Acute Neurological Dysfunction Research Articles

Five‐Year Results of 121 Consecutive Patients Treated With Extracorporeal Membrane Oxygenation at Fu Wai Hospital

Since 2004, our institution has adopted venoarterial (VA) extracorporeal membrane oxygenation (ECMO) for patients who otherwise could not be weaned from cardiopulmonary bypass and patients experiencing cardiogenic shock and/or pulmonary dysfunction unresponsive to conventional treatments. In this study, we reviewed our experience with ECMO support and tried to identify predictors of in-hospital mortality. We retrospectively analyzed the clinical records of 121 consecutive patients receiving ECMO. Patients were divided into adult and pediatric groups and analyzed separately. Demographics, clinical characteristics at the time of ECMO implantation, ECMO-related complications, and in-hospital mortality were collected. Logistic regression analyses were performed to investigate predictors of mortality. A P value ≤ 0.05 was accepted as significant. Sixty-eight adult patients and 53 pediatric patients were included in this study. In adult patients, 52 were weaned from ECMO and 43 survived upon discharge. After univariate analysis, ECMO setup location, receiving cardiopulmonary resuscitation before ECMO, leg ischemia, hemolysis, acute renal failure (ARF), neurological dysfunction, and multiple organ dysfunction syndrome were associated with in-hospital death. In multiple logistic regression analyses, leg ischemia (OR 14.68, 95% CI 1.67-129.1), ARF (OR 12.14, 95% CI 2.5-58.8), and neurological dysfunction (OR 49.0, 95% CI 2.28-1051.96) were risk factors associated with in-hospital mortality. Patients put on ECMO in the operating room had a better chance of survival (OR 0.078, 95% CI 0.013-0.417). In pediatric patients, 30 were weaned from ECMO and 26 survived upon discharge. After univariate analysis, age, weight, and eight ECMO complications were associated with in-hospital death. In multiple logistic regression analyses, ARF (OR 24.0, 95% CI 4.2-137.3) was a risk factor associated with in-hospital mortality. A P value of 0.921 and >0.99 was obtained by the Hosmer-Lemeshow test, and the area under the curve was 0.863 and 0.867 for adult and pediatric patients, respectively. The overall survival rate was 57%. ECMO is a justifiable alternative treatment for refractory cardiac and/or pulmonary dysfunction which could rescue more than 50% of carefully selected patients. Higher survival rates could be achieved by preventing ECMO complications.

Symptomatic paroxysmal dysarthria-ataxia in demyelinating diseases

Paroxysmal dysarthria-ataxia syndrome (PDA) is a rare neurological disorder that can be either primary or symptomatic of acute neurological dysfunction. Episodes of symptomatic PDA are poorly documented and there are no video reports. We describe the cases of two patients with symptomatic PDA related to demyelinating diseases. Detailed studies of the patients' speech disorders showed that the dysarthria and gait disorders were of the ataxic type in both cases. Both patients had midbrain lesions at or below the level of the red nucleus, confirming that this area is critically involved in PDA. The best clinical signs for distinguishing between symptomatic and primary PDA are adult onset and short (<1 min) episodes in the former. If these signs are present, brain MRI should be used to identify a cause of symptomatic PDA.

Injectable interferon beta-1b for the treatment of relapsing forms of multiple sclerosis

