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Intractable Intracranial Hypertension
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
The best studied and understood of these conditions is traumatic cerebral edema, often diffuse, causing intracranial hypertension which is dangerous because it compromises cerebral perfusion [2]. The clinical assessment of these patients is difficult given the pragmatic limitations of associated polytrauma, agitation and pain requiring sedation and analgesia, shock with hemodynamic and respiratory instability, and the non-specific and acute deterioration that occurs prior to a clear clinical herniation syndrome. These difficulties highlight the need for further diagnostic tools to understand what is unfolding in the brain during these critical moments in order to initiate appropriate therapy.
Stroke and Transient Ischemic Attacks of the Brain and Eye
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Medical therapies to reduce cerebral edema have not been shown to improve patient outcome. However, preclinical models of stroke have shown that IV glyburide (glibenclamide) reduces brain swelling and improves survival, a phase II trial in humans showed it is well tolerated,69 and a phase III clinical trial is in progress.
Ornithine transcarbamylase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
The major metabolic characteristic of patients with OTCD is hyperammonemia. Levels found in the classic neonatal form of the disease are usually over 700 μmol/L (1000 μg/dL). Coma is generally present when the concentration exceeds 250 μmol/L (400 μg/dL). In infants dying of the disease, levels may range from 400 to 1700 μmol/L (600–2500 μg/dL). In the presence of levels over 300 μmol/L (500 μg/dL), one sees fixed dilated pupils and complete apnea. Cerebral edema occurs in some patients at these levels. Normal neonatal ammonia is <100 μmol/L, but levels up to 180 can be observed in sick infants without an inherited metabolic disease. Problems in obtaining and handling blood samples invariably raise levels, and exercise such as squeezing a ball, can also raise the level to 150 μmol/L [18]. Thus, a normal level eliminates hyperammonemia, but an abnormal level that does not fit with clinical findings may have to be repeated or confirmed by the presence of an elevated glutamine. Consensus on which specific neonatal level should prompt intravenous (IV) therapy has not been reached or whether mild elevations of ammonia in chronically treated patients should be treated intravenously [18], with the current discussion converging towards an accepted consensus; see the Suggested guidelines for the diagnosis and management of urea cycle disorders [19] (Chapter 25).
Considerations when treating high-grade pediatric glioma patients with immunotherapy
Published in Expert Review of Neurotherapeutics, 2021
Erin Crotty, Kira Downey, Lauren Ferrerosa, Catherine Flores, Bindu Hegde, Scott Raskin, Eugene Hwang, Nicholas Vitanza, Hideho Okada
The neurotoxicity related to CAR T therapy (ICANS) is a distinct entity from CRS, characterized by various neurological symptoms ranging from mild to more severe [65,102,103]. Mild symptoms can include headache, tremor, and dysgraphia. Severe symptoms include aphasia, seizures, and encephalopathy, including fatal cerebral edema. Timing of ICANS can occur within days to weeks after infusion and can co-occur with CRS or present after CRS has resolved [65,102]. While further investigation into the mechanisms of the development of ICANS are needed, data have suggested increased BBB permeability as a potential mechanism [110,111]. In GBM patients, there has been concern about peritumoral inflammatory responses causing potentially severe or fatal neuroinflammation. However, in the existing clinical trials to date, patients have presented with mild to no neurotoxicity [17–19,109]. In the cases where mild symptoms were present, some were secondary to disease progression rather than CAR T related neurotoxicity [17–19,108,109]. The most common symptom secondary to CAR T was seizure but other symptoms included headache, weakness (including facial nerve weakness), and gait changes [17–19,108,109]. One study found increased levels of cytokines in the cerebrospinal fluid (CSF), such as IL-6, IFN-γ, IL-5, IL-10, when patients were experiencing ICANS symptoms without any corresponding increase in serum cytokines or presence of CAR T cells in the blood [17].
Treatment Options for Anti-N-methyl-D-aspartate Receptor Encephalitis
Published in The Neurodiagnostic Journal, 2018
In 2012, Schmitt et al. identified that 30% of patients with anti-NMDAR encephalitis have EDB activity that is representative of cortical dysfunction rather than a seizure (Schmitt et al. 2012). Magnetic resonance imaging (MRI) of the brain usually demonstrates signs of inflammation in the limbic region uni- or bilaterally, more particularly in the mesial temporal lobe (Acién et al. 2014). Swelling of the brain, also referred to as cerebral edema, can occur due to an increase in intracranial pressure (Jha 2003). Symptoms related to an increase in intracranial pressure include headaches, dizziness, difficulty speaking and breathing, and stupor (Jha 2003). Other tests are performed to rule out anti-NMDAR encephalitis such as ovarian or testicular ultrasounds and, if present, the primary treatment is resection of the underlying tumor (ovarian, testicular, or sacrococcygeal; Acién et al. 2014). If the CSF analysis is positive for NMDA receptor antibodies, the Charles-LeMoyne neurological team recommends that treatment begin promptly. If a diagnosis of anti-NMDA receptor encephalitis is suspected, starting immune therapy even before receiving the CSF results is recommended in order to avoid any delays (Dalmau et al. 2011).
Emerging therapeutic targets for cerebral edema
Published in Expert Opinion on Therapeutic Targets, 2021
Ruchira M. Jha, Sudhanshu P. Raikwar, Sandra Mihaljevic, Amanda M. Casabella, Joshua S. Catapano, Anupama Rani, Shashvat Desai, Volodymyr Gerzanich, J. Marc Simard
Cerebral edema is a pathological accumulation of fluid in the brain that increases the net brain-tissue water mass [1–3]. It affects almost all types of acute brain injuries (ABI) commonly seen in neurocritical care units including ischemic stroke, intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), cardiac arrest (CA), traumatic brain injury (TBI), meningitis/encephalitis, central nervous system (CNS) abscesses, acute liver failure, status-epilepticus, primary brain tumors, and metastases, as well as systemic diseases such as diabetic ketoacidosis and sepsis. In many of these primary pathologies, cerebral edema is an independent risk factor for unfavorable prognosis with increased morbidity and mortality, in some cases by more than 80% [1,2,4–8]. There is some degree of molecular overlap in these diseases, with several of the same components, pathways, and networks identified as contributors to cerebral edema. However, there are also important distinctions depending on predominance of specific pathways, spatial location, timing, individual host response, and genetic predispositions. Substantial advances in identifying the underlying molecular machinery of cerebral edema have yielded exciting therapeutic targets to prevent or reduce edema generation. In isolation, these targeted anti-edema agents may not reach their full potential. However, edema therapy based on precision medicine could be optimized by early recognition and serial monitoring of key pathways that are activated/suppressed in individual patients using complementary tools like biomarkers, imaging, multimodal monitoring, and genetic predispositions.