A patient with leg numbness and micturition symptoms

A 37-year-old man presented with an acute loss of sensibility and a gait disorder, caused by a vitamin B12 deficiency due to nitrous oxide use. A spinal cord MRI showed an inverted V sign. Repeated use of nitric oxide blocks the remethylation of homocysteine to methionine, which, in turn, leads to demyelination. Vitamin B12 deficiency, or signs of it in physical examination or diagnostic procedures, is rare in young and otherwise healthy individuals. Therefore, the use of nitrous oxide as a party drug must always be considered as a cause of the deficiency in this particular group of patients, particularly since the popularity of its use is rapidly increasing. Our patient was treated with intramuscular vitamin B12 injections, which significantly improved his gait disorder and sensory symptoms

Hyperglycemia in bacterial meningitis: a prospective cohort study

ABSTRACT: BACKGROUND: Hyperglycemia has been associated with unfavorable outcome in several disorders, but few data are available in bacterial meningitis. We assessed the incidence and significance of hyperglycemia in adults with bacterial meningitis. METHODS: We collected data prospectively between October 1998 and April 2002, on 696 episodes of community-acquired bacterial meningitis, confirmed by culture of CSF in patients >16 years. Patients were dichotomized according to blood glucose level on admission. A cutoff random non-fasting blood glucose level of 7.8 mmol/L (140 mg/dL) was used to define hyperglycemia, and a cutoff random non-fasting blood glucose level of 11.1 mmol/L (200 mg/dL) was used to define severe hyperglycemia. Unfavorable outcome was defined on the Glasgow outcome scale as a score <5. We also evaluated characteristics of patients with a preadmission diagnosis of diabetes mellitus. RESULTS: 69% of patients were hyperglycemic and 25% severely hyperglycemic on admission. Compared with non-hyperglycemic patients, hyperglycemia was related with advanced age (median, 55 yrs vs. 44 yrs, P<0.0001), preadmission diagnosis of diabetes (9% vs. 3%, P=0.005), and distant focus of infection (37% vs. 28%, P=0.02). They were more often admitted in coma (16% vs. 8%; P=0.004) and with pneumococcal meningitis (55% vs. 42%, P=0.007). These differences remained significant after exclusion of patients with known diabetes. Hyperglycemia was related with unfavorable outcome (in a hockey stick-shaped curve) but this relation did not remain robust in a multivariate analysis. Factors predictive for neurologic compromise were related with higher blood glucose levels, whereas factors predictive for systemic compromise were related with lower blood glucose levels. Only a minority of severely hyperglycemic patients were known diabetics (19%). The vast majority of these known diabetic patients had meningitis due to Streptococcus pneumoniae (67%) or Listeria monocytogenes (13%) and they were at high risk for unfavorable outcome (52%). CONCLUSIONS: The majority of patients with bacterial meningitis have hyperglycemic blood glucose levels on admission. Hyperglycemia can be explained by a physical stress reaction, the central nervous system insult leading to disturbed blood-glucose regulation mechanisms, and preponderance of diabetics for pneumococcal meningitis. Patients with diabetes and bacterial meningitis are at high risk for unfavorable outcom

Validation of a Dutch Risk Score Predicting Poor Outcome in Adults with Bacterial Meningitis in Vietnam and Malawi

We have previously developed and validated a prognostic model to predict the risk for unfavorable outcome in Dutch adults with bacterial meningitis. The aim of the current study was to validate this model in adults with bacterial meningitis from two developing countries, Vietnam and Malawi. Demographic and clinical characteristics of Vietnamese (n = 426), Malawian patients (n = 465) differed substantially from those of Dutch patients (n = 696). The Dutch model underestimated the risk of poor outcome in both Malawi and Vietnam. The discrimination of the original model (c-statistic [c] 0.84; 95% confidence interval 0.81 to 0.86) fell considerably when re-estimated in the Vietnam cohort (c = 0.70) or in the Malawian cohort (c = 0.68). Our validation study shows that new prognostic models have to be developed for these countries in a sufficiently large series of unselected patients

