2007
DOI: 10.1016/j.jflm.2007.01.006
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A fatal case of pontine hemorrhage related to methamphetamine abuse

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Cited by 14 publications
(9 citation statements)
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“…Methamphetamine is a potent sympathomimetic that increases the release of dopamine, norepinephrine, epinephrine, and serotonin, 15 which result in acute hypertension and tachycardia, 16 and chronic hypertension with chronic use. 17 Methamphetamine abuse is a well-known cause of spontaneous ICH, [18][19][20][21][22][23][24][25][26][27] although the exact mechanism is unclear. Some postmortem studies have suggested acute necrotizing angiitis, leading to fibrinoid necrosis, thinning of the tunica media and intima, and microaneurysm formation.…”
Section: Study Proceduresmentioning
confidence: 99%
See 1 more Smart Citation
“…Methamphetamine is a potent sympathomimetic that increases the release of dopamine, norepinephrine, epinephrine, and serotonin, 15 which result in acute hypertension and tachycardia, 16 and chronic hypertension with chronic use. 17 Methamphetamine abuse is a well-known cause of spontaneous ICH, [18][19][20][21][22][23][24][25][26][27] although the exact mechanism is unclear. Some postmortem studies have suggested acute necrotizing angiitis, leading to fibrinoid necrosis, thinning of the tunica media and intima, and microaneurysm formation.…”
Section: Study Proceduresmentioning
confidence: 99%
“…Some postmortem studies have suggested acute necrotizing angiitis, leading to fibrinoid necrosis, thinning of the tunica media and intima, and microaneurysm formation. 19,[27][28][29][30][31][32] However, other studies have shown no evidence of inflammation or vasculitis, [33][34][35] suggesting that much of Meth-ICH may be attributable to cumulative burden of methamphetamine-induced high blood pressure. In fact, 96% of Meth-ICHs in our study had hematoma in a location that is consistent with hypertensive ICH, suggesting that this may be an accelerated hypertensive pathology.…”
Section: Study Proceduresmentioning
confidence: 99%
“…Postmortem studies showed that cerebral edema [27] or brain stem hematoma [15] is a common clinical phenotype in patients died of METH intoxication. The present study demonstrated that damage to RVLM in the form of necrotic cell death is a contributing factor to METH-induced mortality.…”
Section: Discussionmentioning
confidence: 99%
“…Cerebrovascular pathology, most commonly hypoxia and hemorrhage, is present in 20% of cases in METH-elicited death [4], [15]. Of particular interests is that our laboratory found previously in experimental brain death models that the degree of tissue hypoxia in RVLM is a crucial determinant of the severity of central circulatory regulatory dysfunction [14], [16].…”
Section: Introductionmentioning
confidence: 99%
“…Basal ganglia and white matter changes occur following poisoning due to carbon monoxide, methanol, ethylene glycol, cyanide, hydrogen sulfide, mercury, manganese, heroine, barbiturates, and solvents [12, 13]. …”
Section: Introductionmentioning
confidence: 99%