Multiple sclerosis (MS) is chronic inflammatory and demyelinating disease with either a progressive (10%-15%) or relapsing-remitting (85%-90%) course. The pathological hallmarks of MS are lesions of both white and grey matter in the central nervous system. The onset of the disease is usually around 30 years of age. The patients experience an acute focal neurologic dysfunction which is not characteristic, followed by partial or complete recovery. Acute episodes of neurologic dysfunction with diverse signs and symptoms will then recur throughout the life of a patient, with periods of partial or complete remission and clinical stability in between. Currently, there are several therapeutic options for MS with disease-modifying properties. Immunomodulatory therapy with interferon beta-1b (IFN-β1b) or -1a, glatiramer and natalizumab shows similar efficacy; in a resistant or intolerant patient, the most recently approved therapeutic option is mitoxantrone. IFN-β1b in patients with MS binds to specific receptors on surface of immune cells, changing the expression of several genes and leading to a decrease in quantity of cell-associated adhesion molecules, inhibition of major histocompatibility complex class II expression and reduction in inflammatory cells migration into the central nervous system. After 2 years of treatment, IFN-β1b reduces the risk of development of clinically defined MS from 45% (with placebo) to 28% (with IFN-β1b). It also reduces relapses for 34% (1.31 exacerbations annually with placebo and 0.9 with higher dose of IFN-β1b) and makes 31% more patients relapse-free. In secondary-progressive disease annual rate of progression is 3% lower with IFN-β1b. In recommended doses IFN-β1b causes the following frequent adverse effects: injection site reactions (redness, discoloration, inflammation, pain, necrosis and non-specific reactions), insomnia, influenza-like syndrome, asthenia, headache, myalgia, hypoesthesia, nausea, paresthesia, myasthenia, chills and depression. Efficacy of IFN-β1b in relapsing-remitting MS is higher than that of IFN-β1a, and similar to the efficacy of glatiramer acetate. These facts promote IFN-β1b as one of the most important drugs in the spectrum of immunological therapies for this debilitating disease.

Clinical management of canine babesiosis

To review and summarize current information regarding epidemiology, pathogenesis, and pathophysiology leading to the various clinical syndromes associated with canine babesiosis. Diagnosis, treatment, preventative strategies, and zoonotic implications are discussed. Babesiosis is caused by hemoprotozoa of the genus Babesia. Numerous species of Babesia exist worldwide. An increased incidence of babesiosis is described, especially in North America. The babesial organism spends the majority of its life cycle within the erythrocyte of the definitive host, resulting in hemolysis, with or without systemic complications. Definitive diagnosis depends on direct visualization of the organism on blood smear or polymerase chain reaction. A positive serologic antibody test indicates exposure with or without active infection. Antiprotozoal drugs, antimicrobials, and supportive care are the mainstays of babesiosis therapy. Prognosis depends on the severity of disease, which in turn depends on both organism and host factors. Clinical syndromes associated with a poorer prognosis include red biliary syndrome, acute renal failure, acute respiratory distress syndrome, neurologic dysfunction, acute pancreatitis, cardiac dysfunction, and hypoglycemia.

The Role of Head Computer Tomographic Scans on the Management of MICU Patients With Neurological Dysfunction

Neurological dysfunction is common in patients admitted to the medical intensive care unit (MICU). However, the indications for head imaging in those patients are unclear. The objective of this study was to assess whether clinical variables would be useful in selecting patients who are likely to have an abnormality on head computerized tomographic (CT) scanning and to determine the impact of such scans on management decisions. We reviewed the charts of 740 patients admitted to our MICU between October 2002 and July 2004. A total of 123 patients (16.6%) had a head CT scan performed, with a new finding being present in 26 (21.1%) patients. In the patients with a new CT finding, there was a change in diagnosis in 11 (42%) patients and a change in treatment in 6 (23%) patients. Logistic regression analysis failed to determine any clinical characteristic that could predict a new finding on the CT scan. This study suggests that clinicians should have a low threshold for ordering a CT scan in MICU patients with acute neurological dysfunction.

Nutrition Support After Neonatal Cardiac Surgery

Congenital heart disease is the most common birth defect in the United States, with an estimated frequency of approximately 12-14 of 1000 live births per year. Neonates with congenital heart disease often need palliative or corrective surgery requiring cardiopulmonary bypass during the first weeks of life. The neonate undergoing cardiopulmonary bypass surgery experiences a more profound metabolic response to stress than that seen in older children and adults undergoing surgery. However, compared with older children and adults, the neonate has less metabolic reserves and is extremely vulnerable to the negative metabolic impact induced by stress, which can lead to suboptimal wound healing and growth failure. There are complications associated with the metabolic derangements of neonatal surgery requiring cardiopulmonary bypass, including but not limited to acute renal failure, chylothorax, and neurological dysfunction. This article discusses the importance of nutrition and metabolic support for the neonate undergoing cardiopulmonary bypass and the immediate postoperative nutrition needs of such a patient. Also, this article uses a case study to examine the feeding methodology used at one particular institution after neonatal cardiac surgery. The purpose of the case study is to provide an illustration of the many factors and obstacles that clinicians often face in the provision and timing of nutrition support.

