Iatrogenic Cerebral Amyloid Angiopathy Post Neurosurgery: Frequency, Clinical Profile, Radiological Features, and Outcome
Prion-like transmission of amyloid-ß through cadaveric dura, decades after neurosurgical procedures, has been hypothesized as an iatrogenic cause of cerebral amyloid angiopathy (CAA). We investigated new and previously described patients to assess the clinical profile, radiological features, and out...
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| Vydané v: | Stroke (1970) Ročník 54; číslo 5; s. 1214 |
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| Hlavní autori: | , , , , , , , , , , |
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| Jazyk: | English |
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01.05.2023
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| ISSN: | 1524-4628, 1524-4628 |
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| Abstract | Prion-like transmission of amyloid-ß through cadaveric dura, decades after neurosurgical procedures, has been hypothesized as an iatrogenic cause of cerebral amyloid angiopathy (CAA). We investigated new and previously described patients to assess the clinical profile, radiological features, and outcome of this presumed iatrogenic CAA-subtype (iCAA).
Patients were collected from our prospective lobar hemorrhage and CAA database (n=251) with patients presenting to our hospital between 2008 and 2022. In addition, we identified patients with iCAA from 2 other Dutch CAA-expertise hospitals and performed a systematic literature-search for previously described patients. We classified patients according to the previously proposed diagnostic criteria for iCAA, assessed clinical and radiological disease features, and calculated intracerebral hemorrhage (ICH)-recurrence rates. We evaluated the spatial colocalization of cadaveric dura placement and CAA-associated magnetic resonance imaging markers.
We included 49 patients (74% men, mean age 43 years [range, 27-84]); 15 from our database (6% [95% CI, 3%-10%]; 45% of patients <55 years), 3 from the 2 other CAA-expertise hospitals, and 31 from the literature. We classified 43% (n=21; 1 newly identified patient) as probable and 57% (n=28) as possible iCAA. Patients presented with lobar ICH (57%), transient focal neurological episodes (12%), or seizures (8%). ICH-recurrence rate in the new patients (16/100 person-years [95% CI, 7-32], median follow-up 18 months) was lower than in the previously described patients (77/100 person-years [95% CI, 59-99], median follow-up 18 months). One patient had a 10 year interlude without ICH-recurrence. We identified no clear spatial relationship between dura placement and CAA-associated magnetic resonance imaging markers. During follow-up (median, 18 months), 20% of the patients developed transient focal neurological episodes and 20% cognitively declined.
iCAA seems common in patients presenting with nonhereditary CAA under the age of 55. Clinical and radiological features are comparable with sCAA. After diagnosis, multiple ICH-recurrences but also long symptom-free intervals can occur. Harmonized registries are necessary to identify and understand this potentially underrecognized CAA-subtype. |
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| AbstractList | Prion-like transmission of amyloid-ß through cadaveric dura, decades after neurosurgical procedures, has been hypothesized as an iatrogenic cause of cerebral amyloid angiopathy (CAA). We investigated new and previously described patients to assess the clinical profile, radiological features, and outcome of this presumed iatrogenic CAA-subtype (iCAA).
Patients were collected from our prospective lobar hemorrhage and CAA database (n=251) with patients presenting to our hospital between 2008 and 2022. In addition, we identified patients with iCAA from 2 other Dutch CAA-expertise hospitals and performed a systematic literature-search for previously described patients. We classified patients according to the previously proposed diagnostic criteria for iCAA, assessed clinical and radiological disease features, and calculated intracerebral hemorrhage (ICH)-recurrence rates. We evaluated the spatial colocalization of cadaveric dura placement and CAA-associated magnetic resonance imaging markers.
