- A disease caused by viral destruction of the anterior horn cells in the spinal cord and brain stem motor nuclei
- The hallmark is motor weakness with normal sensation
Epidemiology
- Eliminated from the western hemisphere
- Vaccine-related poliomyelitis is responsible for most modern day cases
- More common in tropical countries – in late summer months
Etiology
- Caused by the poliovirus
- RNA virus from the picornaviridae family
- Serotype 1, 2 and 3 are disease causing
- Faecal-oral transmission – by ingestion of contaminated food/water
- Incubation period is 6-20 days
- Risk factors – immune deficiency, malnutrition, pregnancy
Pathophysiology
- Poliovirus enters the body through oral ingestion
- Then enters and replicates in the gastrointestinal tract – gains entry by binding to CD155 (the poliovirus receptor)
- Continues to replicate in enterocytes for about a week
- From there it spreads to the tonsils, Peyer’s patches and the deep cervical and mesenteric lymph nodes
- Subsequently absorbed into the bloodstream (viremia) – leads to widespread dissemination in the body
Spinal polio
- Due to viral invasion of the motor neurons of the anterior horn cells (grey matter)
- Invasion leads to inflammation of the nerve cells, causing damage and destruction of motor neuron ganglia
- Leads to muscle atrophy, and eventually paralysis
- Sensation in the paralysed limbs is preserved
Bulbar polio
- Due to viral invasion and destruction of the nerves within the bulbar region of the brainstem
- Most commonly infected cranial nerves – glossopharyngeal n. (CN IX), vagus n. (CN X) and accessory n. (CN XI)
- Causes paralysis of the muscle groups innervated by these nerves, especially those of the soft palate and pharynx
Bulbospinal polio
- Both bulbar and spinal symptoms
- Virus affects C3-C5 and the phrenic nerve
- Leads to paralysis of the diaphragm – patient is unable to breathe without a ventilator
Clinical features – 3 presentations
Asymptomatic/mild illness – 95% of cases
- Sore throat, fever, nausea, vomiting, abdominal pain, flu-like symptoms
Non-paralytic aseptic meningitis
- Headache, nuchal rigidity, abdominal pain
- Fever, vomiting, lethargy
Paralytic polio
- Spinal – affects muscles of the trunk, limbs and the intercostals muscles
- Asymmetric flaccid paralysis – worsens over hours to days
- Paralysis is usually more severe in proximal muscles than in distal
- Bulbar
- Symptoms of encephalitis, dysphagia, dyspnoea
- Pooling of secretions in the airways – can cause suffocation
- Facial weakness, double vision
- Bulbospinal
- Respiratory failure
Diagnosis
- Virus culture from stool, CSF or nasopharynx
- CSF analysis (lumbar puncture) – shows lymphocytosis and elevated protein level
- Serology
- MRI of spinal cord
- EMG of affected limb
Complications
- Equinus foot – similar to club foot
- When the muscles that pull the foot down (plantar flexors) are intact – gastrocnemius, soleus, plantaris, FHL, FDL, tibialis posterior
- But the muscles that pull the foot up (dorsi flexors) don’t function – tibialis anterior, EHL, EDL
- Eventually there is tightening of the Achilles tendon
- Osteoporosis
- Increased risk of bone fractures
Treatment
- Antibiotics – to prevent infections in weakened muscles
- Analgesia
- Physiotherapy
- Ventilators
Foot deformities
- Orthoses
- Operative – contracture release, tendon transfer, arthrodesis
Post-polio syndrome
- Occurs in 25-50% of people who have previously recovered from paralytic polio in childhood
- Occurs from 10-40 years after initial polio infection
Pathogenesis
-
- During recovery from polio, neurons in affected muscles re-grow smaller branches (dendrites)
- These dendrites take over the function of neurons destroyed by the virus
- After years of functioning beyond capacity, these neurones weaken and lose ability to maintain the dendrites
- Leads to muscle weakness
Clinical features
- Gradual deterioration of muscle function
- Muscle weakness
- Fatigue, muscle pain, twitching
- Cold intolerance
Treatment
- Walking aides – canes, walkers
- Physiotherapy and gentle exercise (swimming)