Impact of diet on mortality from stroke: results from the U.S. multiethnic cohort study.

OBJECTIVES: Stroke is the fourth leading cause of death in the United States and stroke mortality rates vary by ethnicity. The purpose of this study was to examine the associations between food group consumption and risk of death from stroke among 5 ethnic groups in the United States. METHODS: The Multiethnic Cohort includes >215,000 participants, the majority of whom are African American, Native Hawaiian, Japanese American, Latino, and Caucasian men and women recruited by mail survey in Hawaii and Los Angeles in 1993-1996. Deaths from stroke were identified by linkage to the state death files and the U.S. National Death Index. Diet was assessed using a validated food frequency questionnaire. Associations were examined using multivariable Cox proportional hazards models, stratified by ethnicity and gender. RESULTS: A total of 860 deaths from stroke were identified among the cohort participants. Vegetable intake was associated with a significant reduction in risk for fatal stroke among African American women (relative risk [RR]=0.60; 95% CI: 0.36-0.99). Among Japanese American women only, high fruit intake was significantly associated with a risk reduction for stroke mortality (RR=0.43; 95% confidence interval [CI]: 0.22-0.85), whereas meat intake increased risk (RR=2.36; 95% CI: 1.31-4.26). Among men, a significant reduction in stroke mortality was observed among Native Hawaiians (RR=0.26; 95% CI: 0.07-0.95). After pooling the data for the ethnic groups, the findings support an elevated risk for high meat intake among women overall (RR=1.56; 95% CI: 1.12-2.16); no significant effects of dietary intake on risk for fatal stroke were observed among men. CONCLUSIONS: Although some variations were observed for the associations between diet and stroke mortality among ethnic groups, the findings suggest that these differences are not substantial and may be due to dietary intake of specific food subgroups. Additional investigations including dietary subgroups and nutrients sources are needed to clarify these findings.

Adherence to the USDA dietary recommendations for fruit and vegetable intake and risk of fatal stroke among ethnic groups: a prospective cohort study.

BACKGROUND: Stroke is the fourth leading cause of death in the U.S. and stroke mortality rates differ substantially by ethnic group. The impact of adherence to the USDA dietary guidelines on risk for fatal stroke among different ethnic groups has not previously been examined. METHODS: A prospective cohort design was used to examine associations between adherence with dietary recommendations for fruit and vegetable intake and risk for stroke mortality among 174,888 men and women representing five ethnic groups; African American, Native Hawaiian, Japanese American, Latino, and Caucasian. Dietary intake was assessed using a mailed quantitative food frequency questionnaire. Associations were examined using Cox proportional hazards models. RESULTS: There was no evidence that ethnicity modified associations between fruit and vegetable intake and stroke mortality. When data for different ethnicities were combined, a reduced risk for fatal stroke was observed among women who were adherent with the USDA dietary recommendations for vegetable intake, although this result did not reach statistical significance (RR = 0.84, 95% CI = 0.68-1.04). No associations were observed among men. CONCLUSIONS: The results of this study do not provide evidence that dietary intake of fruits and vegetables differentially impacts risk for stroke mortality among different ethnic groups.

ICU management of aneurysmal subarachnoid hemorrhage.

INTRODUCTION: Aneurysmal subarachnoid hemorrhage (SAH) has very high morbidity and mortality rates. Optimal intensive care unit (ICU) management requires knowledge of the potential complications that occur in this patient population. METHODS: Review of the ICU management of SAH. Level of evidence for specific recommendations is provided. RESULTS: Grading scales utilizing clinical factors and brain imaging studies can help in determining prognosis and are reviewed. Misdiagnosis of SAH is fairly common so the clinical symptoms and signs of SAH are summarized. The ICU management of SAH is discussed beginning with a focus on avoiding aneurysm re-rupture and securing the aneurysm, followed by a review of the neurologic and medical complications that may occur after the aneurysm is secured. Detailed treatment strategies and areas of current and future research are reviewed. CONCLUSIONS: The ICU management of the patient with SAH can be particularly challenging and requires an awareness of all potential neurologic and medical complications and their urgent treatments.

The effect of a neurocritical care service without a dedicated neuro-ICU on quality of care in intracerebral hemorrhage.