We included 49 patients (74% men, mean age 43 years [range, 27-84]); 15 from our database (6% [95% CI, 3%-10%]; 45% of patients <55 years), 3 from the 2 other CAA-expertise hospitals, and 31 from the literature. We classified 43% (n=21; 1 newly identified patient) as probable and 57% (n=28) as possible iCAA. Patients presented with lobar ICH (57%), transient focal neurological episodes (12%), or seizures (8%). ICH-recurrence rate in the new patients (16/100 person-years [95% CI, 7-32], median follow-up 18 months) was lower than in the previously described patients (77/100 person-years [95% CI, 59-99], median follow-up 18 months). One patient had a 10 year interlude without ICH-recurrence. We identified no clear spatial relationship between dura placement and CAA-associated magnetic resonance imaging markers. During follow-up (median, 18 months), 20% of the patients developed transient focal neurological episodes and 20% cognitively declined.
iCAA seems common in patients presenting with nonhereditary CAA under the age of 55. Clinical and radiological features are comparable with sCAA. After diagnosis, multiple ICH-recurrences but also long symptom-free intervals can occur. Harmonized registries are necessary to identify and understand this potentially underrecognized CAA-subtype. Prion-like transmission of amyloid-ß through cadaveric dura, decades after neurosurgical procedures, has been hypothesized as an iatrogenic cause of cerebral amyloid angiopathy (CAA). We investigated new and previously described patients to assess the clinical profile, radiological features, and outcome of this presumed iatrogenic CAA-subtype (iCAA).BACKGROUNDPrion-like transmission of amyloid-ß through cadaveric dura, decades after neurosurgical procedures, has been hypothesized as an iatrogenic cause of cerebral amyloid angiopathy (CAA). We investigated new and previously described patients to assess the clinical profile, radiological features, and outcome of this presumed iatrogenic CAA-subtype (iCAA).Patients were collected from our prospective lobar hemorrhage and CAA database (n=251) with patients presenting to our hospital between 2008 and 2022. In addition, we identified patients with iCAA from 2 other Dutch CAA-expertise hospitals and performed a systematic literature-search for previously described patients. We classified patients according to the previously proposed diagnostic criteria for iCAA, assessed clinical and radiological disease features, and calculated intracerebral hemorrhage (ICH)-recurrence rates. We evaluated the spatial colocalization of cadaveric dura placement and CAA-associated magnetic resonance imaging markers.METHODSPatients were collected from our prospective lobar hemorrhage and CAA database (n=251) with patients presenting to our hospital between 2008 and 2022. In addition, we identified patients with iCAA from 2 other Dutch CAA-expertise hospitals and performed a systematic literature-search for previously described patients. We classified patients according to the previously proposed diagnostic criteria for iCAA, assessed clinical and radiological disease features, and calculated intracerebral hemorrhage (ICH)-recurrence rates. We evaluated the spatial colocalization of cadaveric dura placement and CAA-associated magnetic resonance imaging markers.We included 49 patients (74% men, mean age 43 years [range, 27-84]); 15 from our database (6% [95% CI, 3%-10%]; 45% of patients <55 years), 3 from the 2 other CAA-expertise hospitals, and 31 from the literature. We classified 43% (n=21; 1 newly identified patient) as probable and 57% (n=28) as possible iCAA. Patients presented with lobar ICH (57%), transient focal neurological episodes (12%), or seizures (8%). ICH-recurrence rate in the new patients (16/100 person-years [95% CI, 7-32], median follow-up 18 months) was lower than in the previously described patients (77/100 person-years [95% CI, 59-99], median follow-up 18 months). One patient had a 10 year interlude without ICH-recurrence. We identified no clear spatial relationship between dura placement and CAA-associated magnetic resonance imaging markers. During follow-up (median, 18 months), 20% of the patients developed transient focal neurological episodes and 20% cognitively declined.RESULTSWe included 49 patients (74% men, mean age 43 years [range, 27-84]); 15 from our database (6% [95% CI, 3%-10%]; 45% of patients <55 years), 3 from the 2 other CAA-expertise hospitals, and 31 from the literature. We classified 43% (n=21; 1 newly identified patient) as probable and 57% (n=28) as possible iCAA. Patients presented with lobar ICH (57%), transient focal neurological episodes (12%), or seizures (8%). ICH-recurrence rate in the new patients (16/100 person-years [95% CI, 7-32], median follow-up 18 months) was lower than in the previously described patients (77/100 person-years [95% CI, 59-99], median follow-up 18 months). One patient had a 10 year interlude without ICH-recurrence. We identified no clear spatial relationship between dura placement and CAA-associated magnetic resonance imaging markers. During follow-up (median, 18 months), 20% of the patients developed transient focal neurological episodes and 20% cognitively declined.iCAA seems common in patients presenting with nonhereditary CAA under the age of 55. Clinical and radiological features are comparable with sCAA. After diagnosis, multiple ICH-recurrences but also long symptom-free intervals can occur. Harmonized registries are necessary to identify and understand this potentially underrecognized CAA-subtype.CONCLUSIONSiCAA seems common in patients presenting with nonhereditary CAA under the age of 55. Clinical and radiological features are comparable with sCAA. After diagnosis, multiple ICH-recurrences but also long symptom-free intervals can occur. Harmonized registries are necessary to identify and understand this potentially underrecognized CAA-subtype. |
| Author | van Walderveen, Marianne A A Klijn, Catharina J M van Etten, Ellis S Peul, Wilco C Terwindt, Gisela M Kappelle, L Jaap Lemstra, Afina W Wermer, Marieke J H Siegerink, Bob Schreuder, Floris H B M Kaushik, Kanishk |
| Author_xml | – sequence: 1 givenname: Kanishk orcidid: 0000-0003-1429-6853 surname: Kaushik fullname: Kaushik, Kanishk organization: Department of Neurology (K.K., E.S.v.E., G.M.T., M.J.H.W.), Leiden University Medical Center, the Netherlands – sequence: 2 givenname: Ellis S orcidid: 0000-0002-8301-6846 surname: van Etten fullname: van Etten, Ellis S organization: Department of Neurology (K.K., E.S.v.E., G.M.T., M.J.H.W.), Leiden University Medical Center, the Netherlands – sequence: 3 givenname: Bob orcidid: 0000-0002-8454-9142 surname: Siegerink fullname: Siegerink, Bob organization: Department of Clinical Epidemiology (B.S.), Leiden University Medical Center, the Netherlands – sequence: 4 givenname: L Jaap orcidid: 0000-0001-8665-6630 surname: Kappelle fullname: Kappelle, L Jaap organization: Department of Neurology, University Medical Center Utrecht, the Netherlands (L.J.K.) – sequence: 5 givenname: Afina W orcidid: 0000-0002-8933-3260 surname: Lemstra fullname: Lemstra, Afina W organization: Department of Neurology, Alzheimer center Amsterdam, Amsterdam University Medical Center, the Netherlands (A.W.L.) – sequence: 6 givenname: Floris H B M orcidid: 0000-0002-7815-0207 surname: Schreuder fullname: Schreuder, Floris H B M organization: Department of Neurology, Donders Institute for Brain, Cognition and Behavior, Radboud University Medical Center, the Netherlands (F.H.B.M.S., C.J.M.K.) – sequence: 7 givenname: Catharina J M orcidid: 0000-0002-8495-4578 surname: Klijn fullname: Klijn, Catharina J M organization: Department of Neurology, Donders Institute for Brain, Cognition and Behavior, Radboud University Medical Center, the Netherlands (F.H.B.M.S., C.J.M.K.) – sequence: 8 givenname: Wilco C surname: Peul fullname: Peul, Wilco C organization: University Neurosurgical Center Holland, LUMC|HMC|HAGA Leiden & The Hague, the Netherlands (W.C.P.) – sequence: 9 givenname: Gisela M orcidid: 0000-0003-3140-6882 surname: Terwindt fullname: Terwindt, Gisela M organization: Department of Neurology (K.K., E.S.v.E., G.M.T., M.J.H.W.), Leiden University Medical Center, the Netherlands – sequence: 10 givenname: Marianne A A orcidid: 0000-0003-4895-229X surname: van Walderveen fullname: van Walderveen, Marianne A A organization: Department of Radiology (M.A.A.v.W.), Leiden University Medical Center, the Netherlands – sequence: 11 givenname: Marieke J H orcidid: 0000-0002-6838-9521 surname: Wermer fullname: Wermer, Marieke J H organization: Department of Neurology (K.K., E.S.v.E., G.M.T., M.J.H.W.), Leiden University Medical Center, the Netherlands |
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| SubjectTerms | Adult Cadaver Cerebral Amyloid Angiopathy - complications Cerebral Hemorrhage - etiology Female Humans Iatrogenic Disease Magnetic Resonance Imaging - methods Male Neurosurgery Neurosurgical Procedures - adverse effects Prospective Studies |
| Title | Iatrogenic Cerebral Amyloid Angiopathy Post Neurosurgery: Frequency, Clinical Profile, Radiological Features, and Outcome |
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