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POLIOMYELITIS
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Poliomyelitis may be either a monophasic or a biphasic disease The initial symptoms or minor illness are nonspeci c, lasting 1 2 days Symptoms are predominantly
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SECTION II
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TABLE 7 1 DIFFERENTIAL DIAGNOSIS OF POLIO VIRUS INFECTIONS
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Disorder Other viral causes of poliomyelitis
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Clinical Features May be indistinguishable from polio with viral prodrome, followed by aseptic meningitis and acute, asymmetric limb and bulbar paralysis Acute onset of motor > sensory signs and symptoms affecting limbs and cranial nerves dysautonomia
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Diagnosis Cultures of throat, stool, or CSF CSF serology for viruses in Table 7 2 Acute and convalescent serum antibody titers to speci c viruses in Table 7 2 Elevated CSF protein without pleocytosis Demyelinating sensory motor neuropathy on electrodiagnostic examination signal, swelling on spinal cord MR imaging Electrodiagnostic ndings of a presynaptic disorder of neuromuscular transmission Toxin isolation or organism culture from wound, stool, or ingested food History of appropriate exposure Clinical diagnosis in context of appropriate exposure Family history (variable) Increased products of heme synthesis in urine
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Guillain Barre syndrome
Transverse myelitis
Botulism
Acute-onset paraparesis or quadriparesis with sensory level back pain Cranial nerve including extraocular muscle weakness, generalized weakness, and symptoms of cholinergic dysautonomia
Rabies
Porphyria
Spinal epidural abscess
Hypokalemia and hypophosphatemia
Pain, weakness, and sensory symptoms in the bitten limb in 20% of individuals who are affected Prodrome of abdominal pain, encephalopathy including psychosis, followed by acute, proximally predominant motor > sensory neuropathy Back pain Rapidly progressive paraparesis/quadriparesis with sensory level Rapidly progressive, symmetric, and generalized weakness
Imaging of spine Blood cultures
Potassium <2 meq/L Phosphorus <1 mg/dL
course of weeks to months, presumably due to reinnervation occurring from neighboring motor units not affected by the disease The concept of a PPS was rst addressed by Cornil and L pine in 1875 They described the clinical and e postmortem features of an individual who developed progressive weakness following a remote episode of poliomyelitis3 This concept received no more than cursory attention until 1981 when an international
TABLE 7 2 OTHER VIRAL AGENTS CAUSING POLIOMYELITIS
Coxsackie virus group A type 7 Echovirus 6 Enterovirus 70 Enterovirus 71 Japanese encephalitis virus Poliovirus types 1, 2, and 3 Rabies virus West Nile virus
Figure 7 1 Asymmetric pectoralis and severe intrinsic hand muscle wasting in a 67-year-old who contracted polio in 1955 affecting only cervical segments
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POLIOMYELITIS
symposium of experts was convened in Chicago, representing a response to the large numbers of people affected by the epidemics of the early 1940s and early 1950s There is convincing evidence that some individuals with prior polio may develop slowly progressive weakness (average decline 1%/yr) after a protracted period of stability (PPMA)4 How frequently PPMA occurs as a manifestation of PPS is a matter of some controversy In one study, 50 patients with prior polio were selected from a cohort of 300 patients and followed for 5 years5 Sixty percent of this group developed symptoms Of this symptomatic group, only a third had symptoms attributed to musculoskeletal complaints and none of them had measurable evidence of progressive atrophy and weakness When it occurs, PPMA typically manifests in the spinal segments or bulbar regions most severely af icted by the initial illness Ventilatory function may decline, with one study suggesting approximately 2% loss of vital capacity a year, in keeping with the slowly progressive nature of the illness6 Criteria have been established to solidify this diagnosis These include increasing weakness, atrophy, or fatigue in a person previously af icted with a documented polio-like illness This must occur subsequent to a protracted period of stability, absent an alternative explanation Other than for sequential quantitative measures of strength, there is no gold standard to determine which polio victims have developed PPMA Consequently, estimates of the prevalence of PPS have ranged from 22% to 85% Signs and symptoms of PPS have been reported to begin as early as 8 years after the initial illness or as late as 71 years, with an average of 35 years The likelihood of developing PPS seems to correlate with both the age of the patient at the time of the initial illness and its severity7 The limits of what are or are not legitimate components of the PPS remain controversial as well Reactivation of the initial symptoms of infection, including increasing weakness, cramping, and fatigue, are understandable So too are problems readily attributable to the indirect effects of worsening muscle weakness Myalgias may result from what would be otherwise considered routine muscle use, which, in a sense, has now become overused due to weakened state of the involved musculature Orthopedic problems such as adhesive capsulitis are a frequent sequelae of immobilized joints Premature degeneration of joints is commonplace in the postpolio population Presumably, this occurs as a result of compensatory overuse of unaffected limbs, in an attempt to avoid use of their more affected and less reliable counterparts Alternatively, excessive laxity of joints and excessive wear applied to articular and periarticular anatomy may result from lack of muscular support to those joints Additionally, there may be unbalanced vectors of force brought to bear on individual joints,
produced by disproportionate weakness of the muscle groups supporting them Sleep-disordered breathing is another syndrome that is easy to understand as a potential manifestation of late polio Hypopharyngeal muscles, normally relaxed during rapid eye movement (REM) sleep, may further weaken as a consequence of the late effects of polio and contribute to airway obstruction and the symptomatology of disordered sleep Sleep-disordered breathing may also be the result of adverse late effects on the breathing centers in the brainstem reticular formation More dif cult to comprehend are other symptoms that have been ascribed to the late effects of polio Many of these symptoms cannot be readily explained by the known pathology of the initial illness or by the indirect effects of the more readily understandable delayed progressive weakness5 Impaired concentration and the ability to process information with the usual speed are complaints sometimes voiced by postpolio patients This may result as an indirect effect of impaired sleep patterns Alternatively, physicians should be cognizant that adverse psychological effects can result from late polio Patients sense of well-being can be seriously undermined by their realization that their muscles are weakening and that they may be losing control of a disease with which they had formerly believed that they had achieved an equilibrium
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