The natural history of familial cavernous malformations: results of an ongoing study

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✓ Cavernous malformations are congenital abnormalities of the cerebral vessels that affect 0.5% to 0.7% of the population. They occur in two forms: a sporadic form characterized by isolated lesions, and a familial form characterized by multiple lesions with an autosomal dominant mode of inheritance. The management of patients with cavernous malformations, particularly those with the familial form of the disease, remains a challenge because little is known regarding the natural history.

The authors report the results of an ongoing study in which six families afflicted by familial cavernous malformations have been prospectively followed with serial interviews, physical examinations, and magnetic resonance (MR) imaging at 6- to 12-month intervals. A total of 59 members of these six families were screened for protocol enrollment; 31 (53%) had MR evidence of familial cavernous malformations. Nineteen (61%) of these 31 patients were symptomatic, with seizures in 12 (39%), recurrent headaches in 16 (52%), focal sensory/motor deficits in three (10%), and visual field deficits in two (6%). Twenty-one of these 31 patients underwent at least two serial clinical and MR imaging examinations. A total of 128 individual cavernous malformations (mean 6.5 ± 3.8 lesions/patient) were identified and followed radiographically. During a mean follow-up period of 2.2 years (range 1 to 5.5 years), serial MR images demonstrated 17 new lesions in six (29%) of the 21 patients; 13 lesions (10%) showed changes in signal characteristics, and five lesions (3.9%) changed significantly in size. The incidence of symptomatic hemorrhage was 1.1% per lesion per year.

The results of this study demonstrate that the familial form of cavernous malformations is a dynamic disease; serial MR images revealed changes in the number, size, and imaging characteristics of lesions consistent with acute or resolving hemorrhage. It is believed that the de novo development of new lesions in this disease has not been previously reported. These findings suggest that patients with familial cavernous malformations require careful follow-up monitoring, and that significant changes in neurological symptoms warrant repeat MR imaging. Surgery should be considered only for lesions that produce repetitive or progressive symptoms. Prophylactic resection of asymptomatic lesions does not appear to be indicated.

Article Information

Address for Dr. Brown: Division of Neuroradiology, Kaiser Permanente Hospital, Portland, Oregon.

Address for Dr. Rigamonti: Division of Neurological Surgery, University of Maryland Hospital, Baltimore, Maryland.

Address reprint requests to: Joseph M. Zabramski, M.D., c/o Editorial Office, Barrow Neurological Institute, 350 West Thomas Road, Phoenix, Arizona 85013.

© AANS, except where prohibited by US copyright law.

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    Magnetic resonance (MR) T1-weighted (A and B) and T2-weighted (C and D) imaging sections obtained 1 year after surgery in a 45-year-old Hispanic woman (Patient B3 in Fig. 4), who presented with the sudden onset of double vision and severe headache. The MR images at the time of her initial presentation revealed an approximately 1.5-cm acute hemorrhage in the tectum of the left midbrain, as well as multiple other hemorrhagic lesions of varying size and age. The MR findings and a strong family history of seizures were believed to be consistent with a diagnosis of familial cavernous malformations. Gross total resection of the midbrain lesion was carried out using a supracerebellar-infratentorial approach. Pathological evaluation confirmed the diagnosis of cavernous malformation. Sections from this follow-up MR imaging again reveal multiple cavernous malformations including three Type I lesions (straight arrows) and three Type III lesions (curved arrows). In addition, the cystic postoperative remnant of the resected brain-stem lesion is readily apparent (arrowhead). Note that the areas of subacute hemorrhage that characterized Type I lesions are hyperintense on T1-weighted images, but may be hyper- or hypointense on T2-weighted images depending on the age of the hemorrhage (see the Clinical Material and Methods section). Type III lesions (chronic hemorrhage) are iso- or hypointense on T1-weighted images, but are always hypointense on T2-weighted spin-echo sequences because of the presence of hemosiderin and ferritin. In contrast, note that the MR imaging signal of the cystic postoperative defect in the midbrain follows cerebrospinal fluid signal intensity: the small halo of hypointensity that surrounds the cyst on the T2-weighted images betrays its hemorrhagic past. This pattern of cystic change may be seen in areas of chronic resolved hemorrhage of other etiologies; however, it is not characteristic of lesions in patients with intact cavernous malformations.

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    Magnetic resonance (MR) T1-weighted (A and B) and T2-weighted (C and D) follow-up images in a 10-year-old Caucasian boy (Case A16 in Fig. 4). This child was asymptomatic when initially screened in June, 1989, at 8 years of age. An MR image at that time demonstrated four foci consistent with cavemous malformation, including the two lesions demonstrated here in November, 1991. The small hypointense Type III lesion (straight arrow, A and C) in the medial right temporal lobe and the much larger variegated Type II lesion (curved arrow, B and D) in the left temporal-occipital region have remained essentially unchanged. Failure of the left temporo-occipital lesion to resolve to a more chronic form suggests continued (re)hemorrhage and/or thrombosis within the cavernous malformation. Complex partial seizures developed at 9 years of age and have been clearly localized to this left-sided lesion.

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    Gradient-echo magnetic resonance images in a 51-year-old Hispanic man (Case C5, Fig. 4) revealing multiple hypointense lesions “too numerous to count” consistent with cavernous malformations. The Type IV lesions are the small punctate areas of low signal intensity, several of which have been arbitrarily indicated by arrows. Two Type IV lesions at the authors' institution have been confirmed pathologically to be capillary telangiectasias,39 suggesting that these lesions form a continuum in the development of the more typical cavernous malformation.

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    Pedigrees of six families with familial cavernous malformations. In the six pedigrees shown, circles denote females and squares denote males. Open symbols denote normal subjects, and solid symbols denote patients with at least one cavernous malformation on magnetic resonance (MR) imaging. Symbols with diagonal lines represent deceased patients. Arrows designate the propositus in each family. A horizontal bar over a symbol indicates that pathological confirmation of the disorder was obtained. Symbols with solid centers indicate that the patient described a history of seizures, severe headaches, hemiparesis or hemisensory deficits, or visual difficulties; symbols with horizontal bars indicate that the patient exhibited an abnormal neurological examination. The 21 patients with MR imaging and clinical follow-up monitoring described in detail in the text are designated by a letter-number combination, such as A3.

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    Follow-up magnetic resonance T1- (left) and T2-(right) weighted images in a 31-year-old Caucasian woman (Case A3 in Fig. 4). The patient first experienced generalized tonic-clonic seizures at 10 years old; her family history was remarkable for seizures in two of her five siblings. Serial MR images demonstrated a large cavernous malformation in the left insular cortex with the now almost classic MR appearance of a mixed signal intensity core surrounded by a ring of hypointensity (Type II lesion). Her seizures were relatively well controlled until the spring of 1991, when there was an acute exacerbation. Repeat MR imaging, shown here, demonstrated findings consistent with an area of subacute hemorrhage within the insular mass, with a region of hyperintense signal (arrows) on both the T1- and T2-weighted images. Violent almost daily seizures persisted despite maximum medical therapy, and the patient underwent craniotomy with complete resection of a multiloculated cavernous malformation. Post-operative mild right hemiparesis and expressive aphasia have resolved completely, and her seizures are presently well controlled on a single medication.

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