Poliomyelitis Clinical Presentation

Updated: Jul 21, 2020
  • Author: Ashish S Ranade, MBBS, MS, FRCS(Glasg); Chief Editor: Jeffrey D Thomson, MD  more...
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History and Physical Examination

Stages of presentation

Acute stage

Poliovirus is primarily spread by fecal-hand-oral transmission from one host to another. The virus is shed in oral secretions for several weeks and in the feces for several months. It destroys the anterior horn cells in the spinal cord. Poliovirus infections can be divided into minor and major forms. [10]

The minor associated illnesses occur 1-3 days before the onset of paralysis, with gastrointestinal complaints such as nausea and vomiting, abdominal cramps and pain, and diarrhea. There are also systemic manifestations, such as sore throat, fever, malaise, and headache. This stage usually lasts for 2-3 weeks but may extend for up to 2 months; the presence of any tenderness in the muscles is evidence that the acute stage is not over.

The major associated illnesses include all forms of central nervous system (CNS) disease caused by poliovirus, including aseptic meningitis (or nonparalytic polio), polio encephalitis, bulbar polio, and paralytic poliomyelitis, alone or in combination.

The clinical findings associated with an attack of polio are as follows:

  • Fever, neck stiffness (nuchal rigidity), and a pleocytosis in the cerebrospinal fluid (CSF)
  • Profound asymmetrical muscle weakness
  • The initial phase is typically followed by some recovery of muscle strength, but permanent weakness results from necrosis of anterior horn cells
  • Rarely, a transverse myelitis with paraparesis, urinary retention, sensory symptoms and signs, autonomic dysfunction (including hyperhidrosis or hypohidrosis), and decreased limb temperature may occur

Recovery stage

In the recovery stage, also known as the convalescent stage, the acute symptoms and muscle tenderness disappear, and the paralyzed muscles begin to recover. This stage lasts for up to 2 years after the onset of the disease. During this entire period, there is gradual recovery of the muscles; the recovery is rapid in the first 6 months but is slower during the subsequent months.

Residual-paralysis stage

The period beyond 2 years after the onset of the disease is called the residual-paralysis stage. No recovery of muscle power occurs in this stage. Deformities are liable to occur as a consequence of imbalance of muscle power and poor posture. There is also disuse atrophy of muscles and shortening of the leg from interference with growth. In neglected cases, gross fixed deformities of the hip, knee, and foot occur with severe wasting of muscles. Children with extensive paralysis and gross deformities have to crawl on all fours to move from place to place. (See the image below.)

Typical contractures of postpolio residual paralys Typical contractures of postpolio residual paralysis.

Pattern of muscle weakness and deformities

Upper-limb involvement

Late functional deterioration is common in long-term poliomyelitis patients. Whereas upper-limb pain in individual functional regions is common, its overall prevalence and pattern in long-term poliomyelitis are poorly documented. [11]  There are data in support of overuse due to greater mobility and independence as a cause of increasing upper-limb pain in long-term poliomyelitis, especially among severely paralyzed polio patients.

Lower-limb involvement

Typical osseous or soft-tissue abnormalities around the knees associated with poliomyelitis include the following:

  • External rotation of the tibia
  • Excessive valgus alignment
  • Ligamentous laxity
  • Genu recurvatum (see the image below)
Genu recurvatum deformity of right knee. Genu recurvatum deformity of right knee.

With localized wasting, the quadriceps can help compensate for a weak calf. With hamstring weakness, the ability to decelerate the tibia is lost, and therefore, flexion of the knee will persist throughout the stance phase. In order to prevent this, the patient may attempt to compensate with increased quadriceps activity for a longer portion of the stance phase of gait.

In the case of a weak quadriceps and hamstrings, the occurrence of an equinus contracture or a hinged ankle-foot orthosis (AFO) with a dorsiflexion block will prevent excessive ankle dorsiflexion, as well as knee flexion during the stance phase. Lengthening of the Achilles tendon should be avoided in these patients. They may require an ischial weightbearing double upright locked knee orthosis, which helps prevent the knee from buckling during gait.

Common foot and ankle deformities seen include the following:

  • Pes cavovarus (hindfoot cavus) due to evertor paralysis (peroneus brevis and longus)
  • Pronated everted foot due to invertor paralysis (tibialis anterior and posterior)

Foot intrinsics are typically spared in poliomyelitis. Claw toes result from relative overactivity of the long toe flexors and extensors (to compensate for weakness of the triceps).

Spine involvement

Scoliosis is seen in young children with paralysis of trunk muscles and typically involves the thoracic spine. In older children, scoliosis develops gradually and typically involves the lumbar region. The curve may affect walking and sitting ability. [12]


Postpolio Syndrome

Postpolio syndrome (PPS) is the term used for the newly occurring late manifestations of poliomyelitis that develop in patients 30-40 years after the occurrence of the acute illness. It has been estimated that 25-60% of patients who had acute polio may experience these late effects of the disease. The syndrome is characterized by new muscle weakness, muscle fatigability, or both occurring many years after the initial poliomyelitis illness. [13, 14, 15]

The specific cause of PPS is unknown; the etiology has been attributed to pathophysiologic and functional causes. Pathophysiologic causes include the following:

  • Chronic poliovirus infection
  • Death of the remaining motor neurons with aging
  • Premature aging
  • Damage to the remaining motor neurons caused by increased demands or secondary insults
  • Immune-mediated syndromes

Functional causes include the following:

  • Greater energy expenditure as a result of weight gain
  • Muscle weakness caused by overuse or disuse

PPS has been recognized for over 100 years, but it is more common at present because of the large epidemics of poliomyelitis that occurred in the 1940s and 1950s.

PPS is characterized by neurologic, musculoskeletal, and general manifestations. Musculoskeletal manifestations include muscle pain, joint pain, spinal changes such as spondylosis and scoliosis, and secondary root and peripheral nerve compression. General manifestations include generalized fatigue and cold intolerance. The slowly progressive muscle weakness occurs in those muscle groups already involved, such as the quadriceps and calf muscles.

Diagnostic criteria for this syndrome include the following:

  • A prior episode of paralytic poliomyelitis with residual motor neuron loss (which can be confirmed through a typical patient history, a neurologic examination, and, if needed, an electrodiagnostic examination [16]
  • A period of neurologic recovery followed by an interval (usually ≥15 years) of neurologic and functional stability
  • A gradual or abrupt onset of new weakness or abnormal muscle fatigue (decreased endurance), muscle atrophy, or generalized fatigue
  • Exclusion of medical, orthopedic, and neurologic conditions that may be causing the symptoms mentioned in the preceding criterion

A comprehensive clinical evaluation with appropriate investigations is essential to fulfilling the established diagnostic criteria for PPS. PPS is a diagnosis of exclusion, in which a key clinical feature required for the diagnosis is new muscle weakness or muscle fatigability that persists for at least 1 year. Electromyographic and muscle biopsy findings including evidence of ongoing denervation cannot reliably distinguish between patients with PSS and those without PPS. [17]



Postpolio patients are a high-risk group for fracture; therefore, bone-density assessment, review of the risk of falls, and therapeutic intervention should be considered for all patients. Both osteopenia and osteoporosis are associated with increased fracture risk. [18]  

In a study from China, adults with polio (age >48.2 years) were shown to have a higher risk of hip fracture (adjusted hazard ratio [HR], 3.59). This finding calls for a customized hip fracture prevention program to be started early in middle age. [19]