Morphological characteristics of infected subdural hematoma: Comparison with images of chronic subdural hematoma.

OBJECTIVES: Infected subdural hematoma (ISH) is a rare type of subdural empyema, with fewer than 50 cases reported to date. Its radiological features have not been adequately described, making diagnosis challenging. At our institution, two adults presented with ISH, which exhibited a characteristic shape on preoperative imaging. PATIENTS AND METHODS: This study examined ISH cases and chronic subdural hematoma (CSH) cases that underwent surgery at the Ishikawa Prefectural Central Hospital between January 2016 and March 2018. To distinguish ISH from CSH, we focused on three specific radiological features: the biconvex shape of the hematoma, presence of a high-density region at the lower end of the hematoma on plain computed tomography (CT), and presence of a hyper-intense signal within the hematoma on diffusion weighted imaging (DWI). RESULTS: We analyzed 30 ISH (current and previously reported) and 102 CSH cases in our study. We found no statistically significant associations between the hematoma type (ISH or CSH) and the presence of a high-density region at the lower end of the hematoma on plain CT (p = 0.13) or the presence of hyperintensity in the hematoma on DWI (p = 1.00). Conversely, a statistically significant association was found between the hematoma type and the biconvex shape of the hematoma (p < 0.01). CONCLUSION: These results suggest that the shape of the hematoma on imaging provides valuable information that can be used to differentiate ISH from CSH and optimize therapeutic approaches.

Anxiety disorders in acute central nervous system infections.

BACKGROUND: Patients affected by acute central nervous system (ACNS) infectionsmay present different complications, including neuropsychological disorders. Nevertheless, psychopathological impairment has been rarely measured by appropriate and validated tests. MATERIAL AND METHODS: Survivors of childhood ACNS infections admitted to the Bambino Gesù Children's Hospital, Rome, Italy, from June 2013 to June 2015 were re-evaluated at follow-up from June 2016 to June 2017. Both patients and their parents underwent a psychological interview and neuropsychological tests (the Leiter International Performance Scale - revised (Leiter-R), the Child Behaviour Checklist (CBCL), the K-SADS-PL test). RESULTS: Thirty children were included in the study. The mean score of IQ and fluid reasoning was within the normal range. A percentage of 20% of the children enrolled showed criteria for generalized anxiety disorder. CONCLUSION: Our study revealed the importance of follow-up evaluations after ACNS infections, in order to prevent mayor psychological sequelae and to perform treatment or rehabilitation.

Neuropsychiatric Aspects of Infectious Diseases: An Update.

Among the critically ill, infectious diseases can play a significant role in the etiology of neuropsychiatric disturbances. All critical care physicians are familiar with delirium as a secondary complication of systemic infection. This article focuses on key infectious diseases that commonly and directly produce neuropsychiatric symptoms, including direct infection of the central nervous system, human immunodeficiency virus infection, and AIDS.

[Psychiatric aspects of infectious diseases -- a literature review]. / A fertozo betegségek pszichiátriai vonatkozásai -- irodalmi áttekintés.

It is essential for the psychiatrist working in the consultation-liaison field or with comorbid patients to be familiar with the psychiatric aspects of central nervous infectious diseases or infectious diseases with psychiatric symptoms. Authors have reviewed the most important psychiatric aspects of common infectious diseases. Essential knowledge for setting up a diagnosis and starting appropriate treatment has been summarized. The most important interactions of infectological and psychiatric treatments have also been discussed.

[Schizophrenia--a mild encephalitis?]. / Schizophrenie--eine milde Enzephalitis?

The mild encephalitis (ME) hypothesis describes a subgroup of severe psychiatric disorders, with a focus on a subgroup of schizophrenias, in which low-level neuroinflammation (LLNI) represents the core in pathogenesis. LLNI is increasingly recognised in experimental neuroimmunology and is in principle able to explain various types of psychopathology. Epidemiology and course of schizophrenia are well compatible with the ME hypothesis, indirectly indicating that the ME subgroup may be rather large. With the ME model connected is a set of three contributing factors: genes, environment (especially infectious agents) and the immune system. The type of psychopathology observed in the individual case may heavily depend upon other conditions, e. g. pre-existing vulnerabilities. The first large-scale epidemiological study in psychiatry identified two factors during lifetime, severe infectious diseases and autoimmune diseases, as risk factors. This and clinical findings more and more support the ME hypothesis, e. g., activated monocytes or proteome changes in blood and slight CSF pathologies in more than 60 % of therapy-resistant schizophrenia, or activated microglia and dysconnectivity in neuroimaging.

