Cerebral amyloid angiopathy (case report)

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Abstract

Cerebral amyloid angiopathy (CAA) is characterized by β-amyloid deposition in cortical and leptomeningeal arteries of small and medium size that disturbs normal structure of arterial wall. CAA is one of the often causes of peripheral intracerebral hemorrhages and cognitive impairment in old patients. We describe male patient, 52 years with CAA. Clinical picture was characterized by recurrent cortical-subcortical (lobar) hemorrhages, cognitive impairment of subcortiical type and epileptic seizures. MRI revealed superficial posthemorrhagic lesions. Gradient-echo MRI found small multiple asymptomatic hemorrhages in cerebral cortex and subcortical matter. Repeat gradientecho MRI carried out monthes revealed new clinically asymptomatic hemorrhages. Arterial hypertension as a cause of intracerebral hemorrhage was excluded on the base of atypical location of hemorrhage (superficial, but not deep). CAA diagnosis was made according to international Boston criteria: multiple lobar, cortical-subcortical hemorrhages not connected with other definite cause of intracerebral hemorrhage. Gradient-echo MRI is of a great importance in diagnosis of CAA, as it discovers small cortical and superficial hemorrhages, none detected by standard MRI regimes.

 
 

About the authors

Larisa A. Dobrynina

Research Center of Neurology

Author for correspondence.
Email: dobrla@mail.ru
ORCID iD: 0000-0001-9929-2725

D. Sci. (Med.), Head, 3rd Neurology department

Россия, Moscow

Lyudmila A. Kalashnikova

Research Center of Neurology

Email: dobrla@mail.ru
Россия, Moscow

Rodion N. Konovalov

Research Center of Neurology

Email: dobrla@mail.ru
ORCID iD: 0000-0001-5539-245X

Cand. Sci. (Med.), senior researcher, Neuroradiology department

Россия, 125367 Moscow, Volokolamskoye shosse, 80

Albert S. Kadykov

Research Center of Neurology

Email: dobrla@mail.ru
ORCID iD: 0000-0001-7491-7215

D. Sci. (Med.), Professor, senior researcher, 3rd Neurological department

Россия, Moscow

References

  1. Верещагин Н.В., Моргунов В.А., Гулевская Т.С. Патология головного мозга при атеросклерозе и артериальной гипертонии. М.: Медицина, 1997: 202–225.
  2. Калашникова Л.А. Неврологические аспекты сосудистой деменции. Очерки ангионеврологии. М.: Атмосфера. 2005: 277–288.
  3. Калашникова Л.А., Гулевская Т.С., Кадыков А.С. и др. Субкортикальная артериосклеротическая энцефалопатия (клиникоморфологическое исследование). Неврологический журнал 1998; 2: 7–13.
  4. Chao C.P., Kotsenas A.L., Broderick D.F. Cerebral amyloid angiopathy: CT and MR imaging findings. Radiographics 2006; 26 (5): 1517–31.
  5. Chen Y.W., Gurol M.E., Rosand J. et al. Progression of white matter lesions and hemorrhages in cerebral amyloid angiopathy. Neurology 2006; 67 (1): 83–7.
  6. Greenberg S.M., Briggs M.E., Hyman В.Т. et al. Apolipoprotein E e4 is associated with the presence and earlier onset of hemorrhage in cerebral amyloid angiopathy. Stroke 1996; 27: 1333–1337.
  7. Greenberg S.M., Edgar M.A. Case records of the Massachusetts General hospital. N. Engl. J. Med. 1996; 335: 189–196.
  8. Greenberg S.M., Eng J.A., Ning M. et al. Hemorrhage burden predicts recurrent intracerebral hemorrhage after lobar hemorrhage. Stroke 2004; 35: 1415–1420.
