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This is the first published case report of a child with acute lymphatic leukemia developing a fatal mucormycosis during blinatumomab treatment. The patient showed multiple, systemic thromboembolic lesions with ischemia, bleeding and infarction in almost all organs. The child succumbed to increased brain pressure resulting in cerebral herniation. This case particularly illustrates the fulminant progression and huge challenges of diagnosing and treating mucormycosis in children with hemato-oncological diseases during treatment with targeted therapeutic antibodies (blinatumomab).

This article introduces the basic concepts of intracranial physiology and pressure dynamics. It also includes discussion of signs and symptoms and examination and radiographic findings of patients with acute cerebral herniation as a result of increased as well as decreased intracranial pressure. Current best practices regarding medical and surgical treatments and approaches to management of intracranial hypertension as well as future directions are reviewed. Lastly, there is discussion of some of the implications of critical medical illness (sepsis, liver failure, and renal failure) and treatments thereof on causation or worsening of cerebral edema, intracranial hypertension, and cerebral herniation.

Hyperammonemia after lung transplant is a severe complication that can result in cerebral herniation. It is associated with up to 70% mortality in patients who have had solid organ transplantation. We describe a rare case in which hyperammonemia was emergently and successfully treated with plasmapheresis in a re-do double lung transplant patient who developed shocked liver.

This case report discusses an incident of cranial hyperostosis that was discovered after an episode of syncope on imaging. A CT and MRI work-up revealed intracranial volume loss and cerebral herniation into the posterior fossa. Concomitant with the episode of syncope, the patient presented with deficits in delayed short-term memory, which was supported using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) test. As far as we are aware, this is the first report of severe memory dysfunction stemming from chronic herniation of the mesial temporal lobe due to severe hyperostosis. Hyperostosis has been shown to manifest as a wide variety of symptoms, but the delayed short-term memory impairment observed in this case is completely novel.

Resumen Las hernias cerebrales son la causa inmediata del fallecimiento en muchas lesiones neurologicas. Algunos protocolos recientes de actuacion neuroquirurgica han originado nuevas modalidades, como por ejemplo en el llamado sindrome del trefinado. Se requiere, pues, una revision actualizada del tema, maxime cuando tiene importantes implicaciones medicolegales. Nuestro objetivo es revisar las clasificaciones, adaptarlas a los avances en Neurorradiologia y Neurocirugia, y analizar su problematica medicolegal. La actualizacion de la clasificacion y un conocimiento detallado de la fisiopatologia de las hernias cerebrales constituyen la mejor orientacion para la resolucion de problemas forenses en lo relativo a etiologia, causalidad y secuelas de las lesiones encefalicas.

Decompressive surgery with hemicraniectomy and durotomy for malignant MCA infarction remains a salvage procedure but can be associated with reasonable clinical outcomes in highly selected patients. This selection of patients appropriate for intervention is of the utmost importance, but exact criteria remain to be defined; older age and increased numbers of associated medical comorbidities seem to define a group of patients who would not derive long term benefit, however. The determination as to whether or not surgery is equally beneficial for dominant or nondominant hemispheric infarction is hampered by lack of good comparative data, but selected case series suggest that some patients who have dominant hemispheric infarction achieve a reasonable degree of independence. Although a well-defined principle of stroke practice is that "time is brain," there are no clear data as to when intervention should be done, as there are some patients who have large MCA infarction and who may not progress to cerebral herniation. Clinicians managing the growing population of patient status post hemicraniectomy should also be aware of this process of the syndrome of the trephined and the potential for resolution that may prompt earlier cranial reconstruction. At present, the decision to proceed with this aggressive intervention of hemicraniectomy and durotomy for large ischemic infarction remains a case-by-case individualized approach, based on patient and family preferences and clinicians' subjective perspective as to patients' potential for clinical recovery.

Increased intracranial pressure is associated with high morbidity and mortality, but prompt treatment can improve outcomes. Traumatic brain injury is the most common cause of increased intracranial pressure, and it results in many hospitalizations and emergency department visits every year. The optimal treatment of intracranial hypertension is not known, and further clinical studies are needed, particularly in children. However, there are many treatments available for increased intracranial pressure. This article reviews the pathophysiology of increased intracranial pressure, common clinical features of intracranial hypertension and cerebral herniation, and evidence for the treatment of increased intracranial pressure in children.

A number of neurologic and nonneurologic complications of bacterial meningitis have been identified. 23 Dodge and Swartz, 30 in their classic series of articles, give a detailed review of the complications and management. Three decades later, through technologic advances, we have been able to identify the pathologic correlates of some of the complications. The management of these complications has not changed much, however, and is based largely on supportive care. Bacterial meningitis with accompanying bacteremia can lead to a systemic inflammatory response with septic shock, respiratory distress syndrome in adults, and disseminated intravascular coagulation. Intracranial complications may have devastating results. Raised intracranial pressure (ICP) can lead to cerebral herniation, and cerebrovascular involvement may result in incapacitating neurologic deficits. The severity of these complications may lead appropriately to management in the intensive care setting. In this review, we focus on the major complications associated with bacterial meningitis, the pathophysiologic basis of these conditions, their identification, and the proposed management when these situations arise.

Cerebral edema, leading to cerebral herniation, is still a major clinical complication and a common cause of death in patients with FHF. Recording of SEP, an objective parameter of cerebral function, has been proposed to predict the neurological course in patients with FHF. Recently, it has been demonstrated that high arterial ammonia is associated with later death by cerebral herniation. We compared the prognostic accuracy of SEP and arterial ammonia in predicting development of cerebral edema and death from cerebral herniation. We included 54 patients (31 females,aged 36:!:19 years) with FHF. The worst N70 peak latency of SEP and the highest arterial ammonia level within 72 hours after emerge of hepatic encephalopathy grade no was used for analysis. Critical cutoff points were defined as 1.) presence or absence of cortical N70 peaks and 2.) arterial ammonia levels below or above 145 ILmoIIL. 21 patients (39%) developed a loss of the N70 peak and 27 patients (50%) had arterial ammonia levels> 145 ILmoIIL. 26 patients (48%) developed cerebral edema and 16 of those (62%) died from cerebral herniation. Out of 21 patients without N70 peak, all but one developed cerebral edema, but only 13 patients died from cerebral herniation. In contrast, out of 27 patients with arterial ammonia < 145 ILmoIIL, 4 patients developed cerebral edema and only 2 patients died from cerebral herniation. Patients who died from cerebral herniation had higher arterial ammonia concentrations (259:!:167 vs 130:!:106 ILmoIIL; p=O.OOI). The prognostic values of SEP and arterial ammonia are shown in the table. In FHF, recording of SEP has a high predictive accuracy to detect patients at risk of developing cerebral edema but fails to predict later death from cerebral herniation. In contrast, assessment of arterial ammonia fails to identify patients at risk of developing cerebral edema but allows detection of patients without risk of cerebral herniation.