You will be presented with the full text of a biomedical research paper. Please write an abstract for this paper. Your response should include the abstract and no additional text.

Paper text:
cerebral amyloid angiopathy ( caa ) is characterized by the deposition of beta amyloid proteins within the cortical and leptomeningeal vessels .
it is a common pathological finding in elderly patients , regardless of concomitant cognitive impairment , and 1040% of elderly brains have pathological evidence of amyloid deposition .
the most frequent presentation of caa in older patients is intracranial hemorrhage , usually recurrent , sparing regions affected by hypertensive hemorrhage and mainly affecting the cerebral or cerebellar cortex and the cortico - subcortical regions ( reflecting locations of amyloid deposition ) [ 2 , 3 ] .
one of the landmarks in caa history was the development of the boston criteria by greenberg and collaborators in 1996 .
these criteria were created to improve the diagnostic accuracy of caa , to provide an easier method for clinical decision - making , and to facilitate a diagnosis during lifetime ( without the need for postmortem pathological evaluation ) by allowing for probable and possible diagnosis .
these criteria reflect the main defining characteristics of caa ( age > 55 years , presentation with multiple parenchymal hematomas and typical pathological findings ) , but they also accommodate the classical imaging findings of cerebral chronic microbleeds , which represent asymptomatic , small , spontaneous bleedings caused by caa .
recently , superficial siderosis and cortical subarachnoid hemorrhage ( csah ) in patients with transient focal neurological symptoms ( tfns ) , the so - called amyloid spells have been related to the phenotype of caa , and several studies suggest that these findings might predict intracerebral hemorrhages caused by caa in the long run [ 4 , 5 , 6 ] .
we report a patient who suffered a massive intracerebral hemorrhage 48 h after presenting to the emergency department with tfns and csah .
a 71-year - old male with a recent history of recurrent episodes of left arm and face paresthesias was admitted to our department after a first generalized convulsive seizure .
his past medical history disclosed hypertension , hypercholesterolemia and peripheral arterial disease , but no known epilepsy , cerebrovascular events or cognitive impairment .
a general examination was unremarkable , and a neurological examination revealed mild left facial palsy and left visual and tactile extinction .
a ct of his brain showed right parietal and left frontal sulcal cortical subarachnoid hemorrhages ( fig .
his antithrombotic medication was stopped , and the patient was started on phenytoin ( 100 mg t.d.s . ) and perindopril ( 5 mg o.d . ) . despite his treatment , the patient remained confused and agitated and his blood pressure values ranged from 160200 ( systolic ) and 7097 mm hg ( diastolic ) . on day 2 of his hospitalization ,
a brain ct revealed a large left frontoparietal and a circumscribed right parietal parenchymal hemorrhage ( ph ) ( fig .
the patient 's blood pressure was controlled with a low dose of bisoprolol and furosemide , and then , there were no further events . a brain mri at 3 months revealed disseminated superficial siderosis without any microbleeds on t2 * ( fig .
the patient was discharged at 3 months with a modified rankin scale score of 4 but died 1 month later of unknown causes and without any autopsy being performed on him .
despite usually presenting as a ph , caa is also a recognized and important cause for spontaneous csah [ 7 , 8 , 9 ] . on the other hand ,
there have also been several reports of patients without the classical caa findings where blood susceptibility imaging revealed only a superficial siderosis , presumed to be the result of recurrent asymptomatic cortical bleeds [ 7 , 8 , 10 , 11 ] , suggesting that csah can occur not only as a secondary phenomenon in the context of a deep cerebral hemorrhage but also as a primary event [ 11 , 12 ] .
some interest has been found in patients with atypical tfns who have positive or negative transient symptoms ( hemianesthesia or hemiparesis ) , the so - called  amyloid spells [ 4 , 10 , 13 , 14 ] . in these patients ,
blood susceptibility imaging revealed the presence of superficial siderosis , a finding which has been strongly associated with the caa pathology   and which presumably reflects previous spontaneous csah .
there is no clear explanation for these tfns , but it is believed that the presence of superficial siderosis could be the catalyst for an epileptic manifestation or even a migraine aura - like cortical spreading depression ( as proposed by some authors ) .
the finding of superficial siderosis in caa - proven patients , associated with presentations as tfns , supports the claim that some patients with caa do not have the classical clinical picture of ph and cerebral microbleeds on mri , but they can present with tfns and have isolated superficial siderosis as an imaging marker [ 13 , 14 ] , thus reinforcing the need for a revision of the boston criteria .
however , when patients present with tfns , caa is usually disregarded as a possible cause , because most of these patients do not have a cognitive decline , and most of them have other cardiovascular risk factors for transient neurological episodes ( ischemic events being the main suspect )
although the natural history of these patients is not clearly established , several studies suggest that they are at an increased risk of intracerebral bleeding within the next days / months [ 5 , 6 , 14 , 15 ] .
curiously , when these phs occur , they tend to occur in the same location as a pre - existing superficial siderosis ( as it has occurred in our patient ) [ 5 , 12 ] .
it has been suggested that in these patients , the first evidence of bleeding may occur as a csah , which could be seen as a warning sign for future phs [ 5 , 12 ] .
the case reports describing these events show a variable latency period between csah and ph ( range 732 days ) [ 5 , 12 ] , but clearly , and this case seems to have the shortest latency period , the risk can be present since an initial presentation of csah . avoiding antithrombotics
has been emphasized before [ 4 , 14 ] , but vigilance and strict blood pressure control should also be considered due to the risk of developing severe phs .
further studies are needed to understand the natural history of patients with amyloid spells and csah , but lowering the risk of future bleeds seems to be of utmost importance . in summary ,
. some of these patients can present with transient focal neurological symptoms and have evidence of superficial siderosis on susceptibility - weighted mri , which would probably reflect previous spontaneous symptomatic or even asymptomatic csah .
these patients should be tightly monitored , especially regarding their blood pressure profile and because they are at an increased risk of phs , which can occur in the hyper - acute phase .
we present the case of a 71-year - old male , admitted after a generalized tonic - clonic seizure , with a history of recurrent left arm and face paresthesias , associated with sulcal cortical subarachnoid hemorrhages . during the next 48 h 
 , he remained agitated with a high blood pressure profile ; he also suffered a cardiac arrest in relation to a severe left fronto - parietal and a smaller right parietal parenchymal hemorrhage that developed over the subarachnoid hemorrhage locations . 
 there were no intracranial vascular abnormalities . 
 three months later , an mri revealed disseminated superficial siderosis . 
 he was discharged with a modified rankin scale of 4 . 
 he died 1 month later of unknown cause . 
 a diagnosis of probable cerebral amyloid angiopathy was assumed . 
 patients with pathologically proven cerebral amyloid angiopathy that present with transient focal neurological symptoms in relation to cortical bleeds , the so - called  
 myloid spells seem to be at an increased risk of future parenchymal hemorrhages . 
 avoiding antiplatelet agents in these cases has been proposed . 
 our case suggests that these patients should be monitored closely in the hyperacute phase , and tight blood pressure control should be considered as the immediate risk of bleeding may be high , even without a definitive diagnosis of cerebral amyloid angiopathy .