  9. Greenberg S.M., Finklestein S.P., Schaefer P.W. Petechial hemorrhages accompanying lobar hemorrhages: detection by gradienttecho MRI. Neurology 1996; 46: 1751–1754.
  10. Greenberg S.M., Vonsattel J.P., Stakes J.W. et al. The clinical spec trum of cerebral amiloid angopathy: presentation without lobar hemorrhage. Neurology 1993; 43: 2073–2079.
  11. Greenberg S.M., Vonsattel J..P.G. Diagnosis of cerebral amiloid angiopathy. Sensitivity and specificity of cortical biopsy. Stroke 1997; 28: 1418–1422.
  12. Greenberg S.M., Vonsattel J..P.G., Segal A.Z. Association of apolipoprotein E є2 and vasculopathy in cerebral amyloid angiopathy. Neurology 1998; 50: 961–965.
  13. Greenberg S.M. Cerebral amiloid angiopathy. Neurology 1998; 51: 690–694.
  14. Hendricks H.T., Franke C.L., Theunissen P.H. Cerebral amiloidangiopathy: diagnosis by MRI and brain biopsy. Neurology 1990; 40: 1308–1310.
  15. Herzig M.C., Van Nostrand W.E., Jucker M. Mechanism of cerebral betaaamyloid angiopathy: murine and cellular models. Brain Pathol. 2006; 16 (1): 40–54.
  16. Imaoka K., Kobayashi S., Fujihara S. et al. Leukoencephalopathy with cerebral amyloid angiopathy: a semiquantitative and morphomettric study. J. Neurol. 1999; 246: 661–666.
  17. Itoh Y., Yamada M., Hayakava M. et al. Cerebral amiloid angiopathy: a significant cause of cerebellar as well as lobar cerebral hemorrhage in the elderly. J. Neurol. Sci. 1993; 116: 135–141.
  18. Knudsen K.A., Rosand J., Karluk D. et al. Clinical diagnosis of cerebral amyloid angiopathy: Validation of the Boston Criteria. Neurology 2001; 56: 537–539.
  19. Maia L.F., Vasconcelos C., Seixas S. et al. Lobar brain hemorrhages and white matter changes: Clinical, radiological and laboratorial profiles. Cerebrovasc. Dis. 2006; 22 (2–3): 155–61.
  20. Mandybur T.I. Cerebral amiloid angiopathy: the vascular pathology and complications. J. Neuropathol. Exp. Neurol. 1986; 45: 79–90.
  21. McCarron M.O., Nicoll J.A., Stewart J. et al. The apolipoprotein E. epsilon 2 allele and the pathological features in cerebral amyloid angiopathyyrelated hemorrhage. J. Neuropathol. Exp. Neurol. 1999; 58: 711–718.
  22. Oide T., Takahashi H., Yutani C. et al. Relationship between lobar intracerebral hemorrhage and leukoencephalopathy associated with cerebral amyloid angiopathy: clinicopathological study of 64 Japanese patients. Amyloid 2003; 10: 136–143.
  23. Smith E.E., Gurol M.E., Eng J.A. et al. White matter lesions, cognition, and recurrentn hemorrhage in lobar intracerebral hemorrhage. Neurology 2004; 63: 1606–1612.
  24. Thomas T., Thomas G., McLendon C. et al. Betaaamyloidmediated vasoactivity and vascular endothelial damage. Nature 1996: 380 (6570): 168–171.
  25. Vinters H.V. Cerebral amiloid angiopathy: a critical review. Stroke 1987; 18: 311–324.
  26. Yamada M., Itoh Y., Otomo E. et al. Subarachnoid haemorrage in the elderly: a necropsy study of the associaton with cerebral amiloid angiopathy. J. Neurol. Neurosurg. Psychiatr. 1993; 56: 543–547.
  27. Yamada M. Cerebral amyloid angiopathy and gene polymorphisms. J. Neurol. Sci. 2004; 226 (1–2): 41–44.
  28. ZhanggNunes S.X., MaattSchieman M.L., van Duinen S.G. et al. The cerebral betaaamyloid angiopathies: hereditary and sporadic. Brain Pathol. 2006; 16 (1).