Brain Imaging in Intensive Care Medicine

The management of severe brain injury requires a comprehensive approach in which imaging is an indispensable complement to the clinical and physiological information acquired at the bedside. Neuroimaging methods are routinely used in the diagnosis and prognosis of a broad spectrum of patients with acute neurological dysfunction. With incremental theoretical and technological refinements, imaging modalities are helping to unravel fundamental questions regarding the pathophysiology and neuroplasticity associated with critical neurological injury, and it is anticipated that this knowledge will lead to new and effective therapeutic interventions. We review some of the established and emerging structural and physiological imaging methods, and discuss their applications in patients with critical injuries including trauma and encephalopathy due to anoxia, liver failure, and sepsis.

PRO: Anesthesia-Induced Developmental Neuroapoptosis: Status of the Evidence

PRO: Anesthesia-Induced Developmental Neuroapoptosis: Status of the Evidence

Diffuse Cerebral Vasculopathy in a HIV-Positive Patient with Recurrent Strokes

The causes of ischemic stroke in the young adult are diverse. Human immunodeficiency virus (HIV) infection-related vasculopathy is usually not included in the list of differential diagnoses. HIV-positive patients may present with acute neurologic dysfunction of different causes, among which cerebral infarction is an uncommon one. Herein, we report a HIV-infected young man who suffered from recurrent ischemic strokes with evidence of cerebral vasculopathy on serial magnetic resonance images.

Short-Term Neurophysiologic Consequences of Intrapartum Asphyxia in Piglets Born by Spontaneous Parturition

Piglets appear to be neurologically sensitive to intrapartum asphyxia. Our aim was to investigate the short-term neurophysiologic consequences of intrapartum asphyxia in piglets. We studied 10 piglets suffering intrapartum asphyxia and 10 control piglets. Glucose and blood gas levels, tympanic membrane temperature, and body weight were measured within the first 2 min after birth. Animals were followed up for a 5-day period. As surrogated markers of piglets’ neurological function, a viability score and the time elapsed from birth to the first contact with the maternal udder were recorded. In the control group, temperature and blood pH levels at birth were significantly higher (p ≤ .001), whereas calcium, lactate and PCO2 levels were statistically lower (p ≤ .05) than in the piglets experiencing intrapartum asphyxia. Lower temperature and blood pH levels as well as higher blood PCO2 and lactate levels were observed in piglets with lower viability scores and in piglets with prolonged times until first udder contact. At the end of the study, asphyxiated piglets weighed on average 200 g less (p = .023) than control piglets. In conclusion, intrapartum asphyxia in spontaneously born piglets was associated with signs of acute neurological dysfunction and lower weight gain, supporting the hypothesis that they may be used as a naturalistic model for the study of asphyxia in newborns.

Intramedullary spinal arteriovenous malformation in a boy of familial cerebral cavernous hemangioma

The coexistence of spinal arteriovenous malformation (AVM) and a familial cerebral cavernous hemangioma (CCH) is extremely rare. A 9-year-old boy suddenly developed severe paraplegia and urinary dysfunction. Spinal magnetic resonance imaging (MRI) scan revealed a cervical and upper thoracic intramedullary lesion. Due to acute neurological dysfunction, the patient underwent emergency surgical exploration. An intramedullary vascular lesion was found and excised. Pathologically, AVM was noted. After the surgery, the boy was ambulatory with left lower limb stiffness. MRI scan of the brain revealed multiple cerebral cavernous hemangioma. Symptomatic multiple CCH in his mother and grandmother were also noted. We concluded that the presence of spinal AVM should be suspected if the patient with familial CCH develops the signs of space-occupying lesion of the spinal cord, facilitating early diagnosis of the spinal AVM.

Deformable Emboli and Inflammation: Temporary or Permanent Damage?