Do survivors of acute neurologic injury remember their stay in the neuroscience intensive care unit?

BACKGROUND: Patients in medical, surgical, and trauma intensive care units (ICUs) are at risk for later development of symptoms of post-traumatic stress disorder (PTSD). Because acute brain injury can impair recall; we sought to show that neuroscience patients undergoing prolonged neuroscience ICU admission have limited memory of their ICU stay and thus are less likely to develop symptoms of PTSD. METHODS: We surveyed patients >18 years admitted for 10 days or more to our neuroscience ICU over a 10-year period. RESULTS: The survey response rate was 50.5% (47/93). Forty percent (19/47) of respondents presented with coma. Recall of details of the ICU admission was limited. Fewer than 10% of patients who required mechanical ventilation recalled being on a ventilator. Only five patients (11%) had responses suggestive of possible post-traumatic stress syndrome. The most commonly experienced symptoms following discharge were difficulty sleeping, difficulty with concentration, and memory loss. CONCLUSION: Patients requiring prolonged neuroscience ICU admission do not appear to be traumatized by their ICU stay.

Enduring consequences of early-life infection on glial and neural cell genesis within cognitive regions of the brain.

Systemic infection with Escherichia coli on postnatal day (P) 4 in rats results in significantly altered brain cytokine responses and behavioral changes in adulthood, but only in response to a subsequent immune challenge with lipopolysaccharide [LPS]. The basis for these changes may be long-term changes in glial cell function. We assessed glial and neural cell genesis in the hippocampus, parietal cortex (PAR), and prefrontal cortex (PFC), in neonates just after the infection, as well as in adulthood in response to LPS. E. coli increased the number of newborn microglia within the hippocampus and PAR compared to controls. The total number of microglia was also significantly increased in E. coli-treated pups, with a concomitant decrease in total proliferation. On P33, there were large decreases in numbers of cells coexpressing BrdU and NeuN in all brain regions of E. coli rats compared to controls. In adulthood, basal neurogenesis within the dentate gyrus (DG) did not differ between groups; however, in response to LPS, there was a decrease in neurogenesis in early-infected rats, but an increase in controls to the same challenge. There were also significantly more microglia in the adult DG of early-infected rats, although microglial proliferation in response to LPS was increased in controls. Taken together, we have provided evidence that systemic infection with E. coli early in life has significant, enduring consequences for brain development and subsequent adult function. These changes include marked alterations in glia, as well as influences on neurogenesis in brain regions important for cognition.

Acquired brain injury and dementia: a comparison of carer experiences.

OBJECTIVE: As their differential needs are unknown and to inform service planning, this study (a) examined experiences of caring for adults with acquired brain injury (ABI) and (b) compared these with carers of adults with dementia. DESIGN: Cross-sectional postal survey. ABI carer experiences were compared with those of a previously studied group of dementia carers using equivalent instruments. METHODS: Family carers (n = 222) of adults with ABI: TBI (49%), strokes (26%), brain infections (18%) and other (7%) completed validated questionnaires assessing physical dependency and psychological problems of those cared for and carers' own perceived burden, quality-of-life and mental health. RESULTS: Carer burden, quality-of-life and mental health were worse for ABI carers, but were not predicted by gender, relationship, injury type, physical dependency or cognitive problems in either ABI or dementia carers. Behavioural problems of those cared for varied between the two groups and affected carers differently. Aggressive problems significantly predicted greater burden, poor quality-of-life and mental health in ABI carers, whereas passivity/low mood significantly predicted greater burden and worse quality-of-life in dementia carers. CONCLUSIONS: This study revealed different experiences of caring for younger adults with ABI vs. older adults with dementia, thereby supporting targeted development of services to sustain families affected by these conditions.

Are common childhood or adolescent infections risk factors for schizophrenia and other psychotic disorders?

