Restoration of elbow flexion by modified Steindler flexorplasty.
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A modified Steindler flexorplasty was used to restore elbow flexion in 8 patients with post-traumatic flail elbow. In 5 patients there was associated loss of wrist and finger extension, which was treated by tendon transfer and in 2 patients an associated flail shoulder was treated by arthrodesis. The results were not compromised in patients whose flexor tendons had been transferred for wrist and finger extension. All patients had a stable and mobile elbow with marked improvement of upper limb function. Modified Steindler flexorplasty is a simple, effective and reliable procedure for the restoration of elbow flexion. (+info)
Activation of divergent neuronal cell death pathways in different target cell populations during neuroadapted sindbis virus infection of mice.
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Infection of adult mice with neuroadapted Sindbis virus (NSV) results in a severe encephalomyelitis accompanied by prominent hindlimb paralysis. We find that the onset of paralysis parallels morphologic changes in motor neuron cell bodies in the lumbar spinal cord and in motor neuron axons in ventral nerve roots, many of which are eventually lost over time. However, unlike NSV-induced neuronal cell death found in the brain of infected animals, the loss of motor neurons does not appear to be apoptotic, as judged by morphologic and biochemical criteria. This may be explained in part by the lack of detectable caspase-3 expression in these cells. (+info)
Surveillance of patients with acute flaccid paralysis in Finland: report of a pilot study.
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WHO recommends that surveillance of patients with acute flaccid paralysis (AFP) be used to demonstrate the eradication of wild poliovirus. In this article we report the results of a study to assess the frequency of AFP patients referred to Finnish hospitals and whether virological diagnostic coverage could be improved by repeated reminders and active feedback. For this purpose, we sent monthly questionnaires to all neurological and paediatric neurological units in Finland, requesting retrospective reporting on investigated paralytic patients with defined clinically relevant diagnoses, rather than AFP. Reminder letters included a pre-paid return envelope. Virological investigations were offered cost free. Of the 492 reporting forms sent, 415 (84%) were returned, evenly covering both the population and the study period (July 1997 to June 1998). Of the 90 patients reported, 83 were evaluable. The apparent incidences of the diagnoses covered were 1.6 per 100,000 at any age, and 1.0 per 100,000 for under--15-year-olds. Guillain-Barre syndrome was the most common diagnosis (0.80 per 100,000). The two faecal specimens required were virologically investigated in nine out of the 10 patients under 15 years of age, but in only 46% of all patients. Four adenovirus strains, but no polioviruses or other enteroviruses, were isolated. We conclude that a satisfactory monthly reporting system was readily established and that a sufficient number of patients with diagnoses resembling AFP are being referred to Finnish hospitals. Active feedback did not increase the proportion of virologically investigated patients to an acceptable level in all age groups. It is clear that other approaches must be used to quantify the circulation of poliovirus in Finland. (+info)
Excluding polio in areas of inadequate surveillance in the final stages of eradication in China.
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In 1996, China adopted a virological classification of acute flaccid paralysis (AFP) cases for its surveillance system. Only AFP cases with wild poliovirus in stool specimens are confirmed as polio. Cases with adequate stool specimens that are negative for wild poliovirus are not counted. This paper describes a methodology to rule out poliomyelitis in AFP cases with inadequate stool specimens. National surveillance data were analysed using dot maps to detect clusters of AFP cases with high-risk factors for poliomyelitis. The surveillance system and vaccine coverage were assessed during field investigations. Four clusters of AFP cases were identified, but no poliomyelitis cases. Programmatic failures in the identified high-risk areas included low vaccination rates, poor stool specimen collection and inadequate AFP surveillance. Programme strategies were implemented to correct the identified failures. Use of this methodology provides strong evidence consistent with the absence of wild poliovirus in China. (+info)
Poliomyelitis surveillance: the model used in India for polio eradication.
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Poliomyelitis surveillance in India previously involved the passive reporting of clinically suspected cases. The capacity for detecting the disease was limited because there was no surveillance of acute flaccid paralysis (AFP). In October 1997, 59 specially trained Surveillance Medical Officers were deployed throughout the country to establish active AFP surveillance; 11,533 units were created to report weekly on the occurrence of AFP cases at the district, state and national levels; timely case investigation and the collection of stool specimens from AFP cases was undertaken; linkages were made to support the polio laboratory network; and extensive training of government counterparts of the Surveillance Medical Officers was conducted. Data reported at the national level are analysed and distributed weekly. Annualized rates of non-polio AFP increased from 0.22 per 100,000 children aged under 15 years in 1997 to 1.39 per 100,000 in 1999. The proportion of cases with two adequate stools collected within two weeks of the onset of paralysis increased from 34% in 1997 to 68% in 1999. The number of polio cases associated with the isolation of wild poliovirus decreased from 211 in the first quarter of 1998 to 77 in the first quarter of 1999. Widespread transmission of wild poliovirus types 1 and 3 persists throughout the country; type 2 occurs only in Bihar and Uttar Pradesh. In order to achieve polio eradication in India during 2000, extra national immunization days and house-to-house mopping-up rounds should be organized. (+info)
Massive outbreak of poliomyelitis caused by type-3 wild poliovirus in Angola in 1999.
