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The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The meninges is a collective term describing the three membranes that cover and protect the brain and spinal cord. The acronym PAD may help you to remember the names of the meninges. Starting from the surface of the brain and working outwards, the membranes are the pia mater, the arachnoid mater and the dura mater. Inflammation of the meninges is called meningitis (see Figure 9.7).
Diagnostic Approach to Rash and Fever in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Lee S. Engel, Charles V. Sanders, Fred A. Lopez
Meningococcemia can occur sporadically or in epidemics and is more commonly diagnosed during the winter months. Neisseria meningitidis is primarily spread by respiratory droplets that require close, prolonged contact for transmission [15]. The risk of infection is highest in infants, asplenic patients, alcoholics, patients with complement deficiency, and persons who live in dormitories (coeds, military personnel, or prisoners). Initial symptoms include cough, headache, sore throat, nausea, and vomiting. Acute meningococcemia progresses rapidly, and patients typically appear ill, with high spiking fevers, tachypnea, tachycardia, mild hypotension, and a characteristic petechial rash [16,17]. Signs and symptoms of meningeal irritation such as headache, vomiting, and change in consciousness occur in up to 88% of patients with meningococcemia [16,18].
Role of Bacteria in Blood Infections
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Kannan Balaji, Gnanasekaran JebaMercy, K. Balamurugan
Meninges are the membrane layers present in brain and spinal cord. Fluid present in the meninges get infected by bacteria or viruses and cause inflammation in the meninges. This condition is called meningitis. A range of pathogenic bacteria can cause bacterial meningitis. Streptococcus pneumonia is the most common causative pathogen. Other bacterial pathogens like Neisseria meningitides, Haemophilus influenza, Listeria monocytogenes, and Group B Streptococcus also causes meningitis.
Clinical neuroimaging in intracerebral haemorrhage related to cerebral small vessel disease: contemporary practice and emerging concepts
Published in Expert Review of Neurotherapeutics, 2022
Martina Goeldlin, Catriona Stewart, Piotr Radojewski, Roland Wiest, David Seiffge, David J Werring
On MRI, cSS can be identified in T2*-GRE or preferably on SWI sequences as curvilinear signal intensity in the subarachnoid space and/or superficial cortical layers [75]. cSS is described as focal (affecting ≤3 gyri) and disseminated (affecting >3 gyri), based on the assumption that one bleeding focus usually affects at maximum 3 gyri [76]. Focal cSS should further be evaluated regarding multifocality with the recently proposed multifocality score [77]. Histopathologically, cSS corresponds to extracellular haemosiderin depositions in the superficial cortical layers I–III and the subarachnoid space and is associated with higher CAA severity in leptomeningeal vessels and reduced CAA severity in cortical vessels [78]. The same study found a correlation between high cSS severity and cortical microinfarcts [78]. Although the causal relationship is not confirmed, it seems pathophysiologically likely that cSS is the long-term sequelae resulting from acute convexity subarachnoid hemorrhage (cSAH). In a cohort study of CAA patients without previous hemorrhage, prevalence of disseminated cSS was found to be much higher in patients presenting with acute cSAH [79]. Furthermore, cortical subarachnoid hemorrhage associated with CAA can occur remote or even in the absence of CAA-related ICH and was found to be associated with a higher CAA-load in meningeal vessels in an autopsy study [80]. cSS and cSAH are both linked to transient focal neurological episodes (TFNE), sometimes also called ‘amyloid spells’ [79,81,82].
Cerebrospinal fluid leaks secondary to dural tears: a review of etiology, clinical evaluation, and management
Published in International Journal of Neuroscience, 2021
Jason Gandhi, Andrew DiMatteo, Gunjan Joshi, Noel L. Smith, Sardar Ali Khan
The meninges are composed of three membrane structures that encapsulate the brain and spinal cord. The three membranes of the meninges from most superficial to deep are respectively the: dura, arachnoid, and pia mater. The dura mater is also referred to as the pachymeninx or “thick meninx”, while the pia and arachnoid mater collectively are referred to as the leptomeninx or “thin meninx” [5]. The dura itself is composed of three layers: the most superficial layer called the endosteal (i.e. periosteal), the meningeal layer, and the deepest layer called the dural border cell layer [6,7]. The dural border cell layer interacts with the arachnoid barrier cell layer and basement membrane of the arachnoid mater. It is in the arachnoid reticular layer and subarachnoid space that the CSF is contained. The depth of the subarachnoid space is variable depending on the relationship between the arachnoid and pia mater [7].
Temporal lobe contusions on computed tomography are associated with impaired 6-month functional recovery after mild traumatic brain injury: a TRACK-TBI study
Published in Neurological Research, 2018
John K. Yue, Ethan A. Winkler, Ross C. Puffer, Hansen Deng, Ryan R. L. Phelps, Sagar Wagle, Molly Rose Morrissey, Ernesto J. Rivera, Sarah J. Runyon, Mary J. Vassar, Sabrina R. Taylor, Maryse C. Cnossen, Hester F. Lingsma, Esther L. Yuh, Pratik Mukherjee, David M. Schnyer, Ava M. Puccio, Alex B. Valadka, David O. Okonkwo, Geoffrey T. Manley
Prior studies of mild and moderate TBI report that patients with focal cortical contusions differ from patients without focal pathology in behavioral measurements 1 month after injury, resulting in difficulties with professional and psychosocial reintegration fort the affected individuals [19,37]. Therefore, clinical characterization of long-term deficits attributable to specific types and locations of focal pathology is necessary for prognostication and postinjury management. In our patients presenting with parenchymal contusions, we observed that the force of the initial trauma also induces extra-axial hemorrhage in 96% (44 of 46) of subjects; however, in the multivariate analysis, we find that the presence of a meningeal hemorrhage in MTBI patients does not associate with long-term functional impairment. While a majority of patients with focal contusions present with extra-axial injuries such as subdural hematoma or subarachnoid hemorrhage, it is important to highlight that the clinical severity of the meningeal hemorrhage, as is often the case with MTBI, is mild and nonoperative, with no significant implications for long-term outcomes.