Response to Atropine in Down's Syndrome

Mir, G. H.; Cumming, Gordon R.

doi:10.1136/adc.46.245.61

Cited by 24 publications

(7 citation statements)

References 8 publications

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“…Hyper‐reactivity to atropine has been reported in DS, which may suggest an early cholinergic deficit (Harris & Goodman 1968; Mir & Cumming 1971). A serotonergic deficit in DS has been suggested, because the level of serotonin is decreased in DS platelets (Boullin & O'Brien 1971; Enns & McCoy 1980).…”

Section: Physiological Impairments With Potential Neurological Conseqmentioning

confidence: 99%

Understanding mental retardation in Down's syndrome using trisomy 16 mouse models

Galdzicki

Siarey

2003

Genes Brain and Behavior

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Mental retardation in Down's syndrome, human trisomy 21, is characterized by developmental delays, language and memory deficits and other cognitive abnormalities. Neurophysiological and functional information is needed to understand the mechanisms of mental retardation in Down's syndrome. The trisomy mouse models provide windows into the molecular and developmental effects associated with abnormal chromosome numbers. The distal segment of mouse chromosome 16 is homologous to nearly the entire long arm of human chromosome 21. Therefore, mice with full or segmental trisomy 16 (Ts65Dn) are considered reliable animal models of Down's syndrome. Ts65Dn mice demonstrate impaired learning in spatial tests and abnormalities in hippocampal synaptic plasticity. We hypothesize that the physiological impairments in the Ts65Dn mouse hippocampus can model the suboptimal brain function occuring at various levels of Down's syndrome brain hierarchy, starting at a single neuron, and then affecting simple and complex neuronal networks. Once these elements create the gross brain structure, their dysfunctional activity cannot be overcome by extensive plasticity and redundancy, and therefore, at the end of the maturation period the mind inside this brain remains deficient and delayed in its capabilities. The complicated interactions that govern this aberrant developmental process cannot be rescued through existing compensatory mechanisms. In summary, overexpression of genes from chromosome 21 shifts biological homeostasis in the Down's syndrome brain to a new less functional state.

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Section: Physiological Impairments With Potential Neurological Conseqmentioning

confidence: 99%

Understanding mental retardation in Down's syndrome using trisomy 16 mouse models

Galdzicki

Siarey

2003

Genes Brain and Behavior

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“…Down’s syndrome patients have decreased CNS catecholamine levels which may result in decreased minimum alveolar concentration level 2. Atropine hypersensitivity has been noted in these patients; hence, sensitivity to atropine needs to be evaluated before giving a vagolytic dose 3. Due to the presence of muscular hypotonia,1 muscle relaxants need to be used with care.…”

Section: Discussionmentioning

confidence: 99%

Laparoscopic surgery in a paediatric patient with Down's syndrome and patent foramen ovale

Singh

Verma²,

Pandey³

et al. 2011

Case Reports

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“…Several studies found that dilation of the pupil occurred more rapidly in children with Down's Syndrome (Berg et al, 1959;O'Brien et al, 1960;Priest, 1960). The mydriasis was reported by Berg et al (1959) to have a longer duration in the children but Mir and Cummings (1971) disagreed, as they found no difference in the duration of mydriasis in Down's Syndrome children compared to normal children. Lowe (1949) did not find any difference in the rate or duration of dilation produced in children with Down's Syndrome compared to normal.…”

Section: Accommodative Esotropiamentioning

confidence: 99%