Neurologic sequelae after cardiopulmonary bypass have a multi-factorial etiology. Although it is typically thought that a neurologic dysfunction means a focal lesion, symptoms of a brain disorder can be initiated by metabolic disruption such as from hyper- or hypoglycemia, hypercalcemia, renal and hepatic injury, fatigue, and anesthesia. However, one of the most important causes of acute neurologic dysfunction is edema. Brain swelling is associated with the systemic inflammatory response and the passage of deformable microemboli. The larger question is whether acute symptoms associated with brain swelling because of a breakdown of the blood-brain barrier contributes to a long-term negative outcome caused by cell loss.

Bilateral Complete Optic Atrophy and Hemorrhagic Infarction of the Putamen Caused by Methanol Intoxication

Methanol is a potent toxic substance for the optic nerves. Even small amounts of ingested methanol can acute permanent neurological dysfunction and irreversible blindness. Methanol intoxication can cause severe visual dysfunction and death. We present a case of a 25 years old admitted to our clinic with bilateral optical atrophy after drinking eau de cologne.

Minocycline Blocks Acute Bilirubin-Induced Neurological Dysfunction in Jaundiced Gunn Rats

Background: Extreme hyperbilirubinemia is treated with double volume exchange transfusion, which may take hours to commence. A neuroprotective agent that could be administered immediately might be clinically useful. Minocycline, an anti-inflammatory and anti-apoptotic semisynthetic tetracycline, prevents hyperbilirubinemia-induced cerebellar hypoplasia in Gunn rats. Acute brainstem auditory evoked potential (BAEP) abnormalities occur after giving sulfadimethoxine to 16-day-old jaundiced Gunn rats to displace bilirubin into tissue including brain. Objective: To assess whether minocycline is neuroprotective in this model of acute bilirubin encephalopathy. Methods: We recorded BAEPs at baseline and 6 h after injecting sulfadimethoxine. Minocycline 0.5 mg/kg (n = 4), 5 mg/kg (n = 9), 50 mg/kg (n = 9) or 500 mg/kg (n = 3, all died) was administered 15 min before sulfadimethoxine (0 h). Controls received saline followed by either sulfadimethoxine (n = 13) or saline (n = 7). Results: At 6 h total plasma bilirubin decreased from 10.84 ± 0.88 mg/dl (mean ± SD) to 0.70 ± 0.35 mg/dl (p <10^–9) in all sulfadimethoxine-injected groups. At 6 h, there was complete protection against decreased amplitudes of BAEP waves II and III and increased I-II and I-III interwave intervals (brainstem conduction times corresponding to I–III and I–V in humans) with 50 mg/kg minocycline, and partial protection with lower doses. Conclusions: Minocycline 50 mg/kg 15 min prior to an intervention that normally produces acute bilirubin neurotoxicity is neuroprotective in jaundiced Gunn rat pups. Further studies are needed to investigate the temporal course and mechanism of neuroprotection. Minocycline, administered immediately, may be clinically useful in treating extreme neonatal hyperbilirubinemia and preventing kernicterus. We believe our model provides an efficient in vivomodel to screen and evaluate new agents that are neuroprotective against bilirubin toxicity and kernicterus.

Viral myelitis: An update

Viral infections of the central nervous system are uncommon but are important in the differential diagnosis of acute myelopathy. Acute viral myelitis can present as acute flaccid paralysis (poliomyelitis) or neurologic dysfunction due to involvement of the white matter. The latter usually affects only part of the transverse expanse of the spinal cord and manifests as asymmetric motor and sensory symptoms. When both halves of the spinal cord are affected, the entity is referred to as acute transverse myelitis and patients exhibit uniformly symmetric weakness, sensory loss, and urinary bladder involvement. Acute flaccid paralysis is due to cytolytic infection of anterior horn cells. When the involvement is mainly white matter, virus-specific and autoimmune host cellular immune responses are believed to contribute to spinal cord damage. Acute flaccid paralysis is caused by polioviruses-1, -2, and -3; coxsackieviruses A and B; enterovirus-71; and flaviviruses, including West Nile virus. Involvement of spinal cord white matter may be associated with infection by many different viruses; however, in most cases a specific viral cause is never determined. Chronic myelitis may be due to either direct infection of the spinal cord by human T-cell lymphotrophic virus-1 (HTLV-1), or a metabolic disturbance due to HIV-1 infection in AIDS patients; no other human virus is known to chronically infect the spinal cord without involvement of the brain. The principal treatment is antiviral drugs immediately upon virus isolation or the identification of a viral sequence by PCR and, when indicated, high doses of methylprednisolone.

