RESUMO
This is an executive summary of the recent guidance produced by the Scottish Intercollegiate Guidelines Network (SIGN) dementia guideline group with regards to the investigation of suspected dementia. This is a sub-section of the broader SIGN 168 guideline released in November 2023. The guideline group included clinicians with expertise in Old Age Psychiatry, Neurology, Radiology, and Nuclear Medicine supported by colleagues from the SIGN and Healthcare Improvement Scotland teams. There was representation from carers and support organizations with experience of dementia, to ensure the recommendations were appropriate from the perspective of the people being assessed for possible dementia and their carers. As the 2018 National Institute for Health and Clinical Excellence (NICE) dementia review included a review of the evidenced investigation of dementia, the SIGN guideline development group decided to focus on a review on the up-to-date evidence regarding the role of imaging and fluid biomarkers in the diagnosis of dementia. To give context to the consideration of more advanced diagnostic biomarker investigations, the guideline and this summary include the NICE guidance on the use of standard investigations as well as more specialist investigations. The evidence review supports consideration of the use of structural imaging, nuclear medicine imaging, and established Alzheimer's cerebrospinal fluid biomarkers (amyloid and tau) in the diagnosis of dementia. Although routine use of amyloid positron emission tomography imaging was not recommended, its potential use, under specialist direction, in patients with atypical or young-onset presentations of suspected Alzheimer's dementia was included as a clinical good practice point.
RESUMO
Autoimmune encephalitis is emerging as an important and relatively common cause of encephalitis in the developed world. Crucially, early recognition and prompt initiation of a range of immunotherapies is likely to improve the outcomes of patients with autoimmune encephalitis, particularly for those with identifiable antibodies against neuronal cell surface proteins. There are a rapidly growing number of specific autoantibodies and associated syndromes, but many of these remain very rare. The majority of cases comprise anti-N-methyl-D-aspartate (NMDA) receptor encephalitis or anti-leucine-rich glioma-inactivated protein 1 (LGI1) encephalitis with the remaining cases a mixture of over 10 other specific antibodies or being seronegative. The core anti-NMDA encephalitis phenotype is a distinct symptom complex involving psychiatric and neurological features and anti-LGI1 encephalitis presents with cognitive changes and distinct seizure types. Diagnosis can be delayed owing to limited access to specialised laboratory testing or in cases with atypical or limited features.