Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome primarily affects the young and may not be considered first in an older adult with infection-like encephalopathy. Here, we present the case of a patient who suffered from the acute onset of fever, delirium, and epilepsy, mimicking herpes simplex encephalitis (HSE). A 52-year-old woman with diabetes and end stage renal disease (ESRD) regularly took oral anti-diabetic drugs (OADs) and received hemodialysis. She presented with an acute onset of fever, delirium, and epilepsy, mimicking HSE. Further investigation showed a persistent elevated lactate level in the cerebrospinal fluid (CSF). A mitochondrial DNA analysis revealed a point mutation at nucleotide 3243. The clinical presentation and imaging studies of MELAS in adults are variable and may mimic those of HSE. Antiviral therapy should be administered until the diagnosis of MELAS is definitive. Infection and metformin may have also precipitated MELAS manifestation in this patient. Clinicians should avoid potential mitochondrial-toxic drugs in these patients.

Patients with end-stage renal disease (ESRD) have higher risks of subdural hemorrhage (SDH) and subsequent 30-day mortality. However, evidences regarding optimal mode of dialysis therapy during acute management are sparse. We aimed to compare the outcomes of ESRD patients who received continuous peritoneal dialysis (CPD) or extended hemodialysis (EHD) after SDH and determined factors associated with 30-day mortality. We retrospectively reviewed consecutive patients with SDH and ESRD in a medical center. The clinical parameters and outcomes were compared between CPD and EHD groups. Factors associated with 30-day mortality were analyzed. We reviewed 32 patients, including 22 received EHD, 8 received CPD, and 2 received continuous veno-venous hemodialysis. Neurosurgery was done in 9 (28%) of them. There was no significant difference in baseline parameters and outcomes between EHD and CPD groups. The overall 30-day mortality rate was 19%. Lower Glasgow coma scale (GCS, median [interquartile range]: 10 [7-12] vs. 15 [11-15], p = 0.02) and larger changes in absolute mean arterial pressure (MAP: 26.5 [10.5-46.0] vs. 7.5 [2.0-17.8] mmHg, p = 0.01) during the first dialysis therapy were noted in patients with 30-day mortality. In multivariate analysis, consciousness disturbance at presentation was an independent risk factor for 30-day mortality. Among ESRD patients with SDH, the 30-day mortality rates were similar between EHD and CPD groups. MAP change during dialysis might be an important modifiable risk factor for 30-day mortality, though the effect was not significant in multivariate analysis. Further prospective studies with larger sample size are warranted.

Stroke results in high mortality with tremendous health care burden. Malnutrition is frequently observed in patients after stroke. This study was designed to explore the nutritional status in the acute stage of stroke aiming at exploring factors related to malnutrition after stroke. This was a hospital based, prospective, observational study recruiting cerebrovascular diseases patients hospitalized for acute management. Patients suffered from all kinds of cerebrovascular diseases hospitalized for management within 30 days after onset were consecutively recruited in the study hospitals. Stroke severity was evaluated by National Institutes of Health Stroke Scale, functional status by Barthel index, and global outcome by modified Rankin Scale. Cognitive function was evaluated by Mini-Mental State Examination. Nutritional status was assessed by Mini Nutritional Assessment (MNA), stratified by 1) adequate nutritional status, MNA ≥ 24; 2) protein-calorie malnutrition, MNA less than 17; 3) at risk of malnutrition, MNA between 17 and 23.5. There were 231 cerebral infarction patients recruited at 13.5 days (25-75%: 5.0-17.0) after stroke onset with mild stroke severity 71.4% and severe 10.4% with nasogastric tube insertion in 14%. Malnutrition was identified in 12.1% with 54.1% at risk of malnutrition. Factor related to malnutrition was severe stroke severity with dependency. Patients with old age, hypertension, and diabetes mellitus tended to have malnutrition or risk of malnutrition. Nutritional status was poor in stroke patients across all stroke severities within weeks. Further longitudinal outcome studies to identify the poor outcome and the evolution of nutritional status are warranted.

Invasive mycosis caused by the Aspergillus, Fusarium, and Mucor can be fetal, especially in the immunocompromised patients with central nervous system (CNS) involvement. Here we present a case of CNS Fusarium infection, and this is the first reported case of Fusarium brain abscess in Taiwan. A 65-year-old woman presented with fever and conscious disturbance for 3 days. Neurological examination showed stupor consciousness, neck stiffness, multiple cranial nerves palsy, and bilateral Babinski signs. Magnetic resonance imaging showed multifocal lesions involving medulla oblongata, pons, bilateral cerebral peduncles, and bilateral cerebellar peduncles. Cerebrospinal fluid (CSF) study revealed neutrophil predominant pleocytosis, but both blood and CSF culture were negative. We treated patient with ceftriaxone and vancomycin initially as empiric therapy for suspected bacterial meningoencephalitis. However, chronic sinusitis with fungal ball and brain abscess were later found. Despite antifungal treatment and surgical intervention, patient expired 3 months after admission. Fungal culture of the brain abscess disclosed Fusarium species 2 weeks after her death. CNS Fusarium infection should be considered when an immunocompromised patient presenting with fever, conscious change, cranial nerve palsies, and angioinvasion suggested by brain imaging. To properly manage the disease, early effective antifungal therapy and neurosurgical intervention are important.

