"The primary manifestation of leptomeningeal vessel involvement is due to convexity subarachnoid haemorrhage, which can present with transient focal neurological episodes or symptoms (TFNE or TFNS), colloquially known as "amyloid spells" 25. These transient focal neurological episodes are classically described as recurrent, stereotyped, spreading paraesthesias lasting several minutes but there is a wide spectrum of presentations encompassing both positive (e.g. spreading paraesthesia or visual symptoms) and negative (e.g. paresis, aphasia, dysphagia) phenomenology 17,25. These symptoms are most prominent when the convexity subarachnoid haemorrhage is localised to the central sulcus 16, which is in close proximity to the primary motor and sensory cortices 25."
"The primary manifestation of leptomeningeal vessel involvement is due to convexity subarachnoid haemorrhage, which can present with transient focal neurological episodes or symptoms (TFNE or TFNS), colloquially known as "amyloid spells" 25. These transient focal neurological episodes are classically described as recurrent, stereotyped, spreading paraesthesias lasting several minutes but there is a wide spectrum of presentations encompassing both positive (e.g. spreading paraesthesia or visual symptoms) and negative (e.g. paresis, aphasia, dysphagia) phenomenology 17,25. These symptoms are most prominent when the convexity subarachnoid haemorrhage is localised to the central sulcus 16, which is in close proximity to the primary motor and sensory cortices 25."
"ATTR peptide with precursor protein transthyretin (chromosome 18): meningovascular amyloidosis (see cerebral transthyretin-associated amyloidoses)"
"may be indistinguishable from cerebral amyloid angiopathy (especially ARIA-H), but occur in the setting of amyloid lowering therapies for Alzheimer disease"
"A positive amyloid PET demonstrates loss of cerebral grey-white matter differentiation due to increased tracer uptake in the cortical gray matter 48. Differentiating positive findings from those of Alzheimer disease may be challenging, but in cerebral amyloid angiopathy there may be an occipital-to-global amyloid PET uptake ratio >1, compared to patients with Alzheimer disease where this is not the case 46,47."
Expected headings
"Types"
"Sporadic cerebral amyloid angiopathy"
"Familial cerebral amyloid angiopathy"
"Iatrogenic cerebral amyloid angiopathy"
"Associations"
"CT and MRI"
"Amyloid PET"
"There are a number of different proteins that can lead to intravascular amyloid deposition, however, the most common, as is the case in sporadic cerebral amyloid angiopathy, is Aß which is a short 42 amino acid peptide (Aβ42) cleaved from amyloid precursor protein (APP) which is encoded on chromosome 21 20."
"There are no established disease-modifying treatments available 27,46. A number of potential avenues of treatment are being investigated including 39:"
"acute cortico-subcortical lesions that may be asymptomatic and incidental 56; lobar lacunes are 3-15 millimetres in size while cerebral cortical microinfarcts are"
"haemorrhagic metastases (e.g. melanoma)"
"have an appropriate clinical history (e.g. trauma, orthopaedic surgery)"