Postnatal infection may represent a preventable risk factor for onset of psychotic disorders in adolescence and early adulthood. The mechanism of action is likely to involve site-directed triggering of the brain's innate immune system, mediated principally through localised activation of microglial cells. This triggering may occur in response to systemic inflammatory stimuli, without direct involvement of the central nervous system. Microglial activation can represent a primary response or a secondary phenomenon at sites made vulnerable by prior injury; that is, areas containing previously activated microglia will respond more strongly to a new stimulus. The presence of activated microglia is indicative of a recent insult or active disease. It is not characteristic of long-established neurodevelopmental abnormalities. Activated microglia, acting through a variety of cytokine and other signal systems, have the capacity to significantly interfere with synaptic turnover and thus, over time, alter synaptic architecture and function. This pathophysiological path should be investigated more systematically as it may explain a novel "neuroprotective" mode of action for some existing antipsychotic compounds.

[Septic encephalopathy. Diagnosis und therapy]. / Septische Enzephalopathie. Differentialdiagnose und therapeutische Einflussmöglichkeiten.

23% of all septic patients develop septic encephalopathy which is associated with an increased mortality rate. Symptoms such as agitation, confusion and disorientation ranging from stupor to coma often develop in early sepsis. Severe hypotension is significantly associated with the development of septic encephalopathy. Several other factors which may play a role are also discussed: effects of inflammatory mediators on the brain, inadequate cerebral perfusion pressure, blood-brain barrier derangements, disturbances of the cerebral microcirculation, cerebral ischemia e.g. due to hypocapnia,metabolic changes, altered amino acid levels, transmitter imbalances, liver insufficiency, multiple organ failure and infections of the CNS, respectively. Compared to patients with an isolated infection,patients in septic shock have increased levels of aromatic amino acids such as phenylalanine and tryptophan in the plasma and brain as well as decreased levels of branched chain amino acids. Patients who died had higher levels of aromatic amino acids than the survivors. The correlation between aromatic amino acids and the APACHE II score was significant. The tryptophan metabolite quinolinic acid which can be synthesized in activated macrophages could act as an excitatory transmitter on the N-methyl-D-aspartate (NMDA) -receptor. Observations from experimental models indicate that activated NMDA receptors activate the neuronal isoform of the NO-synthase and other calcium dependent enzymes. This releases free radicals which may damage the DNA and activate the nuclear enzyme Poly-ADP-ribose-synthetase (PARS), resulting in energy depletion and cell death. Sepsis is the main cause of metabolic encephalopathies in critically ill patients. The differential diagnoses include hepatic, renal,hypoxic-ischemic or cardiovascular encephalopathies as well as encephalopathies,metabolic disorders and organ dysfunctions of other origin. Therapeutic interventions are numerous,however, so far only investigated in few controlled studies. The primary therapeutic goal is to maintain an adequate perfusion pressure and to prevent hypoxia and hypocapnia. Although the infusion of branched chain amino acids is controversial, experimental investigations demonstrated improvements improvements in an animal model with septic encephalopathy. Further investigations with respect to glutamate receptor antagonists, new radical scavengers, NO- and PARS-inhibitors may show whether these substances are suitable for the prophylaxis or early therapy of septic encephalopathy.

Learning deficits in mice with persistent Borna disease virus infection of the CNS associated with elevated chemokine expression.

Borna disease virus (BDV) is a highly neurotropic RNA virus that causes a CD8(+) T cell-mediated neurological disease in certain mouse strains. We established asymptomatic persistent central nervous system (CNS) infections in mutant C57BL/10J mice that lack functional CD8(+) T cells. When analyzed at adult age for spatial learning abilities in a water maze, BDV-infected mice showed slightly impaired escape performance while their exploratory behavior in an openfield test was indistinguishable from uninfected control mice. Histological and molecular biological analysis revealed extensive viral spread throughout the CNS of infected animals. Most neurons of the hippocampus contained viral antigen, but there was no overt loss of neurons from this structure. We found almost unchanged levels of the proinflammatory cytokines IL-1beta and TNF-alpha, but clearly increased levels of the chemokines IP-10 and RANTES in brains of infected mice. Re-examination of water maze data revealed that only infected mice with IP-10 transcript levels above a certain threshold showed impaired performance, whereas the performance of infected mice with lower IP-10 levels was indistinguishable from uninfected controls. This suggests that BDV infection can disturb the function of the mammalian CNS without causing overt neuronal loss, and that the magnitude of virus-induced chemokine production in the CNS correlates with the degree of impairment.