6533b85bfe1ef96bd12baa51
RESEARCH PRODUCT
Chronic Adult Hydrocephalus
J. PhilipponD. Ancrisubject
Wallerian degenerationmedicine.medical_specialtymedicine.medical_treatmentObstructive hydrocephalusDegeneration (medical)Pressure rangeInternal medicineMedicineNeurochemistryAxonCsf shuntbusiness.industryVentricular dilatationRegeneration (biology)medicine.diseasenervous system diseasesHydrocephalusSurgerymedicine.anatomical_structureAxoplasmAmputationNormal csf pressureCardiologySubarachnoid spacebusinessReinnervationdescription
Knowledge of Wallerian degeneration began in 1852 and, following experimental research on degeneration and regeneration of interrupted nerves, surgeons realized that reinnervation of end organs depended on growth of axons through the interrupted area of nerve. Therefore surgeons tried to reanastomose the stumps. Failures of reinnervation could not be blamed on lack of axoplasma metabolism and flow from cell body to suture line because the clinical observation of amputation neuromas and their constant recurrence demonstrated the unfailing delivery of axoplasma by the nerve cell body; at times to the deep concern of the surgeon, and the constant pain of the patient. The electron microscope showed increased size of nerve cell bodies after their axon had been interrupted. This was taken to mean that the cell body had increased its metabolism in trying to form axoplasma, and later neurochemistry investigations proved this was true. Despite the ability of a nerve cell body to continue production of axoplasma indefinitely, when there is a barrier to the flow of axoplasm peripherally, no reinnervation of end organs can occur.
year | journal | country | edition | language |
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1974-01-01 |