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Imaging of head trauma
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
Brain swelling, intra- and extra-axial haematomas can result in significant brain herniation. The types of herniation are based on direction of the brain shift. Asymmetry between the two sides or effacement of normal CSF planes aid recognition. This topic is discussed in a separate chapter. The syndromes include the following:Subfalcine herniation (Figure 3.33)Descending transtentorial herniation (Figure 3.34)Uncal herniation (Figure 3.34)Tonsillar herniationAscending transtentorial herniationExtracranial herniation
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The brain is surrounded and protected by the skull and the meninges. The section of skull enclosing the brain is called the cranium and is made up of eight bones. Swelling of the brain causes intracranial pressure to rise because the adult skull is unable to expand to accommodate the swelling. Swelling of the brain is termed cerebral oedema, and if not treated, may lead to fatal brain herniation.
Neurosurgery: Supratentorial tumors
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Geriatric Neuroanesthesia, 2019
Monica S. Tandon, Kashmiri Doley, Daljit Singh
Primary central nervous system lymphoma (PCNL) are a relatively uncommon form of extranodal non-Hodgkin lymphoma (Figure 5.3). They are highly aggressive, may be solitary or multiple, and are located superficially in the cortex or may have a deep periventricular location. Typically, they are composed of noncohesive neoplastic lymphocytes that diffusely infiltrate the neural parenchyma and the blood vessels. The prognosis is poor, with an average survival time of approximately a year, despite optimal therapy (1) Tumor resection offers no benefit, except in the rare circumstances of neurologic deterioration due to brain herniation (1). These patients usually undergo a diagnostic biopsy followed by chemoradiotherapy.
Fatal cerebral hemorrhage in a patient with thrombotic thrombocytopenic purpura with a normal platelet count during treatment with caplacizumab
Published in Platelets, 2022
Kim Ditzel, Dirk Jan Mons, Rob Fijnheer
After 15 days of plasmapheresis in total and 5 days of caplacizumab, her platelet count recovered to >150 10^9/l (Figure 1). After 2 days of adequate platelet count, the plasmapheresis was stopped and the caplacizumab was planned to continue for a total of 30 days. She was ready to be discharged 12 days after the start of caplacizumab. Unfortunately, the night before planned discharge, she woke up with a left-sided hemiparesis. A CT-scan showed a massive intracerebral hemorrhage with midline shift and signs of brain herniation. There were no signs of underlying cerebrovascular abnormality. Her platelet count at the time was 606 10^9/l and no coagulation abnormalities were shown. She was given 4000 international units of Haemate-P, a vWF/factor VIII concentrate, to counter the iatrogenic decreased activity of vWF. No platelets were given, since her platelet count was normal and there was no platelet dysfunction. The neurologist consulted with a neurosurgeon, but there were no further therapeutic options. All supportive therapy was stopped and she died a few hours later.
Anatomic variations of the human falx cerebelli and its association with occipital venous sinuses
Published in British Journal of Neurosurgery, 2021
Safiye Çavdar, Bilgehan Solmaz, Özgül Taniş, Orhan Ulas Guler, Hakkı Dalçık, Evren Aydoğmuş, Leyla Altunkaya, Erdoğan Kara, Hızır Aslıyüksek
Brain herniation is a highly mortal complication of space-occupying lesions of the brain (intracranial hemorrhages, tumors, hydrocephalus or any lesion leads to brain edema) and it is related to the compensation capacity of the dural reflections of falx and tentorium cerebelli.6 The dimensions and increased number of folds may contribute to the elasticity of falx cerebelli which may affect the compensation capacity. Early intervention may be considered in posterior fossa tumors or hemorrhages in patients with multiple falx cerebelli. Therefore, being aware of the variations related to dural folds and occipital sinus can be important for neurosurgeons and neuroradiologists as these aberrant structures could cause haemorrhage during suboccipital approaches or may lead to erroneous interpretation during imaging of the posterior cranial fossa.
The Apnea Test: Requiring Consent for a Test That is a Self-Fulfilling Prophecy, Not Fit for Purpose, and Always Confounded?
Published in The American Journal of Bioethics, 2020
Third, there are almost always confounders to the apnea test anyways. First, brain herniation, the pathophysiologic mechanism of brain death, causes potentially reversible high cervical spinal cord injury, and this high cervical spinal cord injury occurs in most cases of brain death (Joffe et al. 2010a). High cervical spinal cord injury is known to cause apnea, and thus is a confounder to the apnea test. Second, primary brainstem injury can theoretically cause a total locked-in syndrome with lack of all brainstem reflexes (including apnea), despite relative sparing of the meso-pontine tegmental reticular formation (and thus potential preserved capacity for consciousness) (Walter et al. 2018). Third, central thyroid deficiency due to hypothalamic-pituitary injury, which should occur in many cases of profound brain injury, can cause coma and hypoventilation with poor respiratory response to hypercarbia, and thus failure of breathing during the apnea test (Joffe et al. 2010b). Finally, global ischemic penumbra, with brain blood flow low enough to cause loss of brain function but not brain destruction, is a mimic of brain death with unknown incidence (Coimbra 1999; Shewmon 2018). These confounders mean that the apnea test cannot be diagnostic in most cases, and only has potential harm. Again, for this reason, I believe that the apnea test is contraindicated, whether consent is provided or not.