BACKGROUND: Introduction of neurocritical care services to dedicated neuro-ICUs is associated with improved quality of care. The impact of a neurocritical care service without a dedicated neuro-ICU has not been studied. METHODS: We retrospectively identified all patients admitted to our institution with intracerebral hemorrhage (ICH) in two 12-month periods: immediately before the arrival of the first neurointensivist ("before") and after the neurocritical care service was established ("after"). There was no nursing team, ICU housestaff/physician extender team, or physical unit dedicated to the care of patients with critical neurologic illness during either period. Using an uncontrolled before-after design, we compared clinical outcomes and performance on quality metrics between groups. RESULTS: We included 74 patients with primary supratentorial ICH. Mortality, length of stay (LOS), proportion of patients with modified Rankin Score 0-3, and destination on discharge did not differ between groups when adjusted for confounders. Time to first two consecutive systolic blood pressure (SBP) measurements <180 mmHg was shorter in the "after" cohort (mean 4.5 vs. 3.2 h, p = 0.001). Area under the curve measurement for change in SBP from baseline over the first 24 h after ED arrival demonstrated greater, sustained SBP reduction in the "after" cohort (mean -187.9 vs. -720.9, p = 0.04). A higher proportion of patients were fed without passing a dysphagia screen in the "before" group (45 vs. 0%, p < 0.001). CONCLUSIONS: Introduction of a neurocritical service without a neuro-ICU at our institution was associated with a trend toward longer ICU LOS and improvement in some key metrics of quality of care for patients with ICH.

Postpartum trifecta: simultaneous eclamptic intracerebral hemorrhage, PRES, and herniation due to intracranial hypotension.

BACKGROUND: In the postpartum patient, sudden depression of consciousness may be caused by a number of etiologies and can result in serious consequences. Rapid, accurate diagnosis allows for specific treatments that optimize outcome, but diagnosis can be challenging in this population. We present a case of postpartum herniation due to intracranial hypotension in a patient with eclampsia, posterior reversible encephalopathy syndrome (PRES), and intracerebral hemorrhage (ICH). METHODS: Case report. RESULTS: A 26-year-old woman developed headache on postpartum day (PD) 1 after cesarean section with epidural anesthesia. Over the next 3 days, she developed progressively worsening headache and hypertension. On PD 5, she had a generalized seizure, leading to endotracheal intubation, propofol infusion, and transfer to our institution. By PD 6, she opened her eyes to voice, followed commands, moved all extremities, and had briskly reactive 4 mm pupils. MRI showed L parasagittal ICH with minimal mass effect, edema consistent with PRES, and brain descent with obliteration of the basal cisterns and tonsillar herniation. Later on PD 6, after diuresis for pulmonary edema, she became unresponsive with a dilated and nonreactive left pupil. She was laid flat for transport to CT, with improvement in arousal and pupil reactivity within 5 min. Intravascular volume was repleted with normal saline and albumin, and she was placed in the Trendelenburg position. Over the subsequent 8 h, she developed a dilated and nonreactive left pupil whenever her head was raised to horizontal. Her head position was gradually successfully raised over 48 h without need for a lumbar epidural blood patch. She was discharged home on PD 13 with only mild left arm dysmetria. CONCLUSIONS: Intracranial hypotension may coexist with other potential causes of cerebral herniation in the postpartum period. Establishing this diagnosis is crucial because its treatment is opposite that of other causes of herniation.

Decompressive laparotomy for refractory intracranial hypertension after traumatic brain injury.

BACKGROUND: Intracranial hypertension is a crucial modifiable risk factor for poor outcome after traumatic brain injury (TBI). Limited evidence suggests that decompressive laparotomy may be an effective treatment for refractory ICH in patients who have elevated intra-abdominal pressure. METHODS: Case report. RESULTS: We present a multi-trauma patient who sustained severe TBI in a motor vehicle collision. Intracranial pressure (ICP) was initially medically managed but became refractory to standard therapies. Emergent decompressive laparotomy performed in the surgical intensive care unit for abdominal compartment syndrome concomitantly improved the patient's ICP. CONCLUSIONS: Elevated intra-abdominal pressure can exacerbate intracranial hypertension in patients with TBI. Recognition of this condition and treatment with decompressive laparotomy may be useful in patients with intracranial hypertension refractory to optimal medical therapy.

