Ye-Ting Zhou

Guillain–Barré syndrome and encephalitis/encephalopathy of a rare case of Northern China acute severe hepatitis E infection

In recent years, cases of Guillain–Barré Syndrome (GBS) in patients with acute hepatitis E virus (HEV) infection were increasingly reported [1–3]. Here, we report a rare case of GBS and encephalitis/encephalopathy simultaneous due to acute severe HEV infection in a Chinese patient. A 64-year-old male was admitted to our hospital, with acute flaccid paralysis for at least 7 days. He had a history of a febrile illness with cough and nasal congestion 12 days previously. He had not being given any hepatotoxic or neurotoxic drugs or vaccinations. His temperature was 36.8 C. He was in mental slowness and short-term memory deficits. Medical examination revealed jaundice and tender hepatomegaly. There was no splenomegaly and free fluid in abdomen. Neurological examination showed bilateral upper limbs weakness of grade 3/5 and lower limbs of grade 2/5, generalized hypotonia and symmetric hyporeflexia in the upper limbs and areflexia in the lower limbs. Pinprick perception was reduced in a glove-and-sock distribution, and plantar responses were flexor. The results of blood tests at the first days admitted to hospital are shown in Table 1. Brain MRI was performed on admission day 1 and a mild high signals was showed in the hippocampus bilaterally. On the next week of his admission, he developed respiratory failure, and was moved to the intensive care unit (ICU) for mechanical ventilation. His temperature was 38.1 C. His consciousness was in confusion state with a GCS of E4V3M4. The results of related tests during the ICU stay are shown in Table 1. Finally, GBS and encephalitis/encephalopathy due to an acute severe hepatitis E was diagnosed and he was given immunoglobulin intravenously. Seven days after admission to ICU, he was gradually weaned from mechanical ventilation as his muscle power improved. Forty days later, he was discharged. On followup, 12 months later, he had complete recovery. Several neurological manifestations, including polyradiculopathy, GBS, bilateral brachial neuritis, proximal myopathy, and encephalitis or encephalopathy, have been described in patients with HEV infection [4, 5]. Acute HEV–GBS reported is still less than 20 cases in the medical literature. The diagnosis of HEV infection was either confirmed by the positive for anti-HEV IgM or by the presence of HEV RNA in the serum. In our patient, the evidence for an acute hepatitis E infection was based on serological analysis to detect the positive for anti-HEV IgM, while no detect positive for others hepatitis. Furthermore, the diagnosis of severe HEV–GBS was confirmed by serological, cerebrospinal fluid (CSF), and electromyography. The prodromal symptoms of GBS are usually the symptoms of upper respiratory tract infection or diarrhea [6]. Although the evidence of a HEV infection in patient’s nasopharynx had not been proven, our patient had upper respiratory infection 12 days before admission. Thus, we think that a prior infection in our patient may be from his nasopharynx. X.-D. Chen J.-J. Zhou Y.-W. Wang D.-M. Tong (&) Department of Neurology, Affiliated Shuyang People’ Hospital, XuZhou Medical College, No. 9, Yingbin Road, Shu town, Jiangsu, China e-mail: tongdaoming@163.com

Metabolic Syndrome Is a Strong Risk Factor for Minor Ischemic Stroke and Subsequent Vascular Events

