ACUTE ANTERIOR POLIOMYELITIS
(Infantile paralysis, Heine-Medin disease)
This disease is caused by a group of related viruses (Picorna viruses) which have a special predilection for the anterior hor cells and their homologues in the brain stem. The infection is mostly acquired by the faecal oral route, and also by fomites, droplet infection and healthy carriers, etc.
Three strains of virus, e.g., type 1 (Brunhilde), type 2 (Lansing), and type 3 (Leon) are responsible for this disease which are antigenically distinct. They reach nervous system by blood or through axis cylinder of peripheral or autonomic nerves. A form of lymphocytic meningitis develops. Gray matter of cortex, brain stem and spinal cord are involved. The anterior horn cells of lumber segments of spinal cord are particularly vulnerable. The incidence of this disease has decreased very much in recent times due to improvement of sanitation and vaccination.
5-35 days, commonly 1-2 weeks.
Onset is sudden
Age: Common in children, but may be seen in all ages. The
disease can be conveniently divided into the following stages:
Inapparent infection may be present in many infected subjects (95%) where no symptom is present. When symptoms are present they include fever, headache, malaise, lassitude, weakness, anorxia, vomiting, sore throat, diarrhoea or constipation, myalgia etc. which may last for 24-28 hours after which in many cases the progress of the disease stops. This is called abortive poliomyelitis (4%-5 %). In a minority of patients the disease proceeds to the major illness after an interval of three to seven days.
This is divided into three stages:
The temperature again rises. Patient complains of occipital headache, vomiting, malaise, weakness, anorexia, diarrhoea, etc. Restlessness and delirium are important features. Muscle spasm is usually present in the extensors of the neck, back, trunk and in hamstrings. Due to this, there will be neck stiffness and positive straight leg raising test beyond 90°. Muscles are tender. This type of disease is called non-paralytic poliomyelitis. All these may disappear after 24-48 hours is Some cases. CSF shows increased cell count mostly polymorphs and protein may be high or normal.
Spinal form: In some of the remaining cases (0.1 % of infected individuals) after a further period of 24-48 hours temperature subsides and paralysis develops. Muscle pain persists. Paralysis is patchy and asymmetrical and is usually seen in the lower limbs. In children below 5 years lower limbs and in those above 5 years upper limbs are usually involved. It is mostly ascending in type, may be descending also. Paralysis of shoulder girdle muscles precedes paralysis of intercostal muscles which leads to diminished expansion of chest and decreased vital capacity. Central cyanosis due to hypoxia and stridor may appear later. Within 24 hours, paralysis is complete. On examination, limbs are flaccid, tremor is present, tone is diminished, plantar reflex is flexor, jerks are absent and gradually wasting develops. Sensory changes are never present, constipation and ileus may be present. After a period of one week some improvement is observed in some muscles which continues for several months.Muscles which show no sign of improvement even after one month usually do not recover.
Bulbar form: In some cases the bulbar nuclei are affected and this is called bulbar poliomyelitis. This may develop de novo or from the spinal form where the pathological changes progress upwards involving respiratory centre, vasomotor centre etc. together with variable amount of features of encephalitis. Cranial nerves IX and X are specially vulnurable. This type is characterised by paralysis of muscles of respiration and deglutition. Respiration rate rises, patient becomes restless, cyanosis appears, alae nasi flare, accessory muscles of respiration come into action and short out-bursts of speech occur. Due to paralysis of intercostal muscles and diaphragm chest expansion as well as vital capacity are diminished. Rocking horse respiration and paradoxical movement may be noticed. Nystagmus and tremor may develop. There may be nasal regurgitation of food and nasal intonation of voice due to palatal palsy. Diplopia, difficulty in chewing, dysphagia, paralysis of sternomastoid, trapezius and flexor muscles of neck may develop. There may be loss of gag reflex, pooling of saliva in the mouth, deviation of tongue and paralysis of vocal cord. The most dreadful aspect is Respiratory paralysis.
Due to paralysis of pharyngeal muscles patients cannot swallow or cough, pharyngeal secretion accumulates and this produces respiratory obstruction and peculiar rattling sound in the throat. This is a grave situation and needs urgent attention. This hypertension), attention. this is to be distinguished from respiratory paralysis. Fluctuating blood pressure (hypotension or hypertension), tachycardia and coma may also develop. Coma is due to either hypoxia or encephalitis. Features of different cranial nerve palsy and lower motor neurone paralysis may also be seen.
Stage of Residual disability
In this stage complete muscular wasting leads to contracture and deformity. Talipes equinovarus and scoliosis may develop. Retardation of bone growth, shortening and deformity of limbs, coldness and cyanosis may also be seen due to trophic changes. Fasciculations are seen in partially paralysed muscles for a long time.
1. Meningitis: There is no lower motor neurone lesion in lower limb, neck rigidity is marked, muscle pain is absent, patient may be unconscious, CSF findings are typical.
2. Rheumatic fever, infantile scurvy and osteomyelitis are also confused sometimes but may be distinguished by appropriate findings.
3. Infective polyneuritis: History of fever, symmetric paralysis of limbs (LMN type) with maximum involvement of proximal muscle group, sensory changes, albumin cytologic dissociation in CSF are seen.
4. Epidemic neurasthenia-clinically resembles poliomyelitis but CSF is normal.
1. Blood examination shows leucocytosis or it may be normal.
2. CSF shows clear colour, increased pressure, rarely cobweb coagulum or standing, increased protein, but sugar and chloride show no change. Pleocytosis with dominant polymorphs in early stages and lymphocytes in later stages are seen. CSF may be nomal in 5% of cases.
3. Throat washings (early), CSF and stool examination (early and late) may be valuable for isolating the causative virus.
4. Serological Test: Neutralising antibodies appear in the 1st week and complement fixing antibodies appear in the 1st and 2nd week of the disease.
3. Pulmonary oedema,
5. Bulbar Palsy
6. Respiratory failure.
7. Post Polio syndrome : It is thought to be due to gradual dysfunction of the neurons compensating the initial neuronal loss. There will be progressive weakness, atrophy and fasciculations. This occurs several years after the initial attack and occurs very very slowly. Initial non-involved muscles and involved muscles show more wasting and atrophy.
Trivalent oral vaccine (TOPV) (Sabin) is used now-a-days In immunodeficient or suppressed cases inactivated killed vaccine (Salk) is used. Following one month after oral polio vaccine no injection should be taken. During the period of epidemic, injection, vaccination, operation, heavy exercise should be avoided, because paralysis may settle down in those muscles.
Persons who have been exposed to infection may be protected by immediate injection of Gamma Globulin.
1. Rest in a polio-bed.
2. Sedatives may be given for restlessness and muscle pain.
3. Gentle passive movement of the paralysed muscles may be done.
4. In bulbar type: Foot end of the bed is raised, secretions are aspirated frequently, artificial respirators with intermittent positive pressure respiration should be used. Clear airway is maintained. Respiratory infection should be controlled. Management is to be done in ITU.
5. Orthopaedic procedures to correct talipes, etc. may be utilised afterwards.