Acute Neuronal Injury: The Role of Excitotoxic Programmed

Denson G. Fujikawa 2+ within the early Eighties it was once famous that over the top Ca inflow, most likely via 2+ 2+ voltage-gated Ca channels, with a resultant elevate in intracellular Ca, used to be linked to neuronal loss of life from cerebral ischemia, hypoglycemia, and standing epilepticus (Siejo 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, producing loose radicals, was once regarded as a possible mechanism wherein neuronal harm happens. In cerebral ischemia and a pair of+ hypoglycemia, strength failure was once regarded as the cause of over the top Ca inflow, while in prestige epilepticus it used to be inspiration that repetitive depolarizations have been accountable (Siejo 1981). in the meantime, John Olney chanced on that monosodium glutamate, the nutrients additive, whilst given to immature rats, was once linked to neuronal degeneration within the arcuate nucleus of the hypothalamus, which lacks a blood-brain barrier (Olney 1969). He up this remark with a chain of observations within the Nineteen Seventies that management of kainic acid, which we now comprehend prompts the GluR5-7 subtypes of glutamate receptor, and different glutamate analogues, prompted not just post-synaptic cytoplasmic swelling, but additionally dark-cell degeneration of neurons, whilst seen via electron microscopy (Olney 1971; Olney et al. 1974).

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Journal of Neurosurgery 77: 29–36. Stanton M (1987) Patient education: Implications for nursing. Today’s OR Nurse 9(6): 16–20. Terry D, Nisbet K (1991) External ventricular drainage. Journal of Neuroscience Nursing (23 December) (6): 347–55. May crc 11/16/03 10:27 AM Page 44 Chapter 3 Spinal abnormalities in children Spina bifida Spina bifida was recognized 2,000 years ago by Prior Tay; most children born with spina bifida at that time died of infection or hydrocephalus. Today, with antibiotic use and the treatment of hydrocephalus, most children born with spina bifida have a long lifespan.

Raised intracranial pressure may result directly from a space-occupying lesion such as a tumour or a haematoma, from cerebral oedema, or due to the presence of hydrocephalus. Typical signs include headache (classically, early morning headache), vomiting and papilloedema (papilloedema will not occur in the baby as his head circumference will expand to compensate). Visual deterioration can be a sign of chronic raised intracranial pressure. Changes in vital signs are a late indicator of acute raised intracranial pressure in children, and irritability, drowsiness and pupil dilatation with a decreased reaction to light, are earlier indicators of neurological deterioration.

Cambridge MA: Blackwell. El Shafer IL, El Rough MA (1987) Ventriculojugular shunt against the direction of blood flow. Role of the internal jugular vein as an antisiphonage device. Child’s Nervous System 3: 282–4. Epstein F, Lapras C, Wisoff JH (1988) Slit ventricle syndrome: etiology and treatment. Pediatric Neuroscience 14: 5–10. Fishman RA (1984) The pathophysiology of pseudotumor cerebri. Archives of Neurology 41: 257–8. Guin S (1995) CNS practice in neurosurgery. Clinical Nurse Specialist (9 January) (1) 3–7.

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