Background Minor ischemic stroke (MIS) represents a major global public health problem worldwide due to high incidence. The aim of this study was to investigate whether metabolic syndrome (MetS) is a strong risk for MIS and subsequent vascular events (SVE). Methods A retrospective cohort study was performed examining symptomatic MIS in a Chinese neurologic outpatient population aged over 25 years without history of stroke. MetS was defined using the International Diabetes Federation criteria. MIS was diagnosed by magnetic resonance imaging-diffusion weighted images or fluid-attenuated inversion recovery. Results Of 1361 outpatients, a total of 753 (55.3%) patients were diagnosed with MIS; of them, 80% had a score of 0 using the MIS had a 0 score on the National Institutes of Health Stroke Scale. Among these, 303 (40.2%) individuals with MIS were diagnosed with MetS. Diagnosed of MIS with MetS significantly correlated with abdominal obesity (30.7% v.s 18.0%), hypertension (91.1% v.s 81.6%), increased blood glucose (6.9±2.4 v.s 5.0±0.4), dyslipidemia (78.2% v.s 48.2%), and SVE (50.5% v.s 11.3%) when compared with the controls group. On adjusted analysis, the risk of SVE was also significantly associated with three additional MetS criterion (RR,9.0; 95% CI, 5.677–14.46). Using Cox proportional analysis, risk of SVE in patient with MIS was significantly associated with MetS (RR, 3.3; 95% CI, 1.799–6.210), older age (RR, 1.0; 95% CI, 1.001–1.048), and high blood glucose (RR,1.1; 95%CI, 1.007–1.187). Conclusions The MetS is a strong risk factor for MIS, and patients presenting with MIS and MetS are at a high risk of SVE. Further studies are required to determine the improvement of Mets prevention in the reduction of MIS and SVE.

Hemorrhagic Pure Sensory Strokes in the Thalamus and Striatocapsular Area: Causes, Clinical Features and Long-Term Outcome

Background: Although there have been sporadic reports of patients with hemorrhagic pure sensory strokes (HPSS) in the thalamus and striatocapsular areas, the causes, clinical featuring and long-term outcome have not been adequately investigated. Methods: We recruited 7 consecutive patients without hemiparetic stroke who had HPSS in the thalamic and striatocapsular areas. A CT scan was performed to verify brain imaging patterns, and their causes, clinical featuring and long-term outcome were observed. Results: We studied 7 patients who had HPSS in the thalamic and striatocapsular areas as seen in CT scans. The 7 patients had hypertension, and small hemorrhages were found in the thalamus of 2 patients and in the posterior quarter of the posterior limb of the internal capsule in 4 patients; only 1 patient had a microhemorrhage in the thalamus. The volume of the hemorrhages ranged from 0.3 to 6.3 ml, with a mean of 2.3 ± 1.9 ml. Three patients showed a decreased sense of spinothalamic modality, and position and vibration senses were spared. Four patients showed a sensory deficit of both spinothalamic and medial lemniscal type. The outcomes were excellent and without post-stroke pain in all patients. Conclusion: HPSS in the thalamus and striatocapsular area are usually small hemorrhages or microhemorrhages from rupturing of the microvessels or the branches of small vessels. HPSS only have an impact on the adjacent sensory nucleus or pathway, and have a good outcome without post-stroke pain.

Early Prediction and Outcome of Septic Encephalopathy in Acute Stroke Patients With Nosocomial Coma

Background Septic encephalopathy (SE) is the most common acute encephalopathy in ICU; however, little attention has been focused on risk of SE in the course of acute stroke. Our aim is to investigate the early prediction and outcome of SE in stroke patients with nosocomial coma (NC). Methods A retrospective cohort study was conducted in an ICU of the tertiary teaching hospital in China from January 2006 to December 2009. Ninety-four acute stroke patients with NC were grouped according to with or without SE. Risk factors for patients with SE were compared with those without SE by univariate and multivariate analysis. Results Of 94 stroke patients with NC, 46 (49%) had NC with SE and 48 (51%) had NC without SE. The onset-to-NC time was significant later in stroke patients with SE than those without SE (P < 0.01). There was a significant difference in body temperature, heart rate, respiratory rate, white blood cell (WBC), systolic blood pressure (SBP), diastolic blood pressure (DBP), systemic inflammatory response syndrome (SIRS), acute respiratory failure, septic shock, hypernatremia, and sequential organ failure assessment (SOFA) score between the SE and non-SE group (P < 0.05). On a repeat head imaging, vasogenic edema (P = 0.023) and subcortical white matter lesions (P = 0.011) were significantly higher in patients with SE than those without SE, while hematoma growth (P = 0.000), infarction progress (P = 0.003), and recurrent subarachnoid hemorrhage (SAH) (P = 0.011) were significantly lower in patients with SE than those without SE. Patients with SE had higher adjusted rates of fever ≥ 39 °C (odds ratio (OR): 2.753; 95% confidence interval (CI): 1.116 - 6.794; P = 0.028) and SIRS ≥ 3 items (OR: 6.459; 95% CI: 2.050 - 20.351; P = 0.001). The 30-day mortality in stroke patients with SE was higher than those without SE (76.1% vs. 45.8%, P = 0.003). Conclusion High fever and severe SIRS are two early predictors of stroke patients with SE, and survival rates were worse in stroke patients with SE than those without SE.

