Twenty-Year Follow-up of Chronic Encapsulated Intracerebral Hematoma

Twenty-Year Follow-up of Chronic Encapsulated Intracerebral Hematoma

Case Report Twenty-Year Follow-up of Chronic Encapsulated Intracerebral Hematoma Maya Kono, MD,* Satoshi Takahashi, MD, PhD,* Dai Kamamoto, MD,* Kats...

520KB Sizes 0 Downloads 34 Views

Case Report

Twenty-Year Follow-up of Chronic Encapsulated Intracerebral Hematoma Maya Kono, MD,* Satoshi Takahashi, MD, PhD,* Dai Kamamoto, MD,* Katsura Emoto, MD, PhD,† and Kazunari Yoshida, MD, PhD*

This is the first case report of a patient with chronic encapsulated intracerebral hematoma who developed excessive perifocal edema and symptoms 20 years after his initial diagnosis. Key Words: Chronic encapsulated intracerebral hematoma— collagenous membrane—hematoma—intracerebral hemorrhage—cerebral cavernous malformation. Ó 2015 by National Stroke Association

Chronic encapsulated intracerebral hematoma (CEIH) is usually revealed by gradually progressive neurologic sequealae and is immediately surgically addressed.1 For this reason, the long-term natural course of CEIH has not been fully described.

3 years (Fig 1, C). The lesion was totally removed through a right parietal craniotomy (Fig 1, F). Pathologically, the lesion was an old hematoma enclosed by a collagenous fibrous membrane and was, thus, diagnosed as CEIH (Fig 1, G). The patient’s sensory disturbance and perifocal edema rapidly improved after surgery (Fig 1, E).

Clinical Presentation A 73-year-old man complained of sensory disturbance in his left lower extremity. Magnetic resonance imaging revealed an enhanced mass lesion in his right parietal lobe with evidence of a relatively recent hemorrhage and excessive perifocal edema (Fig 1, D). The lesion was incidentally identified 20 years earlier before surgical resection of a vestibular schwannoma and was conservatively observed under a diagnosis of cerebral cavernous malformation (Fig 1, A,B). It had become symptomatic along with perifocal edema progression in the previous

From the *Department of Neurosurgery, Keio University School of Medicine; and †Division of Diagnostic Pathology, Keio University Hospital, Tokyo, Japan. Received January 14, 2015; revision received April 11, 2015; accepted April 15, 2015. Address correspondence to Maya Kono, MD, Department of Neurosurgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail: [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2015.04.043

Discussion CEIH was originally reported as slowly progressive intracerebral hematoma without obvious vessel anomalies.2 It is pathologically characterized as a hematoma enclosed by a fibrous membrane comprising a collagenous outer layer and granulated inner layer. The etiology and natural course of CEIH remain to be elucidated as it is usually surgically removed to ameliorate neurologic symptoms; most of the reported cases were only followed for weeks or months before surgical resection. The lesion described here was incidentally identified during presurgical assessments for a right vestibular schwannoma, and the patient was followed for about 20 years. Interestingly, he had complained of sensory disturbance only 3 years before CEIH resection. Magnetic resonance imaging taken 2 years later revealed spreading perifocal edema. Notably, the edema resolved after surgical removal of the CEIH. Because the lesion was relatively small, we speculate that the underlying reason for the edema was chemical effect rather than a mechanical one.

Journal of Stroke and Cerebrovascular Diseases, Vol. 24, No. 9 (September), 2015: pp e255-e256

e255

M. KONO ET AL.

e256

The etiology of CEIH remains to be elucidated. One hypothesis is that they are caused by intracerebral vascular malformations.2 We cannot exclude the possibility that any of the pathologic features of a previous intracerebral vascular malformation were destroyed by the repeated hemorrhaging before surgery.3 Indeed, our intraoperative examination showed several pial feeding arteries surrounding the CEIH that resembled cerebral cavernous malformation. This is the first long-term report of a patient with CEIH who was followed up for 2 decades. The findings shed light on the natural course of CEIH.

References 1. Nishiyama A, Toi H, Takai H, et al. Chronic encapsulated intracerebral hematoma: three case reports and a literature review. Surg Neurol Int 2014;5:88. 2. Hirsh LF, Spector HB, Bogdanoff BM. Chronic encapsulated intracerebral hematoma. Neurosurgery 1981; 9:169-172. 3. Greiner-Perth R, Neubauer U, Schenke H. Chronic encapsulated intracerebral hematoma—a well-defined disease. Report on two cases and review of the literature. Neurosurg Rev 1997;20:231-238.

Figure 1. (A) A fluid-attenuated inversion recovery magnetic resonance (FLAIR-MR) image taken 15 years ago showed low-intensity mass in a right parietal lobe. It was considered as cerebral cavernous malformation. (MR image taken 20 years is not available; however, the lesion had not changed from 20 to 15 years ago according to the medical record.) (B) A T1-weighted MR imaging with gadolinium contrast agent taken 15 years ago showed homogenous contrast-enhanced mass lesion. (C) FLAIR MR image obtained 3 years before chronic encapsulated intracerebral hematoma resection revealing a right parietal mass lesion comprising new and old hematoma and a small perifocal edema. (D) Preoperative FLAIR-MR image showing a right parietal mass lesion with a relatively new hemorrhage and perifocal edema. (E) Postoperative FLAIR-MR image showed removal of the lesion and improved perifocal edema. (F) Intraoperative findings. The lesion was covered with a yellowish membrane. (G) Low magnification of a hematoxylin- and eosinstained section. The old hematoma (*) was surrounded by a fibrous membrane comprising an outer layer (arrow head) and inner layer (arrow).