Asymmetric posterior reversible encephalopathy syndrome complicating hemodynamic augmentation for subarachnoid hemorrhage-associated cerebral vasospasm.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is a rare complication of hemodynamic augmentation for subarachnoid hemorrhage (SAH)-associated vasospasm. The roles of hyperperfusion and hypoperfusion in the genesis of PRES remain uncertain. METHODS: Case report. RESULTS: We admitted a 35-year-old woman with Hunt & Hess grade II SAH secondary to rupture of a right middle cerebral artery (MCA) aneurysm. This was surgically clipped. Beginning on hospital day 3, she developed recurrent symptomatic vasospasm of the right MCA despite hemodynamic augmentation to a MAP as high as 130 mmHg and endovascular therapy. On hospital day 7, after 36 h of sustained MAP 120-130 mmHg, her level of arousal progressively declined, culminating in stupor and two generalized tonic-clonic seizures. MRI showed widespread, yet markedly asymmetric changes consistent with PRES largely sparing the right MCA territory. After the MAP was decreased to 85-100 mmHg, she had no further seizures. 2 days later she was fully alert with mild left hemiparesis. CONCLUSIONS: PRES is a rare complication of hemodynamic augmentation that should be considered in the differential diagnosis of delayed neurological decline in patients with aneurysmal SAH-associated cerebral vasospasm. The markedly asymmetric distribution of PRES lesions with sparing of the territory affected by vasospasm supports the hypothesis that hyperperfusion underlies the pathophysiology of this disorder.

Intensive versus conventional insulin therapy in critically ill neurologic patients.

BACKGROUND: Previous studies of glycemic control in non-neurologic ICU patients have shown conflicting results. The purpose was to investigate whether intensive insulin therapy (IIT) to keep blood glucose levels from 80 to 110 mg/dl or conventional treatment to keep levels less than 151 mg/dl was associated with a reduction of mortality and improved functional outcome in critically ill neurologic patients. METHODS: Within 24 h of ICU admission, mechanically ventilated adult neurologic patients were enrolled after written informed consent and randomized to intensive or conventional control of blood glucose levels with insulin. Primary outcome measure was death within 3 months. Secondary outcome measures included 90-day modified Rankin scale (mRS) score, ICU, and hospital LOS. RESULTS: 81 patients were enrolled. The proportion of deaths was higher among IIT patients but this was not statistically significant (36 vs. 25%, P = 0.34). When good versus poor outcome at 3 months was dichotomized to mRS score 0-2 versus 3-6, respectively, there was no difference in outcome between the two groups (76.2 vs. 75% had a poor 3-month outcome, P = 1.0). There was also no difference in ICU or hospital LOS. Hypoglycemia (<60 mg/dl) and severe hypoglycemia (<40 mg/dl) were more common in the intensive arm (48 vs. 11%, P = 0.0006; and 4 vs. 0%, P = 0.5, respectively). CONCLUSION: There was no benefit to IIT in this small critically ill neurologic population. This is the first glycemic control study to specifically examine both critically ill stroke and traumatic brain injury (TBI) patients and functional outcome. Given these results, IIT cannot be recommended over conventional control.

Weakness in the ICU: Guillain-Barré syndrome, myasthenia gravis, and critical illness polyneuropathy/myopathy.

BACKGROUND: Weakness in the ICU may be caused by a number of disorders. Guillain-Barré syndrome (GBS) and myasthenia gravis (MG) are examples of conditions that might lead to an ICU admission. The most likely cause of weakness after ICU admission is critical illness polyneuropathy/myopathy (CIP/M). REVIEW SUMMARY: Studies have attempted to determine both clinical and pulmonary function criteria for the proper timing of intubation in severe GBS and MG. Optimizing medical management of patients with GBS, MG, and CIP/M is essential in reducing the high morbidity and mortality associated with these conditions. This includes measures to prevent deep venous thrombosis, gastric and decubitus ulcer prophylaxis, and chest physiotherapy. Both intravenous immunoglobulin (IVIG) and therapeutic plasma exchange (TPE) are probably equal in efficacy for the treatment of GBS, although relapse rates may differ. Treatment of MG crisis with TPE or IVIG must be followed by long-term immunosuppression. Studies suggest possible preventative measures for CIP/M such as tighter glycemic control but there are still no definitive treatments. CONCLUSION: Research to advance our knowledge of the pathogenesis of GBS, MG, and CIP/M is clearly needed to develop more specific and more effective treatments in the future. In the meantime, measures that optimize medical management can be instituted to improve outcomes in patients with these conditions, preferably in a specialized neuroscience ICU setting.