Long-term outcome in patients with subarachnoid hemorrhage with negative CT scan.

Despite improvements in diagnostic imaging, the initial interpretation of third-generation head CT scans to detect subarachnoid hemorrhage (SAH) has not reached 100% sensitivity [1,2]. The proportion of patients with SAH and a negative CT scan was 3.3% within 0 to 3 days of onset and 3.0% within 4 to 14 days of onset [3]. Another study showed that the proportion of patients with SAH and a negative CT may be close to 7% within 3 days [4].This indicates that SAH with a negative CT scan is not rare. Recurrent hemorrhage remains a serious consequence of aneurysmal SAH, with a fatality rate of approximately 70%, but it may be the most preventable cause of poor outcomes [5]. However, the recently published guidelines by the American Heart Association do not clear and definie the long-term outcome for patients who have SAH with a negative CT scan [5].This study addresses the longterm outcomes of SAH with a negative CT scan. A prospective study of outcomes of consecutive patients with SAH with a negative CT scan from January 1995 to September 2009 was commenced at a university teaching hospital in China. Twenty-eight patients included in the study did not have SAH visible on head CT, and the diagnosis of SAH was based on the results of a lumbar puncture (LP) with the xanthrochromia of the cerebrospinal fluid. Patients with spontaneous aneurysmal and nonaneurysmal SAH were included. Individuals with SAH caused by trauma, traumatic taps, arteriovenous malformation or other secondary causes were excluded. A cerebral angiography was performed within 3–5 days after admission in some patients. We divided these patients into two groups based on whether they agree or rejected angiography: an angiography group and a nonangiography group. Nine of 17 patients of the angiograpphy group showed an aneurysmal pattern of hemorrhage. In addition to eight patients for surgery therapy, the other one patient was not to receive surgery therapy. Those patients who were surviving 30 days after onset of the initial SAH were followed continuously. Rehemorrhage after the initial SAH was defined as a sudden headache with or without coma, and the new bleed was confirmed by head CT or LP. Follow-up was begun on October 10, 2009. Patients or their surrogates were interviewed either by telephone or in person. Subarachnoid hemorrhage and data regarding any rehemorrhages include the date, postmortem reports, and imaging data. Global outcome and functional status were assessed with the modified Rankin Scale (mRS = 0–6; 0 = no symptoms or disability; 6 = dead). Data for the survival and rehemorrhage analyses were extracted in April 2010. Data for the overall death and rehemorrhage analyses were compiled for the initial hospitalization after the primary SAH and from the date of the first SAH until the end September of 2009. A P value <0.05 was considered to be statistically significant. Twenty-eight patients who underwent an initial SAH with a negative CT were enrolled during their first hospitalization. One (fatal rehemorrhage) of 11 patients in the nonangiography group died during the first hospitalization. Therefore, the 27 remaining patients were enrolled and contacted for further follow-up. Table 1 shows the baseline characteristics of the patients in this study. As of April 2010, there were 15 survivors in the angiography group (including the eight patients for surgery therapy) and five survivors (except one lost to follow-up and four died) in nonangiography group. The rate of complete loss of follow-up was

Sepsis Associated Encephalopathy Predicts Poor Outcome among Acute Supratentorial Intracerebral Hemorrhage with Coma

