Paralytic Poliomyelitis

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.

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.

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.

Paralytic poliomyelitis must be differentiated from other causes of Acute Flaccid Paralysis.

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

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.

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.

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.

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).

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.