Application of the neuropsychological evaluation in vocational planning after brain injury
Robert T. Fraser, David C. Clemmons in Traumatic Brain Injury Rehabilitation, 2017
The brain is fully supplied by blood and oxygen. To get blood and oxygen to brain tissue, a complex system of arteries is needed. Unfortunately, this affords much opportunity in brain injury for contusions and hematomas to occur and cause tissue damage since the brain contains so many arteries and blood vessels. In the case of a hematoma, a collection of blood can occur in several spaces in the brain resulting in brain tissue being compressed and, therefore, damaged in that area. When this happens to a great extent, surgery may be required to evacuate this hematoma. A collection of blood in the brain can result in increased pressure inside of the brain. This is called increased intracranial pressure (ICP). Intracranial pressure can also increase due to swelling of brain tissue. This is caused by increased blood volume going to the brain. As is true in other body tissues, swelling occurs in the area of injury. In the brain, this is referred to as brain edema. Many of these types of problems are treated in the trauma unit, emergency room, or intensive care unit. Such difficulties may further be treated while on a neurosurgery or neurology unit or in an acute hospitalization phase. Once medically stable, the client may be transferred to the first phase of rehabilitation.
Stroke
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
Subarachnoid hemorrhage causes aseptic meningitis. This usually increases intracranial pressure for days to weeks. Focal brain ischemia may be due to secondary vasospasm. Approximately 25% of affected patients develop signs of an ischemic stroke or transient ischemic attack. There is significant brain edema. Risks for vasospasm and infarction, known as angry brain, are highest between 72 hours and 10 days. Another common development is secondary acute hydrocephalus. Another rupture may occur. When it does, it is usually within 1 week. The incidence of nonaneurysmal subarachnoid hemorrhage is high in patients with type 1 diabetes. Of cerebrovascular deaths in this group of patients, 23% are due to hemorrhagic strokes. The association of type 2 diabetes with subarachnoid hemorrhage from a ruptured saccular intracranial aneurysm is unclear.
Complications after Craniotomy
Stephen M. Cohn, Matthew O. Dolich in Complications in Surgery and Trauma, 2014
Brain edema [31] during the postoperative period can be caused by excessive intraoperative retraction, intra-operative trauma, arterial or venous occlusion, and associated with a neoplastic process [32]. On further evaluation with CT scanning, edema will appear as an area of decreased density and may be associated with sulcal effacement or brain shift. Brain edema is commonly associated with intracerebral hemorrhage and contusion. Edema associated with cerebral infarction generally indicates severe stroke and may lead to herniation. All of these causes may be seen during the postoperative period (Figure 36.1). When accompanying a neoplastic process, the most typical cause is a meta-static lesion; however, primary brain tumors such as glioblastoma and meningioma may also cause significant edema following resection.
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).
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].
Diffuse large B cell lymphoma primarily presenting as acute liver failure in a surviving patient
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Jumpei Shibata, Shingo Kurahashi, Takehito Naito, Isamu Sugiura
The underlying cause of ALF was unknown. The patient started treatment with vitamin K and multivitamin infusion. However, on the 2nd day of hospitalization, the patient developed asterixis and deteriorated prothrombin time, and underwent steroid pulse therapy, plasmapheresis, and hemodiafiltration. Liver transplantation was considered a treatment option. As we believed that the thickened gastric wall indicated the possible presence of tumors, esophagogastroduodenoscopy was performed, which revealed depressed lesions on the gastric fundus (Figure 2(a,b)). Biopsies were taken from the lesions in the stomach, but not from the liver, because of persistent coagulopathy. Despite intensive care, encephalopathy progressed, and on the 4th day, the patient became unconscious. Brain CT revealed cerebral edema. In addition to the cerebral involvement, pulmonary vascular permeability deteriorated, indicating heart failure, probably because of the increased volume of circulating plasma.
Related Knowledge Centers
- Brain Herniation
- Edema
- Intracranial Pressure
- Subdural Hematoma
- Subarachnoid Hemorrhage
- Stroke
- Headache
- Brain
- Epidural Hematoma
- Intracerebral Hemorrhage