Background: Both sepsis associated encephalopathy (SAE) and supratentorial intracerebral hemorrhage (SICH) are a significant cause of coma and death throughout the world. The aim of this study was to investigate whether the presence of SAE among acute SICH with coma would predict a poor outcome. Methods: A retrospective of consecutive patients was selected for study. All registered an adult intensive care unit (ICU) of university teaching hospital between June, 2013 and July, 2015. Brain computed tomography (CT) scans were analyzed on admission and at coma onset or after coma onset. Univariate and Cox regression analyses were performed. Results: A total of 379 SICH with coma was studied. Among these, 245 (64.6%) SICH patients with coma due to SAE and 134 (35.4%) SICH with coma no SAE was compared. Our data showed that the frequency of the SAE in SICH patients increased at about double the proportion over the four SIRS criteria. The SICH patients with SAE were more likely to present with infection (100% vs 35.8%) and multiple organ failure (1.2 ± 0.9 vs 0.1 ± 0.3), especially nosocomal brain failure (60.4%). The 30 days mortality was significantly higher in the SAE group than those who did not (60.8% vs 11.2%). In Cox multivariate logistic analysis, the SAE (RR, 4.4; 95% CI, 2.296 - 8.422; P = 0.000) was more likely to related to risk on death in SICH patient with coma. Conclusions: SAE is a frequent complication of SICH, which greatly increased risk of death among SICH patients with coma.

Risk factors for nosocomial nontraumatic coma: sepsis and respiratory failure.

Background Coma’s are a major cause of clinical deterioration or death. Identification of risks that predispose to coma are important in managing patients; however, the risk factors for nosocomial nontraumatic coma (NNC) are not well known. Our aim was to investigate the risk factors in patients with NNC. Methods A retrospective case–control design was used to compare patients with NNC and a control group of patients without coma in a population-based cohort of 263 participants from the neurological intensive care unit in Shuyang County People’s Hospital of Northern China. Coma was diagnosed by a Glasgow Coma Scale score ≤8. Adjusted odds ratios for patients with NNC were derived from multivariate logistic regression analyses. Results A total of 96 subjects had NNC. The prevalence of NNC was 36.5% among the subjects. Among these, 82% had acute cerebrovascular etiology. Most of the NNC usually occurred at day 3 after admission to the neurological intensive care unit. Patients with NNC had higher hospital mortality rates (67.7% vs 3%, P<0.0001) and were more likely to have a central herniation (47.9% vs 0%, P<0.001) or uncal herniation (11.5% vs 0%, P<0.001) than those without NNC. Multiple logistic regression showed that systemic inflammatory response syndrome-positive sepsis (odds ratio =4, 95% confidence interval =1.875−8.567, P<0.001) and acute respiratory failure (odds ratio =3.275, 95% confidence interval =1.014−10.573, P<0.05) were the factors independently associated with a higher risk of NNC. Conclusion Systemic inflammatory response syndrome-positive sepsis and acute respiratory failure are independently associated with an increased risk of NNC. This information may be important for patients with NNC.

Transient and persistent symptoms in patients with lacunar infarction: results from a prospective cohort study

Background The transient symptoms with lacunar infarction (TSI) and persistent symptoms with lacunar infarction (PSI) are the most common forms of symptomatic lacunar infarction (LI). The aim of this study was to compare the differences in TSI and PSI of symptomatic LI. Methods A prospective cohort study was conducted in the neurologic outpatients of the tertiary teaching hospital in Northern China between February 2011 and February 2012. The TSI and PSI in participants aged 35 years or over were assessed. Patients were followed up and their outcomes were compared. Results Of the 453 symptomatic outpatients, 251 patients with LI were diagnosed by magnetic resonance imaging. Approximately 77.3% (194/251) of the patients with LI at this time had TSI. and the remaining 23.7% had PSI. After the adjusted odds ratios, only middle age (risk ratio [RR], 1.1; 95% confidence interval [CI], 1.157–1.189), lower National Institutes of Health Stroke Scale score (RR, 20.6; 95% CI, 6.705–13.31), smaller lacunae on brain images (RR, 2.9; 95% CI, 1.960–4.245), and LI frequently in the anterior circulation territory (RR, 0.2; 95% CI, 0.079–0.721) were independently associated with TSI. During a mean follow-up of 6 months, survival rate was significantly higher among patients with TSI than among those with PSI (log rank, 6.9; P=0.010); estimated unadjusted incidence of vascular subsequent events (30.9% vs 54.4%, P=0.001) was significantly lower in TSI than in PSI. Conclusion The TSI has a higher prevalence and is associated with a lower risk of vascular subsequent events and death than PSI. The implications of these findings for TSI and PSI may require different interventions.