VascularA restricted subarachnoid hemorrhage in the cortical sulcus in cerebral amyloid angiopathy: could it be a warning sign?
Introduction
Cerebral amyloid angiopathy is a well-known disease that is predominantly recognized in elderly people and repeatedly causes large subcortical hemorrhages. These hemorrhages may be derived from vessel wall weakness and are very difficult to anticipate or control.
We report on 2 cases of CAA with huge subcortical hematomas. The patients presented with epileptic seizure and were found to have a restricted subarachnoid hematoma in the cerebral sulcus on MRI before their subcortical hemorrhages occurred.
A restricted SAH with epileptic seizure could be a warning sign of a huge subcortical hemorrhage in CAA.
Section snippets
Case patient 1
A 74-year-old woman presented herself to the Hokkaido Neurosurgical Memorial Hospital because of transient left hemiparesis and sensory disturbance. Neurologic deficit disappeared 30 minutes later. On MRI, there was no abnormality; however, she noted numbness in the left side of her body 7 days after her first visit. Although the numbness disappeared after 15 minutes, a restricted SAH in the right frontal lobe was observed on MRI (Fig. 1).
Because epileptic waves were found on electric
Case patient 2
A 73-year-old man was admitted to the Hokkaido Neurosurgical Memorial Hospital because of repeated left hemiparesis that lasted for approximately 10 minutes. Neurologic examination disclosed slight left hemiparesis. On MRI, a restricted SAH was noted in the right frontal sulcus (Fig. 4).
Sodium valproate was prescribed, and the repeated episodes of left hemiparesis disappeared.
We thought the patient might have had CAA when he presented with a restricted SAH on MRI; therefore, we paid close
Discussion
Cerebral amyloid angiopathy is caused by the deposition of Aβ in the walls of cortical and leptomeningeal arteries. As a rule, veins and capillaries tend to be affected less frequently than arteries [3], [4]. Finally, the layers of smooth muscle cells disappear, resulting in vessel weakness.
Although the etiology of this condition remains unknown, Weller and Nicoll [6] suggested that Aβ deposits in vessel walls because of a loss of function in the periarterial interstitial fluid drainage
References (6)
- et al.
Commentary on “Subcortical hematoma caused by cerebral amyloid angiopathy: does the first evidence of hemorrhage occur in the subarachnoid space?”
Neuropathology
(2003) - et al.
Commentary on “Subcortical hematoma caused by cerebral amyloid angiopathy: does the first evidence of hemorrhage occur in the subarachnoid space?”
Neuropathology
(2004) - et al.
Cerebral amyloid angiopathy as a cause of recurrent intracerebral hemorrhage
Conn Med
(2002)
Cited by (43)
Amyloid accumulation in cases of suspected comorbid cerebral amyloid angiopathy and isolated cortical venous thrombosis
2024, Journal of the Neurological SciencesOutcomes after clipping and endovascular coiling for aneurysmal subarachnoid hemorrhage among dual-eligible beneficiaries
2021, Journal of Clinical NeuroscienceCitation Excerpt :Compared to 1990, there was an increase of 4.0% in the global lifetime risk of hemorrhagic stroke [4]. Intracranial hemorrhage may be epidural, subdural, intracerebral, intraventricular, and subarachnoid [5–12]. Although the most common cause of subarachnoid hemorrhage is trauma, aneurysmal rupture accounts for up to 85% of non-traumatic subarachnoid hemorrhage [13].
Cerebral amyloid angiopathy-related transient focal neurological episodes: A transient ischemic attack mimic with an increased risk of intracranial hemorrhage
2019, Journal of the Neurological SciencesCitation Excerpt :Interestingly, all 4 cases had cSS—whether isolated or in combination with CMB—in the previous cerebral MRI. Several case reports and series have associated cSS with a significantly increased risk of bleeding [26,29]. A previous study suggests that the presence of cSS is closely associated with a hemorrhagic phenotype of CAA, whereas a lower presence of cSS is associated with a non-hemorrhagic form, with a predominance of cognitive impairment [30].
Cerebral amyloid angiopathy – The modified Boston criteria in clinical practice
2018, Journal of the Neurological SciencesCitation Excerpt :Given these non-classical presentations, Linn et al. have recently proposed a revision of the Boston criteria, that considers superficial hemossiderin deposits, presumed to be the result of recurrent assymptomatic cortical bleeds [5,9–11], as a part of diagnostic criteria for CAA, with a (non-significant) increase in sensitivity without changing the specificity [11]. Identifying both typical and atypical patients is important in clinical practice given the high propensity for intracerebral bleeds in CAA patients [8,12–16], and the need to avoid antithrombotic therapy. With this issue in mind, we aimed to assess the impact of applying the modified Boston criteria particularly regarding use of antithrombotic therapy.
Acute Convexity Subarachnoid Hemorrhage Related to Cerebral Amyloid Angiopathy: Clinicoradiological Features and Outcome
2016, Journal of Stroke and Cerebrovascular DiseasesCitation Excerpt :The primary location of bleeding in the brain parenchyma itself cannot be excluded because 2 patients developed ICH distant from cSAH. Because of this high rate of ICH occurrence, acute cSAH may be considered a marker of CAA severity and a warning sign for future ICH.31,32 A recent study reported that disseminated cSS in CAA-related symptomatic ICH was associated with an increased risk of subsequent symptomatic lobar hematoma, when compared with patients without cSS.33
Convexity subarachnoid hemorrhage in ischemic stroke
2015, Journal of the Neurological Sciences