Neurons labeled from locomotor-related ventrolateral funiculus stimulus sites in the neonatal rat spinal cord.

Spinal cord/brainstem preparations from 5- to 8-day-old rats, maintained in vitro, were used to determine the cells of origin and regions of termination of fibers in the superficial ventrolateral funiculus (VLF) at a site from which rhythmic locomotor-like activity can be induced. Rhythmic locomotor-like activity was recorded from lumbar ventral roots after short trains of stimuli (50 Hz for 0.5-2 seconds) delivered to the VLF. Field potential mapping revealed that single VLF stimuli elicited responses in the ipsilateral ventrolateral medulla. Tract-tracing experiments by using biocytin, pressure-injected into the VLF, showed that only a small number of brainstem neurons were labeled and these were scattered bilaterally in the ventrolateral and lateral medulla. Dense concentrations of nerve terminals were found in the lateral reticular nucleus ipsilateral to the stimulation site. Labeled spinal cord neurons included a primary population of large cells distributed bilaterally in lamina VII from T13 to L4, with peak numbers in L2 ipsilaterally and in L3 contralaterally. Intracellular recordings revealed that some L2 and L3 neurons with rhythmic responses to VLF stimulation could be activated antidromically from the VLF, with latencies of less than 1.0 msec. These observations led us to speculate that the superficial VLF carries a locomotor-related tract originating bilaterally in lumbar lamina VII and terminating in the ipsilateral medulla, including the lateral reticular nucleus. This pathway may be part of the spinoreticular or spinoreticulotectal pathway that has been described in many species, the function of which has only loosely been ascribed.

Serotonin syndrome associated with clozapine withdrawal.

IMPORTANCE: We describe a case of serotonin syndrome secondary to clozapine withdrawal and concomitant use of citalopram hydrobromide, a phenomenon that has been rarely reported. OBSERVATIONS: This is a case report of a 47-year-old woman admitted to an academic medical center intensive care unit with coma, hypersalivation, hyperreflexia, and stimulus-induced clonus. The patient received a diagnosis of serotonin syndrome attributed to abrupt clozapine withdrawal with concomitant use of citalopram. She improved only minimally with supportive treatment (intravenous fluids, benzodiazapines, and withdrawal of selective serotonin-reuptake inhibitor) and received cyproheptadine hydrochloride on her third day of symptoms. Four hours after she received the loading dose of cyproheptadine, she was alert and oriented and at her baseline mental status, although some clonus remained. CONCLUSIONS AND RELEVANCE: Serotonin syndrome can result from the abrupt withdrawal of a 5-hydroxytryptamine receptor 2A antagonist from a treatment regimen that also includes a medication that increases serotonin availability.

Intensive care management of acute ischemic stroke.

Despite the success of acute reperfusion therapies for the treatment of acute ischemic stroke, only a minority of patients receive such treatment. Even patients who receive reperfusion therapy remain at risk for further neuronal death through progressive infarction and secondary injury mechanisms. The goal of neurocritical care for the patient with acute ischemic stroke is to optimize long-term outcomes by minimizing the amount of brain tissue that is lost to these processes. This is accomplished by optimizing brain perfusion, limiting secondary brain injury, and compensating for associated dysfunction in other organ systems. Because of the rapid and irreversible nature of ischemic brain injury, it is crucial for best neurocritical care practices to begin as early as possible. Therefore, this chapter will discuss optimal, pragmatic neurocritical care management of patients with acute ischemic stroke during the "golden" emergency department hours from the perspective of the neurointensivist. Major topics include cerebral perfusion optimization; management of cerebral edema; post-thrombolytic care; acute anticoagulation; treatment of commonly associated cardiac and pulmonary complications; fluid, electrolyte and glucose management; the role of induced normothermia and therapeutic hypothermia; and prophylaxis against common complications.

Surfers' myelopathy: a case series of 19 novice surfers with nontraumatic myelopathy.

