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Sunday, August 2, 2009

released into bloodstream, as also endogenous pyrogens and other toxins from necrotlc cells

supervenes, (i) CSF -Clear or ground glass Pressure increased. Protein-normal at first, rises to 100-200 mg. per 100 ml during second week Sugar normal. Cells 60-100. mostly polymorphs at first, later lymphocytes Rarely normal fluid. Signs - (a) Pulse fast and out of proportion to rise of Temperature, (b) Excessive perspiration, (c) Patient is alert 3 Paralytic stage - usually develops between 2nd and 5lh days after onset of signs of Involvement of nervous system May set in without initial symptoms Characteristics are - (\) Usually appears while there Is still fever (ii) Maximum al onset (ill) Distribution often asymmetrical (iv) Usually begins within 1 to 5 days after onsal of illness, progresses for 1 to 3 days, remains stationary for about a week and then shows rapid improvement for some weeks and then slower ev) Absence of sensory loss DISTRIBUTION OF PARALYSIS - usually patchy, may produce monoplegia, paraplegia and quadriplegla. (a) Lower limbs - more frequently affected Usually quadriceps. tibialis anterior and peroneal group (b) Upper limbs - most commonly deltoid, (c) Trunk - abdominal muscles, muscles of back, intercostals or diaphragm (d) Respiratory disturbances - due to paratysis of daphragm and intercostal muscles, or affection of respiratory centre in bulbar type - anxiety. Increasing weakness of voice, cough, sucking In of epigastric or intercostal spaces with increasing use of accessory muscles of respiration, cfmlnulion in the numbers a palient can count after one inspiration, andcyanosis 4. Convalescence -India! paralysis usually diminlshes to some extant after two or more weeks, and improvement may continue for several monihs The allected muscles become flaccid white contraction will tend to produce severe deformities unless these are prevented When chronic stage is reached six months to a year atler inilial Infection, no further spontaneous improvement can bs expected. Clinical types - Infection of a susceptible Indvrdual may result In one of clinical manifestations -1 Inapparent infection - in majority of cases Does not progress beyond involvement at regional lymphnodes However replication of virus in lymphoid tissue stlmufales the Immune system 2 Abortive illness-occurs In4-8%cases. Infection reaches virerric phase and foreign protein from virus is released into bloodstream, as also endogenous pyrogens and other toxins from necrotlc cells. This is results in (a) Abortive poliomyelitis - Presumptive diagnosis during epidemic. Brief Influenza-like illness with one or more of the following symptoms - malaise, anorexia, nausea, vomiting, headache, sore throat, constipation and localised abdominal pain Fever seldom more than 103°F Coryza and cough uncommon, (b) Non-paralytic poliomyelitis - Subjective symptoms as In abortive type but headache, nausea, vomiting more intense, and soreness and stiffness of posterior muscles o( neck, trunk and limbs Fleeting paralysis of bladder not uncommon 3. Paralytic poliomyelitis - (a) Spinal form - Paralysis of flrccid Type usually asymmetrical and scattered in distribution, Though more severe in one extremity Legs most frequently Involved. Respiratory paralysis may result from involvement of daphragrn and intercostal muscles Transient bladder involvement in some (b) Bulbar form - Muscles supplied by bulbar nuclei Involved alone or with spinal musculature Facial, palatal and sometimes pharyngeal paralysis causes change in voice, difficulty in swallowing, nasal regurgiiation and choking

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