Neurological Manifestations Induced by Nitrous Oxide Abuse: A Case Series and Review of Literature.

INTRODUCTION: Nitrous oxide (NO) abuse is increasing among young people. This can result in severe neurological disorders such as myelopathy and/or peripheral neuropathy. We report the clinical presentations, biological, radiologic and electrophysiological findings of 5 patients hospitalized with neurological symptoms consecutive to NO abuse. In addition, a literature review was conducted to describe the neurological characteristics and to identify factors associated with a poor recovery. CASE REPORT: Among the 5 patients included, 2 had a myeloneuropathy, 2 had a sensorimotor neuropathy, and 1 had a normal spinal cord magnetic resonance imaging and electromyography despite neurological manifestations consistent with myeloneuropathy. After vitamin B 12 supplementation, recovery was reported in 4 patients, and 1 was lost to follow-up.From the literature review, 154 patients were included [94 males; median age 22 (19 to 26) y; NO exposure 9 (3 to 18) mo]. A myelopathy was identified in 116 patients (75%) and a peripheral neuropathy was documented in 89 patients (58%). Compared with patients who recovered, those with sequelae were more likely to have a motor deficit at presentation ( P <0.001), to use NO regularly ( P <0.001), to have a lower vitamin B 12 level ( P =0.04), and a higher concentration of homocysteine ( P =0.04). A less extensive myelopathy was more frequently found in the group with favorable outcomes ( P =0.002). CONCLUSION: Neurological disorders caused by NO may be challenging with severe clinical patterns. We identified several factors associated with a poor recovery, to make clinicians aware of NO-induced neurotoxicity.

[Intracerebral haemorrhage in young adults]. / Hémorragie cérébrale de l'adulte jeune.

In Western countries, less than 5 % of strokes occur in adults less than 50 years. Most of these strokes are cerebral infarctions, but 10 to 30 % are intracerebral hemorrhages (ICH). The causes of ICH in young adults are wider than in the elderly. Vascular malformations and lipohyalinosis of small vessels weakened by hypertension constitute the most frequent causes. Management of ICH is an emergency and these patients should be hospitalized in specialized units. Compared to cerebral infarction the prognosis of patients with ICH is poor with a risk of death between 40 % and 50 % during the first year. Survivors are left with severe disability in 20 % of cases. The risk of recurrence of ICH in young adults depends of the underlying cause.

Thrombolytic therapy for the treatment of acute ischaemic stroke in adults with homozygous sickle cell disease.

Stroke is a significant cause of morbidity and mortality in patients with homozygous sickle cell disease (SCD). A specific large-vessel vasculopathy is often responsible for both haemorrhagic and ischaemic strokes in patients with SCD. Although intravenous thrombolysis has been considered as a therapeutic option for acute ischaemic strokes in SCD, its use remains debated because of an increased risk of spontaneous intracranial haemorrhage reported in this disease. This risk of haemorrhage is mainly supported by the presence of a Moyamoya syndrome often associated with the specific vasculopathy in patients with homozygous SCD. We report two cases of patients with homozygous SCD treated with intravenous thrombolysis for an acute ischaemic stroke without haemorrhagic transformation. Our cases suggest that reperfusion strategy in acute ischaemic stroke in patients with homozygous SCD can be considered once associated Moyamoya syndrome has been ruled out. An international registry would be of interest as these situations are rare.

Low fetal hemoglobin percentage is associated with silent brain lesions in adults with homozygous sickle cell disease.

Silent white matter changes (WMCs) on brain imaging are common in individuals with sickle cell disease (SCD) and are associated with cognitive deficits in children. We investigated the factors predictive of WMCs in adults with homozygous SCD and no history of neurological conditions. Patients were recruited from a cohort of adults with homozygous SCD followed up at an adult sickle cell referral center for which steady-state measurements of biological parameters and magnetic resonance imaging scans of the brain were available. WMCs were rated by consensus, on a validated age-related WMC scale. The prevalence of WMCs was 49% (95% confidence interval [CI], 39%-60%) in the 83 patients without vasculopathy included. In univariable analysis, the patients who had WMCs were more likely to be older (P = .003) and to have hypertension (P = .02), a lower mean corpuscular volume (P = .005), a lower corpuscular hemoglobin concentration (P = .008), and a lower fetal hemoglobin percentage (%HbF) (P = .003). In multivariable analysis, only a lower %HbF remained associated with the presence of WMCs (odds ratio [OR] per 1% increase in %HbF, 0.84; 95% CI, 0.72-0.97; P = .021). %HbF was also associated with WMC burden (P for trend = .007). Multivariable ordinal logistic regression showed an inverse relationship between WMC burden (age-related WMC score divided into 4 strata) and HbF level (OR for 1% increase in %HbF, 0.89; 95% CI, 0.79-0.99; P = .039). Our study suggests that HbF may protect against silent WMCs, decreasing the likelihood of WMCs being present and their severity. It may therefore be beneficial to increase HbF levels in patients with WMCs.

Mortality in patients treated by intra-venous thrombolysis for ischaemic stroke.

In patients treated by intravenous (i.v.) thrombolysis, mortality rates range from 10 to 20 % at 3 months. The objective of this study was to determine the timing, causes and predictors of early (within 7 days) and delayed (8 days to 3 months) death after i.v. thrombolysis for cerebral ischaemia. We analyzed timing, causes and predictors of early and delayed mortality in a hospital-based registry of consecutive patients treated by i.v. thrombolysis for cerebral ischaemia. Of 500 patients (246 men; median age 71 years; median baseline National Institutes of Health Stroke Scale score 12; median onset-to-needle time 148 min), 76 (15.2%; 95% confidence interval [CI]: 12.3-18.6%) died within 3 months. Of 29 patients with early death, 21 (72.4%; 95% CI: 54.3-85.3%) died from neurovascular causes. Factors independently associated with early death were neurological complications and having had transient ischaemic attacks within the last 7 days. Of 47 patients with delayed death, 24 (51.1%; 95 % CI: 37.2-64.7%) died from infection, all but 1 having a modified Rankin scale >4 at 7 days. Factors independently associated with delayed death were pre-existing conditions and infections. Early and delayed mortality in ischaemic stroke patients are is highly dependent on the neurological status and response to thrombolysis. The target for reducing mortality is therefore to improve response to thrombolysis by any means, which can currently be achieved only by reducing delays.