"T2/FLAIR:"
"T1 C+ (Gd):"
"SWI: may have microhaemorrhages 1"
"DWI/ADC: areas of ischaemia/cytotoxic oedema result in restricted diffusion"
"CBF: increased perfusion"
"MR spectroscopy:"
"because some of the MRI features of ICANS can be non-specific, having a pre-therapy baseline scan to compare to may be helpful 12"
"The pathophysiology of ICANS is not fully understood but it is thought to involve cytokine-mediated inflammation and disruption of the blood-brain barrier 1,3. Some of the cytokines that have been implicated in ICANS include interleukin-6 (IL-6), interferon-gamma (IFN-gamma), granulocyte-macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor-alpha (TNF-alpha), and IL-213. These cytokines may activate microglia and astrocytes in the central nervous system and cause neuroinflammation 3."
"The mortality rate of ICANS has been reported to range from 0-11% depending on the study population and definition used. Factors that have been associated with poor outcome include older age higher grade longer duration and delayed onset."
Expected headings
"Grading"
"Brain"
"Spine"
"Immune effector cell-associated neurotoxicity syndrome (ICANS), previously known as cytokine release encephalopathy syndrome (CRES) or chimeric antigen receptor (CAR) T-cell-related encephalopathy syndrome (CRES), is a neuropsychiatric syndrome that can occur days to weeks following the administration of certain types of immunotherapy, especially immune effector cell and T-cell engaging therapies (e.g. chimeric antigen receptor (CAR) T-cell therapy, bispecific T-cell engagers (BiTE)) 1-4. It can result in life-threatening cerebral oedema."
"The pathophysiology of ICANS is not fully understood but it is thought to involve cytokine-mediated inflammation and disruption of the blood-brain barrier 1,3. Some of the cytokines that have been implicated in ICANS include interleukin-6 (IL-6), interferon-gamma (IFN-gamma), granulocyte-macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor-alpha (TNF-alpha), and IL-213. These cytokines may activate microglia and astrocytes in the central nervous system and cause neuroinflammation 3."
"ICANS has a heterogeneous and non-specific clinical presentation and may manifest as encephalopathy/delirium, headache, myelopathy, aphasia, lethargy, difficulty concentrating, agitation, tremor, seizures, and symptoms of increased cranial pressure 1,4,6,10. In a minority of cases, progression to obtundation, coma and death can be rapid 1. Onset tends to be within days or weeks (most within 1 week) of CAR T-cell infusion, but this depends on the exact product used 1."
"ICANS has a heterogeneous and non-specific clinical presentation and may manifest as encephalopathy/delirium, headache, myelopathy, aphasia, lethargy, difficulty concentrating, agitation, tremor, seizures, and symptoms of increased cranial pressure 1,4,6,10. In a minority of cases, progression to obtundation, coma and death can be rapid 1. Onset tends to be within days or weeks (most within 1 week) of CAR T-cell infusion, but this depends on the exact product used 1."
"The treatment of ICANS depends on its severity and on the underlying cause. Many therapies are supportive and aimed to control specific manifestations (e.g. antiseizure medications for seizures)."