Ischaemic brain

Andersen SN and Skullerud K (1999). Hypoxic/ischaemic brain damage, especially pallidal lesions, in heroin addicts. Forensic Science International, 102, 51-59. 

Kokaia Z, Lindvall O (2003) Neurogenesis after ischaemic brain insults. Curr Opin Neurobiol 13 127-132... 

Lorente de No R (1934) Studies on the structure of the cerebral cortex. II. Continuation of the study of the Ammonic system. J Psychol Neurol 46 113-177 Love S, Barber R, Wilcock GK (1998) Apoptosis and expression of DNA repair proteins in ischaemic brain injury in man. Neuroreport 9 955-959 Love S, Barber R, Wilcock GK (1999) Neuronal accumulation of poly(ADP-ribose) after brain ischaemia. Neuropathol Appl Neurobiol 25 98-103 Luskin MB (1993) Restricted proliferation and migration of postnatally generated neurons derived from the forebrain subventricular zone. Neuron 11 173-189 Magavi SS, Leavitt BR, Macklis JD (2000) Induction of neurogenesis in the neocortex of adult mice. Nature 405 951-955... 

JennettW. B. (1970) Secondary ischaemic brain damage after head injury./. Clin. Pathol. Suppl. 4,172-175. 

Li P A, Shamloo M, Katsura K et al 1995 Critical values for plasma glucose in aggravating ischaemic brain damage correlation to extracellular pH. Neurobiology of Disease 2 97-108... 

Matsuo, Y., Onodera, H., Shiga, Y., Nakomura, M., Ninomija, M., Kihora, T., and Kogure, K., Correlation between myeloperoxidase-quantified neutrophil accumulation and ischaemic brain injury in the rat, Stroke, 25, 1469, 1994. 

Yamasaki, Y., Matsuura, N., Shozuhara, H., Itoyama, Y., andKogure, K., Interleukin-1 as a pathogenic mediator of ischaemic brain damage in rats, Stroke, 26, 676, 1995. 

Lee J-M, Zipfel GJ, Choi DW. The changing landscape of ischaemic brain injury mechanisms. Nature 1999 399(supp.) A7-A14. 

Strong, A.J. and Dardis, R. (2005) Depolarisation phenomena in traumatic and ischaemic brain injury. Adv. Tech. Stand. Neurosurg., 30 3-49. 

In infants who have suffered perinatal hypoxic-ischaemic brain injury (birth asphyxia), P spectra obtained within a few hours of birth show no abnormalities. However, in many cases a delayed secondary energy failure (SEP) develops within 24 h. The Pi signal increases, accompanied by reduced PCr and, in severe cases, low NTP. Furthermore, in contrast to the profound acidosis seen during acute hypoxia-ischemia, an intracellular alkalosis may be detected. Additionally, localized spectroscopy shows elevated lactate levels for several weeks following SEE. Both PCr/Pi and lactate/N-acetylaspartate (Lac/NAA) ratios have proved to be extremely useful indices of the severity of hypoxic-ischaemic injury, with strong prognostic capabilities. 

Recent findings imphcate apoptosis in neuronal degeneration after ischaemic brain injury in animal models of stroke (Mattson et al. 2000). Apoptotic cascades involve increased levels of intraceUular oxyradicals and calcimn induction of expression of proteins such as Par-4 (prostate apoptosis response-4), which act by promoting mitochondrial dysfunction and suppressing antiapoptotic mechanisms mitochondrial membrane depolarisation, calcium uptake, and release of factors (e.g. cytochrome c) that ultimately induce nuclear DNA condensation and fragmentation activation of cysteine proteases of the caspase family activation of transcription factors such as AP-1 that may induce expression of killer genes . 

Branston, N. M., Bayhan, M., Harris, R. J., Watson, A., Symon, L., 1981 Indomethacin increases ischaemic brain oedema in the primate. J. Cereb. Blood Flow Metab. (Suppl. 1) 1, S143-S144. 

Hallenbeck, J. M., Furlow, T. W., 1979 Prostaglandin 12 and indomethacin prevent impairment of post-ischaemic brain reperfusion in the dog. Stroke 10, 629-637. 

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