Vancomycin Resistant Enterococcus (VRE) Bloodstream Infections (BSI) in Patients with Hematological Malignancies: Is the Sick Getting Sicker?.

Patients with hematologic malignancies and hematopoietic stem cell transplant (HSCT) recipients are at high risk for bacterial BSI. Data describing the prognosis and outcomes of VRE BSI in this patient population is limited. We performed a retrospective chart review of all cases of VRE BSI occurring between February 1996 and December 2002 on the Leukemia/HSCT unit at Barnes-Jewish Hospital. 68 episodes of VRE BSI were observed in 60 patients with acute (53%) or chronic (8%) leukemia, NHL (22%), or other malignant hematologic disorders (17%).46 were autologous (13%), related (32%) and URD (32%) transplant recipients. Forty days prior to the VRE BSI, 70% were colonized with VRE, 95% had broad-spectrum antibiotic exposure and 42% had non-VRE BSI, 35% pneumonia, 22% CMV reactivation, 10% fungal infection. At the time of the VRE BSI, 42% of allograft recipients had active acute GVHD and 32% chronic GVHD. Only 57% were neutropenic, 52% had refractory/relapsed malignancy, and 60% had end organ dysfunction with a median APACHE II score of 17. VRE was easily eradicated from the bloodstream after initiation of anti-VRE therapy (median time to clearance 1 (range 1–9) day). 3 patients died within 48 hours of the VRE BSI from causes unrelated to the BSI. Median survival after VRE BSI was 19 days. Only 4 deaths were directly attributable to the VRE BSI. Age, ECOG PS ≥ 2 on admission, HSCT, pneumonia, mechanical ventilation, acute neurologic dysfunction, receipt of anti-fungal drugs, and low APACHE II score were significant factors associated with death by univariate analysis, while pneumonia, receipt of anti-fungal drugs, and low APACHE II score at the time of the VRE BSI remained significant after multivariate analysis.In summary, our analysis suggests that in patients with hematological malignancies, VRE does not have the microbiologic behavior of a virulent pathogen. VRE BSI may simply be a marker of these patients's already existing critical medical condition.

Reliability of clinical balance tests and subjective ratings in dizziness and disequilibrium

The aim was to assess (i) the test–retest and inter-rater reliability of, and (ii) the relationships between, commonly used clinical balance tests and subjective ratings in subjects with dizziness and disequilibrium. Fifty subjects (26 men and 24 women, mean age 63 years) with dizziness and disequilibrium following acute unilateral vestibular loss or central neurological dysfunction were tested with static and dynamic clinical balance tests, visual analogue scales (VAS), University of California Los Angeles Dizziness Questionnaire (UCLA-DQ), Dizziness Beliefs Scale (DBS), European Quality of Life questionnaire (EQ-5D), Dizziness Handicap Inventory (DHI), and Hospital Anxiety and Depression Scale (HADS). Most tests showed good test–retest and inter-rater reliability. Few correlations were seen between objective and subjective tests, but several correlations were found between the different subjective instruments. Sharpened Romberg's test eyes closed, standing on foam eyes closed, standing on one leg eyes open and walking in a figure-of-eight are recommended as reliable and appropriate clinical balance tests in subjects with dizziness and disequilibrium. Subjects with central lesions may have difficulties when rating their symptoms on VAS. Total scores rather than scores for separate items are recommended for UCLA-DQ and DHI.

Cannabis use and cerebrovascular disease.

