1H MR spectroscopy of gray and white matter in carbon monoxide poisoning

Abstract

Carbon monoxide (CO) intoxication leads to acute and chronic neurological deficits, but little is known about the specific noxious mechanisms. (1)H magnetic resonance spectroscopy (MRS) may allow insight into the pathophysiology of CO poisoning by monitoring neurochemical disturbances, yet only limited information is available to date on the use of this protocol in determining the neurological effects of CO poisoning. To further examine the short-term and long-term effects of CO on the central nervous system, we have studied seven patients with CO poisoning assessed by gray and white matter MRS, magnetic resonance imaging (MRI) and neuropsychological testing. Five patients suffered from acute high-dose CO intoxication and were in coma for 1-6 days. In these patients, MRI revealed hyperintensities of the white matter and globus pallidus and also showed increased choline (Cho) and decreased N-acetyl aspartate (NAA) ratios to creatine (Cr), predominantly in the white matter. Lactate peaks were detected in two patients during the early phase of high-dose CO poisoning. Two patients with chronic low-dose CO exposure and without loss of consciousness had normal MRI and MRS scans. On follow-up. five of our seven patients had long-lasting intellectual impairment, including one individual with low-dose CO exposure. The MRS results showed persisting biochemical alterations despite the MRI scan showing normalization of morphological changes. In conclusion, the MRS was normal in patients suffering from chronic low-dose CO exposure; in contrast, patients with high-dose exposure showed abnormal gray and white matter levels of NAA/Cr, Cho/Cr and lactate, as detected by (1)H MRS, suggesting disturbances of neuronal function, membrane metabolism and anaerobic energy metabolism, respectively. Early increases in Cho/Cr and decreases of NAA/Cr may be related to a poor long-term outcome, but confirmation by future studies is needed.

Longitudinal changes in the dopamine transporter and cognition in suicide attempters with charcoal burning

“…To the best of our knowledge, only one case report showed recovery the level of DAT availability in CO-poisoning patients at a 14-month follow-up (Kondziella et al, 2009). DAT receptors are located on the dendrites of the nerve cells projecting to the striatum from the substantia nigra.…”

“…The clinical symptoms of CO poisoning are non-specific and varied, including cognitive dysfunctions, personality changes, urine and fecal incontinence, gait disturbances, parkinsonism and other movement problems, depression, anxiety and mutism (Ernst and Zibrak, 1998;Hurley et al, 2001;Kesler et al, 2001;Hay et al, 2002;Parkinson et al, 2002;Porter et al, 2002;Weaver et al, 2002;Pulsipher et al, 2006;Kondziella et al, 2009;Weaver, 2009;Chang et al, 2010;Ku et al, 2010;Yang et al, 2011). The cognitive impairment caused by CO poisoning involves multiple domains, such as attention, visual and verbal memory, executive function, calculation, and visuospatial function (Hurley et al, 2001;Kesler et al, 2001;Hay et al, 2002;Parkinson et al, 2002;Porter et al, 2002;Weaver et al, 2002;Pulsipher et al, 2006;Kondziella et al, 2009;Chang et al, 2010Chang et al, , 2011. Cognitive impairment is one of the most serious sequelae of CO poisoning because it may prevent the full recovery of pre-morbid functions in CO poisoning patients (Hurley et al, 2001;Weaver et al, 2002).…”

The Role of MR Imaging in Assessment of Brain Damage from Carbon Monoxide Poisoning: A Review of the Literature

“…When attention is focused on the period in which each metabolite appears, these studies reported that the Cho/Cr ratio increased earliest in metabolites and decreased in the late period of the chronic phase, the NAA/Cr ratio began to decrease at the earliest from 3 to 4 weeks, and lactate began to appear at the earliest from 1 to 2 months after CO poisoning in patients with chronic symptoms. 56,[61][62][63][64][65][66][67] It is noteworthy that declines in NAA levels have been proposed as a good prognostic factor, as the NAA/Cr ratio correlates with symptom development, and the presence of lactate acts as a marker of irreversible brain damage because it has been observed in patients with severe chronic symptoms such as akinetic mutism and apallic state. MR spectroscopy findings by 3T MR imaging in the subacute phase in 29 patients with CO poisoning found that the Cho/Cr ratio in the centrum semiovale was slightly but significantly higher in patients with subsequent chronic-phase symptoms than in patients with transient symptoms in the acute phase.…”

1H-magnetic resonance spectroscopy indicates damage to cerebral white matter in the subacute phase after CO poisoning

“…Some authors have mentioned the occurrence of inflammation in association with demyelination of the CNS in the acute phase among CO poisoned patients 8 9. Furthermore, previous studies in the chronic phase have reported increased Cho/Cr ratio in patients both with and without chronic neuropsychiatric symptoms 11 21 22 24. The present study showed that the mean Cho/Cr ratio in patients with chronic symptoms (both Groups P and D) was significantly higher than in patients with acute symptoms only (Group A) (figure 4).…”