Aldehydes-induced toxicity has been implicated in many neurodegenerative diseases. Exposure to reactive aldehydes from (1) alcohol and food metabolism; (2) environmental pollutants, including car, factory exhausts, smog, pesticides, herbicides; (3) metabolism of neurotransmitters, amino acids and (4) lipid peroxidation of biological membrane from excessive ROS, all contribute to 'aldehydic load' that has been linked to the pathology of neurodegenerative diseases. In particular, the α, β-unsaturated aldehydes derived from lipid peroxidation, 4-hydroxynonenal (4-HNE), DOPAL (MAO product of dopamine), malondialdehyde, acrolein and acetaldehyde, all readily form chemical adductions with proteins, DNA and lipids, thus causing neurotoxicity. Mitochondrial aldehyde dehydrogenase 2 (ALDH 2) is a major aldehyde metabolizing enzyme that protects against deleterious aldehyde buildup in brain, a tissue that has a particularly high mitochondrial content. In this review, we highlight the deleterious effects of increased aldehydic load in the neuropathology of ischemic stroke, Alzheimer's disease and Parkinson's disease. We also discuss evidence for the association between ALDH2 deficiency, a common East Asianspecific mutation, and these neuropathologies. A novel class of small molecule aldehyde dehydrogenase activators (Aldas), represented by Alda-1, reduces neuronal cell death in models of ischemic stroke, Alzheimer's disease and Parkinson's disease. Together, these data suggest that reducing aldeydic load by enhancing the activity of aldehyde dehydrogenases, such as ALDH2, represents as a therapeutic strategy for neurodegenerative diseases.

Co-occurrence of Guillain-Barré syndrome (GBS) and other autoimmune diseases is rare. We present the case of a patient with co-occurrence of GBS and primary Sjögren syndrome (pSS). An 82-year-old woman presented with acute ascending flaccid paralysis and acute respiratory failure. Nerve conduction studies and cerebrospinal fluid analysis confirmed the diagnosis of GBS of acute inflammatory demyelinating polyradiculoneuropathy subtype. The initial unresponsiveness to plasma exchange therapy raised the suspicion of other potential diseases. She was later proved to have underlying pSS. Her neurological deficits and respiratory failure improved dramatically with combination therapy of intravenous immunoglobulin (IVIg) and immunosuppressive agent. pSS should be considered as a possible cause of refractory GBS, particularly in elderly women. Combination therapy with IVIg and immunosuppressive agent may be beneficial.

Polydipsia is one of the most serious and complicated problems causing morbidity and mortality in chronic mental health institutes. The pathophysiology of polydipsia in chronic schizophrenia remains unclear; as a result, no effective methods exist to deal with this serious problem. This report describes a patient with schizophrenia with polydipsia and seizures who benefitted from a behavioral modification program at a chronic mental health institute. A 56-year-old schizophrenic man did not have a history of physical illnesses or seizures and developed seizures following polydipsia. Despite drug adjustment, his polydipsia was uncontrolled and he suffered from generalized tonic convulsions. After introducing a "water restriction program," his polydipsia and seizures were controlled. The "water restriction program" consisted of daily body weight monitoring and frequent checking of electrolyte data, both of which are inexpensive and simple. This program can be carried out by untrained nursing staff, who are the primary caregivers in chronic mental health institutes. Our case highlights an effective and inexpensive behavior modification program to deal with the difficult and complicated problems of polydipsia and seizures in chronic mental health institutes.

Status epilepticus was rarely reported as the initial manifestation of intracranial dural arteriovenous fistulas. Successful treatment with endovascular intervention has not been reported in the literature. We report three cases of dural arteriovenous fistulas initially presenting with various types of status epilepticus, including generalized tonic-clonic status epilepticus, complex partial status epilepticus, and nonconvulsive status epilepticus. The status epilepticus of these patients was successfully terminated through aggressive endovascular intervention in conjunction with antiepileptic drugs. These cases highlight the importance of intracranial dural arteriovenous fistulas in diagnosing patients with status epilepticus. Moreover, directly treating dural arteriovenous fistulas plays a crucial role in addition to anti-epileptic drugs therapy in controlling seizures in patients with dural arteriovenous fistulas related status epilepticus.