Een man met een doof gevoel in de benen en mictieklachten

A 37-year-old man presented with an acute loss of sensibility and a gait disorder, caused by a vitamin B12 deficiency due to nitrous oxide use. A spinal cord MRI showed an inverted V sign. Repeated use of nitric oxide blocks the remethylation of homocysteine to methionine, which, in turn, leads to demyelination. Vitamin B12 deficiency, or signs of it in physical examination or diagnostic procedures, is rare in young and otherwise healthy individuals. Therefore, the use of nitrous oxide as a party drug must always be considered as a cause of the deficiency in this particular group of patients, particularly since the popularity of its use is rapidly increasing. Our patient was treated with intramuscular vitamin B12 injections, which significantly improved his gait disorder and sensory symptoms

Community-acquired bacterial meningitis in adults

Despite the availability of effective antibiotics, vaccination programmes and skilled acute-care facilities, there is still a significant mortality and morbidity from bacterial meningitis. Neurologists are often called on to "rule out bacterial meningitis", which can be difficult with the history and physical examination alone. In this review the authors will discuss the epidemiology, diagnosis and treatment of acute community-acquired bacterial meningitis in adults, focussing particularly on the management of patients with neurological complications, and stressing the importance of adjunctive dexamethason

Diffuse Cerebral Intravascular Coagulation and Cerebral Infarction in Pneumococcal Meningitis

There is a widely held belief that cerebral infarction after bacterial meningitis is always caused by vasculitis; however, evidence is weak. We hypothesized that diffuse cerebral intravascular coagulation is an additional explanation of cerebral infarction in patients with pneumococcal meningitis. Sixteen brains of adults who died from pneumococcal meningitis were investigated. Clinical data were collected, and brain sections were scored for signs of inflammation and activation of coagulation. Patients with and without cerebral infarction on autopsy were compared. In total, 38% of patients had focal neurological deficits. Patients died at a median of 7 days (range, 0-32 days) after admission. On autopsy, the nine patients (56%) with cerebral infarctions more often had arterial thrombosis (p = 0.04) than patients without infarction. Patients with infarction tended to have more inflammatory infiltrations of brain parenchyma, microvascular proliferation, small vessel vasculitis/endarteritis obliterans, blood clotting/vessel clogging, and venous thrombosis. None of the patients had large vessel vasculitis. Five patients had cerebral infarctions without vasculitis or endarteritis obliterans. Although four patients with cerebral infarctions had small vessel vasculitis or endarteritis obliterans, areas of infarction could not be localized to the blood flow distribution of these vessels. Blood clotting/vessel clogging was seen in all four patients with vasculitis or endarteritis obliterans, but this was also observed in 10 patients without vasculitis or endarteritis obliterans. None of the patients developed disseminated intravascular coagulation. Our results suggest that diffuse cerebral intravascular coagulation is an additional explanation of cerebral infarction complicating pneumococcal meningiti

Cerebral Infarction in Adults with Bacterial Meningitis

To evaluate clinical features and prognostic factors of cerebral infarctions in adults with community-acquired bacterial meningitis. An observational cross-sectional study, including 696 patients of whom 174 had cerebral infarction, from a prospective nationwide cohort of community-acquired bacterial meningitis (period, 1998-2002), confirmed by culture of cerebral spinal fluid (CSF) in patients aged over 16 years. Two investigators independently determined the presence of infarction. Cerebral infarction occurred in 174 episodes (25%), with a high inter-rater agreement for determining the presence of cerebral infarction (kappa 0.95). Cerebral infarctions occurred in 128 of 352 patients (36%) with pneumococcal meningitis, in 22 of 257 (9%) with meningococcal meningitis and in 24 of 87 patients (28%) with meningitis caused by other bacteria. Patients with infarctions were older (P <0.001) and often presented with predisposing conditions, such as otitis and/or sinusitis (P = 0.001) or an immunocompromised state (P = 0.003) compared to those without infarction. Patients with infarctions presented with lower scores on the Glasgow Coma Scale (P <0.001), lower CSF white cell counts (P = 0.001), and higher serum erythrocyte sedimentation rate (ESR) (P <0.001). Unfavorable outcome occurred in 108 (62%) patients with infarctions. In a multivariate analysis, infarction was related with unfavorable outcome (odds ratio 3.37; 95% confidence interval 2.19-5.21; P <0.001). We identified lower CSF white cell counts and high ESR to be independent risk factors for cerebral infarction. Cerebral infarction is a common and severe complication in adults with community-acquired bacterial meningitis. Preventing cerebral infarctions will be important in reducing the high morbidity and mortality rate in adults with community-acquired bacterial meningiti