  30. Greenberg S.M., Vonsattel J.P., Stakes J.W. et al. The clinical spec trum of cerebral amiloid angopathy: presentation without lobar hemorrhage. Neurology 1993; 43: 2073–2079.
  31. Greenberg S.M., Vonsattel J..P.G. Diagnosis of cerebral amiloid angiopathy. Sensitivity and specificity of cortical biopsy. Stroke 1997; 28: 1418–1422.
  32. Greenberg S.M., Vonsattel J..P.G., Segal A.Z. Association of apolipoprotein E є2 and vasculopathy in cerebral amyloid angiopathy. Neurology 1998; 50: 961–965.
  33. Greenberg S.M. Cerebral amiloid angiopathy. Neurology 1998; 51: 690–694.
  34. Hendricks H.T., Franke C.L., Theunissen P.H. Cerebral amiloidangiopathy: diagnosis by MRI and brain biopsy. Neurology 1990; 40: 1308–1310.
  35. Herzig M.C., Van Nostrand W.E., Jucker M. Mechanism of cerebral betaaamyloid angiopathy: murine and cellular models. Brain Pathol. 2006; 16 (1): 40–54.
  36. Imaoka K., Kobayashi S., Fujihara S. et al. Leukoencephalopathy with cerebral amyloid angiopathy: a semiquantitative and morphomettric study. J. Neurol. 1999; 246: 661–666.
  37. Itoh Y., Yamada M., Hayakava M. et al. Cerebral amiloid angiopathy: a significant cause of cerebellar as well as lobar cerebral hemorrhage in the elderly. J. Neurol. Sci. 1993; 116: 135–141.
  38. Knudsen K.A., Rosand J., Karluk D. et al. Clinical diagnosis of cerebral amyloid angiopathy: Validation of the Boston Criteria. Neurology 2001; 56: 537–539.
  39. Maia L.F., Vasconcelos C., Seixas S. et al. Lobar brain hemorrhages and white matter changes: Clinical, radiological and laboratorial profiles. Cerebrovasc. Dis. 2006; 22 (2–3): 155–61.
  40. Mandybur T.I. Cerebral amiloid angiopathy: the vascular pathology and complications. J. Neuropathol. Exp. Neurol. 1986; 45: 79–90.
  41. McCarron M.O., Nicoll J.A., Stewart J. et al. The apolipoprotein E. epsilon 2 allele and the pathological features in cerebral amyloid angiopathyyrelated hemorrhage. J. Neuropathol. Exp. Neurol. 1999; 58: 711–718.
  42. Oide T., Takahashi H., Yutani C. et al. Relationship between lobar intracerebral hemorrhage and leukoencephalopathy associated with cerebral amyloid angiopathy: clinicopathological study of 64 Japanese
  43. patients. Amyloid 2003; 10: 136–143.
  44. Smith E.E., Gurol M.E., Eng J.A. et al. White matter lesions, cognition, and recurrentn hemorrhage in lobar intracerebral hemorrhage. Neurology 2004; 63: 1606–1612.
  45. Thomas T., Thomas G., McLendon C. et al. Betaaamyloidmediated vasoactivity and vascular endothelial damage. Nature 1996: 380 (6570): 168–171.
  46. Vinters H.V. Cerebral amiloid angiopathy: a critical review. Stroke 1987; 18: 311–324.
  47. Yamada M., Itoh Y., Otomo E. et al. Subarachnoid haemorrage in the elderly: a necropsy study of the associaton with cerebral amiloid angiopathy. J. Neurol. Neurosurg. Psychiatr. 1993; 56: 543–547.
  48. Yamada M. Cerebral amyloid angiopathy and gene polymorphisms. J. Neurol. Sci. 2004; 226 (1–2): 41–44.
  49. ZhanggNunes S.X., MaattSchieman M.L., van Duinen S.G. et al. The cerebral betaaamyloid angiopathies: hereditary and sporadic. Brain Pathol. 2006; 16 (1).

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Copyright (c) 2008 Dobrynina L.A., Kalashnikova L.A., Konovalov R.N., Kadykov A.S.

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