Cannabis is the most commonly abused illicit drug and is often considered innocuous. However, cases of acute onset neurologic dysfunction occurring in relation to cannabis use have been described and corresponding cerebral imaging studies have documented focal ischemic changes and vessel abnormalities. This article reviews all reported cases of presumed cannabis related cerebral ischemic events in the medical literature, as well as pertinent human and animal experimental studies on the cardiovascular and cerebrovascular effects of cannabis. Cannabis use seems to have been causally related to several instances of cerebral ischemia and infarction. Proposed etiologic mechanisms have included cerebral vasospasm, cardioembolization, and systemic hypotension with impaired cerebral autoregulation, but most of the available data points to a vasospastic process. The exact relation of cannabis to cerebrovascular disease remains to be determined.

Necrosis estriatal bilateral infantil

Necrosis of the basal ganglia (NBG) is an uncommon condition in childhood. Cases of NBG have been reported in connection with metabolic disorders, infections, degenerative conditions, intoxications, head injuries and hypoxic-ischemic encephalopathies. The commonest clinical features include alteration of consciousness, chorea-athetoic or dystonic movements, spasticity, contractures of the limbs and convulsions. We describe the case of an eight year old girl, who after having clinical gastroenteritis, developed acute neurological dysfunction, associated with images on cranial computerized axial tomography (CAT) showing a possible intracranial tumour and magnetic resonance (MR) studies showing bilateral hypodensity of the basal ganglia. Three months later magnetic resonance showed that these lesions had almost completely disappeared. This supports the diagnosis of post-infectious lesions. The clinical course is very variable. Cases with a previous history of infection have a better prognosis. In our patient treatment was started with corticosteroids. She made a good recovery and was sent home with no sequelae five days later. The new imaging techniques (CAT and MR) have led to more cases of selective involvement of the basal ganglia being diagnosed. MR is the most specific technique for diagnosis in these patients. Although there is no effective specific treatment, treatment with biperidine, thyrotropic hormone and corticosteroids have been used with no apparent effect on the course of the disorder.

Brain injury after cerebral arterial air embolism in the rabbit as determined by triphenyltetrazolium staining.

Microscopic cerebral arterial air embolism (CAAE) occurs commonly during cardiac surgery and causes acute and chronic nonfocal neurologic dysfunction. Nevertheless, most neuroimaging studies do not detect brain injury after cardiac surgery. Using a rabbit model, the authors hypothesized they could detect and quantitate severe brain injury and infarction 24 h after microscopic CAAE using the vital stain triphenyltetrazolium chloride. Experiments were conducted in methohexital anesthetized New Zealand white rabbits. Surgical shams (n = 5) underwent surgery but had no neurologic insult. Positive controls (n = 3) received 200 microl/kg of intracarotid air. Other animals were randomized to receive either 50 microl/kg intracarotid air, which produces microscopic CAAE (n = 18), or 300 microl intracarotid saline (control, n = 18). Outcomes included somatosensory evoked potential amplitude at 90 min, neurologic impairment score at 4 and 24 h (0 [normal] to 99 [coma]), and percentage of nonstaining brain at 24 h using color-discrimination image analysis. Severely injured or infarcted brain does not stain with triphenyltetrazolium chloride. Surgical shams had little neurologic impairment and a small amount of nonstaining brain at 24 h (5.2 +/- 2.4%; mean +/- SD). Positive controls had profound neurologic impairment and large amounts of nonstaining brain (40-97%). Ninety-minute somatosensory evoked potential amplitude was less in animals receiving 50 microl/kg air versus saline: 38 +/- 28% versus 102 +/- 32%, respectively, P < 1 x 10(-7). Neurologic impairment scores were greater in animals receiving 50 microl/kg air versus saline: at 4 h, 43 +/- 16 versus 23 +/- 9, P < 1 x 10(-7); at 24 h, 24 +/- 12 versus 15 +/- 8, P = 0.013. Nevertheless, there was no difference between 50 microl/kg air and saline in nonstaining brain: 5.5 +/- 2.9% versus 6.8 +/- 5.4%, P = 0.83. Neurologic injury after CAAE is dose-dependent. Although microscopic CAAE causes somatosensory evoked potential abnormalities and neurologic dysfunction, severe cerebral injury or infarction is not present at 24 h. The author's findings are consistent with clinical imaging studies that suggest microscopic CAAE causes neurologic dysfunction even though overt infarction is absent.