OBJECTIVE: We report the clinical characteristics of the largest series of nontraumatic spinal cord injury in novice surfers (surfers' myelopathy). METHODS: A retrospective review of the electronic medical record was performed in patients with nontraumatic spinal cord injury associated with surfing identified upon admission to the largest tertiary referral hospital in Hawaii from June 2002 to November 2011. Classification by the American Spinal Injury Association Impairment Scale (AIS) was performed upon admission and at follow-up. Clinical management, including blood pressure measurements and optimization, use of corticosteroids, and diagnostic evaluations, were reviewed. Follow-up information was obtained by clinic visits, telephone interviews, and electronic mail up to 3 years after injury. RESULTS: In 19 patients (14 male) aged 15-46 years, all patients complained of sudden onset of low back pain while surfing, followed by bilateral leg numbness and paralysis progressing over 10-60 minutes. All patients were novice surfers; 17 of 19 were surfing for the first time. On T2-weighted MRI, all patients had hyperintensity from the lower thoracic spinal cord to the conus medullaris. Six of 10 patients who underwent spinal diffusion-weighted MRI showed restricted diffusion in this region. Patients presenting with worse AIS scores had minimal improvement at follow-up. Blood pressure, corticosteroids, and imaging results were not associated with severity of neurologic deficits at follow-up. CONCLUSIONS: Although the cause of surfers' myelopathy is unclear, the rapid onset and presence of restricted diffusion suggest ischemic injury. Admission severity appears to be most predictive of neurologic outcome.

Patterns of increased intracranial pressure after severe traumatic brain injury.

INTRODUCTION: Secondary brain injury due to increased intracranial pressure (ICP) contributes to post-traumatic morbidity and mortality. Although it is often taught that increased ICP begins early after traumatic brain injury, some patients develop increased ICP after the first 3 days post-injury. We examined our data to describe temporal patterns of increased ICP. METHODS: This is a retrospective review of prospectively collected physiologic and demographic data. RESULTS: Seventy-seven patients were included. We identified four patterns of increased ICP: beginning within 72 h (early), beginning after 72 h (late), early increases with resolution, and then a second rise after 72 h (bimodal), and continuously increased ICP. Late increases in ICP occur in 17% of this cohort. Peak day of swelling was day 7 for the "late" rise group and day 4 for the other patients with increased ICP. Forty-four percent of patients showed enlargement of cerebral contusions on follow-up imaging at 24 h post-injury. CONCLUSIONS: Late rises in ICP were not rare in this cohort. This is clinically relevant as it may impact decisions about ICP monitor removal. Differences between groups in age, CT patterns of injury, fluid therapy, osmotic use, and fever were not statistically significant.

Advances in the management of Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is the most common cause of acute paralysis, yet the pathogenesis has still not been fully elucidated and specific evidence-based consensus management guidelines have not been developed. This paper reviews the research of the past year dedicated to determining the pathogenesis of GBS, optimizing current management, and searching for more efficacious treatment alternatives. Several recent studies have investigated whether there are any particular factors that might predict the course of illness and, thereby, dictate the optimal treatment. Proposed evidence-based guidelines for elective intubation, admission to the intensive care unit, and overall management of GBS are summarized. Therapeutic plasma exchange and intravenous immunoglobulin are both treatments that have been shown to have a beneficial effect on the course of GBS. Various modifications of plasmapheresis, as well as other alternative therapies, are currently being investigated.

Suppression of cytochrome P450 2E1 promoter activity by interferon-gamma and loss of response due to the -71G>T nucleotide polymorphism of the CYP2E1*7B allele.

The CYP2E1*7B allele is defined by two nucleotide sequence polymorphisms, -71G>T and -333T>A. The CYP2E1 promoter sequence flanking the -71G nucleotide is consistent with a gamma-interferon activated sequence. Inflammation and interferon (IFN)-gamma suppress expression of CYP2E1 in vivo; however, the exact mechanism is not known. The objectives of this study were to determine whether the CYP2E1 promoter is regulated by IFN-gamma and to examine the influence of the nucleotide substitutions on this function. Treatment of HepG2 cells with IFN-gamma, after transient transfection with a luciferase reporter gene bearing the native CYP2E1 (-71G) promoter sequence resulted, in a dose-dependent reduction of luciferase activity. In contrast, no suppression was observed in cells transfected with the *7B allele promoter (-333A and -71T) nor a CYP2E1 plasmid containing only the -71T polymorphism. These data indicate that IFN-gamma suppresses native CYP2E1 promoter activity and that the -71G is critical for this response.