear but rapidly shifts to lymphocytic.
- Electrophysiology: Nerve Conduction Studies (NCS) and Electromyography (EMG) demonstrate an abnormal anterior horn cell disease pattern (neuropathic).
- Magnetic Resonance Imaging (MRI): MRI of the spine is usually normal.
Management
Acute Phase
- Specific antiviral treatment is not available.
- Strict Bed Rest: Absolute bed rest is mandatory during the acute phase.
- Contraindications: Intramuscular injections and massage are strictly prohibited as they exacerbate muscle damage.
- Supportive Care: Analgesics for myalgia, warm fomentation for muscle pain, and optimal positioning of limbs to prevent early contractures.
Indications For Hospitalisation
- Progressive weakness or rapid ascending paralysis.
- Respiratory deterioration (increased respiratory rate, decreased single breath count, decreased chest expansion).
- Bulbar involvement manifesting as pooling of saliva, nasal regurgitation, or dysphagia.
- Signs of carbon dioxide narcosis (altered sensorium, sweating, increased pulse rate).
Rehabilitation And Recovery
- Recovery typically begins within 10 days after maximum weakness is reached.
- Passive physiotherapy must be initiated once muscle pain subsides to prevent contractures.
- Later rehabilitation necessitates the use of calipers and braces to promote ambulation and correct severe asymmetrical skeletal deformities.
- The child must receive full polio immunization 3 to 4 weeks after the paralytic attack.