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Poliomyelitis is a viral infection that causes the death of motor neurons in the Anatomy spinal cord and brainstem. During the acute phase of the infection, the virus may infect the cortex, thalamus, hypothalamus, reticular formation, brainstem motor and vestibular nuclei, cerebellar nuclei, and motor neurons of the anterior and lateral horns of the spinal cord, causing an inflammatory reaction.

Death of motor neurons may result, leading to muscle atrophy. The motor neurons that survive recover fully and may reinnervate denervated muscle.

Paralytic poliomyelitis is characterized by an initial period of muscle pain and Symptoms spasms, followed by muscle weakness that peaks in severity by one week after the onset of symptoms. Patients do not experience sensory impairment, but may complain of paresthesias.

Bulbar symptoms occur in some patients and include dysphagia, dysarthria, hiccups, and respiratory weakness leading to anxiety and restlessness. In adults, bulbar disease is found in conjunction with spinal disease, but children (especially those without tonsils or adenoids) may present with a pure bulbar poliomyelitis.

Urinary retention is common during the acute phase. Patients may also complain of neck and back stiffness and pain, from meningeal inflammation.

Muscle weakness is asymmetric and typically proximal. Lumbar segments are Signs usually more severely affected, with trunk muscles being largely spared. Tendon reflexes may be initially brisk, but become diminished or absent. Muscles progressively and permanently atrophy over a period of 2-3 months. Loss of bulbar motor neurons occurs in some patients and can lead to paralysis of the facial muscles (unilaterally or bilaterally), pharynx, larynx, tongue, and mastication muscles.

If infection strikes the reticular formation, severe respiratory and autonomic impairment may result. Breathing and swallowing difficulties, as well as loss of vasomotor control, are serious risks for mortality and warrant intensive life support.


Acute poliomyelitis is caused by infection with one of three forms of entero- Acute poliomyelitis virus, a single-stranded, encapsilated RNA virus in the picornavirus family. Enteroviruses spread by fecal-oral transmission. Rare cases have been attribut-

Minor or abortive poliomyelitis

Non-paralytic or preparalytic poliomyelitis

Paralytic poliomyelitis ed to live attenuated virus in the polio vaccine. The replication phase takes place 1-3 weeks post-infection in the pharynx and lower gastrointestinal tract. Secretion of the virus occurs in the saliva and feces. The severity of infection is variable, and can be classified into several categories:

Most patients (95%) are asymptomatic, or exhibit pharyngitis or gastroenteritis. After this initial phase, up to 5% of infected patients may show signs of nervous system involvement.

Nervous system involvement is preceded by a flu-like set of symptoms, including fever, headache, muscle aches, pharyngitis, anorexia, nausea, and vomiting. Neurological signs and symptoms include restlessness, irritability, and signs of meningitis (back/neck stiffness, Brudzinski and Kernig signs). This situation may then proceed to paralytic poliomyelitis.

Paralytic poliomyelitis develops in only 1-2% of infected patients, anywhere from 4 days to 5 weeks following initial infection. Factors believed to predispose a patient to paralytic disease include muscle damage from recent strenuous exercise or muscle injections, increased age, tonsillectomy, weakened B-cell function, and pregnancy. Acute paralytic poliomyelitis causes fatal respi-

Fig. 4. Postpolio syndrome, with polio in early infancy. A and B Foot deformity reveas early onset. C Very often involvement of the lower limbs is asymmetric (om this case right calf is more atrophic than left)

ratory or cardiovascular problems in 5-10% of cases, or as high as 60% of cases with bulbar involvement.

Encephalitic poliomyelitis is extremely rare and has a high mortality associated Encephalitic poliomyelitis with autonomic dysfunction. Patients present with confusion and agitation, which may progress to stupor and coma.

Post-polio syndrome (PPS) occurs 10 years or longer after the initial polio Post-polio syndrome infection, and is characterized by slowly progressive, asymmetric increases in weakness and muscle atrophy (Fig. 4). Patients may complain of joint and muscle pain, and fatigue. PPS is not caused by the virus itself. It is believed that surviving motor neurons that have reinnervated muscle fibers become incapable of maintaining all the connections in their enlarged motor units, and begin to lose some connections. Some clinicians have suggested that excessive exercise aimed at keeping diseased muscles strong leads to this "burn-out", but studies show that the primary associative factor for PPS is the severity of disease during the acute phase of the infection. PPS may lead to weakness in muscle groups previously thought to be unaffected, but typically these muscles were originally affected and the patient developed sufficient strength and adaptation to mask the deficits until the onset of PPS.

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