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The largest outbreak of poliomyelitis ever recorded in Africa (1093 cases) occurred from 1 March to 28 May 1999 in Luanda, Angola, and in surrounding areas. The outbreak was caused primarily by a type-3 wild poliovirus, although type-1 wild poliovirus was circulating in the outbreak area at the same time. Infected individuals ranged in age from 2 months to 22 years; 788 individuals (72%) were younger than 3 years. Of the 590 individuals whose vaccination status was known, 23% had received no vaccine and 54% had received fewer than three doses of oral poliovirus vaccine (OPV). The major factors that contributed to this outbreak were as follows: massive displacement of unvaccinated persons to urban settings; low routine OPV coverage; inaccessible populations during the previous three national immunization days (NIDs); and inadequate sanitation. This outbreak indicates the urgent need to improve accessibility to all children during NIDs and the dramatic impact that war can have by displacing persons and impeding access to routine immunizations. The period immediately after an outbreak provides an enhanced opportunity to eradicate poliomyelitis. If continuous access in all districts for acute flaccid paralysis surveillance and supplemental immunizations cannot be assured, the current war in Angola may threaten global poliomyelitis eradication. (+info)
Type C botulism in dairy cattle from feed contaminated with a dead cat.
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Four hundred twenty-seven of 441 adult Holstein dairy cattle from a 1,200-cow dairy died over a 1-week period during early spring 1998. Affected animals were from 4 late lactation pens, one of which included the bull string. Signs included weakness, recumbency, watery diarrhea, and death. Eighty animals from the 4 pens were dead approximately 8 hours after the first ill cows were noted. Affected cows would collapse on stimulation and extend all 4 limbs with moderate rigidity. Several lacked lingual tonus and had abdominal breathing patterns. The animals had been fed a load of total mixed ration that included a rotten bale of oat hay containing a dead cat. No common toxicants were identified, and pathologic examination revealed no consistent lesions. Testing of tissue from the cat carcass found in the feed sample using mouse protection bioassay identified the presence of type C botulinum toxin. Samples of feed, tissue from affected animals, cat tissue from feed, milk, and serum were also tested using an enzyme-linked immunosorbent assay (ELISA) specific for type C botulinum. Two samples of rumen contents were tested and found to be positive for botulism by ELISA, and 1 of 3 liver samples had a weak positive finding. No botulinum toxin was found in milk or sera using the ELISA. (+info)
Mechanisms of dysphagia in suprabulbar palsy with lacunar infarct.
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BACKGROUND AND PURPOSE: The objective of the present study was to investigate the neural mechanisms of dysphagia in suprabulbar palsy (SBP) with multiple lacunar infarct. METHODS: We evaluated the swallowing disorders of patients with SBP (n=34) and age-matched healthy control subjects (n=35) by means of an electrophysiological method that recorded the oropharyngeal swallowing patterns. With this method, dysphagia limit, the triggering of voluntarily initiated swallows, duration of laryngeal relocation time, and total duration of oropharyngeal swallowing were recorded and measured. In addition, the EMG behavior of the cricopharyngeal (CP) muscle of the upper esophageal sphincter was also assessed. RESULTS: In patients with SBP, the dysphagia limit in all except 1 patient was pathological with limits of <20-mL bolus volume, which is contrary to normal subjects, in whom the dysphagia limit exceeds the 20-mL bolus volume. Either triggering of swallowing reflex was delayed (P<0.04), or the swallow could hardly be triggered in 7 patients on the voluntary attempts for 3 mL water. Whenever the reflex swallowing could be triggered, it was slow and prolonged (P<0.01). The CP muscle of the upper esophageal sphincter appeared to have become hyperreflexic and incoordinated with laryngeal movements during swallowing. CONCLUSIONS: It was proposed that the progressive involvement of the excitatory and inhibitory corticobulbar fiber systems linked with the bulbar swallowing center is mainly responsible for the triggering difficulties of the swallowing reflex and for the hyperreflexic/incoordinated nature of the CP sphincter. In addition, the dysfunction of the extrapyramidal system has a specific role in the slowing of oropharyngeal swallowing and the accumulation of saliva in the mouth. (+info)