Was the thalidomide tragedy preventable?
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Biomedical subjects
Publications and source records attributed to E M Critchley.
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The purpose of this article is to examine the success and motivation of a small but remarkable group of severely handicapped individuals.
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Botulism can arise from preformed toxin, wound infection or intestinal toxico-infection. All three forms can occur in humans as well as in animals. The examination of botulism in veterinary practice can alert the medical profession to the hazards which can occur with the introduction of dietary alterations and hermetic sealing of foodstuffs. There is also the possibility that the development of pica through lack of essential nutrients could lead to the ingestion of contaminated substances rendering the child (or even adult) susceptible to botulinum intoxication. A positive gain has been that research leading to the elimination of shaker foal disease has provided a comprehensive analysis of factors which may underline the risk of toxico-infection in infants.
The survival of Clostridium botulinum spores in improperly processed foods varies considerably with pH and temperature. The greatest risk arises from commercial or home-prepared condiments, vegetables, non-acid fruits and preserved raw fish. Clinical problems with botulism arise from the rapidity of development, unexpected manifestations involving the autonomic nervous system, including paralytic ileus, gastric dilatation and hypotension, and the need to ensure ventilation.
The clinical features of 27 patients identified in an outbreak of botulism in Lancashire, England, and North Wales are reviewed. All but 1 of the patients (age range 14 months to 74 years) were admitted to hospital: 12 were treated in intensive care units, and 8 received positive pressure ventilation. 1 patient died with an aspiration pneumonia. The clinical presentations contained several unusual features, with evidence of segmental demyelination in some patients and drowsiness, sore throats, and fever in others. The widely dispersed source of intoxication with patients presenting singly to several hospitals added to the difficulties of diagnosis. Successful clinical management depends on full and early recognition both of the dangers of impaired oropharyngeal function and of the rapid neurological changes in botulism.
A 40-yr-old woman, K.S., is reported, who shows a severe loss of memory for people following a history of epilepsy and right anterior temporal lobectomy. Despite this memory problem, K.S. is not clinically amnesic, has a Memory Quotient of 122 on the Wechsler Memory Scale in line with her IQ of 119, and performs well on conventional tests of recognition and recall. She does not have a generalized semantic memory deficit for living things, but her deficit extends beyond people to include famous animals, buildings and product names. Autobiographical memory is good, except where memory for people is concerned. The nature of the memory store that is impaired in K.S. is discussed, as are the implications of her case for theories of the organization of long-term memory.
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Patients are often told of the diagnosis of a neurological disability in less than ideal circumstances such that they may not fully comprehend it. Clinicians must be able to sense when the patient's understanding is imperfect even if superficially he or she appears to take in what has been said and its implications. A programme of further counselling is often required to follow this up. A critical look at current procedures will show how these problems arise. It is suggested that improvements in the care of neurologically disabled patients would follow from improved communication between the many agencies that the concerned in their care and from providing books and other material explaining disability and its treatment. A logical development would be for disabled living centres to be established adjacent to existing neuroscience units.
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